Acute Coronary Symptoms

Aetiology and Pathophysiology

Acute coronary syndromes (ACS) such as myocardial infarction (MI) are usually the end result of atherosclerosis of the coronary arteries. Atherosclerosis is a chronic immunoinflammatory, fibroproliferative disease of medium- to large arteries that is characterised by the formation of lipid-rich plaques in blood vessel walls.¹

Atheromatous plaques sometimes become unstable or inflamed, causing them to rupture or crack, exposing circulating blood to their highly thrombogenic contents.^1,2 Subsequent activation of platelets and the coagulation cascade leads to the development of a thrombus at the site of the rupture or fissure.²

The clinical consequences of coronary thrombosis depend on the size of the thrombus, its location in the coronary vasculature, and its longevity.² In ST-segment elevation myocardial infarction (STEMI), thrombi are fibrin-rich and cause complete vessel occlusion; in non-ST-segment elevation ACS (NSTE-ACS), however, they are platelet-rich and only partially or intermittently occlusive.^1,3 There is often a delay between the rupture of an atherosclerotic plaque and the development of clinical sequelae.⁴

Although thrombosis is the main cause of vessel occlusion in ACS, other contributory factors may include coronary vasoconstriction and microembolism.⁵ In some individuals, ACS may be due entirely to vasospasm rather than thrombosis.²

Severe occlusion of a coronary vessel, regardless of the cause, will result in myocardial ischaemia and, within 15-30 minutes, myocardial necrosis.⁵ Necrosis begins in the subendocardium and progresses to the subepicardium in a time-dependent fashion.⁵

Figure 1. Key stages in the development of coronary atherothrombosis