Aetiology

MI is usually a consequence of coronary artery disease. Atherosclerosis with plaque fissuring or rupture and thrombus formation is the underlying aetiology for STEMI in most patients. A small proportion of patients present with STEMI caused by coronary spasm reducing myocardial perfusion, coronary embolism, or following chest trauma or spontaneous coronary or aortic dissection.

Pathophysiology

Atherosclerotic plaques form gradually over years.[13] They begin with the accumulation of low-density lipoprotein cholesterol and saturated fat in the intima (the inner layer) of blood vessels. This is followed by the adhesion of macrophages to endothelium, then diapedesis and entry into the intima, where they accumulate lipids and become foam cells. Foam cells are a rich source of proinflammatory mediators. The lesion up to this point is referred to as a fatty streak, and may be reversible to a certain extent.

Subsequent evolution involves migration of smooth muscle cells from the media, and their proliferation and deposition of extracellular matrix, including proteoglycans, interstitial collagen, and elastin fibres.[13] Some of the smooth muscle cells in advanced plaques exhibit apoptosis. Plaques often develop areas of calcification as they evolve. The plaque initially evolves with the artery remodelling outwards, followed by encroachment on the arterial lumen. Eventually the stenosis can limit flow under conditions of increased demand, causing angina.

STEMI typically occurs after abrupt and catastrophic disruption of a cholesterol-laden plaque. This results in exposure of substances that promote platelet activation and aggregation, thrombin generation, and thrombus formation, causing interruption of blood flow. If the occlusion is severe and persistent, myocardial cell necrosis follows.

On interruption of blood flow in the coronary artery, the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work. Early hyperkinesis of the non-infarcted zones occurs, probably as a result of acute compensatory mechanisms including increased sympathetic activity and Frank-Starling mechanism. As necrotic myocytes slip past each other, the infarction zone thins and elongates, especially in anterior infarction, leading to infarction expansion.

If a sufficient quantity of myocardium undergoes ischaemic injury, left ventricular (LV) systolic function becomes depressed; cardiac output, stroke volume, blood pressure, and compliance are reduced; and end systolic volume increases. Clinical heart failure occurs if 25% of myocardium has abnormal contraction, and cardiogenic shock occurs on loss of >40% of LV myocardium. Decreased compliance and increased LV end diastolic pressure give rise to diastolic dysfunction.

Classification

Acute coronary syndrome

Acute coronary syndrome (ACS) encompasses a spectrum of conditions, including patients presenting with recent changes in clinical symptoms or signs, with or without changes on 12-lead electrocardiogram (ECG) and with or without acute elevations in cardiac troponin (cTn) concentrations.[2]​ Historically ACS has been divided into three clinical categories according to the presence or absence of ST-segment elevation on a presenting ECG and on elevations of cardiac troponin T or I.[3][4]​​

1. ST-elevation myocardial infarction (STEMI): ECG shows persistent ST-segment elevation in at least two anatomically contiguous leads.

2. Non-STEMI (NSTEMI): ECG does not show ST-segment elevation, but cardiac biomarkers are elevated. The ECG may show ischaemic changes such as ST-segment depression, T-wave inversion, or biphasic T waves.

3. Unstable angina pectoris: non-specific ischaemic ECG changes, but cardiac biomarkers are within the normal range.

Fourth Universal Definition of Myocardial Infarction[1]

In the contemporary setting MI can also be classified according to variations in pathological, clinical, and prognostic factors, alongside the different management strategies recommended for each type.[1]

  • Acute myocardial infarction (types 1, 2, and 3 MI)

    • Defined as acute myocardial injury with clinical evidence of acute myocardial ischaemia and with detection of a rise and/or fall of cardiac troponin values with at least one value >99th percentile of the upper reference limit (URL)

    • A type 1 MI is characterised by identification of a coronary thrombus by angiography (or autopsy)

      • Includes STEMI and NSTEMI

    • In type 2 MI there is evidence of an imbalance between myocardial oxygen supply and demand that is not associated with an acute atherothrombotic event

      • Includes vasospasm, coronary microvascular dysfunction, and non-atherosclerotic coronary dissection

    • A type 3 MI is cardiac death in a patient with symptoms of myocardial ischaemia and new ischaemic ECG changes prior to a cardiac troponin level becoming abnormal or available

  • Coronary procedure-related MI (types 4 and 5 MI)

    • Type 4a MI – related to percutaneous coronary intervention

    • Type 4b MI – related to stent thrombosis

    • Type 4c MI – related to stent restenosis

    • Type 5 MI – related to coronary artery bypass graft surgery

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