Etiology

Myocardial infarction is usually a consequence of coronary artery disease. Atherosclerosis with plaque fissuring or rupture and thrombus formation is the underlying etiology for ST-elevation myocardial infarction (STEMI) in most patients. A small proportion of patients present with STEMI caused by coronary spasm reducing myocardial perfusion, or following chest trauma or spontaneous coronary or aortic dissection.

Pathophysiology

Atherosclerotic plaques form gradually over years.[12] 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 leukocytes 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 fibers.[12] 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 remodeling outward, 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 noninfarcted 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 ischemic injury, left ventricular (LV) pump 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

Myocardial injury, myocardial infarction, and acute coronary syndrome

The term myocardial injury is used when there is evidence of elevated cardiac troponin values with at least one value above the 99th percentile upper reference limit. If there is a rise and/or fall of the troponin values, the injury is considered to be acute.[2]

Acute coronary syndromes encompass a spectrum of conditions, including patients presenting with recent changes in clinical symptoms or signs, with or without changes on 12-lead ECG and with or without acute elevations in cardiac troponin (cTn) concentrations.[3]

The term myocardial infarction (MI) refers to acute myocardial injury with clinical evidence of acute myocardial ischemia (elevated cardiac troponin values with at least one value above the 99th percentile upper reference limit) and at least one of the following:[2]

  • Symptoms of myocardial ischemia

  • New ischemic ECG changes

  • Development of pathologic Q wave

  • Imaging evidence of new loss of viable myocardium or new wall motion abnormality

  • Identification of coronary thrombus by angiography or autopsy

MI caused by atherothrombotic coronary artery disease is designated as type 1 MI. Based on ECG changes, these may be further characterized as STEMI or non-STEMI (NSTEMI).

Classically acute coronary syndrome has been divided into three clinical categories according to the presence or absence of ST-segment elevation on presenting ECG, and on elevations of myocardial biomarkers such as troponin.[2][4]

1. STEMI: ECG shows persistent ST-segment elevation in two or more anatomically contiguous leads.

2. NSTEMI: ECG does not show ST-segment elevation, but cardiac biomarkers are elevated. The ECG may show nonspecific ischemic changes such as ST-segment depression or T-wave inversion.

3. Unstable angina pectoris: nonspecific ischemic ECG changes, but cardiac biomarkers are normal.

To reflect the pathophysiologic continuum between NSTEMI and unstable angina, the American Heart Association/American College of Cardiology guidelines have grouped these conditions under the single term "non-ST-elevation acute coronary syndromes."[5]​​

In the contemporary setting, MI can also be classified according to variations in pathologic, clinical, and prognostic factors, alongside the different management strategies recommended for each type.[1][2]

  • Acute MI (types 1, 2, and 3 MI)

    • Defined as acute myocardial injury with clinical evidence of acute myocardial ischemia 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 characterized 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 nonatherosclerotic coronary dissection

    • A type 3 MI is cardiac death in a patient with symptoms of myocardial ischemia and new ischemic 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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