Reduced reactive hyperemia in HIV-infected patients

Background: Given that several pathology-based studies reported some degree of coronary and arterial vasculopathy in HIV-infected patients, we investi gated whether abnormal vascular reactivity may also be found in these patie nts. Methods: Vascular reactivity was assessed noninvasively using finger-skin b loodflow monitoring by laser-Doppler flow measurement in 10 HIV-infected-pa tients (mean CD4 T-cell count, 350 +/- 84 cells/mm(3)) with cardiac symptom s (previous myocardial infarction or left-ventricular dysfunction) and/or H IV-related protease inhibitor-induced hyperlipemia (group 1, symptomatic), 19 HIV-infected patients free of cardiac disease, hyperlipemia, and previou s opportunistic infections (mean CD4 T-cell count, 333 +/- 175 cells/mm(3); group 2, asymptomatic), and 19 healthy control subjects (group 3). Laser-D oppler flow was measured at baseline, during postocclusive hyperemic respon se following transient interruption of brachial blood flow (reactive hypere mia), during transcutaneous delivery of acetylcholine (Ach) using iontophor esis (endothelium-dependent dilation) and after sublingual nitroglycerin ad ministration (endothelium-independent dilation). Results: During reactive hyperemia, the absolute increase in flow was found to be lower in asymptomatic HIV-infected patients than in controls (median values [25th-75th percentile]: asymptomatic: 300 [200-400]; versus control s: 600 [400-750] arbitrary units [AU]; p less than or equal to .0001). This abnormality was more pronounced in symptomatic patients (100 [100-200]; p less than or equal to .0001). There was also a reduced peak/baseline flow r atio (symptomatic: 1.14 [1.1-1.2]; asymptomatic: 1.40 [1.25-1.5]; versus co ntrols: 1.83 [1.6-2.2]; p < .0001 for both comparisons) and a reduced hyper emic response, as assessed by the curve of area under the flow versus time from deflation to the end of the hyperemic response (symptomatic: 1850 [110 0-2225]; asymptomatic: 6000 [2850-7950]; versus controls: 23,735 [16,000-31 ,800] AU x sec; p < .0001 for both comparisons). Although there was no stat istically significant difference in acetylcholine (Ach)-induced increases i n flow between asymptomatic HIV patients and controls (peak/baseline flow r atio: 6 [4.3-10] versus 5.3 [4-8]; p = .47), a trend to lower values was se en in symptomatic patients (4.3 [1.2-5]; p = .06). Administration of 0.4 mg sublingual nitroglycerin resulted in increases in flow without statistical ly significant difference between patients and controls: peak/baseline flow ratio for symptomatic: 2.4 [1.9-2.7]; asymptomatic: 2.1 [1.75-2.34] versus controls: 1.97 [1.8-2.4]; p = .2 and .83, respectively). Conclusions: Postischemic reactive hyperemia is reduced in HIV-infected pat ients. In addition, there was is trend for a reduced response to Ach only i n those with cardiac disease and/or hyperlipemia.