Abstract

Structural changes in the aortic wall have been reported to be present in aortic dissection (AD), while there have been no investigations concerning peripheral vasomotion characteristics. Peripheral arterial stiffness is an important factor in the regulation of the central aortic pressure because it produces excessive wave reflection. The present study investigated in AD patients endothelium-dependent peripheral vasodilation and the reactive hyperemic response which is considered to be altered by the structural abnormality of the peripheral resistance artery. Forearm blood flow (FBF) changes induced by intra-arterial infusion of acetylcholine (ACh), sodium nitroprusside (SNP), and by occlusion-induced reactive hyperemia (RH) were measured plethysmographically in 10 AD patients, 7 healthy volunteers, and 7 patients with uncomplicated hypertension (UHT). There were no significant differences in the peak FBF response to ACh and SNP infusion for the three groups (ACh, 14.2 +/- 1.8 vs 17.2 +/- 4.5 vs 15.7 +/- 2.3 ml/min/dl tissue, NS; SNP 9.5 +/- 1.3 vs 10.6 +/- 1.7 vs 11.9 +/- 0.8 vs ml/min/dl tissue, NS). In the case of RH, however, peak FBF and maximum conductance were significantly lower in AD patients than in healthy volunteers and UHT patients (21.1 +/- 2.6 vs 36.1 +/- 4.7 and 32.4 +/- 2.6 ml/min/dl tissue volume, p < 0.01, and 0.25 +/- 0.03 vs 0.46 +/- 0.06 and 0.37 +/- 0.03 ml/min/dl per mmHg, p < 0.05, respectively). Peripheral vasodilatory function depending on the endothelium and smooth muscle in AD patients was not significantly different from that in healthy volunteers and UHT patients. However, reactive hyperemic vasodilatory reserve, which is a well-established, noninvasive measure of arterial structure, was significantly impaired in AD. These findings indicate that arterial structural abnormalities rather than systemic atherosclerotic changes represented by endothelial dysfunction may be present. We speculated that this aspect of peripheral resistance artery might possibly have an unfavorable effect on the postonset aortic conditions in AD patients.

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