Paper II
Question
Types and pathogenesis of myocardial infarction
Answer
Myocardial infarction (MI) is the necrosis of cardiac muscle resulting from prolonged ischaemia, most commonly due to coronary artery occlusion.
Types
Transmural infarction
- Involves the full thickness of the ventricular wall (endocardium to epicardium)
- Usually caused by occlusion of a major epicardial coronary artery, typically from acute thrombosis over a ruptured/eroded atherosclerotic plaque
- Corresponds to ST-elevation MI (STEMI) clinically
Subendocardial (non-transmural) infarction
- Limited to the inner one-third to one-half of the ventricular wall, the region most vulnerable to ischaemia (last to receive perfusion, highest wall tension/oxygen demand)
- Usually results from severe, prolonged reduction in coronary perfusion without complete/prolonged total occlusion (e.g., severe hypotension/shock superimposed on stable coronary atherosclerosis, or transient/incomplete occlusion)
- Corresponds to non-ST-elevation MI (NSTEMI) clinically
Pathogenesis
- The typical sequence begins with an atherosclerotic plaque undergoing sudden change — rupture, fissuring, or superficial erosion — exposing thrombogenic subendothelial collagen and plaque contents to the bloodstream
- Platelets adhere, aggregate, and become activated, releasing thromboxane A2, ADP, and serotonin, causing further platelet aggregation and vasospasm
- Activation of the coagulation cascade leads to thrombus formation, which may progress to complete vessel occlusion within minutes to hours
- Myocardium supplied by the occluded vessel becomes ischaemic; if occlusion persists beyond approximately 20–30 minutes, irreversible cell injury (coagulative necrosis) begins, progressing as a “wavefront” from the subendocardium outward toward the epicardium over the following hours if reperfusion is not achieved
- Reperfusion (spontaneous or therapeutic) can salvage some myocardium if achieved early, but may also cause reperfusion injury (additional damage from oxidative stress, calcium overload, and inflammatory response upon reintroduction of oxygenated blood)