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The frequently observed de-endothelialization of venous coronary bypass grafts prepared using standard methods exposes subendothelial prothrombotic cells to blood components, thus endangering patients by inducing acute thromboembolic infarction or long-term proliferative stenosis. Our aim was to gain deeper histological and physiological insight into these relations. An intricate network of subendothelial cells, characterized by histological features specific for true pericytes, was detected even in healthy vessels and forms, coupled to the luminal endothelium, a second leaflet of the macrovascular intima. These cells, and particularly those in the venous intima, express enormous concentrations of tissue factor and can recruit additional amounts of up to the 25-fold concentration within 1 h during preincubation with serum (intimal pericytes of venous origin activate 30.71 ± 4.07 pmol coagulation factor x∙min-1∙10-6 cells; n = 15). Moreover, decoupled from the endothelium, they proliferate rapidly (generation time, 15 ± 2.1 h, n = 8). Central regions of atherosclerotic plaques, as well as of those of restenosed areas of coronary vein grafts, consist almost completely of these cells. In stark contrast with the prothrombogenicity of the intimal pericytes, intact luminal endothelium recruits high concentrations of thrombomodulin (CD 141) specifically within its intercellular junctions, activates Protein C rapidly (42 ± 5.1 pmol/min∙106 venous endothelial cells at thrombin saturation; n = 15), can thus actively prevent coagulatory processes, and never expresses histologically detectable and functionally active tissue factor. Given this strongly prothrombotic potential of the intimal pericytes and their overshooting growth behavior in endothelium-denuded vascular regions, they may play important roles in the development of atherosclerosis, thrombosis, and saphenous vein graft disease. [ABSTRACT FROM AUTHOR]

Since August 1981, 33 orthotopic heart transplantations were performed in our hospital. Three of these patients (9%) had sinus bradycardias with rates as low as 30 beats/min; they were treated by implantation of a dual chamber pacemaker. Those patients had two atria as a result of orthotopic heart transplantation, but only the donor atrium was suitable for positioning the atrial lead. In the postoperative period, some nonsurgical complications were observed in one patient who developed atrial fibrillation which we treated with drugs. A cyclosporin-evoked tremor produced several asystoles due to false inhibition by myopotential interference in the VVI mode. During an episode of acute rejection combined with renal insufficiency, loss of atrial and ventricular sensing occurred. The other patients showed no pacemaker-related complications. Our findings in this unique population of pacemaker patients are discussed. [ABSTRACT FROM AUTHOR]