Overview of acute coronary syndrome

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Last reviewed: 10 Feb 2026

Last updated: 04 Mar 2026

This page compiles our content related to acute coronary syndrome. For further information on diagnosis and treatment, follow the links below to our full BMJ Best Practice topics on the relevant conditions and symptoms.

Acute coronary syndrome (ACS) refers to a spectrum of acute myocardial ischemia and/or infarction. Acute chest pain is the leading presenting symptom; all patients with chest pain require urgent evaluation. ECG should not be delayed in the patient with suspected ACS. Myocardial biomarkers, such as high-sensitivity cardiac troponins, play a complementary role in the diagnosis; subsequent/serial measurements may be needed. Other tests are indicated according to clinical context.[1]

Classically ACS has been divided into three clinical categories.[2][3] In ST-elevation myocardial infarction (STEMI) the ECG shows persistent ST-segment elevation in two or more anatomically contiguous leads. Unstable angina and non-ST-elevation myocardial infarction (NSTEMI) represent a continuum of pathology, differing mainly by the presence of markers of myocardial damage in NSTEMI.[1] Therefore some guidelines have grouped unstable angina and NSTEMI as “non-ST-elevation acute coronary syndromes”.

Strong risk factors for ACS include smoking, hypertension, diabetes mellitus, obesity and metabolic syndrome, sedentary behavior and physical inactivity, dyslipidemia, chronic kidney disease, atherosclerosis, family history of premature coronary artery disease, age >60 years, cocaine use, and depression.

Condition	Description
Unstable angina (UA)	go to our full topic on Unstable angina (UA) UA is defined as myocardial ischemia at rest or on minimal exertion in the absence of acute cardiomyocyte injury/necrosis.[1] UA is characterized by specific clinical findings of prolonged (>20 minutes) angina at rest; new onset of severe angina; angina that is increasing in frequency, longer in duration, or lower in threshold; or angina that occurs after a recent episode of myocardial infarction.[1] Myocardial biomarkers (no dynamic elevation of cardiac troponin above the 99th percentile) rule out acute myocardial infarction. T-segment depression and T-wave changes may be seen on ECG in patients with UA. Alternatively, the initial ECG may show transient ST elevation, or may be normal.[1]
Non-ST-elevation myocardial infarction (NSTEMI)	go to our full topic on Non-ST-elevation myocardial infarction (NSTEMI) NSTEMI is an acute ischemic event causing irreversible myocyte necrosis. It is usually the result of a transient or near-complete occlusion of a coronary artery or an acute factor that deprives the myocardium of oxygen. NSTEMI is differentiated from UA by a dynamic elevation of troponin above the 99th percentile.[1] Patients with NSTEMI may also be clinically unstable (e.g., low blood pressure, shock, left ventricular failure) which is not a feature of UA. The initial ECG may show ischemic changes such as ST depression, T-wave changes, or transient ST elevation; however, ECG may also be normal or show nonspecific changes.
ST-elevation myocardial infarction (STEMI)	go to our full topic on ST-elevation myocardial infarction (STEMI) STEMI is the irreversible necrosis of heart muscle, usually caused by complete atherothrombotic occlusion of a coronary artery. Persistent ST-segment elevation in two or more anatomically contiguous ECG leads is the hallmark ECG pattern. A rise in cardiac-specific troponins confirms the diagnosis. Treatment should, however, be started immediately in patients with a typical history and ECG changes, without waiting for laboratory results.[1]

Condition

Description

Unstable angina (UA)

go to our full topic on Unstable angina (UA)

UA is defined as myocardial ischemia at rest or on minimal exertion in the absence of acute cardiomyocyte injury/necrosis.[1] UA is characterized by specific clinical findings of prolonged (>20 minutes) angina at rest; new onset of severe angina; angina that is increasing in frequency, longer in duration, or lower in threshold; or angina that occurs after a recent episode of myocardial infarction.[1] Myocardial biomarkers (no dynamic elevation of cardiac troponin above the 99th percentile) rule out acute myocardial infarction. T-segment depression and T-wave changes may be seen on ECG in patients with UA. Alternatively, the initial ECG may show transient ST elevation, or may be normal.[1]

Non-ST-elevation myocardial infarction (NSTEMI)

go to our full topic on Non-ST-elevation myocardial infarction (NSTEMI)

NSTEMI is an acute ischemic event causing irreversible myocyte necrosis. It is usually the result of a transient or near-complete occlusion of a coronary artery or an acute factor that deprives the myocardium of oxygen. NSTEMI is differentiated from UA by a dynamic elevation of troponin above the 99th percentile.[1] Patients with NSTEMI may also be clinically unstable (e.g., low blood pressure, shock, left ventricular failure) which is not a feature of UA. The initial ECG may show ischemic changes such as ST depression, T-wave changes, or transient ST elevation; however, ECG may also be normal or show nonspecific changes.

ST-elevation myocardial infarction (STEMI)

go to our full topic on ST-elevation myocardial infarction (STEMI)

STEMI is the irreversible necrosis of heart muscle, usually caused by complete atherothrombotic occlusion of a coronary artery. Persistent ST-segment elevation in two or more anatomically contiguous ECG leads is the hallmark ECG pattern. A rise in cardiac-specific troponins confirms the diagnosis. Treatment should, however, be started immediately in patients with a typical history and ECG changes, without waiting for laboratory results.[1]

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