Gross pathology image of a human heart cross-section (short-axis/transverse) from a 73-year-old female with a history of arterial hypertension, chronic smoking, and three-vessel coronary artery disease. The specimen reveals chronic myocardial infarction scar throughout the myocardium with areas of subacute necrosis on both ventricles. The ventricles show concentric hypertrophy characterized by thickened ventricular walls and reduced cavity size, consistent with long-standing pressure overload. On cut surface, extensive fibrous replacement tissue is seen in the LV and RV walls, with pale, firm areas indicating scar tissue; endocardial surfaces may show thinning in infarcted zones. The presence of bilateral ventricular involvement suggests diffuse ischemic injury, possibly past infarcts with replacement fibrosis. The gross morphology corresponds to ischemic cardiomyopathy spectrum; pathophysiology includes atherosclerotic CAD, hypertension-induced hypertrophy, and chronic subendocardial ischemia. This combination results in remodeling and scar formation, predisposing to arrhythmias and heart failure. The image is from pathorama.ch, illustrating classic post-infarction changes: myocardial scar, subacute necrosis, and hypertrophic remodeling. Clinically, such pathology would correlate with prior chest pain episodes, elevated troponin in the past, and radiographic evidence of cardiomegaly; autopsy or pathology reporting would emphasize chronic infarct burden, LV dysfunction, and risk stratification for sudden cardiac death. Suitable for education on myocardial infarction progression and necrosis patterns.

Gross pathology image of an extracted human heart cut in transverse section to expose the ventricles. Modality: macroscopic inspection during autopsy or surgical specimen; technique: serial cross-sectional dissection of the ventricles revealing infarcted and fibrotic zones. Anteriorly in the anteroseptal left ventricular wall there is a partially healed infarction with thinning, scar formation and mottled pallor consistent with prior ischemic injury. In the anterolateral/lateral left ventricular wall, a subacute infarct is evident, showing fibrous connective tissue with adjacent edema and discoloration. The right ventricle demonstrates marked fibrosis and myocardial remodeling with patchy, firm trabeculations. Overall, the myocardium exhibits biventricular hypertrophy with thickened walls and increased myocardial mass; left ventricular wall thickening may appear concentric but can reflect remodeling from chronic hypertension and ischemic injury. The combination of age (82-year-old female) and cardiovascular risk factors-smoking, essential hypertension, dyslipidemia—supports a long-standing coronary atherosclerotic disease. Notable clinical context includes postmenopausal elevation of coronary risk. The image highlights the structural consequences of myocardial infarction, scar replacement, and concentric/eccentric hypertrophy in the setting of ischemic cardiomyopathy. This resource is useful for education on infarct evolution, ventricular remodeling, and CAD risk assessment in aging female patients. Correlation with clinical history strengthens diagnostic interpretation and teaching value.

Gross pathology photograph of a human heart in transverse mid-ventricular section, illustrating macroscopic features of cardiac amyloidosis. The myocardium appears pale, waxy, and firm, consistent with amyloid deposition replacing normal myocardial tissue. Concentric left ventricular hypertrophy is evident, with thickened LV wall while chamber cavity is reduced in caliber relative to normal. The right ventricle is less involved in this cut, and the endocardial surfaces show smooth contour without focal infarction. These findings reflect an infiltrative cardiomyopathy process where extracellular amyloid proteins infiltrate the interstitium, causing stiff, noncompliant myocardium and diastolic dysfunction. The gross resemblance to waxy infiltration, in combination with preserved coronary architecture, supports a diagnosis of cardiac amyloidosis rather than primary hypertrophic hypertrophy or hypertensive remodeling alone. This image serves educational and diagnostic contexts for surgical pathology, cardiology, and radiology reviews, and is useful for teaching about late-stage restrictive cardiomyopathy. In clinical practice, these macroscopic cues prompt confirmatory microscopic evaluation, immunohistochemical typing, and systemic evaluation for underlying plasma cell dyscrasia or transthyretin amyloidosis. Potential uses include medical education, pathology correlation, radiology-pathology conferences, and research on infiltrative heart disease and cardiomyopathy phenotypes. Correlative clinical data and ancillary testing guide prognosis and treatment choices in suspected infiltrative cardiomyopathy patients today.