Simvastatin may improve myocardial perfusion abnormality in slow coronary flow.

BACKGROUND: The slow coronary flow (SCF) phenomenon is a coronary microvascular disorder characterized by the delayed passage of contrast in the absence of obstructive epicardial coronary disease. Recent studies showed the possible role of endothelial dysfunction, diffuse atherosclerosis and inflammation in the pathogenesis of this phenomenon. We aimed to investigate the effect of statin on myocardial perfusion in patients with SCF. METHODS AND RESULTS: The study population consisted of 97 patients with SCF. Coronary flow patterns of the cases are determined by thrombolysis in myocardial infarction (TIMI) frame count method. Single-photon emission computed tomographic myocardial perfusion imaging studies and lipid parameters of the patients were obtained before and after 6 months of simvastatin treatment period. During the study, daily single dose of 40 mg simvastatin has been given to each subject. We found a significant positive correlation between mean TIMI frame count and basal reversibility score (r = 0.84, p = 0.0001). In addition, analysis of the reversibility scores demonstrates that simvastatin treatment has significantly improved the myocardial perfusion abnormality at the end of the follow-up period. CONCLUSION: Present findings allow us to conclude that simvastatin improved myocardial perfusion in patients with SCF.

Oxidative stress parameters in patients with slow coronary flow.

INTRODUCTION: We investigated the probable role of free-radical damage in the pathogenesis of slow coronary flow (SCF) by using oxidative stress parameters. METHODS: Sixty-four patients with angiographically proven SCF and 63 patients with normal coronary flow (NCF) pattern with similar risk profiles were enrolled in this study. We measured erythrocyte superoxide dismutase (SOD), reduced glutathione (GSH), serum malondialdehyde (MDA), catalase and myeloperoxidase (MPO) levels in all subjects. RESULTS: There were statistically significant differences in the levels of erythrocyte SOD, GSH and serum MDA between the 2 groups. Serum MDA (P = 0.003) and erythrocyte SOD levels (P = 0.0001) were increased in the SCF group. The level of erythrocyte GSH (P = 0.010) was lower in patients with SCF. There were no differences between the groups' serum catalase (P = 0.682) and MPO levels (P = 0.070). CONCLUSION: Our data showed that in patients with SCF, serum MDA and erythrocyte SOD levels were increased while erythrocyte GSH levels were decreased significantly, compared with NCF patients. These results indicate that free-radical damage may play a role in the pathogenesis of SCF.

Effects of CPAP on left ventricular structure and myocardial performance index in male patients with obstructive sleep apnoea.

BACKGROUND: Obstructive sleep apnoea (OSA) has the potential to cause heart failure. We aimed to determine the effects of nasal continuous positive airway pressure (CPAP) therapy on left ventricular structure and myocardial performance index (MPI) in severe OSA patients. METHODS: Sixty-seven subjects without any cardiac or pulmonary disease had overnight polysomnography and echocardiography. In 33 males with severe OSA, thickness of interventricular septum (IVS) and posterior wall (LVPW) were measured by M-mode. Left ventricular MPI was calculated as (isovolumic contraction time+isovolumic relaxation time)/aortic ejection time by Doppler. RESULTS: Eight males were non-compliant with CPAP. Mean age was 47.9+/-8.2 years, and 20 of 25 patients (80.0%) were hypertensive. Patients had high body mass index (BMI: 31.0+/-3.9 kg/m(2)), but there was no change in BMI from baseline after 6 months. Thickness of IVS (11.0+/-1.1mm) and LVPW (11.0+/-1.0mm) at baseline were significantly decreased after 6 months of CPAP therapy (10.5+/-0.9 mm, P<0.001 and 10.4+/-0.7 mm, P<0.0001, respectively). Left ventricular MPI (60.1+/-13.8%) significantly decreased (53.0+/-10.7%, P<0.0001) after CPAP usage. CONCLUSIONS: In male patients with severe OSA, CPAP therapy significantly decreases left ventricular wall thickness and improves global function even with 6 months of usage.

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 (fT4), 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 (microIU/ml) levels of the two groups were similar (p > 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 fT3 and 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.

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 (micromol/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.

Right coronary artery arising as a terminal extension of the circumflex artery (a rare coronary artery anomaly).

A single coronary artery is a very rare type of coronary artery anomaly that may present in various forms. A patient is presented in whom the right coronary artery coursed as the terminal branch of the left circumflex artery. This is the second case of this anomaly in the literature.

Sudden painless visual loss after initiation of antihypertensive therapy: case report.

Sudden, painless visual loss occurs in retinal disorders that stem from primary ocular as well as systemic diseases. Vascular insufficiency is one of the leading causes of sudden painless unilateral loss of vision. Early recognition of ischemic optic neuropathy, and rapid correction of hypotension, might improve the recovery from ischemic optic neuropathy. The case of a 40-year-old man who, after antihypertensive therapy for malign hypertension, developed sudden, painless loss of vision in both his eyes is discussed.

Carotid intima-media thickness in coronary slow flow: relationship with plasma homocysteine levels.

BACKGROUND AND OBJECTIVE: Coronary slow-flow phenomenon is characterized by delayed opacification of coronary vessels in a normal coronary angiogram. Although clinical and pathological features have been previously described, the underlying pathophysiology has not been fully elucidated. Thus, it still remains to be determined whether either microvascular or epicardial diffuse atherosclerotic disease is related to slow flow. In this study, we aimed to determine the carotid artery intima-media thickness, which is a marker of atherosclerosis in patients with coronary slow flow, and its possible relationship with the total homocysteine level. METHOD: The study population consisted of 88 patients who underwent coronary angiography because of typical and quasi-typical symptoms of angina. Forty-four patients with angiographically proven coronary slow flow and 44 individuals with normal coronary flow pattern with similar risk profiles were enrolled in the study. Coronary flow patterns of the latter were determined by the thrombolysis in myocardial infarction frame count method. Intima-media thickness was measured by recording ultrasonographic images of both the left and the right common carotid artery with a 12-MHz linear array transducer. Plasma homocysteine, folate and B12 levels were measured from blood samples. RESULTS: Plasma homocysteine levels (mumol/l) and carotid intima-media thickness (mm) of patients with coronary slow flow were found to be significantly higher than that of controls (12.4+/-4.9 vs. 8.5+/-2.8, P=0.0001; 0.75+/-0.08 vs. 0.69+/-0.06, P=0.0001, respectively). The plasma folate level (ng/ml) was lower in coronary slow-flow patients than in controls (13.8+/-4.4 vs. 16.5+/-5.6, P=0.014). The plasma homocysteine level was significantly positively correlated with the mean thrombolysis in myocardial infarction frame count and intima-media thickness of the carotid artery in correlation analysis (r=0.58, P=0.0001; r=0.41, P=0.0001; respectively). CONCLUSION: 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.

Time and frequency domain analyses of heart rate variability in patients with epilepsy.

Heart rate variability (HRV) is a useful tool for the detection of sympathetic-parasympathetic balance of autonomic nervous system in patients at risk of sudden death (SD). SD is more common in patients with epilepsy and the exact mechanisms of SD are unknown. Autonomic nervous system involvement in patients with epilepsy has rarely been studied and has shown conflicting results. Our purpose was to determine if HRV showed any changes in patients with epilepsy in comparison with normal population. A short period analysis of HRV was performed for both the frequency and time domain in 43 epilepsy patients who had generalized tonic-clonic seizures (GTCS) and who were not taking any medications and also in 43 age and sex matched controls. In the time domain analysis, patients displayed higher SDNN (standard deviation of all R-R intervals), SDANN (standard deviation of mean NN intervals in 5 min recordings) and HRV triangular index than did healthy subjects (p < 0.0001). Patients tended to display higher pNN50 (number of R-R intervals differed by > 50 ms from adjacent interval divided by the total number of all R-R intervals) and RMSSD (root-mean-square of successive differences) values than did healthy subjects, but the differences were not statistically significant (p > 0.05). In the frequency domain analysis, the spectral measures of HRV showed a reduction of high frequency (HF) values (is a marker of parasympathetic activity) and an increase of low frequency (LF) values (is a measure of sympathetic activity); as a result, the ratio between low and high frequencies (LF/HF) was significantly increased (p < 0.0001, p < 0.0001 and p < 0.001, respectively). Our data suggests an increase in the sympathetic control of the heart rate in epilepsy patients who have GTCS. This increased sympathetic activity could play a key role in the development of ventricular tachyarrhythmias in patients with epilepsy and may be related to the higher incidence of sudden death in this disorder as compared to controls.

Do female patients with metabolic syndrome have masked left ventricular dysfunction?

OBJECTIVE: Metabolic syndrome (MS) is a condition, which is recognized as raising the risk of cardiovascular disease. The aim of our study is to estimate the left ventricular functions by atrioventricular plane displacement (AVPD), myocardial performance index (MPI) and conventional methods in patients with MS who were diagnosed according to NCEP (ATP III) criteria. METHODS: Fifty-three female patients with MS (mean age 53.1+/-6.9 years) and 30 healthy female subjects (mean age 52.8+/-6.3 years, p>0.05) underwent complete echocardiographic assessment. All of the subjects had no heart and pulmonary diseases. The systolic mitral AVPD was recorded at 4 sites (septal, lateral, anterior, and posterior) by M-mode echocardiography and left ventricle ejection fraction (LVEF) was calculated from the AVPD-mean (EF-AVPD). The LVEF was also established by biplane Simpson's (EF-2D) and Teichholz's methods (EF-T). Left ventricular MPI was calculated as (isovolumic contraction time + isovolumic relaxation time) / aortic ejection time by Doppler echocardiography. RESULTS: Patients with MS showed mild left ventricular diastolic dysfunction (DD) in comparison to healthy subjects. The EF-2D and EF-T in patients with MS and healthy subjects were not different significantly and were within normal limits. Patients with MS showed LV global dysfunctions compared to healthy subjects (MPI: 0.56+/-0.12 and 0.46+/-0.11 respectively, p<0.01). Both the septal, anterior, lateral and posterior part of the atrioventricular plane values and also AVPD-mean during systole were statistically lower in patients with MS (12.85+/-1.76 mm) as compared with controls (14.65+/-2.19 mm, p<0.05). The EF-AVPD in patients with MS was statistically lower (65.58+/-11.95%) as compared with healthy subjects (74.45+/-11.07%, p<0.01). CONCLUSION: Female patients with MS had both left ventricular DD and a global dysfunction with an increased MPI. The EF-2D and EF-T were not different significantly between patients and controls, but patients with MS had a relatively reduced EF-AVPD. The AVPD method may indicate a systolic dysfunction with a relatively lower AVPD-mean and relatively lower EF-AVPD. The presence of global dysfunction in patients with MS may lead to heart failure.

The association between coronary flow rate and impaired heart rate recovery in patients with metabolic syndrome: A preliminary report.

BACKGROUND: The aim of this study is to evaluate heart rate recovery (HRR) and association between coronary flow rate and HRR in patients with metabolic syndrome (MS) who had morphologically normal coronary angiogram. METHODS: Study population included 43 patients with MS and 37 control subjects without MS. All patients were selected from individuals who had recently undergone coronary angiography in our hospital and were diagnosed as having angiographically normal coronary arteries. Exercise stress test results obtained prior to coronary angiography were evaluated for calculating HRR and other parameters. In addition, coronary flow was objectively evaluated for each major coronary artery in each subject using TIMI frame count method. RESULTS: All HRR values calculated were detected significantly lower in MS group compared to controls (HRR first: 32 ± 9 vs. 37 ± 10; p = 0.01, second: 46 ± 11 vs. 52 ± 11; p = 0.03, third: 51 ± 12 vs. 59 ± 12; p = 0.00, fourth: 54 ± 13 vs. 61 ± 2; p = 0.02). TIMI frame counts for each major epicardial coronary artery and mean TIMI frame count were also found to be significantly higher in MS group compared to controls (left anterior descending artery:51 ± 24 vs. 39 ± 15; p = 0.009, left circumflex artery: 32 ± 11 vs. 24 ± 7; p = 0.001, right coronary artery: 33 ± 14 vs. 24 ± 10; p = 0.003, mean TIMI frame count: 38 ± 15 vs. 29 ± 9;p = 0.002). Additionally, significant negative correlations were also detected between HRR first minute and coronary TIMI frame count values in patients with MS. None of MS parameters did not affect HRR values, however mean TIMI frame count independently associated with HRR first minute (p = 0.04) in patients with MS. CONCLUSIONS: Impaired coronary blood flow occurring in MS might be a clue of autonomic dysfunction in addition to previously known endothelial dysfunction.

Early sign of atherosclerosis in slow coronary flow and relationship with angiotensin-converting enzyme I/D polymorphism.

Increase in carotid artery intima-media thickness (IMT) is an early sign of atherosclerosis. Slow coronary flow (SCF) is characterized by delay of opacification of coronary arteries in coronary angiography in the absence of any evident obstructive lesion, but its etiopathogenesis remains unclear. Genes that regulate the renin angiotensin system also play a role in developing cardiovascular system disorders. The presence of deletion (D) allele in angiotensin converting enzyme (ACE) gene polymorphism is associated with coronary artery disease. The aim of this study was to investigate the carotid artery IMT measurement, as an early sign of atherosclerosis, in patients with SCF and without SCF and also to assess the effect of the renin-angiotensin gene system on carotid IMT. Forty-four patients with angiographically proven SCF and 44 cases with normal coronary flow (NCF) pattern with similar risk profile were enrolled in the study. Coronary flow patterns of the cases were determined by thrombolysis in myocardial infarction (TIMI) frame count method. Intima-media thickness was measured by recording ultrasonographic images of both the left and right common carotid artery with a 12-MHz linear array transducer. ACE I/D polymorphism and Angiotensin II tip 1 receptor (AT1R) A/C gene polymorphism were determined by polymerase chain reaction (PCR) amplification. Demographic characteristics and coronary artery disease risk factors of SCF and NCF groups were similar. Mean TIMI frame count and carotid IMT (mm) were significantly higher in the SCF group than controls (45.9 +/- 12 vs 23.3 +/- 3.7, P = 0.0001; 0.75 +/- 0.08 vs 0.69 +/- 0.06, P = 0.0001, respectively). Mean TIMI frame count was positively correlated with IMT of carotid artery in correlation analysis (r = 0.45, P = 0.0001). When analyzed in regard to ACE genotype in all subjects, IMT values were statistically different (0.78 +/- 0.06 for DD genotype, 0.72 +/- 0.05 for ID genotype, and 0.64 +/- 0.06 for II genotype, P = 0.0001). This difference remained significant in subgroup analyses for each genotype. No association could be observed between the AT1R A/C(1166) polymorphism and IMT of carotid artery measurement (P > 0.05). Lack of association was still observed with analysis carried out when genotype effect was assumed to be inherited as additive (CC versus AA versus AC) or dominant (AA versus AC+CC). Increased IMT in patients with SCF shows that subclinical atherosclerosis may play role in this phenomenon. This increase was most marked in the presence of D allele of ACE genotype, which is associated with vascular hypertrophy.

Elevated homocysteine levels in patients with slow coronary flow: relationship with Helicobacter pylori infection.

BACKGROUND AND OBJECTIVE: Elevation of plasma homocysteine (Hcy) level has been implicated in the pathogenesis of slow coronary flow (SCF) as it can severely disturb vascular endothelial function. Helicobacter pylori chronically infect the human stomach and causes malabsorption of vitamin B(12) and folate in food, leading ultimately to an increase in circulating Hcy levels. METHODS: Forty-three patients with angiographically proven SCF (group I) were enrolled in this study; 43 cases with normal coronary flow pattern (group II) served as controls. Fasting plasma levels of Hcy, vitamin B(12), and folate were measured in all subjects. Presence of H. pylori infection was defined as positive 14 C urea breath test. Coronary flow patterns for each major epicardial coronary artery were determined with the Thrombolysis in Myocardial Infarction (TIMI) frame count method. RESULTS: Mean TIMI frame count was 46.3 +/- 8.7 in group I and 24.3 +/- 2.9 in Group II (p = .0001). Vitamin B(12) levels were similar, whereas folate levels were dramatically reduced in group I compared to group II (13.2 +/- 4.3 vs. 17.1 +/- 5.2, p = .0001). Plasma Hcy levels were significantly higher in group I compared to group II (13.4 +/- 5.6 vs. 7.9 +/- 2.5, p = .0001) as was the prevalence of H. pylori infection (90.7% in group I vs. 58.1% in group II, p = .001). Hcy levels were elevated (11.7 +/- 5.3 vs. 7.5 +/- 2.7, p = .0001) and folate levels were reduced (13.9 +/- 4.7 vs. 18.6 +/- 4.9, p = .0001) in patients with H. pylori infection, while vitamin B(12) levels were similar in patients with and without H. pylori infection. Correlation analysis revealed a significant negative correlation between plasma folate and Hcy levels and also between folate levels and mean TIMI frame counts (r = -.33, p = .002 vs. r = -.33, p = .003). Moreover, there was a significant positive correlation between plasma Hcy levels and mean TIMI frame counts (r = .66, p = .0001). In addition, the folate level was the only significant determinant of the variance of Hcy in multiple regression analysis (r = -.21, p = .03). CONCLUSION: Our data showed that plasma folate levels were decreased and plasma Hcy levels were increased in patients with SCF compared to controls. Also, the prevalence of H. pylori infection was increased in patients with SCF. These findings suggest that elevated levels of plasma Hcy, possibly caused by H. pylori infection, and/or a possible disturbance in its metabolism may play a role in the pathogenesis of SCF.

An asymptomatic case with single atrium.

Single atrium or common atrium is a rare, isolated defect. We report here an adult patient with single atrium detected by transthoracic echocardiography.

Effect of obstructive sleep apnea on aortic elastic parameters: relationship to left ventricular mass and function.

BACKGROUND: Obstructive sleep apnea (OSA) syndrome has a critical association with cardiovascular mortality and morbidity. Aortic elastic parameters are important markers for left ventricular (LV) function and are deteriorated in cardiovascular disease. METHODS AND RESULTS: Aortic elastic parameters and LV functions and mass were investigated in 40 patients with OSA (apnea - hypopnea index (AHI) >or=5) (mean age 51.3 +/-9 years, 32 males) and 24 controls (AHI <5) (mean age 51.9+/-5.2 years, 19 males). All subjects underwent polysomnographic examination and recordings were obtained during sleep. They also underwent a complete echocardiographic examination and systolic and diastolic aortic measurements were noted from M-mode traces of the aortic root. There were no significant differences in the demographic data of the patients with OSA and the controls. Subjects with OSA demonstrated higher values of aortic stiffness (7.1+/-1.88 vs 6.42+/-1.56, p=0.0001), but lower distensibility (9.47+/-1.33 vs 11.8+/-3.36, p=0.0001) than the controls. LV ejection fraction was significantly lower in patients with OSA when compared with the control group (61.3+/-5.2% vs 65.9+/-8.4%, p=0.0001). LV diastolic parameters were also compared and were worse in the subjects with OSA than in the control subjects (mitral E/A: 0.91 +/-0.42 vs 1.35+/-0.66, p=0.001; Em/Am: 0.86+/-0.54 vs 1.23+/-0.59, p=0.021). Respiratory disturbance index had a positive correlation with aortic stiffness (r=0.63, p=0.0001 and negative correlation with distensibility (r=-0.41, p=0.001). CONCLUSION: Aortic elastic parameters are deteriorated in OSA, which has an extremely high association with cardiovascular disease. Increased aortic stiffness might be responsible for the LV systolic and diastolic deterioration in OSA syndrome.

Aortic stiffness, flow-mediated dilatation and carotid intima-media thickness in obstructive sleep apnea: non-invasive indicators of atherosclerosis.

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) > or =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 cm(2)/dyn/10(6)) 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.

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.