title: HIV-positive patients treated with protease inhibitors have vascular changes resembling those observed in atherosclerotic cardiovascular disease.
abstract: A metabolic syndrome associated with atherosclerosis and cardiovascular disease has been described in HIV-positive individuals. In the present study we investigated whether HIV-positive individuals and CAD (coronary artery disease) patients have similarities in their vascular function and structure. In a case-control study, we compared measurements of carotid artery IMT (intima-media thickness) and brachial artery FMD (flow-mediated vasodilation) in HIV-positive individuals with age- and sex-matched controls with similar risk factors and patients with established CAD. Seventy-one HIV patients, age 42+/-13.9 years (91% male), were compared with 29 CAD patients and 25 controls. HIV patients had higher IMT than controls and similar IMT to CAD patients (0.64+/-0.2 compared with 0.55+/-0.05 and 0.66+/-0.08 mm respectively; F=4.2, P=0.01). Patients taking protease inhibitors had higher IMT (0.69+/-0.2 compared with 0.57+/-0.15 mm; P=0.01), blood pressure, cholesterol and triacylglycerols than those not taking protease inhibtors (P<0.05). In multiple regression analyses, increasing blood pressure (beta: 0.37, P=0.001), glucose (beta: 0.26, P=0.016), cholesterol (beta: 0.24, P=0.033), duration of HIV disease (beta: 0.33, P=0.008) and use of protease inhibitors (beta: 0.27, P=0.04) were the most important determinants of IMT respectively. FMD was associated only with triacylglycerol measurements. Patients with HIV present arterial changes resembling those found in patients with atherosclerotic cardiovascular disease. These vascular changes are closely related to protease-inhibitor-induced changes of metabolic parameters. Thus intensive treatment of these metabolic parameters might retard atherosclerosis in HIV patients.
authors.affiliation: 2nd Department of Cardiology, Attikon University Hospital, University of Athens Medical School, Athens, Greece.
authors.forename: John
authors.initials: J
authors.lastname: Lekakis
authors.forename: Sotirios
authors.initials: S
authors.lastname: Tsiodras
authors.forename: Ignatios
authors.initials: I
authors.lastname: Ikonomidis
authors.forename: John
authors.initials: J
authors.lastname: Palios
authors.forename: Garyfalia
authors.initials: G
authors.lastname: Poulakou
authors.forename: Loukianos
authors.initials: L
authors.lastname: Rallidis
authors.forename: Anastasia
authors.initials: A
authors.lastname: Antoniadou
authors.forename: Periklis
authors.initials: P
authors.lastname: Panagopoulos
authors.forename: Antonios
authors.initials: A
authors.lastname: Papadopoulos
authors.forename: Helen
authors.initials: H
authors.lastname: Giamarellou
authors.forename: Dimitrios T
authors.initials: DT
authors.lastname: Kremastinos
mesh_terms: D000328:Adult; D023241:Antiretroviral Therapy, Highly Active / Q000009:adverse effects; D050197:Atherosclerosis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D001916:Brachial Artery / Q000503:physiopathology; D002340:Carotid Artery Diseases / Q000139:chemically induced / Q000000981:diagnostic imaging / Q000473:pathology; D016022:Case-Control Studies; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D005260:Female; D015658:HIV Infections / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D017320:HIV Protease Inhibitors / Q000009:adverse effects* / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D017539:Tunica Intima / Q000000981:diagnostic imaging / Q000473:pathology; D017540:Tunica Media / Q000000981:diagnostic imaging / Q000473:pathology; D014463:Ultrasonography; D019562:Viral Load
chemical_list: D017320:HIV Protease Inhibitors