Cross section of the ventricles showing subendocardial infarcts in the anterior and posterolateral walls that extend into the septum. The infarcts have a gelatinous texture and the red areas represent granulation tissue. Bordering the infarcts, there are subtle areas of white gray discoloration which represent areas of early scar formation. Also note the infarct in the anterolateral papillary muscle.

Cross section of the ventricles fixed in formalin after incubation in nitroblue tetrazolium chloride . Nitroblue tetrazolium is transformed to blue/purple dye by lactic dehydrogenase, indicating viable tissue. This image shows two distinct infarcts (lack of blue/purple staining) in the posterior wall of the left and right ventricles. This stain accurately detects infarcts less than 4 h in evolution, before any reliable histologic finding can be seen.

The myocardiu m shows a yellow demarcation between the viable subepicardial myocardium and infarcted subendocardial myocardium on the left. The infarct becomes transmural on the right side of the field. The paler yellow border represents the zone of maximal infiltration of neutrophils at 2–3 days.

An extensive transmural anteroseptal left ventricular infarct shows thinning of the myocardium with gelatinous change consistent with early scar formation between 7 and 14 days. Islands of necrotic myocardium may persist in large infarcts as seen in the anterior wall in this case. A healed infarct with white scar is present in the posterolateral wall.

Surgical specimen showing a segment of mitral valve and a ruptured papillary muscle secondary to myocardial infarction. Note the pale myocardium with hemorrhages and the ragged edges of the papillary muscle head.

Acute transmural infarction in the posterior wall evolved into a rupture site. The image shows a serpiginous hemorrhagic path of the blood dissecting through the necrotic myocardium.

A pseudoaneurysm with laminated thrombus is shown surrounded by fibrous tissue and pericardium. A pseudoaneurysm results from a contained rupture of the ventricular wall and communicates with the ventricular cavity through a narrow neck. In comparison, a true ventricular aneurysm results from dilatation of the scarred myocardium.

Coagulation necrosis of the myocardium showing hypereosinophilic sarcoplasm of the myocytes with indistinct or frankly blurred striations and loss of nuclei.

Colliquative myocytolysis showing large vacuolated sarcoplasm of myocytes due to hydropic change. It usually occurs in subendocardial location. It may also be seen in areas of “hibernating” myocardium in chronic ischemic injury.

Contraction band necrosis showing transverse hypereosinophilic bands alternating with pale granular spaces along the length of the myocytes. The transverse bands result from overlapping of hypercontracted sarcomeres within a myocyte. For comparison the myocytes in the lower portion of the field do not show contraction band necrosis.

An early morphologic change in acute myocardial infarction is the appearance of wavy and thinned fibers. Note the capillary congestion in these areas, lack of polymorphonuclear infiltration, and presence of hypereosinophilic fibers in the myocytes.

Margination of polymorphonuclear leukocytes is one of the earliest unambiguous changes in myocardial infarcts. It is seen as early as 4–6 h postinfarction.

Once the polymorphonuclear leukocytes marginate inside capillaries near the infarcted area, they begin to diapedese into the extracellular space and infiltrate the surrounding myocardium. This change usually starts at around 6–8 h and increases with time as more polymorphonuclear leukocytes are chemoattracted to the infarcted myocardium.

The top panel shows frank infiltration of the interstitium by further diapedesis of polymorphonuclear leukocytes. The myocardium shows coagulation necrosis. This amount of polymorphonuclear leukocyte infiltration occurs at around 24 h of evolution of the infarct. The nuclei of the myocytes are not staining, but striations can still be identified in the sarcoplasm. The middle panel shows extensive karyorrhexis of the polymorphonuclear leukocytes, which imparts a “dusty” basophilic appearance and is observed at 3–4 days postinfarct. The lower panel shows a zone of basophilia representing polymorphonuclear cells undergoing karyorrhexis between the zone of coagulative necrosis on the left and viable myocardium on the right.

In the deepest areas of a large infarct, the acute inflammatory infiltrate may not reach and promote lysis of the myocytes. Thus, dead myocytes appear eosinophilic, but do not show nuclei (karyolysis). Similarly the endothelial cells of the capillaries undergo karyolysis. However, as the repair response approaches this core, it shows abundant fibroblasts, and hemosiderin-and-lipofuscin laden macrophages become ubiquitous (inset and lower image). This infarct is about 7 days in evolution.

Another pattern commonly seen is the disappearance of myofibrils from the sarcoplasm, which leaves empty spaces bounded by the sarcolemma resulting in an alveolar pattern with scattered macrophages. This pattern is usually seen in small areas of infarction or in the outer zone of a large infarct. The lower image shows a healing transmural infarct with pale and dark blue zones of collagen deposition. Note the mural thrombus with the red fibrin in a trichrome stain (red).

A healed transmural infarct of the anterior septum and a small portion of the anterior left ventricular wall appear as dense white scar with focal calcification. There is an apical thrombus. Note the fine areas of gray white fibrosis in the noninfarcted myocardium. The right ventricle shows a segment of a pacing lead with a fibrous tissue cuff surrounding it.

A case of dilated cardiomyopathy with enlargement of all four chambers, most severe in the left ventricle which appears globular. The wall thickness may be normal as the hypertrophy is masked by the dilatation. The right ventricle shows a segment of a pacing lead well anchored in the apex of this chamber.

This heart shows marked hypertrophy of the interventricular septum which is twice as thick as the left ventricular free wall. There is dilatation of the other chambers as well with a white organizing thrombus in the right atrial appendage.

In hypertrophic cardiomyopathy, the hallmark of the disease is “disarray.” Disarray occurs at the fascicle level, myocyte level, and sarcomere level. At the myocyte level, the myocyte sarcoplasm is disorganized forming branches in contrast to a normal parallel arrangement in sections taken from the interventricular septum. The disarray is also evident in the myofibrils within individual myocytes. This is often accompanied by interstitial fibrosis as shown in the trichrome stain.

The intramural coronary arteries in the septum of hearts with hypertrophic cardiomyopathy are often abnormal. The lumen is narrowed, and the wall is thickened by an increase in the smooth muscle cells and ground substance in the media.

The outflow tract of the left ventricle in the obstructive type of hypertrophic cardiomyopathy shows endocardial thickening with fibrosis and elastosis evident in the Movat stain.

Transilluminated specimen shows loss of the compact zone in the right ventricle which appears translucent in a case of arrhythmogenic right ventricular cardiomyopathy. Also note the thinning of the left ventricular wall and interventricular septum toward the apex due to fibrofatty replacement.

The right ventricular wall of the same heart in Fig. 27.23 is shown. The compact zone is discontinuous with fatty infiltration and fibrous replacement. The trabecular myocardium is relatively spared.

In addition to the marked thinning of the wall of the right ventricle (shown on the right) due to fibrofatty replacement in arrhythmogenic right ventricular cardiomyopathy, involvement of the left ventricle with fatty infiltration producing a “moth-eaten” appearance is seen in almost half of the cases. Note the irregular contour of the subepicardium of the left ventricle in this example.

Section of the right ventricular wall with extensive adipose tissue replacement of the compact zone and trabecular myocardium as shown in an H&E stain and corresponding Movat stain. The Movat stain highlights the fibrous tissue in yellow.

In extensive cardiac amyloidosis, the atria are enlarged, and the endocardium of both atria shows fine yellow-ochre granular surface due to amyloid deposition. These deposits are also seen in the tricuspid and mitral valve leaflets. The ventricular myocardium shows subtle areas of pallor which correspond to amyloid deposits.

Amyloid infiltration in the heart shows “amorphous” eosinophilic material accumulating in the extracellular space. The amyloid is deposited throughout the interstitium surrounding individual myocytes (top panel). In advanced disease, there is more pronounced myocyte atrophy with accumulation of the interstitial deposits into a nodular pattern (bottom panel).

Interstitial amyloid shows apple-green birefringence on polarization microscopy (top panel) when stained with Congo red. Amyloid deposits also appear fluorescent with thioflavin-S or thioflavin-T staining viewed under fluorescence microscopy. This is a more sensitive and reproducible stain than Congo red.

Immunohistochemical staining is useful for typing of cardiac amyloidosis. The top panel shows focal deposits of transthyretin in a coarse interstitial pattern and forming small nodules. The bottom panel shows a diffuse interstitial perimyocytic pattern of deposition in light-chain amyloidosis where lambda light chains are at least twice as frequently seen compared to kappa light-chain deposition.

The myocytes are enlarged with pale sarcoplasm due to massive accumulation of glycogen that stain PAS positive in a case of Pompe disease (top panel). In the adult, glycogen storage disease may appear as irregular vacuoles associated with interstitial fibrosis (bottom panel).

A few myocytes show accumulation of basophilic material in the sarcoplasm that is intensely positive with PAS. This type of glycogen deposition can be seen in type IV glycogen storage disease and in hearts of patients older than 65 years of age (basophilic degeneration).

The myocytes contain dark yellow-to-brown granular deposits mostly in perinuclear location (top panel) which are readily identified as iron on a Prussian blue stain (bottom panel) in a case of hemosiderosis.

In Fabry disease, there is marked vacuolation of the myocytes. The myofibrils are displaced to the periphery by the deposits occupying the central clear to finely granular area (top panel). On toluidine blue stain of a semithin section, the glycolipid deposits are evident as dark blue metachromatic deposits. Ultrastructural examination demonstrates that the metachromatic deposits are in fact the characteristic lamellar bodies seen in Fabry disease.

Giant cell myocarditis showing an aggressive inflammatory infiltrate notable for the presence of multinucleated giant cells and variable amount of eosinophils in both images. Well-formed granulomas are absent.

A case of cardiac sarcoidosis with marked biventricular dilatation of the heart. There is sclerotic white “waxy” appearing formation of scars in the interventricular septum and posterior right ventricular wall. Mural thrombi are present in the right ventricle.

Cardiac sarcoidosis showing discrete noncaseating granuloma in the myocardium (top panel). Small granulomas and multinucleated giant cells typically persist within dense fibrosis in areas of gross scarring (bottom panel).