The aim of this study was to determine the applicability of the polymerase chain reaction (PCR) for routine diagnostic use and for the detection of persistent enteroviral infections. To this end, general primers were selected in the highly conserved part of the 5'-noncoding region of the enteroviral genome. They were tested on 66 different enterovirus serotypes. A specific fragment was amplified from 60 of 66 serotypes. An amplification product was not observed from coxsackievirus types All, A17, and A24 and echovirus types 16, 22, and 23. Enteroviral RNA was detected by the PCR in routinely collected throat swabs and stool specimens that were found to be positive for enterovirus by isolation in tissue culture. Enteroviral RNA was detected in one of five myocardial biopsy specimens from patients with dilated cardiomyopathy, implicating virus persistence. No amplification product was obtained from eight control samples. Our results demonstrate the significance of the PCR for the detection of enteroviral RNA and, in particular, for the demonstration of persistent enteroviral infections.

Electrophysiologic and histologic studies were performed on Langendorff-perfused human hearts from patients who underwent heart transplantation because of extensive infarction. In nine hearts, 15 sustained ventricular tachycardias could be induced by programmed stimulation. In all hearts, mapping of epicardial and endocardial electrical activity during tachycardia was carried out. Histologic examination of the infarcted area between the site of latest activation of one cycle and the site of earliest activation of the next cycle revealed zones of viable myocardial tissue. In two hearts in which the time gap between latest and earliest activation was small, surviving myocardial tissue constituted a continuous tract that traversed the infarct. In three other hearts in which the time gap was large, surviving tissue consisted of parallel bundles that coursed separately over a few hundred micrometers, then merged into a single bundle and finally branched again. The direction of the fibers within the bundles was perpendicular to the direction of the activation front in that area. A similar type of inhomogeneous anisotrophy and activation delay was found in an infarcted papillary muscle removed from one of the explanted hearts and studied in a tissue bath during basic stimulation. Histologic examination of this preparation revealed that the delay was caused by a zigzag route of activation over branching and merging bundles of surviving myocytes separated by connective tissue.

To determine the incidence of active cytomegalovirus (CMV) infection after organ transplantation and its relationship with the immune system, 55 renal and 14 cardiac transplant recipients were closely monitored for active CMV infection (expression of CMV immediate early antigen in granulocytes-antigenemia-and positive cultures) and immune parameters. All 19 CMV-seronegative recipients with seronegative donors remained seronegative, showing that no CMV transmission occurred by leukocyte-depleted blood products. Primary CMV infection occurred in 4 of 11 (36%) patients with positive donors and was symptomatic in 1 (9%) patient. Active CMV infection was found in 29 of 39 (74%) seropositive patients and was symptomatic in 3 (8%) patients. CMV antigenemia was always the first indication of active CMV infection (antigenemia, on average, at day 45 ± 15; immunoglobulin G rise at day 71 ± 36; and positive cultures at day 70 ± 17). Cellular immunity, as measured by lymphocyte proliferation (LPT), proved to be of importance in the prevention of active CMV infection, as 14 of 15 patients with negative LPT obtained active CMV infections with antigenemia and positive cultures, whereas 1 of 10 patients with positive LPT did so (P < 0.0001).

Objective-To describe the causes and circumstances of death regarding patients who died in 1994 and 1995 while on a waiting list for cardiac surgery in the Netherlands. Design-Retrospective multicentre case study. (Heart 1999;81:593-597) Setting-11