Enhanced cytomegalovirus infection in atherosclerotic human blood vessels

Human cytomegalovirus (CMV) is a possible co-factor in atherogenesis and vascular occlusion, but its ability to actively infect medium and large blood vessels is unclear. A vascular explant model was adapted to investigate CMV infection in human coronary artery, internal mammary artery (IMA), and saphenous vein (SV). Vascular explants were inoculated with CMV Towne or low-passage clinical isolate and examined in situ for CMV cytopathic effect and immediate-early and early antigens, as indicators of active infection. At 5 to 7 days after inoculation, we found that CMV Towne actively infected eight of eight different atherosclerotic blood vessel explants (coronary artery, n = 4; SV and IMA grafts, n = 4), whereas it only infected 2 of 14 nonatherosclerotic blood vessel explants (SV, n = 10; IMA, n = 4) (P = 0.001). The CMV clinical isolate actively infected none of six sets of nonatherosclerotic SV explants at 5 to 7 days after inoculation. The active CMV infections involved adventitial and, less frequently, intimal cells. A small subset of infected cells in atherosclerotic tissue expresses the endothelial cell marker CD31. Smooth muscle cells residing in both atherosclerotic and nonatherosclerotic blood vessels were free of active CMV infections even after all vascular tissue layers were exposed to the virus. In contrast, active CMV Towne infection was evident at 2 days after inoculation in smooth muscle cells and endothelial cells previously isolated from the SV tissues. We conclude that active CMV infection is enhanced in atherosclerotic blood vessels compared to atherosclerosis-free vascular equivalents, and this viral activity is restricted to subpopulations of intimal and adventitial cells.     

Irregular atrial activation during atrioventricular nodal reentrant tachycardia: evidence of an upper common pathway

Controversy continues regarding the precise nature of the reentrant circuit of AV nodal reentrant tachycardia, especially the existence of an upper common pathway. In this case report, we show that marked variation and irregularity in atrial activation (maximum AA interval variation of 80 msec) can exist with fixed and constant activation of the His bundle and ventricles during AV nodal reentrant tachycardia in a 45-year-old female patient. We propose that irregular atrial activation is due to variable and inconsistent conduction from the AV node to the atria through the perinodal transitional cell envelope extrinsic to the reentrant circuit. Our observations support the concept of an upper common pathway, at least in some patients with AV nodal reentrant tachycardia.     

Inadvertent positioning of pacemaker leads in the pericardium

A patient had a dual chamber pacemaker with endocardial leads implanted chronically. The lead position on chest X ray and the ECG pattern indicated lead malposition, but a CT scan and transesophageal echocardiography were nondiagnostic. Venography indicated that both leads were in the mediastinal and pericardial space.