Myocarditis

Myocarditis is documented at autopsy in up to 50% of AIDS patients who died from non­cardiac causes [2] and in 31-83% of patients with clinical signs of congestive heart failure [1].

Pathologic Findings

On gross examination, a marked dilation of the cardiac chambers is almost always pres­ent. In most cases, owing to the focal distri­bution of inflammation and myocyte necro­sis, the myocardium is not flabby as it is in hearts with a diffuse inflammatory response. Heart weight is within normal limits. According to the Dallas criteria [4], active myocarditis is characterized by multi­focal or diffuse interstitial inflammatory infiltrates associated with degenerative changes or frank myocyte necrosis (Fig. 1). Histological findings in HIV-infected patients with myocarditis do not substan­tially differ from those observed in seroneg­ative patients. However, the degree of inflammatory infiltrate is generally milder. This is believed to result from the impaired efficiency of cell-mediated immunity [2]. In addition, the inflammatory infiltrate is mainly made by CD8+ lymphocytes, and aberrant expression of class II human leuko­cyte antigens (HLA) by cardiac myocytes is much rarer than in HIV-negative myocardi­tis [5]. The severity of clinical symptoms is not always related to the degree of myocar­dial inflammation and damage.

Histology and immunohistochemistry rarely detect the presence of viruses in the myocardium. However, in situ hybridization or polymerase chain reaction studies reveal a high frequency of either cytomegalovirus or HIV-1, or both, in AIDS patients with lym­phocytic myocarditis and severe left ventric­ular dysfunction [1, 6] (Fig. 2). These data support the hypothesis that, at least in a subset of patients, HIV-1 has a pathogenic action and possibly influences the clinical evolution towards dilated cardiomyopathy [2,3].

Fig. 1 AIDS-related active lymphocytic my­ocarditis. There is a marked interstitial lym­phocytic infiltrate and myocyte necrosis. H&E, x20

Opportunistic myocardial infection is generally part of systemic infections. Fun­gal lesions are visible on gross examination as multiple, small, rounded plaques of whitish color, often hemorrhagic. On histol­ogy, the pathogens most frequently observed are protozoa such as T. gondii, or fungi such as Candida albicans, Cryptococcus neoformans, and Aspergillus spp. [2,3]. Myocardial and cerebral toxoplasmosis are often associated; histological examination shows “pseudocysts” packed with the proto­zoa within cardiac myocytes [2, 3]. Bacterial myocarditis is not infrequent in HIV-infect­ed drug addicts with infective endocarditis. It is a consequence of coronary emboliza­tion from valve vegetations [2].