Author + information
- Received March 7, 2000
- Revision received June 23, 2000
- Accepted August 7, 2000
- Published online December 1, 2000.
- ↵*Reprint requests and correspondence: Dr. Melvyn Rubenfire, University of Michigan Health System, 24 Frank Lloyd Wright Drive, Ann Arbor, Michigan 48106-0363
We designed a study to determine the carotid artery (CA) response to sympathetic activity and to determine whether the response correlates with coronary risk and is independent of wall thickness (IMT).
Brachial artery reactivity in response to wall stress correlates with coronary risk and coronary disease (CAD). The reactivity of the CA, which is susceptible to atherosclerosis, has not been evaluated.
The change in diameter of the CA (ΔCAdiam) during a cold pressor test and after nitroglycerin and IMT were measured with ultrasound in 93 men and women at average risk, high risk and with CAD.
At 90 s during a cold pressor test average-risk subjects increased CAdiam by 7.9 ± 3.3%, which was significantly less in the high-risk group (1.5 ± 1.8%), and vasoconstriction occurred in the group of subjects with CAD (−6.9 ± 2.7%) (p < 0.01 for comparisons). There were no differences in response to nitroglycerin. Coronary risk was an independent predictor of the %ΔCAdiam (p < 0.0001). Wall thickness, age, systolic pressure and triglycerides each correlated negatively, and high-density lipoprotein cholesterol correlated positively with %ΔCAdiam. The major variable associated with the %ΔCAdiam was group (p = 0.0001). After adjusting for smoking, age and high-density lipoprotein cholesterol, there was no association between the %ΔCAdiam, and IMT and %ΔCAdiam, but not IMT, was predictive of groups.
The CA response to a sympathetic stimulus is altered in the presence of coronary risk factors and CAD and appears to reflect endothelial function independent of IMT. Carotid artery reactivity may be a valuable adjunctive noninvasive method to assess coronary risk.
☆ Supported, in part, by a donation from Harold and Kay Peplau and an unrestricted grant from Bristol-Myer Squibb.
- Received March 7, 2000.
- Revision received June 23, 2000.
- Accepted August 7, 2000.
- American College of Cardiology