Objectives: We assessed the value of carotid intima-media thickness (CIMT) and thoracic aorta intima-media thickness (AoIMT) in ruling out significant coronary artery disease (CAD) in patients scheduled for heart valve surgery.
Background: Evaluation of CAD is needed in most patients undergoing heart valve surgery because of the high surgical morbidity in patients with significant CAD, raising the need for sensitive tests to exclude CAD. Coronary angiography is the reference standard, but this invasive procedure is not cost-effective, because more than two-thirds of these patients do not have significant CAD.
Interactions between the endothelium and erythrocytes may contribute to the vascular complications of sickle cell disease (SCD). Endothelium-derived nitric oxide (NO) plays a major role in the regulation of vasomotor tone in response to wall shear stress (WSS) variations and pharmacologic stimuli. However, little is known about endothelial NO production in patients with steady-state SCD.
View Article and Find Full Text PDFArch Mal Coeur Vaiss
September 2000
This study was undertaken to determine the vascular effects of bradykinin and its modes of action on the resistive circulation of the forearms of coronary patients and healthy volunteers. Two groups were studied: Group I comprising 8 coronary patients with normal left ventricular function and Group II with 8 healthy volunteers. The method of measurement of forearm blood flow was occlusive venous plethysmography with a mercury strain gauge.
View Article and Find Full Text PDFFlow-mediated vasodilation (FMD) of human blood vessels is essential to adaptation and regulation of peripheral blood flow, and is mediated by endogenously produced nitric oxide. Endothelial function is impaired in many pathologic states, especially in coronary heart disease. We questioned in this study whether exogenous nitric oxide (NO) would restore endothelial dysfunction in peripheral arteries of patients with coronary artery disease (CAD).
View Article and Find Full Text PDFAngiotensin-converting enzyme (ACE) inhibition potentiates bradykinin and acetylcholine endothelium-mediated vasodilation. Three groups were studied. Group I (n = 10) was the reference group; group II was composed of nine patients with coronary artery disease; and group III of seven patients with coronary artery disease and left ventricular dysfunction.
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