Fig 13.9 Photomicrograph of an 8-day-old boy with positive PCR for Enterovirus in myocardium. There is a heavy inflammatory cell infiltrate with loss of myocytes. Lymphocytes predominate but eosinophils and neutrophils are also present.

Fig 13.10 Same case as Fig 13.9 stained with anti-CD3 antibody. There are large numbers of positive T-cells in the myocardium.

Fig 13.11 Same case as Fig 13.9 stained with anti-CD79a antibody. There are only scattered B-cells.

Fig 13.12 Same case as Fig 13.9 stained with antibody to CD68. There are large numbers of macrophages in the inflammatory cell infiltrate.

Fig 13.13 Photomicrograph of an 8-year-old girl with Parvovirus B19 myocarditis. There is a lymphocytic infiltrate and the myocytes show disintegration and necrosis.

Fig 13.14 Same case as Fig 13.9 stained for fat. Note extensive accumulation of lipid droplets in the myocyte cytoplasm. In this context, the finding of abundant cytoplasmic lipid does not indicate a disorder of fatty acid oxidation. (Frozen section stained with Oil-red-O)

Fig 13.15 Photomicrograph of heart from an 8-year-old boy with severe cardiomyopathy. Biopsy at the time of insertion of ventricular assist device. There is giant cell myocarditis. The giant cells are multinucleate and there is a heavy background lymphocytic infiltrate as well as extensive myocyte destruction. Contraction bands are evident in the lower field.

Fig 13.16 Photomicrograph of heart from a 3-day-old female infant with eosinophilic myocarditis. PCR for viruses negative. There are numerous eosinophils in the myocardium with flocculation of the myocyte cytoplasm.

Fig 13.17 Photomicrograph of an endomyocardial biopsy from a 12-year-old girl with acute heart failure secondary to anti-phospholipid syndrome. A small myocardial artery shows thrombotic occlusion. Other small arteries in the specimen were also occluded.

Fig 13.29 Same case as Fig 13.6. Electron photomicrograph of a cardiac myocyte showing a huge mitochondrion with tubular cristae and dense inclusion.

Fig 13.30 Macroscopic photograph of the explanted heart from a 14-year-old boy with arrhythmogenic right ventricular cardiomyopathy. A transverse section of the heart shows both ventricles with fibrosis and fatty infiltration.

Fig 13.51 A 17-year-old who underwent heart transplant 5 years previously for dilated cardiomyopathy. Macroscopic photograph of the right atrioventricular groove with right coronary artery. There is concentric luminal narrowing. The thickened wall is bright yellow around half of its circumference. There is chronic allograft vasculopathy and also acute cellular rejection.

Fig 13.52 Same vessels as in Fig 13.51. Photomicrograph showing increased adventitial collagen. The tunica media is fibrotic. There is focal disruption of the internal elastic lamina and there is concentric intimal fibroelastic thickening. The appearance is typical of chronic allograft vasculopathy. (Elastic van Gieson)

Fig 13.53 Same vessel as in Figs 13.51 and 13.52. Photomicrograph showing chronic allograft vasculopathy. A section through the vessel wall in which the adventitia is to the left and the intima to the right. There is fibrous replacement of much of the medial smooth muscle with a focal lymphocytic infiltrate. There is intimal fibrous thickening. There is an infiltrate of foam cells throughout the wall. This is in contrast to atherosclerosis where the foam cells are largely confined to the intima.

Fig 13.61 Photomicrograph of an endomyocardial biopsy showing antibody mediated rejection, with interstitial edema, swelling of endothelial cells and intravascular accumulation of inflammatory cells. The endothelium stained positively for C4d. The diagnosis of antibody mediated rejection requires combined evidence of graft dysfunction, the presence of alloantibodies, and histological changes, such as present here.

Fig 13.62 Photomicrograph of myocardium with antibody mediated rejection stained with antibody to C4d. There is strong staining of capillary endothelium. A 6-year-old girl four years after transplant with deteriorating cardiac function; there was no evidence of cell mediated rejection on biopsy. In many cases the significance of positive staining for C4d is uncertain and the result must be interpreted in the light of the clinical condition. (immunohistochemical staining for C4d)

Fig 13.72 Segment of neonatal aorta removed for coarctation. The tubular segment of aorta is viewed end on and demonstrates the pinpoint lumen.

Fig 13.73 Photomicrograph of a segment of aorta with coarctation. The proximal resection margin is to the left of the picture. There is narrowing of the lumen by a sling of ductal tissue (recognizable by its loose pale appearance). Distally, there is elastic thickening of the aortic intima. (Elastic van Gieson)

Fig 13.75 Photomicrograph of the renal artery from Fig 13.74. The muscular media is irregularly thinned and very fibrotic. There is disruption of the internal elastic lamina and variable intimal fibroelastic thickening. (Elastic van Gieson)

Fig 13.76 Macroscopic photograph of the mural leaflet of the mitral valve from a 16-year-old with Marfan’s syndrome and severe mitral regurgitation and heart failure. The leaflet is irregular and thickened, with redundant tissue. The tendinous cords are stretched and thin. The sutures from the previous annuloplasty are visible above the leaflet.

Fig 13.77 Photomicrograph of the valve from Fig 13.76. The valve fibrosa is visible toward the upper part of the photo. The spongiosa shows some myxoid thickening and the atrial aspect shows laminar accretions of fibrous and elastic tissue. (Elastic van Gieson)

Fig 13.78 Photomicrograph of the aorta removed during aortic root repair in a patient with Marfan’s syndrome. The adventitia is to the right of the field. There is near complete loss of the normal parallel array of elastic fibers with replacement by collagen. This process is most severe in the center of the field. (Elastic van Gieson).

Fig 13.81 Photomicrograph of cardiac rhabdomyoma in which the constituent cells are large, much larger in diameter than normal cardiac myocytes. They show central nuclei and have clear cytoplasm. The nucleus is sometimes connected to the cell membranes by thin strands of cytoplasm; so-called ‘spider cells’.

Fig 13.82 Photomicrograph of the myocardium of a heart with histiocytoid cardiomyopathy. Note the histiocytoid cells are small, smaller than the normal cardiac myocytes, and have cytoplasm containing multiple small vacuoles, rather than the enlarged and clear cytoplasm of rhabdomyoma cells.

Fig 13.83 Macroscopic photograph of a cardiac fibroma. The specimen has a firm whorled, white cut surface, resembling a uterine fibroid.

Fig 13.84 Photomicrograph of a cardiac fibroma. The constituent cells are spindle-shaped with wavy nuclei and indistinct cell borders. There are set in a fibrillary collagenous background.

Fig 13.85 Photomicrograph of a cardiac fibroma with a focus of extramedullary hematopoiesis. A collection of erythroid and myeloid precursor cells are present in an otherwise typical fibroma.