Aetiology
Coronary artery disease is the underlying cause in nearly all patients with acute myocardial ischaemia. The most common cause of unstable angina is coronary artery narrowing caused by a thrombus that develops on a disrupted atherosclerotic plaque and is usually non-occlusive.[2]
A less common cause is intense vasospasm of a coronary artery (variant or Prinzmetal's angina, ischaemia and no obstructed arteries [INOCA], or secondary to cocaine use). This intense vasospasm can be caused by vascular smooth muscle or by endothelial dysfunction in INOCA.
Pathophysiology
The initiating lesion in coronary artery disease (CAD) is a fissure in the vessel endothelial lining over an underlying cholesterol plaque, which results in a loss in the integrity of the plaque cap. Plaques that fissure or rupture tend to have a thin fibrous cap, a high lipid content, few smooth muscle cells, and a high proportion of macrophages and monocytes.[13][14]
The fissure or plaque rupture leads to exposure of subendothelial matrix elements (such as collagen), stimulating platelet activation and thrombus formation. Release of tissue factor directly activates the coagulation cascade and promotes the formation of fibrin.
If an occlusive thrombus forms, the patient may develop an acute ST-segment-elevation myocardial infarction (STEMI) unless the affected myocardium is richly collateralised. If the thrombus formation is not occlusive, the patient may develop unstable angina or non-specific ST changes on the ECG (ST depression or T-wave changes).
Arterial inflammation, caused by or related to infection, may cause plaque destabilisation and rupture and precipitate acute coronary syndrome (ACS). Activated macrophages and T lymphocytes located at the shoulder of a plaque increase the expression of enzymes such as metalloproteinase that may cause thinning and disruption of the plaque, leading to ACS.[15]
Myocardial supply and demand mismatch may cause ischaemia without significant CAD. These include:
Increased myocardial oxygen requirements such as fever, tachycardia, thyrotoxicosis
Reduced coronary blood flow: for example, hypotension
Reduced myocardial oxygen delivery such as anaemia or hypoxaemia.
In patients with prior ACS with coronary stents, stent thrombosis or in-stent restenosis may cause STEMI, non-ST-elevation myocardial infarction, or unstable angina. Both stent thrombosis and restenosis have complex causes, triggers, pathophysiology, and risk factors. Of importance, premature cessation of antiplatelet agents in patients with stents (drug-eluting and bare-metal) may trigger an ACS.[1][2]
Classification
Classification of acute coronary syndrome[1][2]
The term acute coronary syndrome (ACS) is used to describe the spectrum of conditions that includes unstable angina (UA), non-ST-elevation myocardial infarction (non-STEMI), and ST-elevation myocardial infarction (STEMI).
The classification of patients is based on ECG findings. Patients are divided into 2 categories:
Chest pain with persistent ST-segment elevation on ECG; classified as STEMI
Chest pain with ST-segment depression, or T-wave changes, or no ECG changes at presentation; classified as non-ST-elevation ACS.
Further categorisation of non-ST-elevation ACS is by measurement of cardiac biomarkers:
Elevated: non-STEMI
Non-elevated: UA.
Use of this content is subject to our disclaimer