Hypertension, Vol 24, 212-219, Copyright © 1994 by American Heart Association
I Antony, E Aptecar, G Lerebours and A Nitenberg
Hypertensive patients with angiographically normal coronary arteries may
have myocardial ischemia when metabolic demand increases. Abnormal
epicardial coronary artery vasomotion in response to sympathetic
stimulation may contribute to ischemia in such patients. We studied the
vasomotor response of smooth coronary arteries to a cold pressor test in 10
hypertensive patients without other risk factors and in 9 control subjects.
Vessel dimensions were measured by quantitative angiography, and blood flow
was calculated using an intracoronary Doppler catheter in the left anterior
descending coronary artery. In response to cold pressor stimulation,
arteries of control subjects dilated 13.0 +/- 5.9% (P < .001), and they
constricted 8.2 +/- 8.5% in hypertensive patients (P < .001).
Rate-pressure product increased from 9466 +/- 1677 to 12,547 +/- 2367 beats
per minute (bpm).mm Hg in control subjects (P < .001) and from 13,720
+/- 1823 to 17,353 +/- 2037 bpm.mm Hg in hypertensive patients (P <
.001). Coronary blood flow velocity and blood flow increased 51 +/- 26% (P
< .05) and 87 +/- 27% (P < .001), respectively, in control subjects
and 68 +/- 52% (P < .05) and 36 +/- 33% (P < .01) in hypertensive
patients. At peak cold pressor test, despite a significant higher
rate-pressure product in hypertensive patients, blood flow was similar in
both groups, suggesting an uncoupling between myocardial metabolic demand
and supply. Thus, hypertension impairs the vasodilator response of
angiographically normal coronary arteries to a cold pressor test. This
abnormal response may be due to enhanced catecholamine reactivity and/or
impairment of endothelial flow-mediated vasodilator response.
ARTICLES
Coronary artery constriction caused by the cold pressor test in human hypertension
Service d'Explorations Fonctionnelles, Centre Hospitalier et Universitaire Xavier Bichat, Paris, France.
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