This composite educational material presents the macroscopic and microscopic features of myocardial infarction following surgical ligation of the left anterior descending (LAD) artery in a mouse model. Panel A is a clinical photograph (gross specimen) of the heart during a surgical procedure. It demonstrates an area of myocardial whitening (pallor) distal to the ligation line, indicated by a black arrow. This visual change represents acute ischemia and initial tissue necrosis. Panel B shows a diagnostic histopathology image of the heart stained with Hematoxylin-Eosin (HE). The cross-section reveals structural changes in the ventricular wall. A black arrow points to an area of significant myocardium thinning, a hallmark of remodeling and tissue loss following infarction. The pink-stained eosinophilic regions highlight the remaining muscular architecture, while the structural thinning indicates the progression of the injury. Together, these images illustrate the correlation between macroscopic ischemic signs (whitening) and microscopic structural pathology (wall thinning) in the context of cardiovascular research and ischemic heart disease models.

This composite educational resource demonstrates the pathology of chronic myocardial infarction through gross and microscopic examination. Image A is a clinical photograph showing a fresh transverse section of the human heart at the ventricular level. The myocardium exhibits a predominantly reddish-brown hue with visible transmural thinning and whitish, fibrotic scarring in the lateral and posterior walls of the left ventricle. A focal area of subendocardial fibrosis is also visible in the anterior ventricle. A 3 cm scale bar is included for morphometric reference. Image B is a light microscopy image at 20x magnification using Gomori trichrome stain, which highlights tissue composition. The viable cardiomyocytes are stained reddish-purple, while dense collagenous scar tissue (fibrosis) is stained bright blue-green, illustrating the replacement of necrotic muscle fibers with connective tissue. This finding is characteristic of a remote or healed myocardial infarct. This material is suitable for cardiovascular pathology education, illustrating the progression from myocardial injury to permanent scarring and ventricular remodeling.

This dual-panel image demonstrates macroscopic and microscopic pathology of acute myocardial infarction with hemorrhagic components. Panel (a) is a clinical photograph of tangential slices from an unfixed human heart, specifically the posterior wall of the left ventricle. It reveals large, irregularly shaped, dark red-to-purple hemorrhagic areas measuring approximately 4 cm x 3 cm and 5 cm x 7 cm, contrasting sharply against the lighter tan-colored myocardium. Panel (b) shows a corresponding histological section stained with Hematoxylin and Eosin (H&E) at 4x magnification. The micrograph depicts eosinophilic (pink) cardiomyocytes with visible structural disruption, including areas of contraction band necrosis and loss of nuclei. Notable pathological features include a prominent longitudinal band of hemorrhage and leukocyte infiltration, which serves to demarcate the necrotic zone from vital muscle. These findings are characteristic of hemorrhagic myocardial infarction and suggest an acute ischemic event followed by vascular rupture or reperfusion injury. The image is intended for medical education in cardiology and pathology to illustrate gross and microscopic signs of myocardial death.

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.

This diagnostic image is a 12-lead electrocardiogram (ECG) demonstrating an acute ST-segment elevation myocardial infarction (STEMI) with extensive involvement. The tracing reveals significant ST-segment elevation in the inferior leads (II, III, and aVF) and the precordial leads (V1 through V5), indicating a combined anterior and inferior wall infarction pattern. Prominent pathological Q-waves are visible in the limb leads I, II, III, and aVF, signifying established myocardial necrosis or a prior infarctive event in those territories. The precordial leads show a 'tombstoning' morphology of the ST segments, particularly from V2 to V4, where the ST elevation merges directly with the T-waves. These findings are consistent with massive myocardial ischemia and infarction, typically necessitating urgent reperfusion therapy. The ECG serves as an educational tool for identifying multivessel or proximal coronary artery occlusion patterns and the evolution of ischemic changes from Q-wave formation to acute ST-segment deviation.

Comparison of three 12-lead electrocardiograms (ECGs) labeled A, B, and C, documenting the progression and persistence of ischemic changes. ECG A, the admission tracing, shows prominent anterolateral ST-segment elevations (2-3 mm) in leads V2-V6, I, and aVL (indicated by black arrows). Significant pathologic QS waves (indicated by red arrows) are visible in leads V2-V4, I, and aVL, while leads V5 and V6 maintain a residual R-wave. This pattern is characteristic of a late-presenting transmural myocardial infarction or a resulting ventricular aneurysm/scar. Tracings B (follow-up) and C (second admission with confirmed left ventricular pseudoaneurysm) demonstrate the persistence of these ST-segment elevations and QS waves without significant morphological evolution over time. The persistent ST elevation in the presence of well-developed Q waves is a classic electrocardiographic sign of ventricular wall dyskinesis or aneurysm formation following an extensive ST-elevation myocardial infarction (STEMI).

This diagnostic image is a 12-lead electrocardiogram (ECG) demonstrating acute ST-segment elevation myocardial infarction (STEMI) patterns. The primary visual abnormality is significant ST-segment elevation (approximately 2.5–3 mm) in the inferior leads (II, III, and aVF). The morphology of the ST segments is convex ('tombstoning') and transitions into upright, prominent T waves. Reciprocal ST-segment depression is visible in the lateral lead aVL. The rhythm is regular and appears to be a normal sinus rhythm with identifiable P waves preceding each narrow QRS complex. There are also deep Q waves present in the inferior leads, suggesting an established or previous inferior wall injury. Precordial leads (V1-V6) show relatively deep S waves and some T-wave flattening, consistent with left ventricular hypertrophy or secondary changes. This tracing is clinically significant for diagnosing an acute inferior STEMI, often associated with right coronary artery (RCA) or left circumflex (LCx) occlusion. It serves as a key educational example for interpreting acute ischemic changes and reciprocal findings on a standard 12-lead ECG.