Acute coronary syndromes (ACSs) represent a spectrum of ischemic heart events that share a common pathophysiology and encompass the following entities: unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI).

ACS usually is caused by an unstable atheromatous plaque that fissures or ruptures in an epicardial coronary artery, which results in the formation of a superimposed platelet and fibrin thrombus.

Unstable plaques associated with ACS are most often lipid-rich, atheromatous lesions with a thin fibrous cap and increased macrophage infiltration, whereas stable plaques causing chronic stable angina generally possess a thick fibrous cap and less lipid core and inflammatory burden.

Most coronary artery unstable plaques leading to ACS were not flow-limiting prior to fissuring or rupture (70% of these plaques have <50% angiographic stenosis).

The differential diagnosis of chest pain encompasses multiple other conditions, some of which can be life-threatening. Aortic dissection and pulmonary embolism are particularly important to consider and diagnose in a timely manner.

When seeing patients with chest discomfort it is helpful to assign patients into one of four categories: a noncardiac diagnosis, chronic stable angina, possible ACS, and definite ACS.

The diagnosis of a STEMI can be made on the basis of electrocardiogram criteria, including ST segment elevation >1 mm in at least two contiguous leads. Reciprocal ST segment depression is an associated and helpful finding that makes the possibility of acute pericarditis mimicking acute STEMI less likely.

Serial testing of serum cardiac enzyme levels should be performed routinely in patients with a suspected ACS.

Troponins T and I are components of the cardiac myocyte contractile apparatus and are highly specific for a cardiac origin. They are also highly sensitive for the detection of myocardial necrosis and are available in rapid assay forms. Troponins begin to rise 3 hours after onset of chest pain and last longer in the circulation (7 to 14 days) than creatine kinase (CK).