In order to determine if cardiac tissue from AIDS patients or patients with seropositivity to HIV-1 might be infected by HIV-1, portions of myocardium obtained postmortem were evaluated for HIV-1 DNA sequences. Cellular DNA was extracted and digested with EcoR1 and Southern blots were performed. One of three AIDS hearts was positive for HIV-1 DNA sequences without amplification, whereas two additional hearts were positive for HIV-1 DNA after amplification. Accordingly, other tissue from the heart positive for HIV-1 without amplification was studied by electron microscopy to localize HIV virions. Unexpectedly, large numbers of proliferating multilamellated membrane bodies were identified in myocytes, predominantly associated with mitochondria. Identical membrane bodies were found in two additional AIDS hearts, and in one heart from a patient with seropositivity to the AIDS virus, but in none of three similarly fixed controls. Immunocytochemistry for HIV core (p24) and envelope (gp120) antigens did not localize gold-labeled antibodies to the membrane bodies. We believe this membranopathy may be an HIV-1- or AIDS-specific abnormality of unknown etiology that may be related to the ultimate development of cardiomyopathy. In addition, our studies provide further support that HIV-1 may be present in AIDS hearts, although as yet we cannot state with certainty where the HIV-1 is located in these tissues.

Studies of normal hearts have revealed a variety of intrinsic connective tissue structures that surround and interconnect myocytes and ventricular mural layers. Among these structures, springlike coiled perimysial fibers, arrayed parallel to myocytes in the interstitial space, have been described in papillary muscle and ventricle. To evaluate the role of the coiled perimysial fibers under perturbed conditions, rat ventricles were filled with barium-gelatin under different pressures and fixed, and then the myocardium was impregnated with silver to visualize the connective tissue. Ventricles were filled at 30, 70 and 100 to 120 mm Hg. The coiled perimysial fibers were studied for their orientation, stretch, integrity and relation to sarcomere length. The coils were noted to embed within the fibrous anulus and to knot into an umbilical-like mass at the apex, thus anchoring them at both ends of the ventricle. They underwent focal straightening even at 30 mm Hg, with generalized straightening and disruption at the highest pressure; changes were most pronounced in the midventricle. Sarcomeres were maintained below 2.2 micron at 30 and 70 mm Hg of cavity pressure in regions of coiled perimysial fiber stretch; only with fiber disruption at 100 to 120 mm Hg were sarcomeres significantly lengthened. Other findings included connective tissue disruption between ventricular wall layers that allowed slippage of myocytes and mural thinning. These observations suggest that coiled perimysial fibers may act as a buffer to protect myocytes from damage under the effects of high cavity pressure.