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Background: The ultrasound assessment of brachial artery flow-mediated vasodilation provides a noninvasive means for measuring endothelial function. The test is performed using either upper or lower arm blood pressure cuff arterial occlusion to induce hyperemia. Upper arm occlusion produces a greater hyperemic stimulus. Brachial artery flow-mediated vasodilation is abnormal in the presence of coronary risk factors., Hypothesis: The study sought to compare the ability of the upper and lower arm occlusion techniques to differentiate endothelial function in subjects with and without risk factors., Methods: We measured brachial artery flow-mediated vasodilation in 20 subjects, 10 without and 10 with a single risk factor (hypertension, hypercholesterolemia, or cigarette smoking) using both the upper and lower arm occlusion techniques (5 min blood pressure cuff occlusion). Using 11 MHz ultrasound, Doppler blood flow velocities were measured before and immediately after cuff deflation. Brachial artery vasodilation was measured 1 min after cuff deflation, compared with baseline, and expressed as a percent increase., Results: The immediately postocclusion hyperemia (% increase in flow) was significantly greater (p < 0.01) using the upper versus the lower arm technique in both the normal (530 +/- 152 vs. 383 +/- 51%) and the risk factor (583 +/- 153 vs. 409 +/- 114%) groups. Flow-mediated vasodilation was significantly greater (p < 0.01) using the upper arm versus the lower arm occlusion technique in both the normal (13.4 +/- 5.3 vs. 5.6 +/- 3.4%) and risk factor (7.9 +/- 3.6 vs. 3.9 +/- 2.2%) groups. Vasodilation was significantly greater (p < 0.01) in the normal subjects than in the risk factor subjects (13.4 +/- 5.3 vs. 7.9 +/- 3.6%) using the upper arm technique, but was not statistically different in the two groups using the lower arm technique., Conclusions: Our study demonstrates that upper arm compared with lower arm cuff occlusion undertaken to induce hyperemia for the assessment of brachial artery flow-mediated vasodilation results in significantly greater hyperemia and vasodilation. Flow-mediated vasodilation obtained using the upper arm technique better separates subjects with and without coronary risk factors.

Impaired endothelium-dependent vasomotion in response to flow-mediated, cholinergic, and cold pressor stimulation has been demonstrated in the presence of both atherosclerosis and cardiac risk factors. This study investigated the effects of different vasoactive stimuli on brachial artery vasomotion with respect to age and gender. Forty healthy subjects (20 men and 20 women), ages 23 to 52 years, were studied. Using 7.5 MHz ultrasound, brachial artery diameter and Doppler flow velocity at baseline, following 5 min of ipsilateral blood pressure cuff occlusion (flow-mediated), during contralateral hand immersion in ice (cold pressor) and after sublingual nitroglycerin administration, were measured in older subjects (> 40 yrs) and younger subjects (< 40 yrs). Among normal subjects, % diameter change in response to the flow-mediated stimulus was less in older men than in younger men (6.8 +/- 3.2% vs. 11.5 +/- 7.4%, p < 0.05); older and younger women had comparable responses (10.0 +/- 5.3% vs. 11.6 +/- 4.3%, p = NS). With cold pressor, normal older men and older women vasoconstricted (-1.2 +/- 0.9%, -2.2 +/- 4.7%) compared with younger subjects who vasodilated (1.4 +/- 2.5%, 0.6 +/- 2.3%, p < 0.02). The cold pressor test elicited comparable responses among older normal subjects. Nitroglycerin, a non-endothelium-mediated stimulus, induced significant vasodilatation in all the groups. In conclusion, endothelium-mediated responses in subjects of varying age and gender are stimulus-dependent. Flow-mediated vasodilatation could not differentiate older premenopausal women from younger women; cold pressor stimulus could.

Previous studies using thallium-201 scintigraphy have suggested that angiographic coronary collaterals can protect against the development of stress-induced perfusion abnormalities, but the effect of collaterals on stress echocardiography (SECHO) has not been determined. In this study, 21 consecutive patients referred for cardiac catheterization underwent SECHO and coronary angiography. Of the 21 study patients, there was a total of 16 significantly obstructed coronary arteries (> or = 70% stenosis) in 14 patients. SECHO revealed stress-induced wall motion abnormalities in the distribution of seven of nine obstructed coronary vessels without angiographic collaterals, but in only one of seven vessels with collaterals (p < 0.05). Six of eight obstructed vessels not associated with a stress-induced wall motion abnormality had collaterals, whereas only one of eight obstructed vessels associated with a stress-induced wall motion abnormality had collaterals. We conclude that (1) angiographically demonstrated coronary collaterals can protect against the development of stress-induced wall motion abnormalities despite the presence of a high-grade coronary artery obstruction, and (2) the lack of a stress-induced wall motion abnormality on SECHO in the perfusion territory of an obstructed vessel may suggest the presence of adequate collateral perfusion.