Myocardial Infarct - Introduction
Clinically, myocardial infardtion is most often due to coronary artery atherosclerosis in over 90% of cases; less often due to coronary vasospasm, coronary artery dissection, coronary thrombosis or embolism.
• Plaque fissure or rupture may cause a totally occlusive thrombosis leading to acute ST-segment elevation MI or a non-occlusive thrombosis leading to unstable angina or non-ST-segment elevation MI.
• Myocardial necrosis occurs in a wavefront phenomenon from the subendocardium to the subepicardial myocardium.
• The extent of myocardial necrosis depends on length of time of occlusion and degree of collateral blood flow.
• Complications of large transmural infarcts include:
- Congestive heart failure – likely to develop if >40% of left ventricle is infarcted
- Arrhythmia – conduction block, bradyarrhythmias, tachyarrhythmias
- Infarct extension/reinfarction – development of new necrosis in the same area of a recent infarction as evidenced by recurrence of chest pain, elevated cardiac enzymes, and electrocardiographic changes
- Infarct expansion and left ventricular aneurysm – the infarcted zone becomes thin and stretched out, forming a regional left ventricular cavity dilatation
- Mural thrombosis/embolism – thrombi can form in expanded akinetic infarcted wall usually in the setting of large anteroapical MI, with risk of systemic embolization
- Right ventricular infarction – associated with posterior wall infarction and high pulmonary pressures
- Cardiac rupture
- free wall rupture leading to hemopericardium, most often in the anterior wall
- interventricular septal rupture leading to left-to-right shunt
- papillary muscle rupture leading to acute mitral regurgitation
- ruptures usually occur in the first 10 days of MI
- pericarditis – may be seen in the area of acute infarction or represent a late postinfarction inflammation (Dressler syndrome) appearing weeks after infarctionMyocardial necrosis in an acute
Gross and microscopic pathology