Abstract 3071: Systemic Abnormalities of Macrovascular and Microvascular Function in Patients with Peripheral Arterial Disease
Objective: Symptoms in patients with peripheral arterial disease (PAD) and intermittent claudication cannot be explained solely by flow limitation from obstructive atherosclerotic lesions. In order to explore other possible contributors to symptomatic PAD, we evaluated macrovascular and microvascular function in the brachial and posterior tibial (PT) arteries of subjects with PAD and intermittent claudication compared to healthy controls.
Methods: High resolution duplex ultrasonography was used to assess macrovascular function, including flow-mediated vasodilation (FMD) and nitroglycerin-mediated vasodilation (NMD) in the brachial artery and FMD in the PT artery. Peak reactive hyperemic blood flow, derived from the Doppler velocity and arterial cross sectional area, was used as a measure of microvascular function.
Results: We studied 46 PAD subjects and 38 healthy controls. PT ultrasound was performed successfully in 16 and 14 subjects in each group, respectively. PAD subjects were older (68.5 vs. 60 years, p<0.0001) and more commonly male (78% vs. 53%, p=0.01). Brachial artery FMD and NMD were lower in PAD subjects compared with controls (mean FMD 7.7 ± 4.8% vs. 11.2 ± 4.3%, p=0.001 and NMD 9.5 ± 7% vs. 13.1 ± 6.2%, p=0.04). Median FMD tended to be reduced in PT arteries of PAD subjects (12.3% [IQR 7–21] vs. 16.1% [12–21], p=ns). PT artery FMD correlated with brachial artery FMD (r=0.44, p=0.015). In addition, peak reactive hyperemic flow was lower in subjects with PAD in both brachial artery of (567 ± 217 vs. 730 ± 343 mL/min, p=0.01) and in the PT artery (335 ± 251 vs. 884 ± 477 mL/min, p=0.001). The increases in flow with reactive hyperemia in the brachial and PT arteries also correlated with one another (r=0.47, p=0.001).
Conclusions: Our findings indicate systemic abnormalities in both macrovascular and microvascular function in patients with PAD and intermittent claudication. These abnormalities cannot be explained on the basis of atherosclerotic stenosis alone and may relate to defects in the synthesis or release of locally acting vasodilator substances, altered vascular smooth muscle signaling, or structural defects. Impaired vascular function could account, in part, for symptomatic limitation in patients with PAD and intermittent claudication.