Background and Objective: Obstructive sleep apnea (OSA) has a critical association with cardiovascular mortality and morbidity. Carotid intima-media thickness (IMT), flow-mediated dilatation (FMD) and aortic stiffness are early signs of atherosclerosis. The presence of subclinical atherosclerosis was assessed in OSA patients using these parameters. Methods: 40 patients with OSA showing an apnea-hypopnea index (AHI) ≧5 (mean age 51.3 ± 9 years, 32 males) and 24 controls (AHI < 5, mean age 51.9 ± 5.2 years, 19 males) were enrolled in the study. In all subjects, polysomnographic examination and recordings were performed during sleep. IMT of the carotid artery, endothelium-dependent/-independent vasodilation of the brachial artery and aortic elastic parameters were investigated using high-resolution Doppler echocardiography. Results: The demographic data of the patients with OSA and controls were not significantly different. Subjects with OSA demonstrated higher values of aortic stiffness (7.1 ± 1.88 vs. 6.42 ± 1.56, respectively) and IMT (0.85 ± 0.13 vs. 0.63 ± 0.11 mm, p = 0.0001, respectively) but lower distensibility (9.47 ± 1.33 vs. 11.8 ± 3.36 cm²/dyn/10⁶) and FMD (4.57 ± 1.3 vs. 6.34 ± 0.83%, p = 0.0001, respectively) than the controls. The respiratory disturbance index correlated positively with aortic stiffness and IMT and negatively with distensibility and FMD. Conclusion: We observed blunted endothelium-dependent dilatation, increased carotid IMT and aortic stiffness in patients with OSA compared with matched control subjects. This is evident in the absence of other diseases, suggesting that OSA is an independent cause of atherosclerosis. These simple and non-invasive methods help to detect subclinical atherosclerosis in OSA.

Background and Objective: Coronary slow-flow (CSF) phenomenon is characterized by delayed opacification of vessels in a normal coronary angiogram, but its etiopathogenesis remains unclear. Plasma homocysteine (Hcy) level can severely disturb vascular endothelial function and may play a role in the pathogenesis of CSF. In our study, endothelial function in patients with CSF and their relationship with Hcy and oxidative stress parameters are investigated. Method: Forty-four patients with angiographically proven CSF and 44 cases with normal coronary flow pattern with similar risk profile were enrolled in the study. Coronary flow patterns of the cases are determined by Thrombolysis in Myocardial Infarction (TIMI) frame count method. Endothelium dependent flow mediated dilatation (FMD) and independent vasodilatation characteristics are evaluated by high frequency ultrasound over the brachial artery. Superoxide dismutase (SOD) and reduced glutathione (GSH) and reduction of oxidative material in the body and the end product of lipid peroxidation, malondialdehyde (MDA) are measured as oxidative stress markers in blood samples. Results: Plasma Hcy level (µmol/l) of patients with CSF was found to be significantly higher than in controls (12.2 ± 4.9 vs. 8.5 ± 2.8, p = 0.0001). FMD was 7.87 ± 2.0% in controls and 4.98 ± 1.1% in patients with CSF (p = 0.0001). GSH was reduced in patients with CSF. SOD and MDA activity were found higher in patients with CSF than control subjects. Plasma Hcy level was significantly positively correlated with mean TIMI frame count and negatively correlated with FMD in correlation analysis (r = 0.58, p = 0.0001; r = –0.41, p = 0.022; respectively). Conclusion: The present findings allow us to conclude that patients with CSF have increased levels of Hcy and oxidative stress markers and impaired endothelial cell function.

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he vascular endothelium plays an important role in the regulation of vascular tone and the maintenance of cardiovascular homeostasis. 1 Importantly, endothelial dysfunction, particularly impaired endotheliumdependent vasodilation, has been linked to the pathogenesis of atherosclerotic vascular disease and acute cardiovascular events. 2 Indeed, reduced endothelial vasodilatory function occurs early in atherogenesis before histological and angiographic evidence. 3,4 Epidemiologic studies have shown that high levels of physical activity and cardiorespiratory fitness reduce cardiovascular morbidity and mortality in the general population, including healthy subjects. 5,6 It is clinically important to select the appropriate kind of exercise. Regular aerobic exercise is associated with beneficial changes in blood pressure, lipid metabolism, glucose metabolism, neurohormonal factors, body weight, and shear stress. 7,8 Although the mechanism of improvement in endothelial function during exercise has not been fully clarified, it is thought that nitric oxide (NO) production is increased by up-regulation of endothelial NO synthase gene expression and vascular endothelial growth factor-induced angiogenesis, as well as decreased NO inactivation with augmented antioxidants, Circulation Journal Vol. 69, September 2005 such as superoxide dismutase and glutathione peroxidase, and attenuation of nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide phosphate (NADH/NADPH) oxidase activity, all leading to an increase in NO bioavailability. 9 Polymorphisms of the angiotensin converting enzyme (ACE) gene, located on chromosome 17, have been found and the polymorphism is characterized by the presence (insertion (I)) or absence (deletion (D)) of a 287-base-pair alu repeat within intron 16. The presence of the D allele has been associated with higher concentrations of circulating and tissue ACE. Increased ACE activity might lead to high Angiotensin II (Ang II) concentrations. 10 Of the several candidate genes for endothelial dysfunction, the ACE gene appears to be a likely one because (1) it is anchored via its carboxyl terminus to the endoluminal side of the endothelial cell plasma membrane, from where it can be released in the bloodstream, 11,12 and (2) the increased plasma ACE activity found in subjects with the D allele could decrease bradykinin bioactivity with ensuing blunting of receptormediated release of NO. 13 Furthermore, even though the literature is variable on whether Ang II effects are increased in subjects with the D allele, 14,15 enhanced Ang II production can increase the concentrations of superoxide through increased activity of NADH/NADPH oxidase activity 16 and thus lower the bioactivity of NO. 17 The balance of vasodilators and vasoconstrictors also plays an important role in the physiologic regulation of vascular tone; 18 However, it is not clear whether the ACE genotype can modify the endothelial response to exercise in athletes.The aim of this study was to investigate the relationship between the...

Homocysteine levels and carotid intima-media thickness increased but folate levels decreased in patients with coronary slow flow. The present findings allow us to conclude that the possible disturbance in the metabolism of homocysteine in patients with coronary slow flow may have a role in the etiopathogenesis of this phenomenon by causing generalized atherosclerosis.