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Pathology - Non-ST-elevation myocardial infarction
Definition: Partial thickness necrosis of a region of the myocardium.
Epidemiology • Extremely prevalent.
Aetiology
• Primarily attributable to coronary artery atherosclerosis.
Pathogenesis
• The rupture or fissuring of an unstable atherosclerotic plaque triggers the development of a platelet-rich thrombus. • This thrombus results in considerable and protracted arterial constriction, leading to ischemic necrosis in a portion of the myocardium supplied by the affected artery.
Presentation
• Acute coronary syndrome characterized by prolonged ischemic cardiac chest discomfort at rest or with minimal exertion. • ECG reveals ischemic alterations without ST-elevation. Biochemistry • Elevated blood troponin levels are observed. Macroscopy • Notable narrowing of the affected coronary artery due to a complex atherosclerotic plaque.
Histopathology
• The initial alteration in myocardial infarction is heightened cytoplasmic eosinophilia and the absence of nuclei in the afflicted myocytes approximately 8–12 hours post-infarction. • Within 24 hours, neutrophils infiltrate the necrotic region, and after several days, granulation tissue is established. • Over the course of many weeks, the granulation tissue is substituted by scar tissue.
Prognosis: Patients have a significant risk of future acute coronary episodes and the subsequent development of left ventricular dysfunction.
Definition: Partial thickness necrosis of a region of the myocardium.
Epidemiology • Extremely prevalent.
Aetiology
• Primarily attributable to coronary artery atherosclerosis.
Pathogenesis
• The rupture or fissuring of an unstable atherosclerotic plaque triggers the development of a platelet-rich thrombus. • This thrombus results in considerable and protracted arterial constriction, leading to ischemic necrosis in a portion of the myocardium supplied by the affected artery.
Presentation
• Acute coronary syndrome characterized by prolonged ischemic cardiac chest discomfort at rest or with minimal exertion. • ECG reveals ischemic alterations without ST-elevation. Biochemistry • Elevated blood troponin levels are observed. Macroscopy • Notable narrowing of the affected coronary artery due to a complex atherosclerotic plaque.
Histopathology
• The initial alteration in myocardial infarction is heightened cytoplasmic eosinophilia and the absence of nuclei in the afflicted myocytes approximately 8–12 hours post-infarction. • Within 24 hours, neutrophils infiltrate the necrotic region, and after several days, granulation tissue is established. • Over the course of many weeks, the granulation tissue is substituted by scar tissue.
Prognosis: Patients have a significant risk of future acute coronary episodes and the subsequent development of left ventricular dysfunction.
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