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(Circulation. 2000;101:11.)
© 2000 American Heart Association, Inc.

Brief Rapid Communications

Previous Cytomegalovirus Infection and Risk of Coronary Thrombotic Events After Stent Placement

Franz-Josef Neumann, MD; Adnan Kastrati, MD; Thomas Miethke, MD; Gisela Pogatsa-Murray, MD; Melchior Seyfarth, MD; Albert Schömig, MD

From the Deutsches Herzzentrum (F.J.N., A.K., G.P.M., M.S., A.S.) and Institut für Medizinische Mikrobiologie, Immunologie, und Hygiene (T.M.) der Technischen Universität München, Munich, Germany.

Correspondence to Franz-Josef Neumann, MD, 1. Medizinische Klinik der Technischen Universität, Ismaningerstraße 22, 81675 München, Germany. E-mail neumann{at}med1.med.tu-muenchen.de

Background—Cytomegalovirus (CMV) infection induces upregulation of tissue factor and loss of anticoagulants, including thrombomodulin, prostacyclin, and tissue plasminogen activator. CMV infection may thereby increase the procoagulant properties of coronary artery plaques. This prospective study investigated the effect of previous CMV infection on the early hazard of coronary stent placement.

Methods and Results—In 551 consecutive patients with successful coronary stent placement, we determined CMV IgG titers. The end point was the composite rate of death, nonfatal Q-wave myocardial infarction, and urgent reintervention during 30-day follow-up. The study population represented the entire spectrum of coronary stenting; an acute coronary syndrome was present in 50% of the patients. A positive CMV IgG titer (1/230) was found in 340 patients (62%). Of these, 10 reached the end point during 30-day follow-up (2 deaths, 4 infarctions, 4 urgent reinterventions). In the group with negative CMV titer, thrombotic events did not occur (P=0.014 versus group with positive CMV titers). After correction for pertinent covariables, a significant relation between positive CMV titer and the 30-day end point prevailed (P<0.001).

Conclusions—Previous CMV infection may increase the risk of coronary thrombotic events after stent placement.

Key Words: viruses • stents • thrombosis

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