Association between Prior Cytomegalovirus Infection and the Risk of Restenosis after Coronary Atherectomy

• Published in: The New England journal of medicine Vol. 335; no. 9; pp. 624 - 630
• Main Authors: Zhou, Yi Fu, Leon, Martin B, Waclawiw, Myron A, Popma, Jeffery J, Yu, Zu Xi, Finkel, Toren, Epstein, Stephen E
• Format: Journal Article
• Language: English
• Published: Boston, MA Massachusetts Medical Society 29.08.1996
• Subjects: Adult; Aged; Angioplasty; Antibodies, Viral - blood; Apoptosis; Atherectomy, Coronary; Biological and medical sciences; Cell cycle; Cineangiography; Coronary Artery Disease - diagnostic imaging; Coronary Artery Disease - surgery; Coronary Artery Disease - virology; Coronary Disease - diagnostic imaging; Coronary Disease - surgery; Coronary Disease - virology; Cytomegalovirus; Cytomegalovirus - immunology; Cytomegalovirus Infections - complications; Cytomegalovirus Infections - immunology; Female; Gene expression; Hepatitis Antibodies - blood; Hepatovirus - immunology; Humans; Immunoglobulin G - blood; Linear Models; Logistic Models; Male; Medical sciences; Middle Aged; Multivariate Analysis; Patients; Prospective Studies; Recurrence; Risk Factors; Serologic Tests; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases; Surgery of the heart; Human; Postoperative; Cytomegalovirus; Atherectomy; Herpesviridae; Coronary artery; Cardiovascular disease; Betaherpesvirinae; Coronary heart disease; Virus; Infection; Restenosis; Treatment; Surgery; Risk factor; Complication; Preoperative
• ISSN: 0028-4793; 1533-4406
• DOI: 10.1056/NEJM199608293350903

Neointimal hyperplasia and arterial remodeling cause restenosis in 20 to 50 percent of patients who have undergone coronary angioplasty. 1 , 2 Although the mechanisms are unknown, previous findings have raised the possibility that cytomegalovirus (CMV) contributes to the development of restenosis in some patients. 3 In approximately one third of patients with restenosis, the lesions contain CMV DNA sequences. Smooth-muscle cells grown from such lesions express IE84, one of the virus's immediate early proteins, and IE84 binds to and inhibits the p53 tumor-suppressor gene product. These effects may enhance the proliferation of smooth-muscle cells or inhibit apoptosis, either of which may contribute . . .