This medical figure illustrates the methodology and visual findings of an experimental myocardial infarction model. Panel A is an anatomical diagram showing a heart with a coronary occlusion placed on a coronary artery distal to the left atrium (LA). A shaded brown region extending inferiorly from the occlusion site represents the infarcted area. The diagram indicates the levels of three transverse ventricular sections labeled Slice 1, Slice 2, and Slice 3. Panel B displays corresponding macroscopic clinical photographs of these three cross-sectional heart slices stained with thioflavin-S under white light. The macroscopic view demonstrates the progression of tissue damage: Slice 1 (proximal) shows a localized area of pale, healthy tissue alongside darker necrotic regions; Slice 2 and Slice 3 (distal) exhibit increasingly larger areas of dark, necrotic tissue, indicating the transmural extent of the infarction throughout the left ventricle. This material is designed for cardiovascular pathology education, specifically illustrating the spatial relationship between arterial ligation and the resulting downstream myocardial necrosis.

This medical illustration depicts a pathophysiology diagram of an intracoronary artery retrograde thrombolysis (ICART) system during a percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI). The primary focus is a longitudinal cross-section of a coronary artery showing total occlusion. A dark reddish-brown, elongated, irregular mass representing a thrombus is visible, situated adjacent to yellowish atherosclerotic plaque material. A thin blue interventional guidewire is shown successfully traversing the occlusion into the distal vessel segment. The distal artery is color-coded green, containing small red patches, indicating the site for retrograde thrombolytic cocktail injection via a microcatheter. The background illustrates the branching coronary vasculature of the heart. This diagram serves as an educational tool to demonstrate the mechanical and pharmacological approach to managing culprit vessel occlusion by delivering thrombolytic agents directly to the distal lumen through a retrograde technique.

Educational medical composite depicting cardiac imaging analysis in a porcine model of myocardial infarction (MI). Figure A shows the experimental timeline: baseline MRI, MI induction via LCx artery occlusion, and follow-up cardiac MRI and epicardial echocardiography. Angiograms highlight the LAD and LCx coronary arteries. Figure B displays diagnostic images and data visualization of regional myocardial function. Left: Longitudinal and circumferential tagging cardiac MRI views with superimposed green and red myocardial contours for strain analysis. Right: A bull's-eye plot (17-segment model) representing peak strain distribution. The myocardial regions are categorized into three distinct areas: the Infarction Zone (IZ) in the inferolateral region (light green segments), the adjacent Border Zones (BZ) (cyan segments), and the healthy Remote Zone (RZ) (dark blue segments covering the remaining anterior and septal walls). The diagram illustrates spatial classification used to study differences in longitudinal and circumferential strain following ischemic injury and subsequent mitral regurgitation development.

This composite image illustrates the creation and treatment of an acute myocardial infarction (AMI) model. Panel A and B are fluoroscopic angiograms showing the left anterior descending (LAD) artery before (A) and during (B) balloon catheter occlusion, indicated by red arrows. Panel C is a clinical photograph of an open-heart surgical procedure where a hypodermic needle is used for direct intramyocardial injection into the exposed heart surface. Surgical retractors and sutures are visible within the thoracic cavity. Panel D is a schematic anatomical diagram of the heart depicting the coronary anatomy and post-infarct zones. It labels the LAD, its diagonal branches (D1, D2), and the distal occlusion site. The diagram highlights the three functional territories: the Infarct Zone (IZ, grey), the Border Zone (BZ, light pink), and the Remote Zone (RZ, red dot). This visual set demonstrates the methodology for translational cardiology research, specifically modeling ischemic injury and subsequent therapeutic cell delivery.

A 12-lead electrocardiogram (ECG) demonstrating an acute anterolateral ST-elevation myocardial infarction (STEMI). The tracing shows significant, convex-upward ST-segment elevation in the precordial leads (V1–V6), consistent with an anterior wall injury. Leads I and aVL also display ST-elevation, indicating lateral involvement. These changes are accompanied by hyperacute, peaked T-waves most prominent in V2 through V4. There is evidence of reciprocal ST-segment depression in the inferior leads (II, III, and aVF). The QRS complexes appear widened in the leads with maximal ST elevation. The heart rhythm is sinus. This ECG pattern is clinically significant for proximal left anterior descending (LAD) artery occlusion, necessitating urgent reperfusion therapy. The visual presentation focuses on teachable hallmarks of cardiac ischemia, including the relationship between anatomical lead distribution and corresponding vascular territories, as well as the identification of reciprocal changes in opposing leads.

A standard 12-lead electrocardiogram (ECG) demonstrating an acute inferior ST-elevation myocardial infarction (STEMI). The tracing shows significant, convex ST-segment elevation in the inferior leads (II, III, and aVF), consistent with an acute transmural injury in the distribution of the right coronary artery or left circumflex artery. Reciprocal changes are evident as ST-segment depression in the high lateral leads (I and aVL) and the precordial leads (V4 through V6). The rhythm appears to be sinus, and the diagnostic imaging is presented on standard grid paper for the assessment of cardiac electrical activity. This visual is highly relevant for medical education concerning cardiovascular emergencies, acute coronary syndromes (ACS), and the interpretation of reciprocal ECG changes.

A 12-lead electrocardiogram (ECG) demonstrating an acute ST-elevation myocardial infarction (STEMI) with characteristic anterior and anterolateral findings. The tracing displays a normal sinus rhythm with a heart rate of approximately 84 beats per minute and normal P wave morphology. Significant pathology is localized to the precordial leads, specifically V2 through V5, which exhibit pronounced ST-segment elevation. This elevation presents with a convex 'tombstoning' morphology, a high-risk indicator of extensive myocardial injury. Additionally, evolving QS waves are visible in leads V2 and V3, indicating necrotic changes or transmural infarction. These findings are clinically consistent with an acute occlusion of the left anterior descending (LAD) coronary artery. The limb leads (I, II, III, aVR, aVL, aVF) show relatively stable baselines, though mild reciprocal changes or secondary ST-T wave abnormalities may be present in the inferior leads. This diagnostic image serves as a classic educational example of early-stage STEMI progression and the visual identification of localized ischemic injury on electrocardiography.

Imaging modality: Light microscopy of hematoxylin-eosin (H&E) stained cardiac tissue. Specimen is paraffin-embedded myocardial section, 5 micron thick, imaged with bright-field optics at high magnification. Anatomic region: left ventricular myocardium with an infarct in the left half of the field. The histology demonstrates pallor of necrotic cardiomyocytes (myocytolysis) produced by sarcolemmal disruption with influx of salt and water and cytoplasmic swelling. In this early post-ischemic stage, fibers lose cross-striations and display increased eosinophilia; nuclei are often absent or pyknotic. The infarct border may show waviness of fibers and mild edema; contraction bands may be present at the margin. Neutrophilic infiltration is typically minimal during the first 24 hours but may begin to appear around this window. The combination of coagulative necrosis, myocytolysis, and pallor indicates an acute myocardial infarction approximately one day old. This histologic pattern correlates with ischemia from coronary occlusion, clinical presentation of acute coronary syndrome, and aligns with diagnostic timelines (0-24 h). Clinically the image supports timing of infarct and helps distinguish acute infarction from myocarditis or chronic scar, serving as an educational reference for pathology, medical education, and research on myocardial injury dynamics. Further confirmed by clinical correlation and education.

Imaging modality and tissue: light microscopy of hematoxylin and eosin stained myocardial tissue from the left ventricle showing acute infarct with myocytolysis. The left half of the field demonstrates pallor of necrotic cardiac myocytes, consistent with early ischemic injury about one day old. Disruption of the sarcolemma and loss of cytoplasmic integrity produce osmotic swelling as salt and water accumulate within myocytes, yielding pale, swollen, eosinophilic cells. Nuclei are pyknotic or obscured, and cross‑striations are variably preserved in some fibers while others show early coagulative necrosis. The surrounding myocardium exhibits preserved architecture with clear demarcation between infarcted and viable tissue. This stage precedes substantial neutrophilic infiltration and precedes macrophage clearance. The histologic features correlate with an acute coronary syndrome of short duration, typically anterior or lateral wall involvement depending on infarct territory, and predict ongoing impairment of contractility in the affected region. Clinically, this finding supports acute myocardial infarction (AMI) within 24 hours, ischemic necrosis, and myocytolysis as a pathologic correlate of severe ischemia. Differential considerations include early myocarditis, reperfusion injury, or artifact; however, the combination of pallor, sarcolemmal disruption, and myocytolysis most strongly supports early infarction. The image is diagnostic for early infarct with histologic confirmation.

Imaging modality: light microscopy of a cardiac tissue section stained with hematoxylin and eosin reveals infarct border-zone myocardium from the left ventricle. The tissue shows parallel, wavy myocardial fibers along the border between viable and necrotic tissue—a hallmark of early coagulative necrosis in myocardial infarction. The fibers appear elongated and noncontractile, with eosinophilic (pink) cytoplasm and loss of distinctive cross-striations; nuclei are scarce or absent in necrotic cells. In the periphery, viable myocytes tug on adjacent fibers during systole, producing the characteristic waviness. The infarct core is hypo-cellular with meshy eosinophilic areas and early inflammatory cells beginning to infiltrate, consistent with the 6–12 hour window after ischemic onset. These histologic changes reflect irreversible injury, rapid necrosis, and initiation of repair processes. Clinically, recognition of wavy fibers and coagulative necrosis supports an acute MI diagnosis and helps estimate timing, guiding anti-ischemic therapy, reperfusion decisions, and prognostic assessment. This image is representative in education and research contexts for teaching infarct evolution, distinguishing acute from subacute tissue changes, and illustrating the border zone pathophysiology in cardiology and pathology education. This micrograph serves as a teaching tool for students, residents, and researchers studying ischemic injury timelines, scar formation, and therapeutic windows in infarcted myocardium.

This composite educational image details a preclinical study on myocardial ischemia-reperfusion (IR) injury and the cardioprotective effects of active YAP (aYAP) modified RNA (modRNA). Panel A illustrates the experimental design: LAD ligation followed by modRNA and red bead injection, with subsequent histological collection. Panel B presents fluorescence microscopy of heart cross-sections with in vivo MF20 labeling (green), a marker for necrotic cardiomyocytes. The vehicle control (Veh+IR) shows significantly more extensive green fluorescence compared to the aYAP+IR group, which is quantified in Panel C as a reduced percentage of MF20-labeled myocardium. Panel D shows Triphenyltetrazolium chloride (TTC) staining of heart slices from base to apex. Viable tissue stains red, while infarcted tissue appears pale/white. The aYAP+IR group demonstrates visibly smaller infarct zones across all levels compared to the Veh+IR group. This is quantified in Panel E, showing a significant reduction in infarct size. Panel F displays a bar graph of serum cardiac Troponin T (cTnT) concentrations, indicating lower levels in the aYAP-treated group at Day 2, reflecting reduced myocardial damage. The content demonstrates pathophysiology, therapeutic intervention, and diagnostic biomarkers of myocardial infarction.

A multi-panel timeline chart illustrating the clinical and biochemical progression of a patient with immune-checkpoint inhibitor (ICI)-induced multiorgan failure, including myocarditis and myasthenia gravis. The top three line graphs track cardiac and muscle biomarkers: Creatine Kinase (U/L), Troponin I (ug/L), and Brain Natriuretic Peptide (BNP, pg/mL). All markers show a sharp peak followed by a rapid decline toward normalization following the initiation of treatment on day 1 (marked by a vertical dashed line). Middle panels consist of a shaded area graph showing an increase in eyelid distance (mm) from 0 to 4mm and a bar chart demonstrating a steady improvement in Grading Muscle Strength from 2 to 5+. The bottom bar chart detail the methylprednisolone dosage (mg/day), starting at 80 mg/day with a gradual taper after day 17. A timeline footer indicates the timing of diagnostic interventions, including electrocardiography (ECG), coronary angiography (CAG), echocardiography, muscle biopsy, electromyography, and pacemaker implantation. This visual data correlates high-dose corticosteroid therapy with the resolution of biochemical markers and clinical improvement in myopathic and cardiac symptoms.

Educational panel illustrating the cardioprotective effects of ZYZ-488 in a murine model of acute myocardial infarction (MI). Section (a) contains three bar graphs showing serum levels of cardiac biomarkers LDH, CK, and AST, which significantly increase post-MI and decrease with ZYZ-488 treatment. Section (b) displays cross-sections of murine hearts stained with triphenyltetrazolium chloride (TTC); viable tissue appears dark red, while infarcted tissue is pale/white. The MI group shows a large infarct, which is reduced in the ZYZ-488 (Low/High) and LEO (positive control) groups. An accompanying bar graph quantifies the infarct area percentage. Section (c) shows H&E-stained histological microphotographs (200x) of the myocardial border zone. The SHAM group exhibits organized myofibers, while the MI group shows significant tissue disruption and inflammatory infiltration. Treatment groups (ZYZ-488 and LEO) show preserved cardiomyocyte arrangement and reduced inflammatory cell presence, indicating therapeutic attenuation of ischemic injury and preservation of myocardial structural integrity.

This composite of cardiac magnetic resonance (CMR) images illustrates various mechanical and ischemic complications following acute myocardial infarction. (A) Two-chamber long-axis post-contrast view showing a contained chronic rupture of the anterior left ventricular (LV) wall (white arrow). (B) Three-chamber long-axis cine frame demonstrating a large pseudo-aneurysm of the mid-cavity inferolateral wall with a narrow 'tunnel-like' connection (white arrowhead) showing active flow. (C) Short-axis post-contrast image identifying myocardial infarction within the papillary muscles. (D) Short-axis post-contrast sequence highlighting right ventricular (RV) inferior wall involvement (black arrow) associated with basal inferior LV infarction. (E, F) Four-chamber long-axis views in early and late gadolinium enhancement phases, respectively, depicting a large apical thrombus. The thrombus is characterized by a persistent low-signal (dark) intensity in both phases due to its avascular nature. These diagnostic images are essential for characterizing structural damage, identifying myocardium at risk, and distinguishing between true and pseudo-aneurysms in the setting of coronary artery disease.

This set of three cardiac MRI (CMR) images in the horizontal long-axis (four-chamber) view illustrates the complications of an old anterior myocardial infarction in a patient with heart failure. Panel (a) is a cine MRI frame and panel (b) is an early contrast-enhanced MRI (ce-MRI), both demonstrating an apical aneurysm of the left ventricle containing a large, hypoenhanced, non-vascularized mural thrombus (indicated by arrows). Panel (c) shows late gadolinium enhancement (LGE) imaging in the same plane, which highlights transmural hyperenhancement of the apical wall (indicated by arrowheads), characteristic of replacement fibrosis and myocardial scarring. The diagnostic images provide a clinical comparison between early post-contrast sequences used to detect intracavitary thrombi and late enhancement sequences used to assess myocardial viability and infarct size. Key educational concepts include ventricular remodeling, post-infarct aneurysm formation, and the imaging characteristics of mural thrombi versus scarred myocardium.