Aortic elastic properties in patients with coronary artery ectasia

Background: The purpose of the present study was to investigate the elastic characteristics of the aorta in patients with coronary ectasia (CE) and the relationship between these characteristics and echocardiographic left ventricular (LV) diastolic functions. Methods and Results: In the first group there were 35 patients with CE, the second group consisted of 35 patients with coronary artery disease (CAD) and the third group consisted of 35 patients with normal coronary arteries. Echocardiographic investigation was carried out for the assessment of the LV diastolic functions. Aortic strain, β index and aortic distensibility were used as aortic elasticity parameters. LV diastolic functions were impaired in both the ectasia group and the CAD group as compared with patients with normal coronary arteries. Beta index and aortic distensibility measurements were similar between the CAD and CE groups. The values obtained for aortic strain, β index and aortic distensibility were lower in the CAD and ectasia groups when compared with the values of the normal group. On performing the stepwise linear multivariable analyses, aortic elastic parameters have been determined to possess the strongest diagnostic power for LV diastolic functions. Conclusions: The results of the current study show that stiffness parameters of aorta are impaired in the patients with CE as in the patients with CAD. The increase in aortic stiffness might be responsible for LV diastolic dysfunction

Interaction of plasma homocysteine and thyroid hormone concentrations in the pathogenesis of the slow coronary flow phenomenon

Background and Objective: The slow coronary flow (SCF) phenomenon is an angiographic observation and a well-recognized clinical entity characterized by delayed opacification of vessels in a normal coronary angiogram due to reasons yet unclear. Thyroid hormones exert significant effects on plasma homocysteine (Hcy) levels and microvascular resistance. Recently, several investigators have consistently reported that elevation of the plasma Hcy level can severely disturb vascular endothelial function and play a role in the pathogenesis of SCF. Accordingly, we investigated the levels of plasma Hcy and thyroid hormones and their relationship in patients with SCF. Method: Forty-four patients with angiographically proven SCF (Group I) (mean age 55.5 ± 10.4 years, 26 males) and 44 cases with normal coronary flow (NCF) pattern (Group II) (mean age 53.9 ± 11 years, 22 males) with similar risk profiles were enrolled in the study. Coronary flow patterns of the cases were determined by the thrombolysis in myocardial infarction (TIMI) frame count method. The coronary TIMI frame counts were calculated separately for each coronary artery and their average was determined as the mean TIMI frame count for each subject. Serum levels of free tri-iodothyronine (fT3), free thyroxine (fT 4), thyroid stimulating hormone (TSH) and Hcy were measured. Patients with thyroid disease or on medications with a potential to affect thyroid functions were excluded. Results: There were no statistically significant differences between the groups concerning the demographic characteristics and major cardiovascular risk factors. Mean TIMI frame counts of SCF and NCF groups were 45.9 ± 12 and 23.3 ± 3.7, respectively. fT4 (ng/dl) and TSH (µIU/ml) levels of the two groups were similar (p ;gt; 0.05). The level of fT3, the active metabolite of the thyroid hormone family, was dramatically reduced in the SCF group when compared to the NCF group (2.3 ± 0.2 vs. 3.0 ± 0.3, p = 0.0001, respectively). Plasma Hcy levels of patients with SCF were found to be significantly higher than controls (12.2 ± 4.9 vs. 8.5 ± 2.9, p = 0.0001, respectively). Correlation analysis showed a significant negative correlation between the plasma fT 3and Hcy levels and the mean TIMI frame counts (r = -0.31, p = 0.003 vs. r = -0.66, p = 0.0001). Moreover, there was a significant positive correlation between the plasma Hcy levels and the mean TIMI frame counts (r = 0.58, p = 0.0001). Also, fT3 was the only significant determinant of the variance of Hcy in multiple regression analysis (r = -0.30, p = 0.005). Conclusion: fT3 levels were decreased and plasma Hcy levels were increased significantly in patients with SCF as compared to controls. This finding suggests that thyroid hormones and/or (?) a possible disturbance in their metabolism may be responsible for the elevated levels of plasma Hcy in patients with SCF and may play a role in the pathogenesis of the SCF phenomenon. Copyright © 2007 S. Karger AG

Effect of homocysteine-induced oxidative stress on endothelial function in coronary slow-flow

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. Copyright © 2007 S. Karger AG

Cigarette smoking induced oxidative stress may impair endothelial function and coronary blood flow in angiographically normal coronary arteries

Background: Smoking contributes to the progression of atherosclerotic heart disease by causing endothelial dysfunction. In the present study the effect of smoking on endothelial functions and coronary flow was investigated, as well as the relationship of these factors with oxidative stress parameters, in subjects with normal coronary arteries. Materials and Results: The study group comprised 87 patients with angiographically normal coronary arteries (36 smokers, 51 nonsmokers). Coronary flow patterns were determined by the Thrombolysis In Myocardial Infarction (TIMI) frame count method. Endothelial function was evaluated by high-frequency ultrasound imaging of the brachial artery. Superoxide dismutase (SOD) and reduced glutathione (GSH) and reduction of oxidative material in the body and the endproduct of lipid peroxidation, malondialdehyde (MDA), were measured as oxidative stress markers. Mean TIMI frame count was significantly higher in smokers than nonsmokers (42.2±16 vs 29.5±9.5, p=0.0001). Endothelium-dependent flow-mediated dilatation was 6.81±1.95% in nonsmokers and 5.7±2.2% in smokers (p=0.0001). The smokers had dramatically higher levels of SOD and MDA and lower levels of GSH than the nonsmoker group. Conclusion: Smoking induced oxidative stress deteriorates coronary blood flow by disturbing endothelial function