presentation of unstable angina

Unstable Angina

(acute coronary insufficiency; preinfarction angina; intermediate syndrome).

• Symptoms and Signs |
• Diagnosis |
• Treatment |
• Prognosis |
• Key Points |

Unstable angina results from acute obstruction of a coronary artery without myocardial infarction. Symptoms include chest discomfort with or without dyspnea, nausea, and diaphoresis. Diagnosis is by electrocardiography (ECG) and the presence or absence of biomarkers. Treatment is with antiplatelets, anticoagulants, nitrates, statins, and beta-blockers. Coronary angiography with percutaneous intervention or coronary artery bypass surgery is often necessary.

(See also Overview of Acute Coronary Syndromes .)

Unstable angina is a type of acute coronary syndrome that is defined as one or more of the following in patients whose cardiac biomarker levels do not meet criteria for acute myocardial infarction (MI):

Rest angina that is prolonged (usually > 20 minutes)

New-onset angina of at least class 3 severity in the Canadian Cardiovascular Society (CCS) classification (see table Canadian Cardiovascular Society Classification System for Angina Pectoris )

Increasing angina, ie, previously diagnosed angina that has become distinctly more frequent, more severe, longer in duration, or lower in threshold (eg, increased by ≥ 1 CCS class or to at least CCS class 3)

Unstable angina is clinically unstable and often a prelude to myocardial infarction or arrhythmias or, less commonly, to sudden death.

Symptoms and Signs of Unstable Angina

Patients have symptoms of angina pectoris (typically chest pain or discomfort) except that the pain or discomfort of unstable angina usually is more intense, lasts longer, is precipitated by less exertion, occurs spontaneously at rest, is progressive (crescendo) in nature, or involves any combination of these features.

Unstable angina is classified based on severity and clinical situation (see table Canadian Cardiovascular Classification System for Angina Pectoris ). Also considered are whether unstable angina occurs during treatment for chronic stable angina and whether transient changes in ST-T waves occur during angina. If angina has occurred within 48 hours and no contributory extracardiac condition is present, troponin levels may be measured to help estimate prognosis; troponin-negative results indicate a better prognosis than troponin-positive.

Diagnosis of Unstable Angina

Serial ECGs

Serial cardiac biomarkers

Immediate coronary angiography for patients with complications (eg, persistent chest pain, hypotension, unstable arrhythmias)

Delayed angiography (24 to 48 hours) for stable patients

(See figure Approach to Unstable Angina .)

Evaluation begins with initial and serial ECG and serial measurements of cardiac biomarkers to help distinguish between unstable angina and acute myocardial infarction (MI)—either non–ST-segment elevation MI (NSTEMI) or ST-segment elevation MI (STEMI). This distinction is the center of the decision pathway because fibrinolytics benefit patients with STEMI but not those with NSTEMI and unstable angina. Also, urgent cardiac catheterization is indicated for patients with acute STEMI but not generally for those with NSTEMI or unstable angina.

ECG is the most important test and should be done as soon as possible (eg, within 10 minutes of presentation) ECG changes such as ST-segment depression, ST-segment elevation, or T-wave inversion may occur during unstable angina but are transient.

Cardiac biomarkers

Patients suspected of having unstable angina should have a highly sensitive assay of cardiac troponin (hs-cTn) done on presentation and 2 to 3 hours later. If a standard Tn assay is used, measurements are done at presentation and 6 hours later.

Creatine kinase MB fraction (CK-MB) is not elevated in unstable angina. Cardiac troponin, particularly when measured using high-sensitivity troponin tests, may be slightly increased but does not meet the criteria for myocardial infarction (above the 99th percentile of the upper reference limit or URL).

Coronary angiography

Patients with unstable angina whose symptoms have resolved typically undergo angiography within the first 24 to 48 hours of hospitalization to detect lesions that may require treatment. Coronary angiography most often combines diagnosis with percutaneous coronary intervention (PCI—ie, angioplasty, stent placement).

After initial evaluation and therapy, coronary angiography may be used in patients with evidence of ongoing ischemia (ECG findings or symptoms), hemodynamic instability, recurrent ventricular tachyarrhythmias , and other abnormalities that suggest recurrence of ischemic events.

Treatment of Unstable Angina

Pharmacologic therapy: Antiplatelet agents, antianginal drugs, anticoagulants, and in some cases other medications

Angiography to assess coronary artery anatomy

Reperfusion therapy: Percutaneous coronary intervention or coronary artery bypass surgery

Post-discharge rehabilitation and chronic medical management of coronary artery disease

Prehospital care

Triage to appropriate medical center

1 ). Early diagnostic data and response to treatment can help determine the need for and timing of revascularization .

Hospital admission

Risk-stratify patient and choose timing of reperfusion strategy

Pharmacologic therapy with antiplatelets, anticoagulants, and other medications based on reperfusion strategy

On arrival to the emergency department, the patient's diagnosis is confirmed. Pharmacologic therapy and timing of revascularization depend on the clinical picture. In clinically unstable patients (patients with ongoing symptoms, hypotension or sustained arrhythmias), urgent angiography with revascularization is indicated. In clinically stable patients, angiography with revascularization may be deferred for 24 to 48 hours (see figure Approach to Unstable Angina ).

Approach to Unstable Angina

Pharmacologic treatment of unstable angina

All patients should be given antiplatelet agents , anticoagulants , and if chest pain is present, antianginals. The specific medications used depend on the reperfusion strategy and other factors; their selection and use is discussed in Medications for Acute Coronary Syndrome . Other medications, such as beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and statins, should be initiated during admission (see table Medications for Coronary Artery Disease ).

Patients with unstable angina should be given the following (unless contraindicated)

Antiplatelet agents

Anticoagulants : A heparin (unfractionated or low molecular weight heparin

Sometimes a glycoprotein IIb/IIIa inhibitor when PCI is done

Beta-blocker

Angiotensin-converting enzyme (ACE) inhibitor

Aspirin reduces short- and long-term mortality risk ( 2 prasugrel and ticagrelor are more rapid in onset and may be preferred.

Either a low molecular weight heparin (LMWH), unfractionated heparin heparin -induced thrombocytopenia.

Nitroglycerin is preferable to morphine , which should be used judiciously (eg, if a patient has a contraindication to nitroglycerin or is in pain despite maximal nitroglycerin therapy). is initially given sublingually, followed by continuous IV drip if needed. Morphine , given 2 to 4 mg IV, repeated every 15 minutes as needed, is highly effective but can depress respiration, can reduce myocardial contractility, and is a potent venous vasodilator. Evidence also suggests that morphine interferes with some P2Y12 receptor inhibitor activity. A large retrospective trial also showed that morphine may increase mortality in patients with acute myocardial infarction ( 4, 5 ). Hypotension and bradycardia may also occur secondary to morphine use, but these complications can usually be overcome by prompt elevation of the lower extremities.

Standard therapy for all patients with unstable angina includes beta-blockers, ACE inhibitors, and statins. Beta-blockers are recommended unless contraindicated (eg, by bradycardia, heart block, hypotension, or asthma), especially for high-risk patients. Beta-blockers reduce heart rate, arterial pressure, and contractility, thereby reducing cardiac workload and oxygen demand. ACE inhibitors may provide long-term cardioprotection by improving endothelial function. If an ACE inhibitor is not tolerated because of cough or rash (but not angioedema or renal dysfunction), an may be substituted. Statins are also standard therapy regardless of lipid levels and should be continued indefinitely.

Reperfusion therapy in unstable angina

Fibrinolytic drugs , which can be helpful in patients with STEMI, do not benefit patients with unstable angina.

Angiography is typically done during admission—within 24 to 48 hours of admission if the patient is stable or immediately in unstable patients (eg, with ongoing symptoms, hypotension, sustained arrhythmias). Angiographic findings help determine whether PCI or coronary artery bypass grafting (CABG) is indicated. Choice of reperfusion strategy is further discussed in Revascularization for Acute Coronary Syndromes .

Pearls & Pitfalls

Rehabilitation and post-discharge treatment

Functional evaluation

Changes in lifestyle: Regular exercise, diet modification, weight loss, smoking cessation

Medications: Continuation of antiplatelets, beta-blockers, ACE inhibitors, and statins

Patients who did not have coronary angiography during admission, have no high-risk features (eg, heart failure, recurrent angina, ventricular tachycardia or ventricular fibrillation after 24 hours, mechanical complications such as new murmurs, shock), and have an ejection fraction > 40% usually should have stress testing of some sort before or shortly after discharge.

The acute illness and treatment of unstable angina should be used to strongly motivate the patient to modify risk factors. Evaluating the patient’s physical and emotional status and discussing them with the patient, advising about lifestyle (eg, smoking, diet, work and play habits, exercise), and aggressively managing risk factors may improve prognosis.

On discharge, all patients should be continued on appropriate antiplatelets, statins, antianginals, and other medications based on comorbidities.

Treatment references

1. Nakayama N, Yamamoto T, Kikuchi M, et al : Prehospital Administration of Aspirin and Nitroglycerin for Patients With Suspected Acute Coronary Syndrome—A Systematic Review.  Circ Rep 4(10):449–457, 2022. doi:10.1253/circrep.CR-22-0060

2. Antithrombotic Trialists' Collaboration : Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients [published correction appears in BMJ 2002 Jan 19;324(7330):141].  BMJ 324(7329):71–86, 2002. doi:10.1136/bmj.324.7329.71

3. Amsterdam EA, Wenger NK, Brindis RG, et al : 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes. J Am Coll Cardiol 64 (24):e139–e228, 2014. doi: 10.1016/j.jacc.2014.09.017

4. Kubica J, Adamski P, Ostrowska M, et al : Morphine delays and attenuates ticagrelor exposure and action in patients with myocardial infarction: the randomized, double-blind, placebo-controlled IMPRESSION trial. Eur Heart J 37(3):245–252, 2016. doi: 10.1093/eurheartj/ehv547

5. Meine TJ, Roe MT, Chen AY, et al : Association of intravenous morphine use and outcomes in acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative. Am Heart J 149(6):1043-1049, 2005. doi 10.1016/j.ahj.2005.02.010

Prognosis for Unstable Angina

Prognosis after an episode of unstable angina depends upon how many coronary arteries are diseased, which arteries are affected, and how severely they are affected. For example, stenosis of the proximal left main artery or equivalent (proximal left arterial descending and circumflex artery stenosis) has a worse prognosis than does distal stenosis or stenosis in a smaller arterial branch. Left ventricular function also greatly influences prognosis; the presence of significant left ventricular dysfunction (even with 1- or 2-vessel disease) warrants a lower threshold for revascularization.

Overall, a substantial proportion of patients with unstable angina have a myocardial infarction within 3 months of onset; sudden death is less common (see table Risk of Adverse Events at 14 Days in Unstable Angina or NSTEMI ). Marked ECG changes with chest pain indicate higher risk of subsequent MI or death.

Unstable angina is new, worsening, or rest angina in patients whose cardiac biomarkers do not meet criteria for myocardial infarction.

Symptoms of unstable angina include new or worsening chest pain or chest pain occurring at rest.

Diagnosis is based on serial ECGs and cardiac biomarkers.

Immediate treatment includes oxygen, antianginals, antiplatelets, and anticoagulants.

For patients with ongoing symptoms, hypotension, or sustained arrhythmias, do immediate angiography.

For stable patients, do angiography within 24 to 48 hours of hospitalization.

Following recovery, initiate or continue antiplatelet agents, beta-blockers, angiotensin-converting enzyme inhibitors, and statins.

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• Diseases & Conditions

Angina (an-JIE-nuh or AN-juh-nuh) is a type of chest pain caused by reduced blood flow to the heart. Angina is a symptom of coronary artery disease.

Angina also is called angina pectoris.

Angina is often described as squeezing, pressure, heaviness, tightness or pain in the chest. It may feel like a heavy weight lying on the chest. Angina may be a new pain that needs to be checked by a healthcare professional, or it may be recurring pain that goes away with treatment.

Angina is relatively common. But some people may not be able to tell it apart from other types of chest pain, such as heartburn. If you have unexplained chest pain, get medical help right away.

There are different types of angina. The type depends on the cause and whether rest or medicine eases symptoms.

Stable angina. Stable angina is the most common form of angina. It usually happens during activity, also called exertion. It goes away with rest or angina medicine. Pain that starts when you're walking uphill or in the cold weather may be angina.

Stable angina is predictable. It is usually similar to previous episodes of chest pain. The chest pain typically lasts a short time, perhaps five minutes or less.

• Unstable angina, which is a medical emergency. Unstable angina is unpredictable and occurs at rest. Or the pain is worsening and occurs with less physical effort. Unstable angina is typically severe and lasts longer than stable angina, maybe 20 minutes or longer. The pain doesn't go away with rest or the usual angina medicines. If the blood flow doesn't improve, the heart doesn't get enough oxygen. A heart attack occurs. Unstable angina is dangerous and needs emergency treatment.
• Variant angina, also called Prinzmetal angina. This type of angina isn't due to coronary artery disease. It's caused by a spasm in the heart's arteries. The spasm temporarily reduces blood flow. Severe chest pain is the main symptom of variant angina. It most often occurs in cycles, typically at rest and overnight. The pain may be relieved by angina medicine.
• Refractory angina. Angina episodes are frequent despite a combination of medicines and lifestyle changes.

• Heart attack

A heart attack occurs when an artery supplying the heart with blood and oxygen becomes blocked. Fatty deposits build up over time, forming plaques in the heart's arteries. If a plaque ruptures, a blood clot can form and block the arteries, causing a heart attack. During a heart attack, tissue in the heart muscle dies due to lack of blood flow through the heart's arteries.

Angina symptoms include chest pain and discomfort. The chest pain or discomfort may feel like:

Pain also may be felt in the arms, neck, jaw, shoulder or back.

Other symptoms of angina include:

• Shortness of breath.

The severity, duration and type of angina can vary. New or different symptoms may signal unstable angina or a heart attack.

Any new or worsening angina symptoms need to be checked immediately by a healthcare professional. The healthcare team can determine whether you have stable or unstable angina.

Angina in women

Symptoms of angina in women can be different from the classic angina symptoms. These differences may lead to delays in seeking treatment. For example, chest pain may not be the only symptom or the most common symptom. Other symptoms of angina in women may include:

• Discomfort in the neck, jaw, teeth or back.
• Stabbing pain instead of chest pressure.
• Stomach pain.

When to see a doctor

Chest pain that lasts longer than a few minutes and doesn't go away with rest or angina medicines may be due to a heart attack. Call 911 or emergency medical help. Only drive yourself to the hospital if there is no other way to get there.

If chest discomfort is a new symptom for you, see a healthcare professional to determine the cause and to get proper treatment. If you have stable angina and it gets worse or changes, seek medical help immediately.

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Angina is caused by reduced blood flow to the heart muscle. Blood carries oxygen, which the heart muscle needs to survive. When the heart muscle isn't getting enough oxygen, it causes a condition called ischemia.

The most common cause of reduced blood flow to the heart muscle is coronary artery disease (CAD). The heart arteries, called the coronary arteries, can become narrowed by fatty deposits called plaques. This condition is called atherosclerosis.

Plaque in a blood vessel may rupture or cause a blood clot. These events can quickly block or reduce flow through a narrowed artery. This can suddenly and severely decrease blood flow to the heart muscle.

The heart muscle may still be able to work during times of low oxygen demand without triggering angina symptoms. An example is when resting. But when the demand for oxygen goes up, such as when exercising, angina can result.

More Information

• Coronary artery spasm: Cause for concern?

Risk factors

The following things may increase the risk of angina:

• Increasing age. Angina is most common in adults age 60 and older.
• Family history of heart disease. Tell your healthcare team if your mother, father or any siblings have or had heart disease or a heart attack.
• Tobacco use. Smoking, chewing tobacco and long-term exposure to secondhand smoke can damage the lining of the arteries. Artery damage can let deposits of cholesterol collect and block blood flow.
• Diabetes. Diabetes increases the risk of coronary artery disease. Coronary artery disease can cause angina.
• High blood pressure. Over time, high blood pressure damages arteries by speeding up the hardening of the arteries.
• High cholesterol or triglycerides. Too much bad cholesterol, called low-density lipoprotein (LDL), in the blood can cause arteries to narrow. A high LDL level increases the risk of angina and heart attack. A high level of triglycerides in the blood also is unhealthy.
• Other health conditions. Chronic kidney disease, peripheral artery disease, metabolic syndrome or a history of stroke increases the risk of angina.
• Not enough exercise. An inactive lifestyle raises the risk of high cholesterol, high blood pressure, type 2 diabetes and obesity. Talk with your healthcare team about the type and amount of exercise that's best for you.
• Obesity. Obesity is a risk factor for heart disease, which can cause angina. Being overweight makes the heart work harder to supply blood to the body.
• Emotional stress. Too much stress and anger can raise blood pressure. Rushes of hormones made by the body during stress can narrow the arteries and worsen angina.
• Medicines. Some medicines tighten blood vessels, which may trigger Prinzmetal angina. An example is certain migraine medicines.
• Drug misuse. Cocaine and other stimulants can cause blood vessel spasms and trigger angina.
• Cold temperatures. Exposure to cold temperatures can trigger Prinzmetal angina.

Complications

The chest pain that occurs with angina can make doing some activities, such as walking, uncomfortable. However, the most dangerous complication is a heart attack.

Warning symptoms of a heart attack include:

• Pressure, fullness or a squeezing pain in the center of the chest that lasts for more than a few minutes.
• Pain extending beyond the chest to the shoulder, arm or back, or even to the teeth and jaw.
• Threatening sense of doom.
• Increasing episodes of chest pain.
• Nausea and vomiting.
• Continued pain in the upper belly area.

If you have any of these symptoms, seek emergency medical attention immediately.

You can help prevent angina by following the same lifestyle changes that are used to treat angina:

• Avoid or limit alcohol.
• Don't smoke.
• Eat a healthy diet.
• Exercise regularly.
• Maintain a healthy weight.
• Manage other health conditions related to heart disease.
• Reduce stress.
• Get 7 to 9 hours of sleep a day.

Also get recommended vaccines to avoid heart complications.

Living with angina?

Connect with others like you for support and answers to your questions in the Heart & Blood Health support group on Mayo Clinic Connect, a patient community.

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• Bonow RO, et al., eds. Stable ischemic heart disease. In: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 12th ed. Elsevier; 2022. https://www.clinicalkey.com. Accessed Dec. 21, 2021.
• Goldman L, et al., eds. Angina pectoris and stable ischemic heart disease. In: Goldman-Cecil Medicine. 26th ed. Elsevier; 2020. https://www.clinicalkey.com. Accessed Dec. 23, 2021.
• Angina. National Heart, Lung, and Blood Institute. https://www.nhlbi.nih.gov/health-topics/angina. Accessed Dec. 21, 2021.
• Angina in women can be different than men. American Heart Association. https://www.heart.org/en/health-topics/heart-attack/angina-chest-pain/angina-in-women-can-be-different-than-men. Accessed Dec. 21, 2021.
• Warning signs of a heart attack. American Heart Association. https://www.heart.org/en/health-topics/heart-attack/warning-signs-of-a-heart-attack/heart-attack-symptoms-in-women. Accessed Dec. 21, 2021.
• AskMayoExpert. Stable ischemic heart disease. Mayo Clinic; 2020.
• Simons M, et al. New therapies for angina. https://www.uptodate.com/contents/search. Accessed Dec. 21, 2021.
• Mankad R (expert opinion). Mayo Clinic. Feb. 24, 2020.
• Ferri FF. Angina pectoris. In: Ferri's Clinical Advisor 2022. Elsevier; 2022. https://www.clinicalkey.com. Accessed Dec. 23, 2021.
• Lopez-Jimenez F (expert opinion). Mayo Clinic. Jan. 21, 2022.

Associated Procedures

• Chest X-rays
• Coronary angiogram
• Coronary artery bypass surgery
• Echocardiogram
• Electrocardiogram (ECG or EKG)
• Nuclear stress test
• Stress test

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Unstable Angina Treatment & Management

• Author: Walter Tan, MD, MS; Chief Editor: Eric H Yang, MD  more...
• Sections Unstable Angina
• Practice Essentials
• Pathophysiology
• Epidemiology
• Patient Education
• Physical Examination
• Braunwald Classification
• Canadian Cardiovascular Society Grading System
• Acute Coronary Syndrome Risk Assessment
• Risk Stratification: TIMI and GRACE Risk Scores
• Approach Considerations
• Basic Blood Studies
• Cardiac Biomarkers
• Electrocardiography
• Echocardiography
• SPECT and MRI
• Myocardial Perfusion Imaging
• Exercise Testing
• Initial Medical Management
• Role of Medical Therapy With Anticoagulation
• Further Medical Management
• Cardiac Catheterization
• Revascularization
• Consultations
• 2023 ESC Guidelines for the Management of ACS
• 2020 ESC Acute Coronary Syndromes Clinical Practice Guidelines
• 2014 AHA/ACC and 2015 ESC Guidelines for the Management NSTE-ACS
• Medication Summary
• Antiplatelet agents
• Lipid-Lowering Agents, Statins
• PCSK9 Inhibitors
• Antiplatelet Agent, Cardiovascular
• Beta-Blockers, Beta-1 Selective
• Beta-Blockers, Beta-1 Selective; Antidysrhythmics, II
• Beta-Blockers, Nonselective
• Beta-Blockers, Nonselective; Antidysrhythmics, II
• Anticoagulant
• Low Molecular Weight Heparins
• ACE Inhibitors
• Thrombin inhibitors
• Nitrates, Angina
• Questions & Answers
• Media Gallery

Management is directed toward (1) reducing myocardial oxygen demands; (2) improving myocardial oxygen supply; and (3) assessing the patient's risk of progression to myocardial infarction or having a complication related to treatment.

Patients who present with new-onset chest pain or other symptoms suggestive of myocardial ischemia need immediate evaluation including electrocardiography (ECG) and levels of biomarkers (preferably high sensitivity [hs] troponin). The need for an urgent (< 2-4 hrs) or early (< 24 hrs) invasive strategy can be determined by the presence of very high-risk or high-risk criteria.

An initial (intensive) medical strategy is recommended for patients with no ongoing symptoms and no very-high risk or high-risk criteria. Noninvasive ischemia testing or anatomic testing (coronary computed tomography angiography [CTA]) should be obtained to determine if an invasive study is indicated.

Patients with unstable angina require admission to the hospital for bed rest with continuous telemetry monitoring. Obtain intravenous (IV) access, and provide supplemental oxygen if evidence of desaturation is noted. Because the course of unstable angina is highly variable and potentially life-threatening, the aggressiveness of the therapeutic approach must be established expeditiously.

Decision on initial treatment strategy: Ischemic guided vs invasive (immediate, early, or delayed)

An invasive strategy refers to the routine use of cardiac catheterization with possible revascularization, and a ischemia-guided strategy refers to initial medical management with the possible use of cardiac catheterization if indicated by failure of medical therapy or objective evidence of ischemia (dynamic ECG changes or abnormal noninvasive stress test results). Determination of the preferred strategy depends on the patient’s clinical characteristics and clinical risk. In the After Eighty trial, in which investigators evaluated the health-related quality of life (HRQOL) in patients with acute coronary syndrome (ACS) (non-ST-elevation myocardial infarction [NSTEMI], unstable angina [UA]) aged 80 years or older who were randomized to either invasive (n = 208) or conservative (n = 216) management, there were only minor differences in HRQOL from baseline to 1-year follow-up between these interventions, as measured by the Short Form 36 health survey (SF-36). [ 46 ]

Specific therapy for primary causes of ischemia should be directed at each pathophysiologic origin of unstable angina: increased myocardial rate-pressure product, coronary vasoconstriction, platelet aggregation, and thrombosis.

The level of care and expertise of the different units vary from hospital to hospital. For example, the intermediate care unit in certain tertiary cardiac centers may be equipped and appropriately staffed for treatment of asymptomatic patients, but high-risk patients with unstable angina would be more appropriately cared for in an intensive care unit (ICU) in a community hospital setting.

Invasive strategy

In patients considered to have UA based on symptoms, ECGs, and levels of biomarkers (preferably hs troponin), an invasive strategy may be indicated. Risk stratification can guide this decision and is recommended by contemporary guidelines.

The European Society of Cardiology (ESC) risk categories include the following [ 47 ] :

• Very high risk:  Presence of hemodynamic instability, cardiogenic shock, recurrent/refractory chest pain despite medical therapy, life-threatening arrhythmias, mechanical complications of MI, acute heart failure clearly related to non-ST elevation acute coronary syndrome (NSTE-ACS), ST depression larger than 1 mm/6 leads plus ST elevation in leads aVR and/or V1
• High risk: Established diagnosis of NSTEMI; dynamic new, or presumably new continuous ST/T changes (symptomatic or silent); resuscitated cardiac arrest without ST elevation or cardiogenic shock; Global Registry of Acute Coronary Events (GRACE) risk score above 140
• Low risk: Absence of any of the very high or high-risk parameters

An urgent invasive strategy (< 2-4 hrs) is recommended for very high-risk patients (ie, with at least one very high-risk criterion) irrespective of ECG and biomarker findings.

An early invasive strategy (< 24 hrs) is recommended for high-risk  patients  (ie, with at least one high-risk parameter). A GRACE score over 140 is one such parameter that favors an early invasive strategy. [ 48 ]

Consider a selective invasive strategy for patients with no recurrent symptoms and no very high-risk or high-risk criteria. Further testing may include ischemia evaluation (stress echocardiography, cardiac magnetic resonance imaging [CMR]), or nuclear perfusion studies) or coronary CTA.

Indications for intensive care

ICU or emergency revascularization disposition is indicated by the following:

TIMI (Thrombolysis In Myocardial Infarction) risk score of 3-7

New ECG changes in two or more leads

ST elevation greater than 1 mm or Q waves 0.04 seconds or longer

ST depression greater than 1 mm or T-wave inversion in the context of angina

New left bundle branch block

Signs and symptoms of incipient or florid heart failure

Syncope or sudden death presentation

Serious new arrhythmias, including second-degree or complete heart block and ventricular tachyarrhythmias

Refractory angina

Positive cardiac enzymes (creatine kinase [CK] or troponin)

Myocardial infarction or coronary stenting within the last 2 weeks

Indications for immediate care

Patients are admitted to intermediate care units when they are asymptomatic but have any of the following conditions:

Atrial arrhythmia, supraventricular tachycardia, or low-grade second-degree atrioventricular block

Isolated basilar rales

Borderline blood pressure

Symptoms with minimal activity

Presence of major comorbidity (eg, severe pulmonary, renal, or hepatic disease; bleeding history; or dyscrasia)

Very advanced age or frailty

Indications for observation

Patients who are otherwise healthy without ischemic ECG changes but who have either of the following should be admitted to observation units:

New-onset symptoms at moderate levels of exertion

Known coronary artery disease (CAD) with a presentation that does not suggest true worsening but for which further observation is thought to be prudent

Medical management of adverse events

Medications that provide symptomatic relief but that have not been shown to affect long-term major events include nitrates (eg, nitroglycerin IV), calcium channel blockers (eg, diltiazem, verapamil), and heparin. Medications that have been convincingly shown to be capable of reducing short- or long-term adverse events are as follows:

Clopidogrel

Beta-adrenergic blocking agents

Lipid-lowering agents (statins)

Angiotensin-converting enzyme (ACE) inhibitors

Glycoprotein (GP) IIb/IIIa antagonists

Unstable angina may require patients to take nothing orally if stress testing or an invasive procedure is anticipated. Otherwise, a diet low in cholesterol and saturated fat is recommended. Sodium restriction should be instituted for patients with heart failure or hypertension.

Medications used in the initial management of unstable angina include the following:

Antiplatelets (aspirin; P2Y12 inhibitors: thienopyridines [clopidogrel, prasugrel]; nonthienopyridines [ticagrelor]; glycoprotein (GP) IIb/IIIa antagonists)

Heparin (discussed in the next section, under Role of Medical Therapy With Anticoagulation )

Direct thrombin inhibitors (discussed in the next section under Role of Medical Therapy With Anticoagulation )

Antiplatelets

Administer chewable aspirin 162-325 mg promptly to patients who are not at high risk for bleeding, who do not have ongoing bleeding, or who do not have true intolerance or allergy. Timeliness of administration is essential, because platelet aggregation is central to acute coronary syndrome (ACS); the peak effect can be observed within as short a time as 30 minutes. Patients with unstable angina/non–ST-segment elevation myocardial infarction (UA/NSTEMI) should continue indefinitely on aspirin, if tolerated. [ 49 ]

Pooled data from more than 2000 patients revealed a reduction in the rate of death or myocardial infarction (MI) from 11.8% to 6% with aspirin in cases of unstable angina. Several studies have shown approximately 40-50% risk reductions for death or MI with aspirin at 30-day follow-up and at up to 1-year follow-up in this patient population.

In the event of percutaneous coronary intervention (PCI), oral aspirin 162-325 mg should be given for at least 1 month after bare metal stent implantation, 3 months after sirolimus-eluting stent implantation, or 6 months after paclitaxel-eluting stent implantation. Thereafter, oral aspirin 75-162 mg should be continued indefinitely.

Thienopyridines

Clopidogrel is recommended as the antiplatelet of choice in patients who are intolerant to aspirin. It is also used as an adjunctive antiplatelet agent in conjunction with aspirin (dual antiplatelet therapy). [ 49 , 50 ]

The Food and Drug Administration approved clopidogrel for the medical management of unstable angina/NSTEMI, STEMI in those receiving fibrinolytic therapy, and for secondary prevention in recent MI, recent stroke, and peripheral artery disease. [ 51 ]

The CURE (Clopidogrel in Unstable angina to prevent Recurrent Events) trial showed that the addition of clopidogrel to aspirin therapy reduced the incidence of cardiovascular death, MI, or stroke from 11.4% to 9.3% at 1 year, with early benefit shown at 24 hours. [ 52 ]  However, the beneficial results of clopidogrel-aspirin treatment came at the cost of a higher rate of major bleeding (3.7%) than that observed in patients on aspirin therapy plus placebo (2.7%).

The PCI-CURE [ 52 ]  and the CREDO (Clopidogrel for the Reduction of Events During Observation) [ 53 ]  trials showed significant benefit from the administration of clopidogrel to patients with unstable angina who undergo coronary intervention; pretreatment with oral clopidogrel 6 hours before intervention was associated with improved outcomes. A loading dose of 600 mg may offer more effective platelet inhibition than one of 300 mg; increasing the loading dose beyond 600 mg has not shown benefit.

Patients who later undergo coronary artery bypass grafting (CABG) (eg, those with multivessel disease) while receiving clopidogrel have an increased risk of major bleeding and are more likely to undergo surgery for bleeding. Because of this increased risk of bleeding, it is recommended that clopidogrel be withheld for at least 5 days before elective CABG. Thus, many physicians choose to hold clopidogrel until the patient’s coronary anatomy is defined during coronary angiography.

Even with the above discussion in mind, patients who are clinically unstable should receive clopidogrel or be taken immediately for coronary angiography. Clopidogrel is a prodrug that must be metabolized into the active form before it is effective. Metabolism of clopidogrel is carried out in the liver by a number of enzymes, including CYP2C19. [ 54 , 55 ]

Numerous variations of CYP are described, with the wild type being CYP2C19*1. Polymorphisms for *2, *3, *4, and *8 are also described and are associated with lower efficacy of therapy. The results of some studies suggest that an additional polymorphism, designated *17, may increase the efficacy of clopidogrel therapy. However, these studies have not been consistently replicated. [ 54 , 55 ]

Studies have been conducted to ascertain viable strategies for overcoming the variability in the metabolism and efficacy of clopidogrel. [ 56 ]  Doubling the dose has been suggested; some studies found this to improve outcomes in poor responders, whereas others failed to show this result. Another suggestion is to add a phosphodiesterase inhibitor, such as cilostazol; some of the initial results of this strategy are promising, and a clinical trial is currently under way.

Finally, switching to more potent inhibiting agents, such as prasugrel (see below), remains a possible strategy. Despite its similarity to clopidogrel, prasugrel is not metabolized by the CYP2C19 system. Consequently, its metabolism would not be influenced by the same genetic factors as that of clopidogrel. [ 56 , 57 , 58 ]  However, Rudolph et al reported that compared to clopidogrel, prasugrel improves endothelial nitric oxide bioavailability and reduces platelet-leukocyte interaction and levels of inflammatory markers in patients with unstable angina undergoing PCI. [ 59 ]

It should be noted that although clopidogrel may be less efficacious than the newer P2Y12 inhibitors, it may carry a slightly lower bleeding risk.

Head-to-head comparison has shown that whereas prasugrel is more effective at reducing clinical events than clopidogrel is, it is also associated with a higher risk of bleeding.

Prasugrel is potentially harmful as part of a dual-platelet regimen in patients with a stroke history for whom PCI is planned. [ 49 ]  Owing to excess bleeding without clinical benefit, the US Food and Drug Administration lists a Black Box warning that does not recommend administration of prasugrel to patients who weigh less than 60 kg as well as those aged 75 years or older, unless the risk of recurrent cardiac ischemia outweighs the elevated bleeding risk. [ 49 ]

It should be noted that prasugrel remains unproven for use in patients with ST-elevation MI (STEMI) or ACS who were treated only medically. In addition, this agent must be withdrawn at least 7 days before planned CABG (compared with 5 days for clopidogrel or ticagrelor).

Prasugrel should not be used prior to coronary angiography. Thus, based on current guidelines, patients with unstable angina being treated with upfront dual antiplatelet therapy should be given either clopidogrel or ticagrelor.

Findings from a 1-year clinical effectiveness retrospective observational comparison of prasugrel with ticagrelor using data from an integrated claims database from 15,788 patients with ACS managed with PCI revealed noninferiority of prasugrel for rates of postdischarge net adverse clinical events (NACEs), major adverse cardiovascular events (MACEs), and rehospitalization for bleeding. [ 60 ]  However, prasugrel use was associated with a significantly lower NACEs and MACEs, mostly driven by heart failure, but with no significant difference in all-cause death, MI, unstable angina, stroke/transient ischemic attack, or bleeding. The investigators noted that physicians preferentially used prasugrel rather than ticagrelor in younger ACS-PCI patients with lower risk of bleeding or comorbidities. [ 60 ]

Nonthienopyridine P2Y12 inhibitor

Ticagrelor is indicated to reduce the rate of thrombotic CV events following ACS. Ticagrelor also reduces the rate of stent thrombosis in patients who have undergone stent placement for treatment of ACS. In September 2015, the indication was expanded to include patients with a history of MI more than 1 year previously. It is used in addition to low-dose aspirin (75-100 mg/day). [ 61 ]

The key points with respect to ticagrelor are (1) that this agent can also be used for STEMI patients and (2) that improved survival is achieved at 1 year, with all-cause mortality reduced from 5.9% to 4.5%. [ 21 ]  This 1.4% absolute risk reduction in the death rate is attributed to a possible increase in endogenous circulating adenosine, in that ticagrelor is known to inhibit its uptake into erythrocytes. This may also be the cause of the agent’s unique side effect of transient dyspnea.

Approval of ticagrelor use beyond 1 year in patients with a history of MI is based on the PEGASUS TIMI-54 study, a large-scale outcomes trial involving over 21,000 patients. [ 62 ]  PEGASUS TIMI-54 investigated ticagrelor 60 mg twice daily plus low-dose aspirin, compared to placebo plus low-dose aspirin, for the long-term prevention of CV death, heart attack, and stroke in patients who had experienced a heart attack 1-3 years prior to study enrollment. In patients with an MI more than 1 year previously, treatment with ticagrelor significantly reduced the risk of CV death, MI, or stroke compared with placebo. [ 62 ]

Glycoprotein IIb/IIIa antagonists

Because of the availability of novel oral P2Y12 platelet inhibitors, IV GP IIb/IIIa inhibitors have been relegated to use in special circumstances when a second antiplatelet agent in conjunction with aspirin cannot be promptly given (as in cases where there is a high likelihood of urgent CABG or where cardiac catheterization is delayed because of consent or staffing issues). [ 49 ] The risk must justify the bleeding risk (as in young diabetics with elevated troponin levels).

All of the currently available GP IIb/IIIa inhibitors (ie, abciximab, eptifibatide, and tirofiban) have been shown to increase the safety of acute PCI, with relative risk reductions in adverse events (including 30-day mortality and infarction) of approximately 30-50% in trials prior to the advent of the newer P2Y12 platelet inhibitors.

However, the GUSTO-IV (Global Utilization of Streptokinase and TPA [tissue plasminogen activator] for Occluded coronary arteries IV) randomized clinical trial did not show any benefit for abciximab in medically treated patients who did not undergo PCI. [ 63 , 64 ] In fact, longer duration of abciximab use was associated with a negative trend in event rates.

Of the currently used GP IIb/IIIa inhibitors, only eptifibatide and tirofiban have been shown to be beneficial in high-risk patients treated with medical management alone. The relative reduction in adverse events observed in this setting is on the order of 5-7%. In addition, a meta-analysis of six randomized trials (with 31,400 patients) failed to show a mortality benefit in patients who did not undergo PCI. [ 65 ] Whether this small benefit offsets the risk of bleeding events is a matter for the physician’s clinical judgment.

Beta blockers

Clinical trials of beta blockers in cases of unstable angina have shown decreases in ischemic symptoms and in the occurrence of MIs. These benefits have to be counterbalanced by the potential complications of heart failure or cardiogenic shock that have been demonstrated when beta blockers are used in hemodynamically compromised patients.

Oral beta blockers (eg, metoprolol) are preferred to IV agents. Studies have associated IV beta-blocker therapy with an increased risk of cardiogenic shock in patients presenting with heart failure or high-risk features. However, IV beta blockers may still be indicated in select patients with tachycardia or hypertension and ongoing chest pain.

In vitro studies have shown inhibition of platelet aggregation with beta blockers.

IV nitrate agents may be used in the treatment of ischemic chest pain, symptoms of heart failure, or hypertension, but these drugs are not associated with appreciable long-term clinical benefit. Nitrate agents are contraindicated for patients with right ventricular infarction, hypertrophic cardiomyopathy (HOCM), and severe aortic stenosis.

The role of medical treatment with anticoagulation (heparin, low molecular weight heparin [LMWH], or direct thrombin inhibitor) and dual antiplatelet therapy (DAPT) should be the same for those being managed with ischemic-guided or invasive strategies.

Because of the risks for bleeding, there is continuous reevaluation and evolving recommendations for anticoagulation and DAPT in patients along the ACS spectrum, especially regarding postdischarge DAPT regimen and duration. Patients with unstable angina (UA) are managed according to ACS protocols that indicate urgent or early invasive strategy for individuals with very–high-risk or high-hisk features and those with an an initial medical (or selectively invasive) strategy in patients with low-risk features.

In patients with unstable angina who undergo revascularization with invasive coronary angiography and who have disease suitable for treatment with either coronary artery stenting or bypass surgery (CABG), postprocedure management of antiplatelet therapy includes DAPT, usually with aspirin, and a P2Y12 inhibitor (ticagrelor or prasugrel) for 12 months. There are studies in progress considering shorter courses of DAPT, particularly for troponin-negative cohorts (6 months, or even 1-3 months), and then following with monotherapy with a P2Y12 inhibitor to replace ASA. However, the enthusiasm for deescalating to aspirin monotherapy or “short (duration) DAPT” is curbed by data showing ongoing and lifelong risk for cardio- and cerebrovascular events and mitigation of these long-term adverse ischemic outcomes with more aggressive antiplatelet regimens beyond aspirin. [ 62 ]

The remainder of coronary treatment program remains essentially the same with use of beta blockers when appropriate, preventive therapy with angiotensin-converting enzyme inhibitors (ACEIs), and lipid -owering therapy, with the cornerstone being high-intensity statin therapy.

A subset of patients with ACS and unstable angina with known or presumed obstructive coronary disease (coronary artery disease [CAD]) may not have coronary anatomy suitable for revascularization or, who, for other reasons (eg, frailty), do not undergo coronary revascularization. These individuals are not well represented in the clinical trials literature, and their management is challenging for the clinician.

While all UA/ACS spectrum patients should receive comprehensive medical treatment and aggressive secondary prevention with or without stenting or CABG, some nonrevascularized patients may benefit from further risk stratification and testing. Address heart failure, ischemia-related ventricular arrhythmia, or other high-risk conditions such as inadequately controlled blood pressure, diabetes, chronic kidney disease, and bleeding risk. Objective measures of increased risk include the following:

• Left ventricular (LV) dysfunction evaluated by transthoracic echocardiogram (TTE)
• Biomarker levels (natriuretic peptides [brain natriuretic peptide (BNP) and N-terminal pro-BNP (NT-pro BNP)], cardiac troponin [cTn])
• Significant ischemia on noninvasive testing
• Extent and severity of CAD and atherosclerosis burden, as evaluated with coronary computed tomography angiography and cardiac calcium (CAC) score. Those with higher ischemic and atherosclerotic risk may merit more intensive medical therapy that may entail more costs or side-effects.

Less routine treatment options that may be of benefit for this high-risk cohort of patients include the following:

• Continue DAPT with aspirin and a P2Y12 inhibitor for not less than 12 months. Alternatively, use low-dose rivaroxaban 2.5 mg twice daily in addition to low-dose aspirin, particularly for patients with heart failure and ACS overlap. Note that these strategies come at the cost of an increased risk of bleeding; an intermediate option is monotherapy with a P2Y12 inhibitor. [ 66 , 67 ]
• Consider proton-pump inhibitors in patients with high bleeding risk.
• Intensive lipid management is needed and includes high-intensity statin therapy to reduce low-density lipoprotein cholesterol (LDL-C) level by at least 50% and a target LDL that is below 70 mg/dL (target < 55 mg/dL or < 1.4 mmol/L in European guidelines). [ 68 ] Adjunctive therapy to high-intensity statins to achieve these goals include ezetimibe, PCSK9 inhibitors, and bempedoic acid. When evaluating lipid profile, also note the patient's triglyceride levels; if they are over 150 mg/dL, consider the use of icosapent ethyl in these patients. Targeting high-density lipoprotein (HDL) cholesterol has not been shown to improve outcomes.
• Consider ACEIs to provide additional cardioprotective benefit even in normotensive patients with normal left ventricular function.
• Low dose colchicine to mitigate inflammation has been used in post ACS cohorts and may be of benefit as well. [ 69 ]

The use of LMWH and the use of intravenous (IV) unfractionated heparin (UFH) are two comparable anticoagulation strategies in the treatment of unstable angina. The many potential benefits of using LMWH include lower bleeding rates, reduced costs, and decreased incidence of heparin-induced thrombocytopenia. However, many interventional cardiologists are uncomfortable using LMWH because anticoagulation activity cannot be measured during percutaneous coronary intervention (PCI). [ 70 ]

In the ESSENCE (Efficacy and Safety of Subcutaneous Enoxaparin in Non–Q-wave Coronary Events) study, when LMWH (enoxaparin) was compared with UFH, the 30-day composite rates of death, myocardial infarction (MI), or recurrent angina were significantly reduced for subjects taking LMWH (19.8% vs 23.3%). [ 71 ]  However, excess minor bleeding occurred in 11.9% of patients in the LMWH group, versus 7.2% of those in the non-LMWH group, many of which were due only to injection site ecchymosis. [ 71 ]  The revascularization rate was intermediate (~30%).

In the SYNERGY (Superior Yield of the New Strategy of Enoxaparin Revascularization and Glycoprotein IIb/IIIa Inhibitors) trial, enoxaparin was associated with more major bleeding episodes (9.1%) than UFH was (7.6%). [ 72 ]  High-risk patients with non-ST-elevated MI (NSTEMI) (including those with unstable angina) were randomized into groups that received either UFH or enoxaparin. All enrolled patients were treated with an early invasive strategy. No difference in the composite endpoint (death or MI by 30 days) was detected in the SYNERGY trial. [ 72 ]  Although more major bleeding episodes occurred in the enoxaparin group, much of this effect was attributed to patients who crossed over to UFH after receiving an initial dose of enoxaparin.

In the OASIS-5 (Organization to Assess Strategies for Ischemic Syndromes-5) trial, which compared fondaparinux and enoxaparin for treatment of UA/NSTEMI, fondaparinux was associated with a low, but increased, rate of guiding catheter thrombus. [ 73 ]  Fondaparinux yielded a lower major bleeding rate at 9 days, as well as significant reductions in MI, stroke, and mortality at 180 days. [ 73 ]  However, this agent is not recommended if urgent PCI is foreseen because of the increased rate of guiding catheter thrombus.

Enoxaparin, fondaparinux, and UFH are safe alternatives for the treatment of unstable angina. Note that switching agents (eg, from LMWH to UFH) is associated with excess bleeding and reduced clinical benefit. If a conservative strategy is intended, LMWH may be preferred.

Reactivation of unstable angina after discontinuance of heparin has been documented among subjects not receiving concomitant aspirin therapy. [ 74 ]

Direct thrombin inhibitors

Direct thrombin inhibitors, such as hirudin, lepirudin (recombinant hirudin), and bivalirudin, are potential alternatives to heparin. These agents are much more costly than conventional anticoagulation agents and may be associated with higher rates of bleeding.

In a large meta-analysis comparing direct thrombin inhibitors and heparin in the treatment of patients with ACS, there was a slightly greater reduction in MI in the inhibitors group (2.8%) than in the heparin group (3.5%). [ 75 ]  Treatment with hirudin was associated with an higher risk of major bleeding than treatment with heparin, whereas treatment with bivalirudin was associated with a lower risk. [ 75 ]

GUSTO (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) IIB investigators compared recombinant hirudin with heparin in 12,142 patients, a third of whom had STEMI. [ 76 ]  The hirudin group had a 9% relative risk reduction in 30-day death or MI rates (8.9% vs 9.8%) but experienced more moderate bleeding events (8.8% vs 7.7%). [ 76 ]

In the international OASIS-2 (Organisation to Assess Strategies for Ischemic Syndromes-2) clinical trial, involving 10,141 patients who were randomly assigned to receive either heparin (activated partial thromboplastin time [aPTT] maintained between 60 and 100 seconds) or lepirudin (0.4 mg/kg bolus, followed by 0.15 mg/kg/hr by IV infusion for 72 hours), investigators found no evidence indicating attenuation of myocardial necrosis (based on creatine kinase or troponin measurements), in contrast with GP IIb/IIIa antagonists. [ 77 ]

The FDA approved lepirudin for use in patients with  heparin-induced thrombocytopenia  (HIT) and associated thrombotic disease. The goal is 1.5-2.5 times the control aPTT values. The dosage must be adjusted for patients with renal impairment.

The benefits of bivalirudin in patients who undergo coronary stent implantation has been demonstrated in the REPLACE-2 (Randomized Evaluation in PCI Linking Angiomax to reduced Clinical Events-2) and ACUITY (Acute Catheterization and Urgent Intervention Triage strategY) trials. [ 77 , 78 ]  At present, however, the data are insufficient to support a recommendation of routine bivalirudin use in patients with unstable angina.

Although direct thrombin inhibitors should not be routinely used in the treatment of unstable angina, they may be of clinical benefit in special circumstances (eg, HIT).

Other considerations

For all ACS or postrevascularization patients, offer cardiac rehabilitation services and counsel in healthy behavior and smoking cessation. The American Heart Association's “Healthy Lifestyle: Life's Essential 8” and "My Life Check" are useful, evidence-based, and understandable tools, and they are available in  English  and  Spanish .

Additional management of unstable angina includes the use of statins (lipid-lowering agents) and angiotensin-converting enzyme (ACE) inhibitors.

HMG coenzyme A reductase inhibitors (statins)

Multiple large, randomized, secondary prevention trials, including the Heart Protection Study, have demonstrated significant mortality benefit from statin therapy in patients with unstable angina.

Results from the MIRACL (Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering) study and the PROVE-IT (Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE-IT) TIMI (Thrombolysis in Myocardial Infarction) trials suggested that early initiation of antilipidemic agents (statins) in patients with acute coronary syndrome (ACS) can decrease adverse events within a relatively short period. [ 79 , 80 ]

The MIRACL trial (including 3086 patients with unstable angina randomized to high-dose atorvastatin vs placebo) demonstrated that therapy with atorvastatin resulted in a reduction in the primary endpoint (ie, death, MI, resuscitated cardiac arrest, severe recurrent symptomatic ischemia) from 17.4% to 14.8% within a relatively short period (4 months) as compared with placebo. [ 79 ] The benefit was mostly for recurrent symptomatic ischemia with objective evidence and requiring emergency rehospitalization (from 8.4% to 6.2%). [ 79 ]

The PROVE-IT TIMI-22 trial demonstrated a benefit from statin therapy even in patients with ACS presenting with relatively low serum low-density lipoprotein cholesterol (LDL-C) levels (< 100 mg/dL), suggesting that the target LDL-C level should be less than 80 mg/dL in these patients. [ 80 ]

To improve patient adherence, statin therapy should be initiated before hospital discharge. Additional clinical benefit may be gained by starting therapy within 24-96 hours of admission.

FDA safety alerts

On June 8, 2011, the FDA notified healthcare professionals of its recommendations for limiting the use of the highest approved dose (80 mg) of simvastatin because of an increased risk of muscle damage. The FDA required that the simvastatin label be changed to add new contraindications and dose limitations for using simvastatin with certain medicines. [ 81 ]

On February 28, 2012, the FDA approved important safety label changes for statins, including removal of routine monitoring of liver enzymes. Information about the potential for generally nonserious and reversible cognitive side effects and reports of increased blood sugar and glycosylated hemoglobin (HbA1c) levels was added to the statin labels. In addition, extensive contraindication and dose limitation updates were added to the lovastatin label in situations when this drug is taken with certain medicines that can increase the risk for myopathy. [ 82 ]

On March 1, 2012, the FDA updated healthcare professionals regarding changes to the prescribing information concerning interactions between protease inhibitors (drugs for management of human immunodeficiency virus [HIV] and hepatitis B virus [HBV] infection) and certain statins. The combination of these drugs may raise the blood levels of statins and increase the risk for myopathy. Rhabdomyolysis, the most serious form of myopathy, can cause kidney damage and lead to kidney failure, which is life-threatening. [ 83 ]

ACE inhibitors

ACE inhibitors are of particular benefit in patients with large anterior infarctions, especially those with compromised left ventricular function (eg, from ST-elevation MI [STEMI]) but without hypotension. The benefit in patients with unstable angina is less clear.

Currently, these agents are recommended in patients with left ventricular dysfunction or congestive heart failure, diabetes, and hypertension. ACE inhibitor therapy may be started within 24 hours of admission and titrated for blood pressure effect.

Other medications

Calcium-channel antagonists, antibiotics against Chlamydia pneumoniae, and fibrinolytic agents currently have no established role in the setting of unstable angina.

Most of the clinical trials of fibrinolytic therapy have shown a tendency toward more nonfatal infarctions attributed to procoagulant effects in the context of a nonocclusive thrombus.

Although the available data suggest that the efficacy of ticlopidine is similar to that of aspirin, the use of ticlopidine in the United States was drastically reduced after reports appeared of associated fatal thrombotic thrombocytopenic purpura.

Ranolazine, trimetazidine, nicorandil, and ivabradine, which have been shown to reduce myocardial ischemia through various means, have received limited testing in patients with ACS. [ 84 ]

Patients with unstable angina and the following clinical characteristics should be referred for immediate cardiac catheterization :

Cardiogenic shock

Severe left ventricular dysfunction

Angina refractory to medical therapy

Acute mitral regurgitation

New ventricular septal defect

Unstable tachyarrhythmias

Invasive versus conservative therapy

It has been questioned whether patients who have unstable angina but lack the clinical characteristics listed above receive greater benefit from an invasive strategy than from conservative management.

Among patients presenting with unstable angina, approximately 15% have 1-vessel CAD, 35% have 2-vessel CAD, and 50% have 3-vessel CAD. The incidence of left main disease is roughly 5-10%. The rate of thrombus detected at coronary angiography varies widely, ranging from less than 10% among those with chest pain in the previous month to more than 50% among those with rest angina in the preceding 24 hours.

This high prevalence of significant disease has led some to advocate routine angiography, whereas the imperfect ability to predict who will develop long-term adverse events has encouraged a tendency toward so-called permissive revascularization.

Older clinical trials, such as TIMI III-B, the VANQWISH (Veterans Affairs Non–Q-Wave Infarction Strategies in-Hospital) study, and the MATE (Medicine versus Angiography in Thrombolytic Exclusion) trial, did not find routine catheterization to be superior to reserving catheterization for patients with recurrent ischemic symptoms or a significantly positive stress test result. Heightened abrupt vessel closure, stent thrombosis, and MI rates were early hazards observed with angioplasty performed in the acute setting of myocardial ischemia. [ 85 , 86 ]

The TACTICS (Treat angina with Aggrastat and determine Cost of Therapy with Invasive or Conservative Strategy)/TIMI-18 study showed a very low 30-day and 6-month results for the composite endpoint of death, MI, or rehospitalization with the early invasive strategy. [ 36 ] The study entailed the administration of IV GP IIb/IIIa (tirofiban), coupled with angiography within 48 hours. The benefit of early invasive strategy was more substantial in intermediate- and high-risk patients (ie, those with a TIMI score of 3).

The FRISC-II (FRagmin during InStability in Coronary artery disease-II) trial showed a significant reduction in death or MI at 6 months in patients with unstable angina who underwent early catheterization and revascularization, as compared with patients who were treated with a noninvasive strategy. [ 87 ]

This treatment difference was primarily driven by a lower rate of MI in the invasive arm (7.8%) than in the noninvasive arm (10.1%). Patients in the invasive arm also had a significant reduction in angina and hospital readmission rates. The treatment benefits were more pronounced in patients with ST-segment depression and cardiac marker elevation. [ 87 ]

Investigators in the RITA-3 (Randomized Intervention Trial of unstable Angina-3) study also reported a benefit with the invasive strategy as opposed to conservative management in intermediate- to high-risk patients with NSTEMI and ischemic changes on ECG or elevated troponin levels. [ 88 ]

In this study, the combined endpoint of death, MI, and refractory angina at 4 months was significantly reduced in the invasive arm (9.6%) as compared with the conservative arm (7.6%). Although the two groups showed no difference in the combined endpoint (death or nonfatal MI) at 1 year, a 5-year follow-up analysis revealed that the invasive strategy was associated with significant reductions in death or nonfatal MI. [ 88 ]

In contrast to these trials, the ICTUS (Invasive vs Conservative Treatment in Unstable coronary Syndromes) trial did not find an early invasive strategy to confer any advantage over a selective invasive strategy in 1200 patients with chest pain and elevated troponin who had either a history of CAD or the presence of ischemic ECG changes. [ 89 ] However, the selective invasive group had a 40% rate of revascularization during initial hospital stay.

Timing of catheterization

With regard to the timing of catheterization, the ISAR-COOL (Intracoronary Stenting Angiographic Results COOLing-off) trial suggested that earlier catheterization provides a significant benefit over later use of the procedure. [ 90 ] Patients with NSTEMI who underwent coronary angiography within 6 hours had a lower rate of death or large MI at 30 days (5.9%) than did patients who underwent the treatment at 3-5 days (11.6%). [ 90 ]

Two meta-analyses (one of which included the ICTUS trial) also supported the use of an early invasive strategy in the management of patients with NSTEMI, with the most prominent benefit occurring in those patients with high-risk features. The weight of the current evidence favors the view that an early invasive strategy benefits high-risk patients with ACS.

Patients at moderate to high risk for adverse events, such as persons with ST depression greater than 1 mm on ECG, troponin positivity or non–Q-wave myocardial infarction (NQMI), or chest pain refractory to medical therapy, should be scheduled for cardiac catheterization with likely revascularization within the next 48 hours. The TACTICS/TIMI-18 trial showed that this early invasive strategy reduced 30-day rates of death, MI, or rehospitalization for unstable angina from 19.4% to 15.9%. [ 36 ]

The FRISC II study showed that even a delayed invasive strategy (mean time to revascularization, 4 days; 71% revascularization rate vs 9% in the conservative arm), coupled with LMWH (dalteparin) therapy, provides durable benefit for individual hard endpoints. [ 87 ] At 1 year, the study’s invasive strategy group had statistically significant reductions in MI (8.6% vs 11.6%) and death (2.2% vs 3.9%), compared with the noninvasive group.

To date, FRISC II is the only randomized clinical trial showing a mortality benefit—probably because of the very strict criteria for revascularization, which resulted in only 9% of the conservative arm receiving PCI or CABG. In the TACTICS/TIMI-18 study and other North American trials, about 50% of the patients in the conservative arm had some form of revascularization, and not all of those in the invasive arm had indications for PCI or CABG. Consequently, the benefits of revascularization appeared less striking.

Notably, by 1 year, a catch-up phenomenon was observed in patients who had initial conservative management. By then, 52% had undergone angiography, and 43% required revascularization (see the image below).

Cost-to-benefit ratio of revascularization

Wallentin et al estimated the cost-to-benefit ratio of an initial invasive approach based on the FRISC II trial. [ 91 ] At the cost of 15 extra CABG and 21 PCI procedures, the benefits per 100 patients per year were as follows:

1.7 lives saved

2 MIs prevented

20 readmissions prevented

Symptoms relieved earlier and better

CABG is usually the preferred method for revascularization in patients with the following conditions:

Left main trunk artery stenosis

Poor left ventricular function

Significant 3-vessel CAD or 2-vessel disease that involves the proximal left anterior descending (LAD) artery

Diabetes mellitus with focal stenosis in more than one vessel

Concomitant severe valvular disease that necessitates open heart surgery

Patient monitoring

Continuous observation by Holter monitoring can provide helpful information. Depending on the criteria of ST-segment deviation, the timing of monitoring relative to disease instability, and the intervening medical therapy, the incidence of abnormal ST-segment shifts has been reported to be 11-66% in unstable angina. As many as 92% of these abnormal ST-segment shifts are asymptomatic; more important, patients who experienced such episodes had an associated higher adverse event rate than those who did not (48% and 20%, respectively).

Other studies have documented unfavorable outcomes at up to 6 months with the presence of at least 1 hour of silent ischemia during initial admission.

Approximately 1-3 months after the acute phase of unstable angina, the risk of major adverse events typically declines to that observed in patients with chronic stable angina. The goals are to prepare patients for resumption of their normal activities as safely as possible, to preserve left ventricular function, and to prevent future events.

Although secondary prevention is the responsibility of the primary care provider and the cardiologist, some centers have specialized teams (eg, cardiac rehabilitation and preventive services) that offer more intensive, and perhaps more effective, counseling and follow-up.

Smoking cessation

Aggressive attempts should be made to convince the patient and the rest of his or her household to cease smoking. The target is for the patient and his or her cohabitants to abstain completely from all tobacco products for 12 months or longer. Patients who have expressed a decision to quit should be supported with counseling, follow-up, and pharmacotherapy, and possibly with acupuncture or hypnosis (if necessary). Patients should avoid secondhand smoke.

Lipid lowering

The target is an LDL-C level of 70 mg/dL or lower, a high-density lipoprotein cholesterol (HDL-C) level higher than 35 mg/dL, and a triglyceride level below 200 mg/dL. Diet modification, exercise, and drug therapy are indicated as per National Cholesterol Education Program (NCEP) guidelines.

Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors (eg, evolocumab, alirocumab) are indicated to not only lower LDL-C but also to reduce the risk of unstable angina requiring hospitalization in adults with established CV disease. [ 92 , 93 ]

Control of hypertension

The target blood pressure is below 140/90 mm Hg or below 130/80 mm Hg if the patient has diabetes mellitus or chronic kidney disease. Diet modification, moderation of sodium and alcohol intake, exercise, smoking cessation, and pharmacotherapy are indicated.

Diabetes mellitus management

Diet modification, exercise, pharmacotherapy (including ACE inhibitor therapy), preventive counseling regarding foot care, and ophthalmic examinations are indicated. [ 94 ]

Weight management and nutritional counseling

The target body mass index (BMI) is below 25 kg/m 2 , in conjunction with a waist circumference of less than 40 inches in men and of less than 35 inches in women. Diet modification with adequate intake of fruits and vegetables, exercise, and behavioral modification and counseling are indicated.

Psychosocial management

The targets in psychosocial management are lifestyle modification, recognition and treatment of substance abuse (whether involving alcohol or psychotropics), management of depression or hostile attitude, and compliance with health maintenance. Education, counseling, support groups, and social or religious resources are indicated.

Activity management

Patients at risk for MI should avoid sudden strenuous activities, especially in cold weather (eg, shoveling snow).

When a clinician is presented with a patient with suspected or confirmed unstable angina, consultation with a cardiologist is indicated to assist in risk stratification and decision making, to expedite further cardiac testing (eg, with echocardiography, stress testing, or angiography), and to treat unstable patients. A critical care or telemetry unit specialist is helpful for acute care and monitoring. A cardiothoracic surgeon should be consulted when coronary artery bypass grafting (CABG) is indicated.

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Rottger E, de Vries-Spithoven S, Reitsma JB, et al. Safety of a 1-hour rule-out high-sensitive troponin T protocol in patients with chest pain at the emergency department. Crit Pathw Cardiol . 2017 Dec. 16(4):129-34. [QxMD MEDLINE Link] .

Driscoll A, Barnes EH, Blankenberg S, et al. Predictors of incident heart failure in patients after an acute coronary syndrome: The LIPID heart failure risk-prediction model. Int J Cardiol . 2017 Dec 1. 248:361-8. [QxMD MEDLINE Link] .

• Unstable Angina. Pathogenesis of acute coronary syndromes.
• Unstable Angina. Thrombolysis in Myocardial Infarction (TIMI) Risk Score correlates with major adverse outcome and effect of therapy with low-molecular-weight heparin. ARD = absolute risk difference; ESSENCE = Efficacy and Safety of Subcutaneous Enoxaparin in Non–Q-wave Coronary Events; No. = number; NNT = number needed to treat.
• Unstable Angina. Algorithm for initial invasive strategy. ASA = acetylsalicylic acid (aspirin); GP IIb/IIIa= glycoprotein IIb/IIIa; IV = intravenous; LOE = level of evidence; UA/NSTEMI = unstable angina/non–ST-segment elevation myocardial infarction; UFH = unfractionated heparin. (Adapted from 2007 ACC/AHA UA/NSTEMI Guidelines.)
• Unstable Angina. Algorithm for initial conservative strategy. ASA = acetylsalicylic acid (aspirin); EF = ejection fraction; GP IIb/IIIa= glycoprotein IIb/IIIa; IV = intravenous; LOE = level of evidence; LVEF = left ventricular ejection fraction; UA/NSTEMI = unstable angina/non–ST-segment elevation myocardial infarction. (Adapted from 2007 ACC/AHA UA/NSTEMI Guidelines.)
• Unstable Angina. Rate and timing of revascularization for patients with unstable angina using invasive versus conservative approach (FRagmin during InStability in Coronary artery disease [FRISC] II).
• Unstable Angina. Time course of elevations of serum markers after acute myocardial infarction. CK = creatine kinase; CK-MB = creatine kinase MB fraction; LDH = lactate dehydrogenase.
• Table 1. Patient Characteristics, GUARANTEE Versus CRUSADE Trials
• Table 2. Demographic Characteristics of Patients in International OASIS-2 Registry
• Table 3. Thirty-Day Clinical Outcome in Patients With Acute Coronary Syndromes in Clinical Trials
• Table 4. Braunwald Classification of Unstable Angina
• Table 5. Recommendations for Selection of Preferred Management Strategy

Contributor Information and Disclosures

Walter Tan, MD, MS Associate Professor of Medicine, Wake Forest University School of Medicine; Director of Cardiac Cath Labs, Wake Forest Baptist Medical Center Walter Tan, MD, MS is a member of the following medical societies: American Association for the Advancement of Science , American College of Cardiology , American Heart Association , American Stroke Association , National Stroke Association , Society for Vascular Medicine , Society of Interventional Radiology Disclosure: Nothing to disclose.

Frederic Ross Kahl, MD, FACC, FAHA Professor of Medicine, Cardiology Section, Department of Medicine, Professor, Department of Radiology, Professor, Translational Science Institute, Design, Epidemiology, Biostatistics, and Clinical Research Ethics Program, Associate Physician, Department of Radiology, Wake Forest University School of Medicine Frederic Ross Kahl, MD, FACC, FAHA is a member of the following medical societies: American College of Cardiology , American College of Physicians-American Society of Internal Medicine , American Heart Association , American Medical Association , Forsyth-Stokes-Davie County Medical Society, North Carolina Medical Society Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Nothing to disclose.

Richard A Lange, MD, MBA President, Texas Tech University Health Sciences Center, Dean, Paul L Foster School of Medicine Richard A Lange, MD, MBA is a member of the following medical societies: Alpha Omega Alpha , American College of Cardiology , American Heart Association , Association of Subspecialty Professors Disclosure: Nothing to disclose.

Eric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic ArizonA Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha Disclosure: Nothing to disclose.

David J Moliterno, MD Professor of Medicine, Jefferson Morris Gill Professor of Cardiology, Chief, Division of Cardiovascular Medicine, University of Kentucky; Vice Chairman of Internal Medicine, Chandler Medical Center; Medical Director, Gill Heart Institute David J Moliterno, MD is a member of the following medical societies: American College of Cardiology , European Society of Cardiology , Association of Professors of Cardiology , American College of Physicians , American Heart Association , American Medical Association Disclosure: Nothing to disclose.

Steven James Filby, MD Fellow in Interventional Cardiology, The Cleveland Clinic Foundation

Disclosure: Nothing to disclose.

Justin D Pearlman, MD, ME, PhD, FACC, MA Chief, Division of Cardiology, Director of Cardiology Consultative Service, Director of Cardiology Clinic Service, Director of Cardiology Non-Invasive Laboratory, Director of Cardiology Quality Program KMC, Dartmouth-Hitchcock Medical Center, Dartmouth Medical School

Justin D Pearlman, MD, ME, PhD, FACC, MA is a member of the following medical societies: American College of Cardiology , American College of Physicians , American Federation for Medical Research , International Society for Magnetic Resonance in Medicine , and Radiological Society of North America

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

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• Angina Pectoris
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Stable vs. Unstable Angina: Differences and Similarities

• Main Differences
• Physical Activity
• Long-Term Management

Angina is a type of chest pain that results from poor blood flow to the heart muscle, typically from blocked coronary arteries. It is a condition marked by localized squeezing pressure, tightness, or a painful "strangling sensation" in the chest, arms, or jaw caused by the heart not getting enough oxygen due to insufficient blood flow .

Stable angina follows a pattern and occurs during physical exertion, while unstable angina doesn't follow a pattern and can occur without physical exertion. Unstable angina is more dangerous and may be a warning that a person is at imminent risk of a heart attack.

Read on to learn what you need to know about the difference between stable and unstable angina, including common versus emergency symptoms, why unstable angina is more intense and serious than stable angina, tests doctors use to confirm unstable angina, treatment options, and more.

RealPeopleGroup / Getty Images

Stable vs. Unstable Angina: Main Differences

Below is a side-by-side comparison list that shows similarities and differences between stable and unstable angina.

Chest pain near the heart

Caused by the heart not getting enough blood flow and oxygen

Symptom of heart disease

Less serious, more common

Not always an emergency

Predictable

"Stable" consistent pattern

Triggered by exertion, exercise, strong emotions, anxiety, eating a big meal, etc.

Rest, relaxation, and calmness typically relieve symptoms

Usually lasts one to five minutes; rarely lasts longer than 15 minutes

Not classified as acute coronary syndrome (ACS)

More serious, deadlier

Always an emergency

Unpredictable

"Unstable" nonexistent pattern

Not triggered by any predictable factors (often occurs out of the blue while reclining or sleeping)

Rest and relaxation do not quickly resolve symptoms

Often lasts longer than 15 minutes; can last 30 minutes or more

Classified as acute coronary syndrome (ACS)

Acute coronary syndrome (ACS) is characterized by an abrupt, life-threatening reduction in the heart's blood supply. Unstable angina is a form of ACS; stable angina is not.

Although stable angina isn't considered an ACS, it can become unstable angina if you don't take steps to slow it.

Common Symptoms

Angina feels like a heavy pressure and tightness in the chest, but the pain or squeezing sensation can also be felt in other locations near the heart, such as the arms, shoulders, neck, or jaw.

Stable and unstable angina cause defects in the heart's functioning and its ability to sufficiently supply the heart with blood. But their seriousness and potential deadliness are different: Unstable angina is much more dangerous and should always be treated with life-or-death urgency as a medical emergency.

Stable and unstable angina symptoms may seem similar at the first sign of chest pain. However, unstable angina is unpredictable and doesn't quickly resolve with rest, relaxation, or the calming of strong emotions. It also causes more severe, longer-lasting symptoms requiring immediate medical attention at a nearby hospital or by calling 911.

Potential Angina Complications

Angina symptoms are caused by myocardial ischemia , a medical term that means “restricted blood supply to the heart.” When the heart doesn’t get enough blood, it can cause complications such as abnormal heart rhythms ( cardiac arrhythmias ), heart failure , heart tissue death (myocardial necrosis ), or heart attacks .

Emergency Symptoms

You should call 911 or go to the emergency room (ER) if your stable angina symptoms seem different than usual or are accompanied by any of the following:

• Previously predictable angina symptoms occur unpredictably
• Symptoms last five minutes or longer
• Chest pain radiates to the arm, upper back, neck, or jaw
• Skin breaks out in a cold sweat
• Shortness of breath

Causes and Risk Factors

The most common underlying cause of stable and unstable angina is atherosclerosis, a condition marked by plaque buildup inside the heart’s arteries, which is a sign of coronary artery disease (CAD) . Other causes include coronary microvascular dysfunction and coronary artery spasm .

Risk factors for both stable and unstable angina include:

• Age (Getting older increases risk)
• Underlying medical conditions ( high blood pressure, cardiomyopathy , diabetes , etc.)
• Hereditary factors (e.g., having a family history of heart disease)
• Smoking cigarettes
• Being overweight
• Drug use (amphetamines can cause angina-inducing heart damage)
• Insufficient sleep or poor sleep quality
• Unhealthy eating habits
• Lack of physical activity
• High levels of low-density lipoprotein (or "bad") cholesterol

How Is Stable vs. Unstable Angina Treated?

Vasodilators are medications that dilate the arteries and veins; they are first-line treatments for both stable and unstable angina. Common vasodilators for treating angina are nitroglycerin and a nitrate medication called Imdur (isosorbide mononitrate). Another relatively new anti-angina drug is Ranexa (ranolazine).

People experiencing chronic angina are usually prescribed two or more of the following types of drugs:

• Beta-blockers
• Calcium channel blockers
• Late sodium current blockers (e.g., Ranexa)

Vasodilation vs. Vasoconstriction

Angina is caused by a narrowing of the arteries, which constricts blood flow (also known as vasoconstriction) to the heart. Nitrates that treat angina improve blood flow by widening coronary arteries (this is also called vasodilation).

Because unstable angina is more serious than stable angina, it requires more aggressive treatment. Most people with stable angina don't need surgery. The gold standard for most people with stable angina is non-invasive medical treatment such as medications and heart-healthy lifestyle changes.

People with unstable angina usually require an invasive surgical procedure such as angioplasty with stenting to unblock clogged arteries. In addition to making lifestyle changes and having a surgical procedure, unstable angina treatment often includes different prescription drugs, including anti-ischemic agents, anticoagulants, and antiplatelets.

Physical Activity and Rehabilitation With Angina

Physical activity is key to making heart-healthy lifestyle choices that reduce angina risk. That said, because strenuous exercise can trigger angina symptoms, it's important to work closely with a trained professional when using physical activity as part of rehabilitation with angina.

Long-Term Management, Follow-Up, and Living Well

Long-term management of stable and unstable angina involves living well by making heart-healthy lifestyle choices and scheduling regular follow-up visits with a healthcare provider for checkups.

Because stable angina symptoms tend to be predictable, the American Heart Association has a downloadable "Cardiac Rehabilitation Angina Log" for tracking the date of any angina attacks, what triggered it, its intensity rating (1–4), how long it lasted, and what you did to alleviate its symptoms. You should share this log with your healthcare provider during follow-up visits.

Long-term management of stable and unstable angina aims to prevent the progression of blockages and to avoid severe consequences associated with coronary artery disease, such as deadly heart attacks. 

Angina means "chest pain." Stable and unstable angina are both caused by plaque buildup, which blocks the heart's blood flow. They share similar symptoms: constricted feelings of heavy pressure, tightness, or a squeezing "strangling sensation" in the chest area near the heart.

Unstable angina is unpredictable and more serious than stable angina. Strenuous exercise and strong emotions can trigger stable angina. But unstable angina doesn't have clear triggers; it can happen anytime, even when someone's relaxed or sleeping.

Sitting down or resting usually relieves stable angina symptoms in less than five minutes. However, taking it easy or relaxing doesn't relieve unstable angina symptoms, which generally last longer than 15 minutes and can lead to a heart attack or death.

Unstable angina is a medical emergency that almost always requires surgery to remove the heart's blockage. Stable angina doesn't necessarily require surgery and is primarily treated with medicine and heart-healthy lifestyle changes. 

European Society of Cardiology. Angina pectoris: how has the clinical presentation evolved? Is it still the same today as it was several years ago?

MedlinePlus. Angina .

American Heart Association. Angina pectoris (stable angina) .

American Heart Association. Unstable angina .

Bhatt DL, Lopes RD, Harrington RA. Diagnosis and treatment of acute coronary syndromes: a review .  JAMA . 2022;327(7):662. doi:10.1001/jama.2022.0358

National Health Service. Angina .

Mount Sinai. Stable angina .

National Heart, Lung, and Blood Institute. What causes angina?

Tan Z, Shang X, Li L, et al. Clinical study of isosorbide mononitrate treatment for angina pectoris in coronary heart disease .  Experimental and Therapeutic Medicine . 2013;5(4):1133-1136. doi:10.3892/etm.2013.958

Salazar CA, Basilio Flores JE, Veramendi Espinoza LE, et al. Ranolazine for stable angina pectoris . Cochrane Heart Group, ed.  Cochrane Database of Systematic Reviews . 2017;2019(1). doi:10.1002/14651858.CD011747.pub2

Bhatt DL, Hulot JS, Moliterno DJ, Harrington RA. Antiplatelet and anticoagulation therapy for acute coronary syndromes .  Circ Res . 2014;114(12):1929-1943. doi:10.1161/CIRCRESAHA.114.302737

American Heart Association. Cardiac Rehabilitation Angina Log .

Braunwald E, Morrow DA. Unstable angina: is it time for a requiem?   Circulation . 2013;127(24):2452-2457. doi:10.1161/CIRCULATIONAHA.113.001258

By Christopher Bergland Bergland is a retired ultra-endurance athlete turned medical writer and science reporter. He is based in Massachusetts.

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StatPearls [Internet].

Unstable angina (nursing).

Amandeep Goyal ; Roman Zeltser ; Anya A. Gunn .

Affiliations

Last Update: September 18, 2022 .

• Learning Outcome

Unstable angina falls along a spectrum under the umbrella term acute coronary syndrome. This public health issue that daily affects a large portion of the population remains the leading cause of death worldwide.

Distinguishing between this and other causes of chest pain that include stable angina is important regarding the treatment and disposition of the patient.

Providers should be aware of the signs and symptoms of acute coronary syndrome as patients rely on health care professionals to make the distinction from other causes of chest pain.

Unstable angina deals with blood flow obstacles causing a lack of perfusion to the myocardium. Initial perfusion starts directly from the heart into the aorta and subsequently into the coronary arteries which supply their respective portions of the heart.

The mainstay of treatment focuses on improving perfusion of the coronary arteries. This is done in several ways. Patients are often treated with aspirin for its antiplatelet therapies, 162 to 325 mg orally, or 300 mg rectally if the patient is unable to swallow.

Nitroglycerin comes in several forms (intravenous, sublingual, transdermal, orally) and improves perfusion by vasodilation of the coronaries allowing improved flow and improved blood pressure. This will decrease the amount of work the heart has to perform, which decreases the energy demand of the heart.

Supplemental oxygen should be given as well via nasal cannula to maintain appropriate oxygen saturation.

• Introduction

Unstable angina falls along a spectrum under the umbrella term acute coronary syndrome. This public health issue that daily affects a large portion of the population remains the leading cause of death worldwide. Distinguishing between this and other causes of chest pain that include stable angina is important regarding treatment and disposition of the patient. Providers should be aware of the signs and symptoms of acute coronary syndrome as patients rely on health care professionals to make the distinction from other causes of chest pain. Often patients will present to the emergency room. However, acute coronary syndrome can be seen in the outpatient setting as well. Over the years, a significant amount of research has gone into determining the appropriate and most effective treatment modalities, as well as the diagnostic tools available, in evaluating unstable angina and the other variants of acute coronary syndrome.  [1] , [2] , [3]

• Nursing Diagnosis
• Short of breath
• Palpitations

Coronary atherosclerotic disease is the underlying cause of unstable angina in nearly all patients with acute myocardial ischemia. The most common cause of unstable angina is due to coronary artery narrowing due to a thrombus that develops on a disrupted atherosclerotic plaque and is nonocclusive.

A less common cause is vasospasm of a coronary artery (variant Prinzmetal angina). Endothelial or vascular smooth dysfunction causes this vasospasm. [4]

• Risk Factors

Coronary artery disease affects a large portion of the population. It is estimated that coronary artery disease causes more than a third of deaths in people over the age of 35. It is the leading cause of death in this particular age group. Roughly 18 million within the United States alone are estimated to be affected by this disease. The incidence is higher in men, but as individuals surpass the age of 75, the incidence of males and females becomes much closer. Other risk factors include obesity, diabetes, hypertension, high cholesterol, smoking history, cocaine or amphetamine abuse, family history, chronic kidney disease, HIV, autoimmune disorders, and anemia. [5]

Patients will often present with chest pain, shortness of breath. The chest pain will often be described as pressure-like, although it is not necessarily limited to this description. Tightness, burning, sharp type of pain can be described. Often patients will report discomfort as opposed to actual pain. The pain will often radiate to the jaw or arms, both left and right sides can be affected. Constitutional symptoms such as nausea, vomiting, diaphoresis, dizziness, and palpitations may also be present. Exertion may worsen pain and rest can ease the pain.  Nitroglycerin and aspirin administration may also improve the pain.  One distinguishing factor of unstable angina is that the pain may not completely resolve with these reported relieving factors. Also, many patients will have already have coronary artery disease. This may be either established coronary artery disease or symptoms they have been experiencing for some time. These patients may have familiarity with the symptoms and may report an increase in episodes of chest pain that takes longer to resolve and an increase in the severity of symptoms. These symptoms indicate unstable angina as the more likely diagnosis, as opposed to stable angina or other causes of chest pain. This is important to note as these difference may indicate impending myocardial infarction, and ST-elevation myocardial infarction (STEMI) and should be evaluated expeditiously as the risk of morbidity and mortality are higher in this scenario versus stable angina. The exam will likely be normal, although the patient may be clutching at their chest, sweating, have labored breathing, their heart sounds may be tachycardic, and rales may be heard due to pulmonary edema.

When a patient presents, he or she should be evaluated quickly.  The patient should have an ECG to evaluate for ischemic signs or possible STEMI. The ECG in unstable angina may show hyperacute T-wave, flattening of the T-waves, inverted T-waves, an ST depression. ST elevations indicate STEMI and these patients should be treated with percutaneous coronary intervention or thrombolytics while they wait on the availability of a catheterization lab. Any number of arrhythmias may be present in acute coronary syndrome including junctional rhythms, sinus tachycardia, ventricular tachycardia, ventricular fibrillation, left bundle branch block, and others. However, most commonly, the patient will be in sinus rhythm, especially in the scenario of unstable angina as opposed to infarcted tissue. The patient should also have lab work that includes a complete blood count evaluating for anemia, platelet count, and basic metabolic profile evaluating for electrolyte abnormalities. A troponin test should be performed to determine if any of the myocardium has infarcted. A pro-brain natriuretic peptide (Pro-BNP) can also be checked, as an elevated level is associated with higher mortality. Coagulation studies may be appropriate if the patient will be anticoagulated or anticoagulation is anticipated. Often, a chest x-ray will show the heart size and the size of the mediastinum so the physician may screen for dissection and other explanations of chest pain. It should be stated here that the history should be screened for other emergent causes of chest pain, shortness of breath, pulmonary embolism, aortic dissection, esophageal rupture, pneumonia, and pneumothorax. The patient should be kept on a cardiac monitor to evaluate for any rhythm changes. Further testing may include any number of cardiac stress tests (walking treadmill stress test, stress echocardiogram, myocardial perfusion imaging, cardiac CT/MRI, or the gold standard, cardiac catheterization). These are typically ordered and performed by inpatient providers and primary care providers, but with observation medicine growing, emergency medicine providers may order these.  [6] , [7]

• Medical Management

The mainstay of treatment focuses on improving perfusion of the coronary arteries. This is done in several ways. Patients are often treated with aspirin for its antiplatelet therapies, 162 to 325 mg orally, or 300 mg rectally if the patient is unable to swallow. Nitroglycerin comes in several forms (intravenous, sublingual, transdermal, orally) and improves perfusion by vasodilation of the coronaries allowing improved flow and improved blood pressure. This will decrease the amount of work the heart has to perform, which decreases the energy demand of the heart. Supplemental oxygen should be given as well via nasal cannula to maintain appropriate oxygen saturation. These 3 actions are the quickest and most important functions to be performed in evaluating and treating for unstable angina. In patients with continued pain or longer recovery time, the patient's response should be evaluated because they are at much higher risk for myocardial infarction. Other potential therapies include anticoagulation with either low or high molecular weight heparin. Beta-blockers also can decrease the energy demand by decreasing blood pressure and heart rate.  [1] , [8] , [9]

• Nursing Management
• Manage chest pain
• Provide oxygen
• Administer aspirin and nitroglycerin
• Place patient with head of the bed elevated at 45 degrees
• Make patient comfortable
• Hook up to monitor
• Check vitals
• Check labs for troponin
• When To Seek Help
• Hypotension
• Unrelenting chest pain
• Arrhythmias
• Fast heart rate
• Altered mental status
• Declining urine output
• Outcome Identification
• No chest pain
• Stable vital signs
• Pain intensity
• Pulse oximetry
• Cardiac enzymes
• Respiration
• Listen to the chest for rales
• Coordination of Care

Unstable angina is a very common disorder that is seen in the emergency room. There are many recommendations on the management of this serious cardiac disorder. Current recommendations are that this disorder should be managed by an interprofessional team that includes primary health care providers, nurse practitioners, physician assistants, pharmacists, cardiologists and emergency room physicians. In addition, a consult from a cardiac surgeon is highly recommended. Both the American College of Cardiology and American Heart Foundation have issued guidelines on the management of unstable angina [10] (Level V). Today most hospitals have healthcare teams that specialize in the management of unstable angina. The members of this team need to be familiar with the latest guidelines and support patients with education on the reduction of risk factors and the benefits of compliance with medications.

Ample evidence exists that quality improvement programs have the lowest morbidity and best outcomes. [11] (Level ll)

• Health Teaching and Health Promotion

The goals of prevention are to enable the patient to resume all daily living activities, preserve myocardial function and prevent future cardiac events. Today, most cardiac centers have specialized teams like cardiac rehab that offer intensive and more effective counseling.

Smoking cessation is mandatory to prevent recurrent cardiac events. This applies to everyone in the household Lipid-lowering should try and obtain a target LDL-C level of 70 mg/dl or lower, an HDL level of at least 35 mg/dl, and a triglyceride level of less than 200 mg/dl.

The patient should exercise and eat a low-fat diet.

Control of Hypertension

The target blood pressure should be below 140/90 mm Hg, at the same time the patient should decrease the intake of sodium and alcohol

Diabetes Mellitus Management

Blood sugar levels may be decreased with diet, exercise or pharmacotherapy.

Weight Management and Nutritional Counseling

The patient should be encouraged to lose weight and achieve a body mass index (BMI) of 25 kg/m

Activity Management

Patients at risk for unstable angina should avoid intense physical activity, especially in cold weather.

• Discharge Planning
• Discontinue smoking
• Maintain a healthy weight
• Exercise regularly
• Control blood pressure and blood glucose
• Lower lipids
• Take medication as prescribed
• Evidence-Based Issues
• Aspirin should be given within 30 minutes to reperfuse the heart
• NTG can open up blood vessels
• Statins can lower lipids and reduce risk of unstable angina
• Pearls and Other issues

Legally, unstable angina and other variants of acute coronary syndrome constitute a large portion of cases brought against providers. Aggressive evaluations of chest pain, in general, have led to over-testing, high admission rates, and often false positives resulting in inappropriate testing. Over the years, several rules have been developed to limit inappropriate admissions and testing. Several of these have variable sensitivity and specificity. With the number of legal cases that are brought on, physicians are often still somewhat aggressive in the management and treatment of chest pain involving potential acute coronary syndrome.

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Types of Angina in the Coronary Artery. The illustration depicts stable angina, unstable angina, and variant angina. Contributed by C Rowe

Disclosure: Amandeep Goyal declares no relevant financial relationships with ineligible companies.

Disclosure: Roman Zeltser declares no relevant financial relationships with ineligible companies.

Disclosure: Anya Gunn declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

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Acute Coronary Syndromes

Chris nickson.

• Mar 4, 2021
• Coronary artery disease accounts for > 30% of death in West and presents acutely as acute coronary syndromes
• Acute coronary syndrome (ACS) is a catch all term that refers to ischemic symptoms resulting from acute coronary occlusion
• All patients who present with a suspected acute coronary syndrome must be assessed in the ED on an urgent (category 2) basis and have an ECG performed within 10 minutes of first acute clinical contact
• A clinician with ECG expertise should review the ECG
• A “CODE STEMI” activation system should be in place in any hospital that has an acute percutaneous coronary intervention service

DEFINITIONS

STEMI (S-T Segment Elevation Myocardial Infarction)

• presentation with clinical symptoms consistent with an acute coronary syndrome together with S-T segment elevation on ECG
• New LBBB may be included in this sub-heading as the treatment approach is similar to STEMI

NSTEACS (non S-T Segment elevation acute coronary syndrome)

• NSTEACS refers to any acute coronary syndrome which does not show S-T segment elevation
• The ECG may show S-T segment depression or transient S-T segment elevation, but often will be normal

Non-STEMI (Non S-T Segment Elevation Myocardial Infarction)

• By definition this will be shown by an elevation of serum troponin levels in the absence of S-T segment elevation

Unstable Angina

• A small but still significant proportion (< 4 %) of patients presenting with possible cardiac chest pain in whom biomarkers and ECGs are normal will have unstable angina due to underlying coronary artery disease
• Note that “unstable angina” is measured against a patient’s usual pattern of “stable angina” which is most commonly classified according to the New York Heart Association’s Functional Classification of Angina
• New onset angina should be considered unstable in the first instance

RISK FACTORS FOR CORONARY ARTERY DISEASE

Risk factors (these are of little diagnostic use in the acute setting):

• diabetes mellitus
• hypertension
• family history
• previous MI
• hormone replacement for menopause

UNIVERSAL CLASSIFICATION OF MYOCARDIAL INFARCTION

• Spontaneous MI
• Spontaneous myocardial infarction related to atherosclerotic plaque rupture, ulceration, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis.
• MI secondary to ischaemic imbalance
• Myocardial injury with necrosis where a condition other than CAD contributes to an imbalance between myocardial oxygen supply and/or demand, e.g. coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachy-/brady-arrhythmias, anemia, respiratory failure, hypotension, and hypertension with or without LVH
• MI resulting in death when biomarker values are unavailable
• Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic ECG changes or new LBBB, but death occurring before blood samples could be obtained, before cardiac biomarker could rise, or in cases cardiac biomarkers were not collected
• MI related to PCI (there are complex specific criteria)
• MI related to stent thrombosis (there are complex specific criteria)
• MI related to CABG MI related to CABG (there are complex specific criteria)

NEW YORK HEART ASSOCIATION FUNCTIONAL CLASSIFICATION OF ANGINA

• Patients with cardiac disease but without resulting limitation of physical activity.
• Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain.
• Patients with cardiac disease resulting in slight limitation of physical activity.
• They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.
• Patients with cardiac disease resulting in marked limitation of physical activity.
• They are comfortable at rest. Less than ordinary activity causes fatigue, palpitation, dyspnea, or anginal pain.
• Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort.
• Symptoms of heart failure or the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.

RISK STRATIFICATION OF PATIENTS WITH CONFIRMED ACS

Very High Risk

• Heart failure/ cardiogenic shock
• Mechanical complications of myocardial infarction
• Life-threatening arrhythmias or cardiac arrest
• Intermittent ST segment elevation
• de Winter T wave changes
• Wellens syndrome (or LMCA syndrome)
• Widespread ST elevation in two or more coronary territories
• Rise and/or fall in troponin level consistent with myocardial infarction
• Dynamic episode of ST segment and/or T wave changes with or without symptoms
• GRACE score >140

Intermediate Risk

• Diabetes mellitus
• Renal insufficiency (glomerular filtration rate < 60mL/min/1.73m2)
• Left ventricular ejection fraction ≤ 40 %
• Percutaneous coronary intervention
• Coronary artery bypass grafting
• GRACE score >109 and <140
• no recurrent symptoms
• no risk criteria (as listed above)

CLINICAL ASSESSMENT OF ACUTE CORONARY SYNDROME

An ECG should be performed as soon as possible in a patient with a presentation consistent with ACS

• If a diagnosis of STEMI or new LBBB is made on ECG a brief and directed history and examination is needed to determine the best reperfusion strategy
• If STEMI or new LBBB is ruled out and the patient has possible NSTEACS, risk stratification assessment into high, intermediate or low risk for an adverse event is performed.
• When did the pain commence?
• Establish the nature of pain and its duration
• ACS may present as a ‘chest pain’ surrogate (e.g. shortness of breath, lethargy); especially in elderly females
• previous coronary interventions or investigations? (e.g. thrombolysis, stent or CABG)
• comorbidities (especially contra-indications to thrombolysis)
• Warfarin, antiplatelet agents or NOACs
• Has an aspirin or other anti-platelet agent already been taken?
• sildenafil (GTN may have an excessive effect if used)
• allergies (especially aspirin)

Examination

• generally unhelpful in establishing the diagnosis of ACS
• Assess any immediate ABC issues
• Vital signs (blood pressure is especially important with respect to the decision to thrombolyse
• Degree of patient anxiety/ distress
• Look for any evidence of heart failure or (e.g. S3/S4, APO, edema, distended tender liver)
• Look for any evidence of cardiogenic shock (altered mental state, poor skin perfusion +/- hypotension)

Clinical Risk Stratification for ACS in Patients Presenting with Chest Pain (i.e. possible not confirmed NSTEACS)

• S-T segment depression ≥ 0.5 mm
• New T wave inversion ≥ 2.0 mm in more than 2 contiguous leads
• Transient S-T segment elevation ≥ 0.5 mm in more than 2 contiguous leads
• ECG changes consistent with critical coronary artery stenosis, e.g. Wellens Syndrome or LMCA stenosis syndrome.
• Systolic blood pressure ≤ 90 mmHg
• Signs of poor peripheral perfusion
• Signs of cardiac failure or frank pulmonary edema, (ie Killip class > 1)
• New onset of mitral regurgitation
• Ongoing pain, or recurrent episodes of pain despite initial treatment whilst in the ED
• Arrhythmias requiring treatment such as sustained ventricular tachycardia
• Diaphoresis
• Elevated serum troponin
• Left ventricular systolic dysfunction (ejection fraction < 0.4)
• Past PCI or CAGS
• Past myocardial infarction
• those presenting with clinical symptoms consistent with ACS but do not have high risk or low risk criteria
• Age < 40 years
• Symptoms that are atypical for angina
• Remain symptom free
• Absence of known CAD
• Normal troponin levels
• Normal ECG (including no transient changes)

Assessment of bleeding risk

• The routine use of a validated risk stratification tool, such as the CRUSADE Score, for bleeding events assists with individual patient clinical decision making
• The CRUSADE Score is available on MDCALC [ CRUSADE Score for Post-MI Bleeding Risk ]
• Systolic Blood Pressure
• Creatinine Clearance
• Signs of CHF at Presentation
• History of Vascular Disease
• History of Diabetes Mellitus

INVESTIGATIONS

• UEC/ glucose (especially K)
• Normal levels are considered vary according to the exact assay that is being used
• In general terms a normal level is considered to be < 99th percentile for the assay
• may persist for 5-14 days post infarction
• Reinfarction can also be assessed via troponin levels (CK/CKMB is now obsolete and not required)
• For the vast majority of patients being investigated for possible MI, a rising pattern is suggestive of the diagnosis of MI
• In patients who present late following MI, troponin elevations may have already peaked and in this context, a falling troponin pattern is significant
• Note that all troponin assays, regardless of their detection sensitivity do not rule out unstable angina or stable coronary ischemia
• Clinical management decisions should not be based solely on troponin levels, but on thorough investigation and risk assessment that includes detailed clinical assessment, observation, repeated ECG tests, and where available functional testing
• Note that some patients that fit specific low risk stratification criteria may be suitable for validated accelerated diagnostic pathways.
• All patients who present with a suspected ACS must have an ECG within 10 minutes of first acute clinical contact
• The immediate decision pathway then involves the ECG stratification of STEMI, from NSTEACS
• ≥ 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
• ≥ 1.5 mm ST elevation in V2-3 in women
• ≥ 1 mm ST elevation in other leads
• New LBBB (LBBB should be considered new unless there is evidence otherwise)
• may be normal
• peaked T waves with ST elevation
• gradual loss of R wave
• development of pathological Q wave and TWI
• Anteroseptal = LAD
• Anterolateral = Cx
• Inferior = RCA
• Posterior = Cx or PDA (off RCA)
• Comparison with old ECGs will be useful
• ≥ 1 lead with ≥1 mm of concordant ST elevation
• ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression
• ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave.
• In cases of LBBB urgent echocardiography may be useful, if readily available, to detect wall motion abnormalities (suggesting myocardial ischaemia) and hence assist in decision making
• This should not be allowed to delay any treatment measures, especially reperfusion therapies.
• If an x-ray is done this should be in the Resus bay, except for stable low risk patients who may be suitable to leave the department for their x-ray, this will need to be judged on a case by case basis.
• Look for cardiomegaly, cardiac failure and differentials of chest pain (e.g. PE, pneumonia, pneumothorax, esophageal rupture, aortic dissection)

Echocardiography (not a routine test in ACS, but may be considered on an urgent basis in selected cases)

• Confirmation of wall motion abnormalities when the diagnosis of ACS is unclear (pericarditis or myocarditis is being considered for example or in cases of LBBB)
• Cardiogenic shock
• Inferior infarction where evidence of right ventricular infarction is being sort
• If secondary complications are suspected, such as cardiac tamponade or valvular disruption

Coronary Angiography

• This is the definitive investigation for any patient with a STEMI who is to undergo a PCI
• Patients with high or very high risk NSTEACS should be referred to cardiology urgently for consideration of a urgent coronary angiogram.
• STEMI management
• NSTEACS management

COMPLICATIONS OF ACUTE CORONARY SYNDROMES

• cardiac failure
• post-infarction ischaemia
• therapy: pericardiocentesis and repair
• therapy: IABP, inotropes, surgery
• therapy: afterload reduction, IABP, inotropes, surgery ASAP
• therapy: IV fluids, inotropes, AV synchrony, IABP, reperfusion
• therapy: correct hypoxia, acidosis, hypovolaemia, K+, Mg2+ (controversial)
• therapy: must get revascularisation (PCI or CABG) within 24 hours
• therapy: mural thrombus -> anticoagulate
• pericarditis and Dressler’s syndrome
• complications of therapy, e.g. haemorrhage, coronary artery dissection, stent thrombosis, surgical complications

References and Links

• Cardiac biomarkers (CCC)
• Buttner R. OMI: Replacing the STEMI misnomer . LITFL 2021

Journal articles

• Chew DP, Scott IA, Cullen L, et al. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Australian clinical guidelines for the management of acute coronary syndromes 2016 . The Medical journal of Australia. 205(3):128-33. 2016
• Chew DP, Scott IA, Cullen L, et al. National Heart Foundation of Australia & Cardiac Society of Australia and New Zealand: Australian Clinical Guidelines for the Management of Acute Coronary Syndromes 2016. Heart, lung & circulation. 25(9):895-951. 2016. [ pubmed ] [ free full text ]
• Delewi R, Zijlstra F, Piek JJ. Left ventricular thrombus formation after acute myocardial infarction. Heart. 2012 Dec;98(23):1743-9. doi: 10.1136/heartjnl-2012-301962. Review. PubMed PMID: 23151669 ; PubMed Central PMCID: PMC3505867 .
• Thygesen K, Alpert JS, Jaffe AS. Third universal definition of myocardial infarction. Circulation. 126(16):2020-35. 2012. [ pubmed ]

FOAM and web resources

• StEmlyns — New STEMI Guidelines (2013)

Critical Care

Chris is an Intensivist and ECMO specialist at the  Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University . He is a co-founder of the  Australia and New Zealand Clinician Educator Network  (ANZCEN) and is the Lead for the  ANZCEN Clinician Educator Incubator  programme. He is on the Board of Directors for the  Intensive Care Foundation  and is a First Part Examiner for the  College of Intensive Care Medicine . He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website,  INTENSIVE .  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the  FOAM  movement (Free Open-Access Medical education) and is co-creator of  litfl.com , the  RAGE podcast , the  Resuscitology  course, and the  SMACC  conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is  @precordialthump .

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JOHN R. MCCONAGHY, MD, MALVIKA SHARMA, MD, AND HITEN PATEL, MD

Am Fam Physician. 2020;102(12):721-727

Related letter: Previous ECG Criteria (Including STEMI Criteria) Overlook Too Many Acute MIs Due to Acute Coronary Occlusion

Author disclosure: No relevant financial affiliations.

Approximately 1% of primary care office visits are for chest pain, and 2% to 4% of these patients will have unstable angina or myocardial infarction. Initial evaluation is based on determining whether the patient needs to be referred to a higher level of care to rule out acute coronary syndrome (ACS). A combination of age, sex, and type of chest pain can predict the likelihood of coronary artery disease as the cause of chest pain. The Marburg Heart Score and the INTERCHEST clinical decision rule can also help estimate ACS risk. Twelve-lead electrocardiography is recommended to look for ST segment changes, new-onset left bundle branch block, presence of Q waves, and new T-wave inversions. Patients with suspicion of ACS or changes on electrocardiography should be transported immediately to the emergency department. Those at low or intermediate risk of ACS can undergo exercise stress testing, coronary computed tomography angiography, or cardiac magnetic resonance imaging. In those with low suspicion for ACS, consider other diagnoses such as chest wall pain or costochondritis, gastroesophageal reflux disease, and panic disorder or anxiety states. Other less common, but important, diagnostic considerations include acute pericarditis, pneumonia, heart failure, pulmonary embolism, and acute thoracic aortic dissection.

Approximately 1% of all ambulatory visits in primary care settings are for chest pain. 1 Cardiac disease is the leading cause of death in the United States, yet only 2% to 4% of patients presenting to a primary care office with chest pain will have unstable angina or an acute myocardial infarction. 2 – 4 The most common causes of chest pain in the primary care population are chest wall pain (20% to 50%), reflux esophagitis (10% to 20%), and costochondritis (13%). 2 Other potential factors include pulmonary etiologies (pneumonia, pulmonary embolism [PE]), psychological etiologies (panic disorder), and nonischemic cardiovascular disorders (congestive heart failure, thoracic aortic dissection). 2 , 3 , 5 , 6 No definitive diagnosis may be found in as many as 15% of patients. 2 Differentiating ischemic from nonischemic causes is often challenging because patients with ischemic chest pain may appear well. As such, the initial diagnostic approach should always consider a cardiac etiology for the chest pain unless other causes are apparent. 7

Initial Evaluation

The first decision point for most physicians is to determine whether the patient needs immediate referral to the emergency department for further testing to determine whether the chest pain is an acute coronary syndrome (ACS) caused by coronary ischemia. 7 ACS is a clinical diagnosis that includes unstable angina, ST segment elevation myocardial infarction, and non–ST segment elevation myocardial infarction. Definitions of chest pain have evolved over time. Typical chest pain or angina is a deep, poorly localized chest or arm discomfort (pain or pressure) associated with physical exertion or emotional stress and relieved with rest or sublingual nitroglycerin within five minutes. 8 Unstable angina is new-onset angina, angina at rest, or angina that becomes more frequent, severe, or prolonged. 9 Acute myocardial infarction is myocardial injury resulting in elevated cardiac biomarkers in the setting of acute ischemia caused by ST segment elevation myocardial infarction or non–ST segment elevation myocardial infarction. 10 The impression of chest pain is often determined by a combination of clinical symptoms at the time of presentation, physical examination, initial electrocardiography (ECG), and risk factors for ACS. 11 Patients often do not use the term pain to describe their symptoms but frequently use other terms such as pressure, aching, discomfort, tightness, squeezing, or indigestion. 12

A meta-analysis of studies that evaluated the role of previous chest pain in diagnosing ACS concluded that chest pain that is pleuritic, positional, or reproducible with palpation and not related to exertion is low risk for ACS. Pain that is described as pressure (similar to that of prior myocardial infarction), worse than prior anginal pain, associated with exertion, accompanied by nausea or diaphoresis, and/or radiates to one or both arms/shoulders is higher risk for ACS. 13

Although individual characteristics generally do not support or rule out a diagnosis, a combination of these may increase diagnostic accuracy. 14 The combination of age, sex, and type of chest pain can predict the likelihood of coronary artery disease (CAD) as the cause of chest pain. 15 Table 1 outlines updated predicted pretest probabilities of CAD in patients with chest pain based on these three factors. 15 U.S. guidelines recommend that patients with a probability of less than 5% be classified as low risk and not undergo further testing. 16 Those with a probability greater than 70% should undergo invasive angiography, and those with a probability of 5% to 70% should undergo noninvasive testing. 16 European guidelines use cutoffs of 15% and 85%, respectively. 15

Validated clinical decision rules can help determine whether chest pain is caused by CAD. One systematic review found that the validated Marburg Heart Score is better than clinical judgment alone for predicting whether chest pain is cardiac in origin. 17 , 18 Table 2 outlines the scoring for this clinical rule and presents the probability of CAD as the cause of chest pain for pretest probabilities of 2%, 10%, and 20%. 18

The INTERCHEST clinical decision rule is a second validated decision rule that can predict the presence or absence of CAD in patients who present with chest pain in the primary care setting  ( Table 3 ) . 19 , 20 Patients with a score of less than 2 have only a 2% chance of having CAD, whereas 43% of patients with a score of 2 or more have CAD, making the test useful for ruling out CAD as a cause of the patient's chest pain. 20

Because history alone usually cannot determine whether a patient is actively experiencing cardiac ischemia, a 12-lead ECG should be performed on all patients in whom cardiac ischemia is suspected. 21 ECG findings that increase the likelihood of ACS include ST segment elevation, new-onset left bundle branch block, presence of Q waves, or new T-wave inversions. 22 Similar ECG findings may be observed in non-ACS conditions, including acute pericarditis and left ventricular hypertrophy. Patients with suspicion of ACS based on clinical presentation (history, physical examination, risk factors) with changes seen on ECG should be transported immediately to the emergency department. 16

For patients with chest pain not requiring immediate referral who have a low to intermediate pretest probability of CAD, exercise stress testing should be considered. 23 Adding myocardial perfusion or echocardiography to the stress test increases test accuracy with a negative predictive value for acute myocardial infarction and cardiac death of 98%. 24 Evaluating with coronary computed tomography angiography (CCTA) decreases the number of nonfatal acute myocardial infarctions 25 and is moderately more accurate than stress ECG in ruling out CAD in patients with chest pain (positive likelihood ratio [LR+] = 5.62; negative likelihood ratio [LR–] = 0.05). 26 As a result, CCTA is becoming a first-line test for patients presenting with chest pain in the emergency department and should be a consideration for family physicians evaluating and managing patients with stable chest pain in the office. Cardiac magnetic resonance imaging may be useful in the evaluation of typical angina. For the evaluation of acute chest pain, cardiac magnetic resonance imaging is comparable to angiography in mortality at one year; however, it results in less need for invasive angiography and fewer subsequent revascularization procedures. 27 Cost is a barrier to the use of CCTA and cardiac magnetic resonance imaging. According to Healthcare Bluebook, the cost of an exercise stress test is $171, whereas the price of CCTA is $667 and cardiac magnetic resonance imaging angiography is $1,075. 28 Consideration should also be given to the harms of radiation and contrast exposure from CCTA.

Other Diagnostic Considerations

If the initial evaluation indicates that ACS is less likely or the diagnostic evaluation for ACS in higher-risk patients is negative, other non-ACS conditions that may cause symptoms similar to coronary ischemia should be considered ( Table 4 ) . Understanding the presentation of these common conditions with the clinical impression will help lead to a correct diagnosis.

CHEST WALL PAIN

Chest wall pain is the most common cause of chest pain in the outpatient setting, accounting for 33% to 50% of chest pain. 29 One prospective cohort study identified four clinical factors that predict a final diagnosis of chest wall pain in patients presenting to the primary care office with chest pain: localized muscle tension, stinging pain, pain reproducible by palpation, and the absence of a cough. In a study population with a prevalence of chest wall pain of 47%, patients with at least two of these findings had a 77% likelihood of chest wall pain as the cause of their discomfort (LR+ = 3.02), and those with none or one of the findings had only an 18% likelihood (LR− = 0.47). 29

COSTOCHONDRITIS

Often considered a subset of chest wall pain, costochondritis is a self-limited condition characterized by pain that is reproducible with palpation in the parasternal costochondral joints. Costochondritis is a clinical diagnosis and does not require specific diagnostic testing in the absence of concomitant cardiopulmonary symptoms or risk factors. 30

GASTROESOPHAGEAL REFLUX DISEASE

Classic symptoms of gastroesophageal reflux disease (GERD) include a burning retrosternal pain, acid regurgitation, and a sour or bitter taste in the mouth. 31 , 32 There are no useful physical examination maneuvers or standard tests to establish the diagnosis or to support or rule it out. A one-week trial of a high-dose proton pump inhibitor is modestly sensitive and specific for GERD, with a 50% reduction in reflux symptoms being moderately accurate for a final diagnosis of GERD (LR+ = 5.5; LR− = 0.24). 33 ACS symptoms can often be mistaken for those of GERD; if clinical suspicion is high for ACS, an ECG should be obtained.

Panic Disorder and Anxiety State

Panic disorder and anxiety states are common. One in four people with a panic attack will have chest pain and shortness of breath. 34 Yet, concomitant panic disorder and chest pain are often not recognized, leading to more testing, follow-up, and higher costs of care. 34 A moderately accurate assessment for detecting panic disorder is had by asking the following validated screening question: “In the past four weeks, have you had an anxiety attack (suddenly feeling fear or panic)?” This question is good at supporting a diagnosis of panic disorder when patients answer yes (LR+ = 4.2) and is good at ruling it out when the answer is no (LR− = 0.09). 35

Less Common, but Important, Diagnostic Considerations

Pericarditis.

Pericarditis manifests as a clinical triad of pleuritic chest pain, a pericardial friction rub, and diffuse ECG ST–T-wave changes often preceded by a viral illness. 36 Acute pericarditis should be considered in patients presenting with new-onset chest pain that increases with inspiration or when reclining and is lessened by leaning forward. 36 ECG usually demonstrates diffuse ST segment elevation and PR interval depression.

Common symptoms of pneumonia include fever, chills, productive cough, and pleuritic chest pain. 37 Egophony (LR+ = 8.6), dullness to percussion of the posterior thorax (LR+ = 4.3), and respiratory rate greater than 20 breaths per minute (LR+ = 3.5) are suggestive of pneumonia. 38 Normal temperature, heart rate, and respiratory rate with a normal pulmonary examination rules out pneumonia (LR− = 0.10). 39 Chest radiography can assist in the diagnosis of pneumonia; however, a Cochrane review suggests that routine chest radiography does not affect outcomes in patients who present with signs of lower respiratory tract infection. 40

HEART FAILURE

Most patients with heart failure present with dyspnea on exertion, although some will present with chest pain. 41 Clinical impression is predictive of heart failure (LR+ = 9.9; LR− = 0.65), as is pulmonary edema on chest radiography (LR+ = 11.0). 41 Patients with acute dyspnea and one or more of the MICE criteria (Male sex, history of myocardial Infarction, basal lung Crepitations, and ankle Edema) likely have heart failure and should be evaluated with echocardiography. 42 , 43

PULMONARY EMBOLISM

Diagnosing PE in the office is challenging because its presentation is highly variable. Although dyspnea, tachycardia, and/or chest pain are present in 97% of those diagnosed with PE, no single clinical feature effectively supports or rules out its diagnosis. 44 Risk of PE can be estimated by using a validated clinical decision rule, such as the Wells criteria ( Table 5 ) . 45 Patients at moderate or higher risk should undergo additional testing with a d-dimer assay, ventilation-perfusion scan, or helical computed tomography of the pulmonary arteries. 45 The Pulmonary Embolism Rule-out Criteria were developed to specifically rule out PE in the primary care setting. 46 Patients meeting all eight criteria (50 years or younger, heart rate less than 100 beats per minute, oxygen saturation greater than 94%, no unilateral leg swelling, no hemoptysis, no surgery or trauma within four weeks, no previous deep venous thrombosis or PE, no oral hormone use) have a less than 1% likelihood of PE and thus do not need d-dimer testing or imaging. 46 , 47

ACUTE THORACIC AORTIC DISSECTION

Patients with acute thoracic aortic dissection may present with chest or back pain. 48 History and physical examination are only modestly useful for supporting or ruling out the diagnosis; acute chest or back pain and a pulse differential in the upper extremities modestly increases the likelihood of an acute thoracic aortic dissection (LR+ = 5.3). 49 Clinical suspicion for thoracic dissection warrants immediate referral to the emergency department.

This article updates previous articles on this topic by McConaghy and Oza 50 and Cayley . 51

Data Sources: A PubMed search was completed using the key terms chest pain, chest pain evaluation, diagnosis, clinical decision rule, differential diagnosis, acute coronary syndrome, and angina. The search included meta-analyses, reviews, randomized controlled trials, point-of-care guides, and clinical trials. We also searched the Cochrane Database of Systematic Reviews, the National Guideline Clearinghouse, Essential Evidence Plus, Database of Abstracts of Reviews of Effects, and Agency for Healthcare Research and Quality Evidence Reports. Search date: literature search was completed on several occasions; last date was October 11, 2020.

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Acute Coronary Syndrome (ACS)

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Introduction

Chest pain is a common presentation, and the diagnosis of acute coronary syndrome  is frequently suspected. Acute coronary syndrome (ACS) encompasses a variety of diagnoses and can be subcategorised into:

• ST-elevation ACS : ST-elevation myocardial infarction (STEMI)
• Non-ST elevation ACS : Non-ST elevation myocardial infarction (NSTEMI) and unstable angina

Two of the three diagnoses that exist under the umbrella of ACS are types of myocardial infarction ( STEMI and NSTEMI ). 

Definition of myocardial infarction (MI)

The European Society of Cardiology’s definition of MI is as follows…

Detection of a rise and/or fall in cardiac biomarker values (preferably troponin ) with at least one value above the 99 th percentile (upper reference limit) with at least one of the following :

• Symptoms of ischaemia (the patient’s history and clinical presentation and the history are vital to guide your interpretation of the tests you are about to perform)
• New or presumed new significant ST segment or T wave changes or new left bundle branch block (LBBB)
• Pathological Q wave changes on the ECG
• Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
• Identification of an intracoronary thrombus by angiography

A ‘new left bundle branch block’ does not mean ‘a left bundle branch block that has just been found because the patient has never had an ECG before’. Nor does it mean ‘a left bundle branch block that is present now but was not present on an ECG in 2006’.

A new LBBB due to ischaemia is the result of an occluded proximal left anterior descending (LAD) or left main stem artery . A large amount of myocardium and conductive tissue needs to be affected to cause this ECG appearance and these patients are usually acutely unwell.

Development of Q waves on the ECG

The Q wave reflects septal depolarisation . This is usually hidden behind the much more forceful and electrically active ventricular wall depolarisation . If the ventricular wall is dead, a ‘window’ is created that allows the septal depolarisation to show up on the surface ECG.

Imaging evidence of new regional wall abnormality

The sequence of changes and signs of ischaemia (the ischaemic cascade) on various tests is shown in Figure 1.

A troponin level is only a number. It is only relevant when applied in the context of other clinical findings.

There are many causes of a raised troponin, including: 1

• Myocardial infarction
• Tachy/bradyarrhythmias
• Aortic dissection
• Severe aortic valve disease
• Hypertrophic cardiomyopathy
• Severe respiratory failure
• Severe anaemia
• Coronary spasm
• Heart failure
• Takotsubo cardiomyopathy
• Renal failure
• Subarachnoid haemorrhage

Classification of myocardial infarctions

Type 1: spontaneous myocardial infarction.

This is your ‘typical’ myocardial infarction. Atherosclerosis originates from damage to the endothelium and a build-up of cholesterol.

The inflammatory reaction to atherosclerosis by macrophages causes a plaque of foam cells, lipids, cellular debris and (eventually) calcium to build up with a fibrous cap on top.

When this cap cracks, the exposed debris triggers thrombus formation in the confines of the affected coronary artery (which are only typically between 2 and 5mm in diameter), causing partial or total occlusion of the artery.

Type 2: myocardial infarction secondary to ischaemia

A type 2 myocardial infarction is a common event in hospitals where patients with stable coronary artery disease +/- previous coronary intervention (PCI or CABG) are unwell and put additional stress on their heart that would not normally be present.

If there is a sufficient imbalance between the supply of blood (e.g. anaemia/hypovolaemia, coronary vasospasm) and demand for blood (e.g. sepsis/hypovolaemic shock, tachyarrhythmia) then the myocardium can become ischaemic without a plaque rupture event .

Type 3 MI: post-mortem

A type 3 myocardial infarction is diagnosed post-mortem .

Type 4a MI: percutaneous coronary intervention

This is related to percutaneous coronary intervention (i.e. caused by an angioplasty procedure blocking a side branch or damaging the main coronary artery causing ischaemia)

Type 4b MI: stent thrombosis

This is related to stent thrombosis . If patients stop anti-platelets early post-angioplasty or continue to smoke, stents can occlude (this usually results in a STEMI if complete sudden thrombosis or NSTEMI if gradual re-stenosis over time).

Type 5 MI: bypass

Type 5 myocardial infarction is related to a bypass graft (CABG) operation.

Clinical features

The clinical features of ACS are similar, regardless of the underlying diagnosis (e.g. NSTEMI, STEMI or unstable angina).

Typical clinical presentations of ACS include: 2

• pain in the chest and/or other areas (for example, the arms, back or jaw) lasting longer than 15 minutes
• chest pain associated with nausea and vomiting, marked sweating and breathlessness
• chest pain associated with haemodynamic instability
• new-onset chest pain, or abrupt deterioration in previously stable angina, with recurrent chest pain occurring frequently and with little or no exertion, and with episodes often lasting longer than 15 minutes.

For more information, see the Geeky Medics guide to a chest pain history .

When ACS is suspected, initial management should be commenced as soon as possible: 2

• Resting 12-lead ECG
• Oxygen: only if low SpO 2
• Nitrates (e.g. glyceryl trinitrate)
• Aspirin (300 mg) and a second rapid-acting antiplatelet such as Ticagrelor or Prasugrel

For more information, see the Geeky Medics guide to the emergency management of ACS .

ST-elevation ACS

St-elevation myocardial infarction (stemi).

Patients with STEMI typically present with acute chest pain and persistent (>20 minutes) ST-segment elevation .

ST elevation is a sign of complete occlusion of an epicardial coronary artery by thrombus causing immediate myocardial death relating to the territory affected:

• Anterior: V1-V4
• Inferior: II, III, aVF
• High lateral: I, aVL
• Low lateral: V5, V6
• Posterior: a dominant R wave in V1-3 with ST depression in V1-3 (the mirror image of an anterior MI)

These patients are at elevated risk of ventricular arrhythmias and myocardial damage can be minimised by rapidly opening the artery.

Management of STEMI 3

The current gold standard treatment option is primary percutaneous intervention (PCI) to allow the vessel to be opened as quickly as possible (as ‘time is muscle’).

Studies have shown that it is beneficial to delay treatment for up to 90 minutes to allow transfer to a primary PCI centre rather than resorting to thrombolysis.

There is a benefit associated with performing primary PCI up to 12 hours from the onset of pain. After that point, the OAT trial suggests that there is limited benefit in opening up the occluded artery as the damage is already done. 4

The recommended treatment used to be thrombolysis to try and break down the clot in the artery. However, this has significant bleeding risks attached to it and often failed to open the artery up requiring the patient to undergo ‘rescue angioplasty’ with higher bleeding risks associated due to the pre-medication.

Non-ST-elevation ACS

Non-st-elevation myocardial infarction (nstemi).

Non-ST elevation myocardial infarctions (NSTEMIs) are often seen as a more ‘routine’ heart attack. However, they have worse long-term outcomes than STEMIs (although a lower risk of death in the short term).

They tend to be associated with partial coronary occlusion .

Diagnosis of an NSTEMI involves a combination of, clinical assessment, serial troponin measurement and ECG analysis (see definition of MI earlier in the article). For more information, see the Geeky Medics guide to NSTEMIs . 

Management of NSTEMI 5

Initiate further medical treatment once a diagnosis of NSTEMI is confirmed (with serial troponin measurement):

• Beta blockade (or alternative rate-limiting agent if contraindicated – aim HR of 50-60 bpm)
• ACE inhibitor (unless contraindicated – aim for a systolic blood pressure of 120 mmHg or less)
• Atorvastatin 80mg OD

Once someone is diagnosed with a type I NSTEMI and commenced on appropriate medical therapy, there are various risk scores that can be calculated to assess the value of invasive angiography .

NICE recommends the use of the GRACE score  which is used to predict in-hospital and post-discharge to 6-month mortality.

Other factors that should be considered before proceeding to angiography include:

• Renal function (there is a risk of contrast nephropathy and this can leave predialysis patients permanently dependent on dialysis)
• Bleeding risk (as above)
• Can the patient lie flat? Although angiography can be performed whilst patients with severe heart failure are sat upright, it is not fun for the operator, cath lab team or the patient. In a non-urgent setting, angiography should be delayed until the patient is able to tolerate lying flat.
• Other significant co-morbidities: patients with poor quality of life and/or short life expectancy (age/dementia/malignancy) may not gain any prognostic benefit from the procedure and should be managed medically.

When to perform angiography

Unstable angina.

Stable (or ‘exertional’) angina is defined as:

• Typical cardiac pain
• Brought on by exertion and relieved by rest
• Lasting less than 20 minutes

Unstable angina is an acute coronary syndrome that is defined by the absence of biochemical evidence of myocardial damage. It is characterised by specific clinical findings of: 6

• prolonged (>20 minutes) angina at rest
• new onset of severe angina
• angina that is increasing in frequency, longer in duration, or lower in threshold
• angina that occurs after a recent episode of myocardial infarction

Diagnosis of unstable angina is based on clinical assessment. Troponin measurements will be normal as there has not been any ischaemic damage (yet) and the ECG may be normal for similar reasons.

Management of unstable angina 5

Management of unstable angina is the same as for NSTEMI discussed above.

Dr Chris Jefferies

• Third Universal Definition of Myocardial Infarction. European Heart Journal (2012) 33 , 2551 – 2567.
• Acute coronary syndromes (including myocardial infarction); NICE Quality Standard, Sept 2014. Available from: [ LINK ]
• NICE Guideline. Myocardial infarction with ST-segment elevation: acute management. Clinical guideline [CG167]. Published date:  10 July 2013. Available from: [ LINK ]
• Yousef ZR, Redwood SR, Bucknall CA, Sulke AN, Marber MS. Late intervention after anterior myocardial infarction: effects on left ventricular size, function, quality of life, and exercise tolerance: results of the Open Artery Trial (TOAT Study). J Am Coll Cardiol 2002;40:869-876
• NICE Guideline. Unstable angina and NSTEMI; NICE Clinical Guideline (March 2010 – last updated November 2013). Available from: [ LINK ]
• Roffi M, Patrono C, Collet JP, et al. 2015 ESC guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). Eur Heart J. 2016 Jan 14;37(3):267-315.

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