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To obtain a valve with better hemodynamic performance and longer durability than the currently available bioprostheses, a single-cusp pericardial xenograft has been developed. This valve has been tested extensively both in vitro, in a pulse duplicator and in a fatigue-testing system, and in vivo, in a series of dogs and sheep. Hemodynamic studies showed improved hemodynamic performance compared with other biological and mechanical valves. Effective orifice areas were larger and performance indexes higher, especially in the small sizes. Accelerated fatigue testing showed durability significantly superior to that of other biological devices. Animal experiments have established that the single cusp remains pliable even after more than two years of insertion. There is a low incidence of calcification and good preservation of the collagen matrix. This preliminary experience demonstrates that the unicusp pericardial xenograft has superior hemodynamics, increased resistance to fatigue-induced lesions, and a low incidence of calcification. These results might indicate an extended in vivo durability for this device.

Ultrastructural studies of the extracellular collagen matrix were made on the "stunned" myocardium using scanning, conventional and high voltage transmission electron microscopy and light microscopy. Regional myocardial dysfunction was produced by 12 sequential 5 minute occlusions of the left anterior descending coronary artery, separated by 10 minute intervals of reperfusion. A final 90 minute reperfusion period documented persistent myocardial dysfunction. At the end of the final reperfusion period, the percent systolic shortening, measured by sonomicrometers, was depressed significantly to 35 +/- 9% of baseline. The heart was then perfusion fixed, and samples were taken from both control and stunned areas. No changes associated with irreversible cellular damage were noted in the stunned region. However, scanning electron microscopy of the stunned area showed that the extracellular collagen matrix underwent profound structural changes. Collagen cables were roughened, uncoiled and discontinuous. Linear grooves on the surface of the myocytes were frequently seen, indicating complete loss of collagen cables. The usual dense collagen weave surrounding myocytes became patchy or absent. Myocyte to myocyte struts were sparse and frequently absent, with remnant nodular or nublike structures indicative of breakage. High voltage electron microscopy of the stunned area showed that the collagen struts were discontinuous and vacuolated with rounded tips. Light microscopy of silver-stained sections of the stunned tissue demonstrated large patchy areas that were devoid of silver, indicating absence of the collagen matrix. There was a progressive increase in percent systolic bulging during each sequential coronary occlusion, suggesting increasing myocardial compliance. These results indicate that the myocardial collagen matrix is severely damaged from reversible ischemic cell injury. The greater myocardial compliance and less effective contractile effort in the stunned myocardium might be explained on a structural basis: disruption of the mechanical coupling function provided by the extracellular collagen matrix.

A 40-year-old homosexual man with the acquired immunodeficiency syndrome (AIDS) presented with dyspnea and renal insufficiency. A chest radiograph showed cardiomegaly and prominent pulmonary arteries, without alveolar infiltrates. Swan-Ganz catheterization revealed pulmonary hypertension and no evidence of left-to-right shunt. Liver function tests were normal. He was treated empirically for Pneumocystis carinii pneumonia, but he died 3 days after admission. At autopsy, membranoproliferative glomerulonephritis type III, P. carinii pneumonia, and plexogenic pulmonary arteriopathy were found. The kidney and lung were studied by electron microscopy and immunohistochemistry. Electron-dense immunoglobulin deposits were identified in glomerular capillaries and were confirmed by immunohistochemistry, but the pulmonary plexogenic lesions were negative. The combination of membranoproliferative glomerulonephritis and plexogenic pulmonary arteriopathy has not been described in AIDS to date.

Primary familial cardiomyopathy, once exclusively associated with hypertrophic disorders, is now recognized to occur in a dilated or congestive form. In some instances, characteristic myocellular inclusions of varying morphologies have been identified. Nemaline rods are inclusions which typically have been linked with a rather benign and nonprogressive congenital myopathy. We report finding myocellular inclusions consistent with nemaline rods in two brother who died with congestive cardiomyopathy. Although there was no history or clinical evidence of a myopathy, characteristic nemaline rod inclusions were also identified in the skeletal muscle of one sibling.