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Pathology - ST-elevation myocardial infarction
Definition: Complete thickness necrosis of a region of the myocardium.
Epidemiology • Extremely prevalent.
Aetiology • Nearly invariably a consequence of coronary artery atherosclerosis.
Pathogenesis
The rupture of an unstable atherosclerotic plaque in a coronary artery induces the creation of an occlusive thrombus rich in fibrin above the plaque. Complete closure of the coronary artery results in transmural necrosis of the myocardial region fed by that artery
Presentation • Persistent severe ischemic cardiac chest discomfort. • Patients frequently report a sensation akin to impending death. • The ECG displays ST-elevation or newly developed left bundle branch block. Biochemistry • Blood troponin concentrations are increased.
Macroscopy • The impacted coronary artery exhibits total obstruction due to a thrombus overlaying an atherosclerotic plaque. The infarcted myocardium becomes apparent approximately 15 hours post-event, presenting as mushy, enlarged, and exhibiting a darker red hue. • Within 24 to 48 hours, the infarct becomes yellow. Over weeks to months, the infarct is substituted by white scar tissue, resulting in a thinner ventricular wall.
Histopathology
The initial alteration in myocardial infarction is cytoplasmic eosinophilia and the loss of nuclei in the afflicted myocytes occurring approximately 8 to 12 hours post-infarction. • Within 24 hours, neutrophils infiltrate the necrotic region, and after several days, granulation tissue is established. • Over the course of weeks to months, the granulation tissue is supplanted by fibrous scar tissue.
Prognosis: Immediate problems encompass ventricular arrhythmias, which can be deadly, and abrupt heart failure in extreme instances. Rupture of the infarcted ventricular free wall results in hemopericardium, leading to fast cardiac tamponade and mortality. A thrombus that develops on akinetic myocardium may dislodge and result in systemic emboli. Subsequent difficulties encompass the creation of ventricular aneurysms and the emergence of left ventricular (LV) issues.
Definition: Complete thickness necrosis of a region of the myocardium.
Epidemiology • Extremely prevalent.
Aetiology • Nearly invariably a consequence of coronary artery atherosclerosis.
Pathogenesis
The rupture of an unstable atherosclerotic plaque in a coronary artery induces the creation of an occlusive thrombus rich in fibrin above the plaque. Complete closure of the coronary artery results in transmural necrosis of the myocardial region fed by that artery
Presentation • Persistent severe ischemic cardiac chest discomfort. • Patients frequently report a sensation akin to impending death. • The ECG displays ST-elevation or newly developed left bundle branch block. Biochemistry • Blood troponin concentrations are increased.
Macroscopy • The impacted coronary artery exhibits total obstruction due to a thrombus overlaying an atherosclerotic plaque. The infarcted myocardium becomes apparent approximately 15 hours post-event, presenting as mushy, enlarged, and exhibiting a darker red hue. • Within 24 to 48 hours, the infarct becomes yellow. Over weeks to months, the infarct is substituted by white scar tissue, resulting in a thinner ventricular wall.
Histopathology
The initial alteration in myocardial infarction is cytoplasmic eosinophilia and the loss of nuclei in the afflicted myocytes occurring approximately 8 to 12 hours post-infarction. • Within 24 hours, neutrophils infiltrate the necrotic region, and after several days, granulation tissue is established. • Over the course of weeks to months, the granulation tissue is supplanted by fibrous scar tissue.
Prognosis: Immediate problems encompass ventricular arrhythmias, which can be deadly, and abrupt heart failure in extreme instances. Rupture of the infarcted ventricular free wall results in hemopericardium, leading to fast cardiac tamponade and mortality. A thrombus that develops on akinetic myocardium may dislodge and result in systemic emboli. Subsequent difficulties encompass the creation of ventricular aneurysms and the emergence of left ventricular (LV) issues.
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