Global impairment of brachial, carotid, and aortic vascular function in young smokers - Direct quantification by high-resolution magnetic resonance imaging

OBJECTIVES The purpose of this study was to assess vascular dysfunction in young smokers by high-resolution magnetic resonance imaging (MRI). BACKGROUND Cigarette smoking is a well-known cause of endothelial dysfunction, reflected by brachial artery reactivity to hyperemia. We hypothesized that smoking induces both peripheral endothelial dysfunction and altered function in central conduit arteries, and that these global changes in vascular function could be directly quantified in a single noninvasive examination using high-resolution MRI. METHODS A total of 22 healthy young volunteers (mean age 31 +/- 2 years; 12 nonsmokers, 10 smokers: cumulative cigarette consumption 11.9 +/- 6.0 pack-years) underwent noninvasive high-resolution MRI to assess central vascular distensibility and pulse-wave velocity (PWV), and cross-sectional flow-mediated dilation (FMD) of the brachial artery. RESULTS Brachial artery FMD was significantly reduced in smokers compared with nonsmokers (73 +/- 2.7% vs. 15.5 +/- 2.0%; p = 0.03), indicating impaired endothelium-dependant relaxation, whereas endothelium-independent responses to sublingual glyceroltrinitrate (400 mug) were identical in both groups. Impaired peripheral endothelial function in smokers was accompanied by striking decreases in central vascular distensibility in both the common carotid arteries (-45.7%; p = 0.02) and at multiple sites in the aorta (ascending aorta -26.9%, p = 0.04; thoracic descending aorta -25.0%, p = 0.01; abdominal descending aorta -25.5%, p = 0.02). Aortic arch PWV in smokers was increased by 19% (p = 0.02). CONCLUSIONS Cigarette smoking induces global changes in both peripheral and central vascular function. Direct quantification of multiple parameters of vascular function using high-resolution MRI will provide powerful new approaches to the assessment of vascular disease pathogenesis, diagnosis, and treatment. (C) 2004 by the American College of Cardiology Foundation.