Cardiovascular

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Figure 42.1 Adriamycin cardiotoxicity, manifesting as vacuolar areas of sarcoplasmic myofiber loss (arrows). This change is apparent in both plastic embedded thick sections stained with toluidine blue O (left) and by transmission electron microscopy (right)

Figure 42.2 Restrictive eosinophilic endomyocardial disease, with organizing mural thrombus in the right ventricle apex (left). The thrombus is eosinophil-rich and there is an associated eosinophilic myocardial infiltrate (right)

Figure 42.3 Arrhythmogenic cardiomyopathy, with primarily right ventricular involvement (by fibrofatty replacement of ventricular myocardium)

Figure 42.4 Left ventricular noncompaction cardiomyopathy with left ventricular hypertrabeculation comprising more than half of the ventricular thickness (highlighted by trichrome staining)

Figure 42.5 Giant Cell Myocarditis. Scattered multinucleated giant cells accompanied by lymphocytes are seen in association with loss of myocardial fibers. There are no granulomas and myocyte damage is widespread, and eosinophils are present in the background

Figure 42.6 Cardiac sarcoidosis with multinucleated giant cells within well-formed granulomas. The surrounding myocytes are relatively intact

Figure 42.7 Pertinent Pathologic Changes in Cardiac Allografts. A, Endomyocardial biopsy with mild acute cellular rejection. There is patchy perivascular lymphocytic infiltrate with no myocyte injury. B, Moderate acute rejection showing inflammation and myocyte damage. C, Antibody-mediated rejection features including "activated intravascular mononuclear cells." D, Positive staining for complement component C4d by immunohistochemistry and immunofluorescence methods in antibody-mediated rejection. E, Acute/subacute ischemic changes including edema, inflammation and "wavy" myocytes showing focal contraction bands. F, Cardiac allograft vasculopathy with concentric narrowing of epicardial coronary artery by fibromuscular intimal proliferation. Note the preservation of internal elastic lamina (Elastic-van Gieson stain)

Figure 42.8 Gross and microscopic features of common mitral valve diseases (note the myxoid expansion of myxomatous disease and well- formed vessels in the valve layers in rheumatic disease)

Figure 42.9 Gross features of aortic stenosis (note the number and proportionality of cusps and presence of commissural fusion help dis- tinguish various disease processes)

Figure 42.10 Gross features of aortic valve endocarditis (active and healed) involving three-leaflet and bicuspid valves

Figure 42.11 Gross Appearance of Cardiac Myxoma. The lesion has a polypoid shape and a hemorrhagic appearance. A portion of atrial septal wall is attached at the "stalk" base

Figure 42.12 Cardiac myxoma showing a concentric arrangement of tumor cells around vascular spaces; highly characteristic of myxoma

Figure 42.13 "Glandular" Myxoma. The glandular epithelium is tall columnar and contains intracytoplasmic mucin. This rare type of myxoma should not be confused with metastatic adenocarcinoma

Figure 42.14 Gross features of papillary fibroelastoma (note how the delicate fronds become apparent when floating in clear liquid)

Figure 42.15 Microscopic features of papillary fibroelastoma with highly branched papillary architecture and dense elastin rich cores lined by flattened endothelium

Figure 42.16 So-Called Cardiac MICE. A, This process is composed of an admixture of plump histiocytes and ribbons of small cuboidal mesothelial cells. B, The immunostain for keratin highlights the mesothelial cell component, which is surrounded by the negative histiocytes and other mononuclear cells

Figure 42.17 So-called cystic tumor of the atrioventricular nodal region. In this case the lining of the cysts had a definite squamoid quality

Figure 42.18 Gross appearance of a large angiosarcoma of the hear

Figure 42.19 Primary synovial sarcoma of heart showing typical biphasic appearance

Figure 42.20 Large metastatic carcinoma in left atrium that was continu- ous with tumor in left pulmonary vein. This mass simulated an atrial myxoma by echocardiography. The primary tumor was a mucoepidermoid carcinoma of left submaxillary gland

Figure 42.21 Comparative histology of muscular (top) and elastic (bottom) arteries

Figure 42.22 Arterial Wall Remodeling in Atherosclerosis. The wall segment underlying the atherosclerotic plaque shows marked thinning (bottom arrow) compared to the normal wall segment opposite the plaque (top arrow)

Figure 42.23 Ruptured Atherosclerotic Plaque and Luminal Throm- bosis (Atherothrombosis). An arrow points to the site of probably plaque rupture (note the inflammatory infiltrate in the plaque and adventitia)

Figure 42.24 Cross section of stented artery, using plastic resin embed- ding techniques, metallic stent sections appear opaque (black). The native plaque as well as neo-intimal plaque formation are apparent

Figure 42.25 Cross Section of Stented Artery, Using Stent Dissolution Techniques. Holes can be seen where the stent struts were situated prior to dissolving (right). Specimen radiography can be helpful in identifying the location of stents, prior to dissolving (left)

Figure 42.26 Routine Histologic Sampling of Bypass Grafts. The anastomotic site should be serially sectioned to locate the joining point of native vessel and graft (arrow). Step sections through the block may be helpful in visualizing this histologically

Figure 42.27 Arterial aneurysm types and their morphologic and clinical association

Figure 42.28 Abdominal aortic aneurysm with mural thrombus (note the presence of atherosclerotic changes and the asymmetric (saccular) configuration of the aneurysm

Figure 42.29 Ascending aortic aneurysm and bicuspid aortic valve. Note the uniform symmetric (fusiform) dilatation of the aneurysm

Figure 42.30 Medial Degenerative Changes in Ascending Aortic Aneurysm. A, "Cystic" change (translamellar mucoid extracellular matrix accumulation). B, More subtle elastic fiber fragmentation and intralamellar mucoid extracellular matrix accumulation

Figure 42.31 Aortitis with (top) and without giant cells (bottom). The inflammatory component is intimately associated with areas of smooth muscle cell nuclear loss and elastic laminal collapse

 Figure 42.32 Intimal tear in the descending thoracic aorta with acute dissection. Histologically, the tear is associated with fibrin coating of the rupture tract

Figure 42.33 Aortic Dissection, Cross Section. Thrombus fills the intra-medial "false" lumen, compressing the true lumen beneath

Figure 42.34 Aortic Coarctation. A discrete segment of marked nar- rowing in the pediatric aorta excised during coarctation repair (top). Sections should be oriented in longitudinal section to the ductus arteriosus (black arrow). Focal intimal thickening can often be seen opposite this (white arrow)

Figure 42.35 Cystic Adventitial Disease. Multiple irregular cystic spaces are seen surrounding the adventitia of this popliteal artery. Some appear to contain mucoid material

Figure 42.36 Fibromuscular Dysplasia (Medial Type). Irregular (fes- tooned) luminal contours are created by disorganized medial smooth muscle arrangements

Figure 42.37 Arteriovenous Malformation. Irregular vascular spaces with varying wall thicknesses are seen in this soft tissue arteriovenous malformation

Figure 42.38 Thromboangiitis Obliterans (Buerger Disease). Hallmark features include transmural inflammation (of veins and arteries), recanalized luminal thrombus, and preservation of the internal elastic lamina

Figure 42.39 Takayasu Aortitis. Marked adventitial fibrosis and patchy lymphoplasmacytic inflammation, characteristic (although not entirely specific for) Takayasu disease

Figure 42.40 Coronary artery involvement by Takayasu arteritis, manifesting as fibrotic wall thickening with lymphoplasmacytic inflammation and intimal multinucleated giant cells (again the clinical context of aortitis with primary branch involvement in a young woman is needed to confirm Takayasu disease)

Figure 42.41 Giant cell aortitis with ribbon-like areas of elastic laminar collapse, cuffed by lymphohistiocytic inflammation including multinucleated giant cells (inset)

Figure 42.42 Giant cell-temporal arteritis showing transmural lympho- histiocytic inflammation with multinucleated giant cells near the internal elastic lamina

Figure 42.43 Coronary (Pseudo)aneurysm in Kawasaki Disease. Coronary angiogram showing a proximal (pseudo)aneurysm (left). The aneurysm wall shows wisps of internal elastic lamina at one edge (confirm- ing contained rupture-pseudoaneurysm)

Figure 42.44 Polyarteritis Nodosa. Vascular lesions in the liver (elastic stains) showing features of active/ subacute fibrinoid necrotizing arteritis (left) and segmental wall destruction with contained rupture (pseu- doaneurysm) (right). Temporal variability (active and healed lesions in the same organ) is a hallmark feature of polyarteritis nodosa

Figure 42.47 Podoplanin (D2-40) staining of breast tissue to evaluate for lymphatic invasion of an adjacent tumor. The lymphatic channel endothelium stains intensely for D2-40, whereas the arterial and venous endothelium does not