Acute coronary syndromes (ACS) include:
Non-ST-elevation myocardial infarction (NSTEMI), and
Unstable angina,
ST-elevation myocardial infarction (STEMI)

Myocardial infarction occurs when cardiac myocytes die due to myocardial ischaemia, and can be diagnosed on the basis of:
appropriate clinical history,
12-lead ECG and
elevated biochemical markers - troponin I and T, creatinine-kinase-MB (CK-MB).

The spectrum of acute coronary syndromes. The relation between ECG changes, biochemical markers of damage and the extent of myocardial necrosis. (CK = creatine kinase)

The above figure explains ECG changes in ischemis with regard to extent of myocardial damage:
Ischemia with no myocardial damage- Unstable angina- ST and T wave changes (like ST depression and T wave inversion)
Ischemia with minimal myocardial damage,
Partial thickness (non ST elevation or non-Q wave) myocardial infraction, and
Full thickness (Q wave myocardial infraction)

The common mechanism to all ACS (Acute coronary syndrome- unstable angina, non ST elevation MI and ST elevation MI) is rupture or erosion of the fibrous cap of a coronary artery plaque.
This leads to platelet aggregation and adhesion, localized thrombosis, vasoconstriction, and distal thrombus embolization.
The presence of a rich lipid pool within the plaque and a thin fibrous cap, are associated with an increased risk of rupture.
Thrombus formation and the vasoconstriction produced by platelet release of serotonin and thromboxane A2, results in myocardial ischaemia due to reduction of coronary blood flow.

Unstable Angina

Unstable angina (UA) is defined as- angina pectoris or equivalent ischemic discomfort with at least one of three features:
(1) it occurs at rest (or with minimal exertion), usually lasting >10 min;
(2) it is severe and of new onset (i.e., within the prior 4–6 weeks); and/or
(3) it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously).

The diagnosis of NSTEMI is established if a patient with the clinical features of UA develops evidence of myocardial necrosis, as reflected in elevated cardiac biomarkers.

Clinical Findings

The clinical hallmark of UA/NSTEMI is (symptoms)
chest pain, typically located in the substernal region or sometimes in the epigastrium, that radiates to the neck, left shoulder, and left arm.
Anginal "equivalents" such as dyspnea and epigastric discomfort may also occur.

The examination resembles that in patients with stable angina and may be unremarkable.
If the patient has a large area of myocardial ischemia or a large NSTEMI, the physical findings can include
pale cool skin,
sinus tachycardia,
a third and/or fourth heart sound,
basilar rales, and
sometimes hypotension, resembling the findings of large STEMI.


ECG- In UA, ST-segment depression, transient ST-segment elevation, and/or T-wave inversion, depending on the severity of the clinical presentation.
T-wave changes are sensitive for ischemia but less specific, unless they are new, deep T-wave inversions.

Cardiac Biomarkers (bichemical test)- Creatinine Kinase (CKMB) and Troponin.
Elevated levels of these markers distinguish patients with NSTEMI from those with UA.
In patients with an unclear history, small troponin elevations may not be diagnostic of an ACS.

A guide to the investigation and treatment of unstable angina and non-ST segment elevation myocardial infarction (NSTEMI).