Impairment of Flow-Dependent Coronary Dilation in Hypertensive Patients : Demonstration by Cold Pressor Test Induced Flow Velocity Increase

In normal coronary arteries, increased flow velocity induces endothelium-dependent dilation, and dilation in response to sympathetic stimulation evoked by the cold pressor test is partly due to increased flow velocity. In arterial hypertension, angiographically normal coronary arteries were constricted by acetylcholine, an endothelium-dependent vasodilator. To assess the epicardial coronary artery response to the increased blood flow velocity induced by the cold pressor test in hypertensive patients with angiographically normal coronary arteries, coronary artery diameters and flow velocity were measured during cold pressor test in 12 untreated hypertensive patients and in 10 control subjects. Diameters were determined by quantitative angiography on proximal and distal segments of the left anterior descending coronary artery, and flow velocity measurements were made by Doppler testing in the distal segment. In control subjects, the proximal and distal segments dilated during cold pressor test by 12.0 ± 4.5% and 13.9 ± 6.5%, respectively (both P< .001), when flow velocity increased by 46.7 ± 26.1% (P> .05). In hypertensive patients, segments were constricted, respectively, by 10.3 ± 8.5% (P< .001) and 7.9 ± 8.6% (P< .01), when the flow velocity was increased by 68.3 ± 48.2% (P< .001). Intracoronary injection of an endothelium-independent dilator resulted in similar dilation in control subjects (proximal: +30.0 ± 12.9%; distal: +32.4 ± 15.2%) and in hypertensive patients (proximal: +22.3 ± 7.5%; distal: +28.8 ± 15.4%). In conclusion, in hypertensive patients with angiographically normal coronary arteries and without any other coronary risk factors, endothelium-dependent flow-mediated coronary dilation evoked by the cold pressor test is impaired. This abnormal response may result in a reduction of the conductance of epicardial vessels during sympathetic stimulation which might be detrimental for myocardial perfusion.