Myocardial Infarction

Myocardial infarction is the death (necrosis) of heart muscle resulting from prolonged ischaemia, most often caused by acute thrombotic occlusion of a coronary artery superimposed on atherosclerosis. This pathology entry describes the cellular and tissue events of ischaemic myocardial injury and the evolving morphology of the infarct, complementing the clinical-syndrome view of the condition.

Definition

Myocardial infarction is ischaemic necrosis of myocardium, defined clinically by the detection of a rise and/or fall of cardiac troponin with at least one value above the 99th-percentile reference limit together with evidence of acute myocardial ischaemia, and characterised pathologically by coagulative necrosis evolving through inflammatory and reparative phases to a fibrous scar.

Scope

The entry covers the pathophysiology of coronary occlusion and ischaemia, the time-course of irreversible myocyte injury, the gross and microscopic evolution of the infarct from coagulative necrosis to granulation tissue and scar, and major complications. It is framed as reference pathology, not as diagnostic or treatment guidance; the clinical-care perspective is held under separate clinical entries.

Core questions

• How does atherosclerotic plaque rupture or erosion lead to coronary thrombosis and ischaemia?
• What determines whether ischaemic injury becomes irreversible, and over what time-course?
• How does the infarct evolve morphologically from acute necrosis to mature scar?
• What complications - arrhythmia, rupture, aneurysm, failure - arise from infarcted and remodelled myocardium?

Key concepts

• Coronary thrombosis on a disrupted plaque
• Ischaemia and the wavefront of necrosis
• Reversible versus irreversible injury
• Coagulative necrosis
• Reperfusion injury
• Infarct healing and scar formation
• Cardiac troponin as a marker of myocyte necrosis

Mechanisms

Most infarcts begin when an atherosclerotic plaque ruptures or erodes, exposing thrombogenic material and triggering occlusive coronary thrombosis. The resulting ischaemia depletes myocyte energy stores; if flow is not restored, injury becomes irreversible, spreading as a wavefront from subendocardium toward epicardium over hours. Necrotic myocardium evolves through recognisable phases: early coagulative necrosis with neutrophilic infiltration, followed by macrophage-mediated removal of debris, granulation tissue, and finally collagenous scar over weeks. Loss of contractile tissue and subsequent remodelling can produce complications including arrhythmia, myocardial rupture, ventricular aneurysm and progression to heart failure. Reperfusion limits infarct size but can itself contribute to tissue injury.

Clinical relevance

Myocardial infarction is a major cause of death and disability and a defining acute manifestation of coronary atherosclerosis; its pathology underlies the biomarkers and morphological findings used to recognise it. This entry describes the disease process for reference and does not provide individualised diagnostic or treatment advice.

Epidemiology

As the dominant acute consequence of coronary atherosclerosis, myocardial infarction is among the leading causes of mortality worldwide; its incidence tracks the prevalence of atherosclerotic risk factors. The standardised universal definition supports consistent ascertainment across populations.

History

Understanding of myocardial infarction advanced from early twentieth-century clinicopathological correlation of coronary thrombosis with myocardial necrosis to the late-twentieth-century recognition that plaque disruption and thrombosis drive most events. The introduction of sensitive cardiac troponin assays reshaped diagnosis, and successive expert consensus documents - culminating in the Fourth Universal Definition (2018) - standardised the definition and classification of infarction.

Key figures

• Kristian Thygesen
• Peter Libby
• Renu Virmani

Seminal works

• thygesen-2018
• libby-2013

Frequently asked questions

What actually dies in a myocardial infarction?

Cardiac muscle cells (cardiomyocytes) in the territory supplied by an occluded coronary artery undergo ischaemic (coagulative) necrosis; the dead tissue is later cleared and replaced by a fibrous scar.

How is this pathology entry different from the clinical heart-attack topic?

This entry focuses on the tissue and cellular pathology - how ischaemia produces necrosis and how the infarct heals - while a separate clinical entry under coronary artery disease addresses presentation and management. They are cross-linked as neighbours.