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The pathophysiology of acute myocardial infarction
1Division of Cardiovascular Medicine, University of Massachusetts Medical School, Worcester 01655.
Insights
Coronary arterial thrombosis causes acute myocardial infarction by rupturing atherosclerotic plaques. Promptly restoring blood flow is crucial for reversible recovery, preventing cell necrosis.
Area of Science:
- Cardiovascular Medicine
- Pathophysiology
- Thrombosis
Background:
- Acute myocardial infarction is directly caused by coronary arterial thrombosis.
- Thrombosis results from atherosclerotic plaque rupture, exposing thrombogenic material and activating platelets and the clotting cascade.
Purpose of the Study:
- To elucidate the mechanisms underlying atherosclerotic plaque rupture.
- To detail the biochemical and physiological alterations in the myocardium due to ischemic events.
Main Methods:
- Review of recent scientific literature on coronary arterial thrombosis and myocardial infarction.
- Analysis of proposed mechanisms for plaque fissure or rupture.
- Description of cellular and physiological changes during myocardial ischemia.
Main Results:
- Plaque rupture exposes thrombogenic material, initiating platelet activation and clotting.
- Potential mechanisms for plaque rupture include platelet factors, vasomotion, mechanical stress, and vasa vasorum issues.
- Myocardial ischemia leads to intracellular acidosis, energy depletion, altered calcium sensitivity, and reduced compliance.
Conclusions:
- Coronary thrombosis is the definitive cause of acute myocardial infarction.
- Reversible myocardial ischemia depends on prompt reperfusion; prolonged ischemia results in necrosis.
Abstract:
Recent work has now clearly established that coronary arterial thrombosis is the direct cause of acute myocardial infarction. This thrombotic event occurs when a pre-existing atherosclerotic plaque ruptures or fissures, thereby exposing underlying thrombogenic material to the circulation. Platelets are thus activated and the clotting cascade is initiated. It is as yet unclear why a previously stable atherosclerotic plaque should fissure or rupture. However, suggested mechanisms include release of vasoactive substances from activated platelets, coronary arterial vasomotion, mechanical stress fatigue of the atherosclerotic plaque, and rupture of vasa vasorum within the atherosclerotic plaque. The resultant cessation of myocardial blood flow produces specific biochemical and physiological alterations secondary to myocardial ischemia. Intracellular acidosis, loss of high-energy phosphates, reduced sensitivity of contractile proteins to calcium, and accumulation of inorganic phosphate and lipid, all occur within the ischemic myocyte. Diastolic compliance is markedly reduced by ischemia followed by cessation of systolic contractile activity. Most of these alterations are reversible if ischemia is relieved promptly. Prolonged ischemia leads to delayed biochemical and physiological recovery and/or cell necrosis.