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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

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