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Background: A persistent left superior vena cava (PLSVC) is a relatively frequent systemic venous anomaly associated with congenital heart defects. This anomaly has been explained with the persistence of the left superior cardinal vein. PLSVC usually drains into the right atrium, via coronary sinus, but it joins the left atrium in approximately 8% of the cases either directly in the setting of atrial isomerism, or via an unroofed coronary sinus, or through a coronary sinus type atrial septal defect. Case report: We describe a case of an adult patient with atria in the situs solitus, PLSVC draining into the left atrium, atresia of coronary sinus without atrial septal defect, and with additional cardiac anomalies (ventricular septal defect and discrete subaortic stenosis). Conclusion: A possible embryological explanation to this case rises from a right partial isomerism of the superior cardinal veins, which gives reason for both the coexistence of the PLSVC draining into the left atrium and the absence of coronary sinus, atrial septal defect, or coronary sinus ostium.

The pathogenesis of dilated cardiomyopathy in acquired immunodeficiency syndrome (AIDS) is poorly understood. We report a case of an HIV-positive, 45-year-old homosexual male treated with high-dose azidothymidine (AZT, 1,200 mg/day) for two years prior to development of AIDS. He subsequently manifested symptoms of congestive heart failure with left ventricle dilation and a 20% ejection fraction. An endomyocardial biopsy showed no active myocarditis, but intramyocytic vacuoles were found. Transmission electron microscopy revealed mitochondrial cristae with distortion and myofibrillar loss. The clinical consideration was dilated cardiomyopathy in AIDS. His AIDS worsened and he died in October 1991. Autopsy revealed a 100-ml pericardial effusion, cardiomegaly, and biventricular dilation. Vacuolar changes in cardiac myocytes were present. Pathologic findings support a diagnosis of AZT-induced cardiotoxicity. Potential mechanisms are discussed.

Seven explanted hearts from a total of 288 heart transplants performed at UCLA Medical Center had histologic evidence of hypersensitivity myocarditis (prevalence = 2.4%). Three patients had a clinical history of drug allergy, and two had a clinically documented drug reaction prior to transplant. Three patients had peripheral eosinophilia prior to transplant. Five patients with hypersensitivity myocarditis had dilated cardiomyopathy, one had congenital abnormalities, and one had ischemic heart disease. In the period up to 3 weeks posttransplant, four patients had episodes of acute rejection (ISHLT grade 2 to 4) with eosinophils histologically. Results suggest that hypersensitivity myocarditis may have an increasing prevalence in the native heart before transplant and in the newly transplanted heart.

Hypersensitivity myocarditis is a well-known complication of pharmaceutical therapy, often requiring heart transplantation. We report the unusual case of pre-transplant hypersensitivity myocarditis with eosinophilic myocardial infiltration in the donor heart, demonstrated by needle biopsy at the time of transplant ('time-zero' biopsy). At first the myocarditic process was temptatively attributed to a pre-transplant pathology in the donor heart, but the close similarity between the pre-transplant and the post-transplant infiltrate and the clinical data of an eosinophilic peak of the recipient during the transplant procedure brought to the diagnosis of early recurrent hypersensitivity myocarditis.