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.