Melatonin Attenuates Contrast-Induced Nephropathy in Diabetic Rats: The Role of Interleukin-33 and Oxidative Stress.

BACKGROUND: Inflammation and oxidative stress (OxS) contribute to the pathogenesis of diabetic kidney disease (DKD) and contrast-induced nephropathy (CIN). Patients with DKD were found to be more prone to CIN. Interleukin-33 (IL-33) is a proinflammatory cytokine, but its role in DKD and CIN is unknown. METHODS: Thirty male Sprague-Dawley rats were enrolled. The first group was comprised of healthy rats (HRs), whereas the other four groups were made up of diabetic rats (DRs), diabetic rats with contrast-induced nephropathy (CIN + DRs), melatonin-treated diabetic rats (MTDRs), and melatonin-treated CIN + DRs (MTCIN + DRs). All groups except the HRs received 50 mg/kg/day streptozotocin (STZ). CIN + DRs were constituted by administrating 1.5 mg/kg of intravenous radiocontrast dye on the 35th day. MTDRs and MTCIN + DRs were given 20 mg/kg/day of intraperitoneal injection of melatonin (MT) from the 28th day for the constitutive seven days. RESULTS: We observed increased IL-33 in the kidney tissue following induction of CIN in DRs. To determine whether MT is effective in preventing CIN, we administered MT in CIN + DRs and demonstrated that kidney tissue levels of OxS markers, inflammatory cytokines, and IL-33 were significantly diminished in MTCIN + DRs compared with other groups without MT treatment (p < 0.05). CONCLUSION: Inhibition of IL-33 with MT provides therapeutic potential in DKD with CIN.

Diabetes mellitus and female gender are the strongest predictors of poor collateral vessel development in patients with severe coronary artery stenosis.

BACKGROUND: Coronary collateral vessel development (CVD), i.e., arteriogenesis, is regarded as one of the most important mechanisms­along with angiogenesis­to result in protection of the myocardium. Coronary CVD is associated with a reduction in infarct size, future cardiovascular events and improved survival in patients with occlusive coronary artery disease by enhancing regional perfusion in the chronically ischemic myocardium. In the present study, we aimed to investigate the relation of cardiovascular risk factors and hematological parameters with collateral development in patients with severely stenotic (≥95%) and totally occluded coronary artery disease including at least one major coronary artery. MATERIALS AND METHODS: The study population was selected from the patients who underwent coronary angiography between January 2008 and March 2009. Five hundred and two patients who had at least one coronary artery stenosis ≥95% (368 men; mean age 59 ± 10 years) comprised the study population. Of the 502 patients, 228 had total occlusion in at least one major epicardial coronary artery. Collateral artery grading was performed by using Cohen-Rentrop method to the vessel with coronary artery stenosis of ≥95% and patients with chronic total occlusions (CTO). Patients with grade 0-1 collateral development were regarded as the poor collateral group, and patients with grade 2-3 collateral development were regarded as the good collateral group. RESULTS: Two hundred and fifty-eight (51%) of 502 patients had poor collateral development, and 244 (49%) had good collateral development. Logistic regression analysis revealed that DM was independently associated with poor CVD in patients with ≥95% stenosis (p < 0.001). Additionally, female gender and DM were found to be independently associated with poor CVD in patients with CTO (p = 0.005 and p < 0.001, respectively). Monocyte count was found to be independent of CVD neither in patients with ≥95% stenosis nor in patients with CTO. CONCLUSION: Our data show that DM is an independent factor for poor coronary CVD both in patients with severe coronary artery stenosis and in patients with CTO. Female gender or being in post-menopausal period is another negative risk factor for poor CVD in addition to DM in patients with CTO.

Predictive Value of Atrial Electromechanical Delay on Long-Term Cardiovascular Outcomes in Hemodialysis Patients.

BACKGROUND: Atrial electromechanical delay (AEMD) times were considered independent predictors of cardiovascular morbidity among the general population. We aimed at evaluating AEMD times and other risk factors associated with 2-year combined cardiovascular (CV) events in HD patients. MATERIAL AND METHODS: Sixty hemodialysis (HD) and 44 healthy individuals were enrolled in this prospective study. Echocardiography was performed before the mid-week dialysis session for HD patients. Data were expressed as mean ± SD. Spearman test was used to assess linear associations. Survival was examined with the Kaplan-Meier method. Multivariate Cox regression analysis was used to determine the predictors of combined CV events in this cohort. RESULTS: At the beginning of the study, left intra-atrial-AEMD times were significantly longer in HD patients compared to the left intra-atrial-AEMD times in healthy individuals. After 24 months, 41 patients were still on HD treatment and 19 (31.6%) had died. Serum triglyceride, total cholesterol and albumin were found to be higher and C-reactive protein (CRP) levels, left intra-atrial EMD time (LIAT) and interatrial EMD times were found to be lower in survived HD patients. With the cut-off median values of 3.5 g/dl for albumin, 0.87 mg/dl for CRP, 157 mg/dl for total cholesterol and 151 mg/dl for triglyceride, the Kaplan-Meier curves demonstrated significant differences in terms of all-cause mortality. We also demonstrated the Kaplan-Meier survival curves of HD patients according to tertile values of LIAT. Cox regression analysis revealed that increased CRP and higher LIAT were found to be independent predictors of combined CV events. CONCLUSIONS: Increased LIAT and inflammation were found to be closely associated with 2 years combined CV events and all-cause mortality in HD patients.

New inflammatory markers for prediction of non-dipper blood pressure pattern in patients with essential hypertension: Serum YKL-40/Chitinase 3-like protein 1 levels and echocardiographic epicardial adipose tissue thickness.

The aim of the present study was to investigate whether YKL-40 levels and epicardial adipose tissue (EAT) thickness were associated with non-dipping pattern in essential hypertension (HT). Age- and sex-matched 40 dipper hypertensive patients and 40 non-dipper hypertensive patients were included in the study. Non-dippers had significantly increased EAT thickness and higher YKL-40 and high-sensitivity C-reactive protein levels than dippers. Multivariate logistic regression analysis showed that the EAT thickness and serum levels of YKL-40 and high-sensitivity C-reactive protein were independent predictors of non-dipping pattern in essential HT. In essential HT, presence of non-dipping pattern is associated with increased inflammatory response.

Serum YKL-40/chitinase 3-like protein 1 level is an independent predictor of atherosclerosis development in patients with obstructive sleep apnea syndrome.

OBJECTIVE: The inflammatory process plays an important role in the development of cardiovascular complications in patients with obstructive sleep apnea syndrome (OSAS). YKL-40/chitinase 3-like protein 1 is a novel biomarker of systemic inflammation. This study aimed to investigate whether carotid intima-media thickness (CIMT), a useful marker for early atherosclerosis, is associated with serum YKL-40/chitinase 3-like protein 1 levels in patients with normotensive and nondiabetic OSAS. METHODS: The study included 40 OSAS patients and 40 age- sex- and body mass index-matched healthy controls. Serum YKL-40 levels were detected by enzyme-linked immunosorbent assay. CIMT was measured by B-mode ultrasound. RESULTS: The patients with OSAS had significantly increased CIMT and higher YKL-40 and high sensitivity C-reactive protein (hsCRP) levels than those of the controls. CIMT was strongly correlated with serum YKL-40 levels (r=0.694, p<0.001), hsCRP (r=0.622, p<0.001), age (r=0.525, p=0.001), and weakly correlated with apnea-hypopnea index (AHI) (r=0.365, p=0.021) and the percentage of recording time spent (PRTS) of oxygen saturation<90% (r=0.488, p=0.001). Moreover, it was detected that serum YKL-40 levels were strongly correlated with AHI (r=0.617, p<0.001), and weakly correlated with SaO2<90% of PRTS (r=0.394, p=0.012) and hsCRP (r=0.486, p=0.001). In multiple regression analyses, age and serum levels of YKL-40 and hsCRP were found to be independent predictors of CIMT. CONCLUSION: In patients with OSAS, CIMT was increased. This increase was associated with serum YKL-40 level. Increased serum level of YKL-40 may be an early predictor of atherosclerosis development in patients with OSAS.

Relationship of left atrial global peak systolic strain with left ventricular diastolic dysfunction and brain natriuretic peptide level in patients presenting with non-ST elevation myocardial infarction.

BACKGROUND: In patients presenting with non-ST elevation myocardial infarction, we investigated the relationship of left atrial deformational parameters evaluated by 2-dimensional speckle tracking imaging (2D-STI) with conventional echocardiographic diastolic dysfunction parameters and brain natriuretic peptide level. MATERIAL AND METHODS: We enrolled 74 non-ST segment elevation myocardial infarction patients who were treated with percutaneous coronary intervention and 58 healthy control subjects. Non-ST segment elevation myocardial infarction patients had echocardiographic examination 48 h after the percutaneous coronary intervention procedure and venous blood samples were drawn simultaneously. In addition to conventional echocardiographic parameters, left atrial strain curves were obtained for each patient. Average peak left atrial strain values during left ventricular systole were measured. RESULTS: BNP values were higher in non-ST segment elevation myocardial infarction patients compared to controls. Mean left atrium peak systolic global longitudinal strain in Group 2 (the control group) was higher than in the non-ST segment elevation myocardial infarction group. Left atrium peak systolic global longitudinal strain was significantly correlated with left ventricular ejection fraction. There was a significant inverse correlation between left atrium peak systolic global longitudinal strain and brain natriuretic peptide level, left atrium volume maximum, and left atrium volume minimum. CONCLUSIONS: Our study shows that Left atrium peak systolic global longitudinal strain values decreased consistently with deteriorating systolic and diastolic function in non-ST segment elevation myocardial infarction patients treated with percutaneous coronary intervention. Left atrium peak systolic global longitudinal strain measurements may be helpful as a complimentary method to evaluate diastolic function in this patient population.

Effect of slow coronary flow on electrocardiographic parameters reflecting ventricular heterogeneity.

QT interval dispersion reflects regional variations in ventricular repolarization and cardiac electrical instability. Previous studies have showed that QT interval dispersion changes during episodes of myocardial ischemia. Slow coronary flow (SCF) in epicardial coronary arteries is a rare and unique angiographic finding. Whether this pattern of flow is associated with electrocardiographic abnormalities is unknown. Therefore, this study was designed to investigate whether SCF results in electrocardiographic (ECG) changes compared to normal coronary flow. For this aim 24 patients with angiographically proven SCF who had no obstructive coronary lesion (group I) and 25 patients without coronary artery disease (group II) were included in the study. Both groups underwent a routine standard 12-lead surface electrocardiogram recorded at 50 mm/s during rest. QT dispersion (QTd), corrected QT (QTc), and corrected QT dispersion (QTcd) were calculated. Distributions of sex, age, body mass index (BMI), and cardiac risk factors were similar in the 2 groups. Mean heart rate was similar in the 2 groups (74 +/-8 vs 77 +/- 7 p > 0.05). Mean QRS interval durations were similar in the groups (92 +/-7 vs 90 +/-6 ms p > 0.005). In group I, QTd, QTcd, and QTc, were significantly higher than in group II (QTd: 73 +/-14 vs 40 +/-14; QTcd: 71 +/-15 vs 42 +/-9; QTc: 414 +/-14 vs 388 +/-13, respectively p <0.05). In conclusion, SCF was found to be associated with prolonged QT interval and increased QT dispersion. Ischemia in microvascular level and/or altered autonomic regulation of the heart may be responsible mechanisms.

Increased high sensitive CRP level and its significance in pathogenesis of slow coronary flow.

Previous studies have suggested that microvascular abnormalities cause slow coronary flow (SCF). The role of inflammation has not been investigated, to date. The purpose of this study was to determine the role of inflammation in pathogenesis of SCF. The study included 32 patients with angiographically proven SCF (mean age 49 +/-9 years) (group I) and 30 subjects with normal coronary flow (mean age 48 +/-8 years) (group II). Blood samples were collected for high sensitive CRP (hs-CRP) measurements. Thrombolysis in myocardial infarction frame count (TFC) was compared in both groups. Distribution of sex, age, body mass index (BMI), arterial blood pressure, and ejection fraction were similar in the 2 groups. TFC was significantly higher in group I than in group II for each artery including left anterior descending coronary artery (LAD), left circumflex artery (Cx), and right coronary artery (RCA) (38.9 +/-6.6 vs 22.1 +/-1.8 frames, p = 0.0001; 39.6 +/-4.9 vs 22.3 +/-1.8 frames, p = 0.001 ; 39.0 +/-3.8 vs 22.0 +/-1.8 frames, p = 0.001, respectively). In group I, serum hs-CRP concentration was significantly higher than that of group II (0.6 +/-0.58 vs 0.24 +/-0.1 mg/dL p = 0.03). Correlation analysis showed a positive correlation between hs-CRP level and TFC for each artery (for CTFC(LAD), r = 0.36 p = 0.004; for TFC(Cx), r = 0.42 p = 0.003; and for TFC(RCA), r = 0.42, p = 0.0001 respectively). Increased hs-CRP level suggests that inflammation may be associated with pathogenesis of SCF or at least in part contributes to its pathogenesis. Increased hs-CRP level may also be an early marker of impaired coronary blood flow.

Determinants of Chronic Total Occlusion in Patients With Peripheral Arterial Occlusive Disease.

Chronic total occlusion (CTO) is a common finding in 40% of the patients with peripheral arterial disease (PAD). The aim of this study was to investigate the determinants of CTO in patients with PAD. The study included a total of 211 nonanemic patients with PAD. All patients were categorized according to the Fontaine classification. In lower extremity angiography cohorts, CTO- patients were designated as group 1 and CTO+ patients were designated as group 2. Patients with CTO had significantly higher red cell distribution width (RDW), neutrophil-lymphocyte ratio, uric acid, and high-sensitivity C-reactive protein compared to patients without CTO ( P ≤ .001, P = .036, P ≤ .001, and P = .015, respectively). Albumin, total bilirubin, and direct bilirubin were significantly lower in the patients with CTO compared to patients without CTO ( P = .023, P ≤ .001, and P = .049, respectively). Multivariate logistic regression analysis showed that RDW, uric acid, and total bilirubin were independent predictors of CTO in patients with PAD. We demonstrated that increased RDW and uric acid levels and lower total bilirubin values were independently associated with CTO in patients with PAD.

Myocardial deformation and total atrial conduction time in the prediction of cardiac involvement in patients with pulmonary sarcoidosis.

AIMS: In this study, we aim to evaluate the left atrial global longitudinal strain (LAGLS), total atrial conduction time (TACT) and left ventricle (LV) functions in recently diagnosed pulmonary sarcoidosis (PS) patients. METHOD: Fifty recently diagnosed PS patients (group 1) and a control group of 50 healthy individuals (group 2) were evaluated in the study. Two-dimensional echocardiography images were obtained from LV apical 4-chamber (4C), long-axis (L) and 2-chamber (2C) views. Peak longitudinal strain and strain rate (SR) were obtained from 4C, L and 2C views. Mean values of the three views were calculated. LV global longitudinal strain and LV-SR torsion were determined as the net differences in the mean rotation between the apical and basal levels. LAGLS and TACT values were calculated. RESULTS: The study found that LAGLS was significantly lower in group 1 than in group 2 (P < 0.05). TACT was also significantly longer in group 1 than in group 2 (respectively group 1: 111.6 ± 15.1 ms; group 2: 103.4 ± 5.8 ms, P < 0.001). There was a significant moderate negative correlation between LAGLS and TACT (r = -0.36, P < 0.05). Patients with sarcoidosis had significantly lower LV longitudinal strain and SR measurements than the control group. Although LV basal rotation (LVR) values were similar in both groups, LVR-apical and LV-torsion (LVTR) values were significantly higher in the patient group (group 1). CONCLUSION: The identification of left atrial and left ventricular myocardial deformation using speckle tracking echocardiography in patients with PS allows subclinical LV dysfunction and subclinical electrophysiologic changes to be detected earlier.

Beneficial Effects of Ozone Therapy on Oxidative Stress, Cardiac Functions and Clinical Findings in Patients with Heart Failure Reduced Ejection Fraction.

The aim of study was to determine the effects of ozone therapy on the oxidative stress, cardiac functions and clinical findings in patients with heart failure reduced ejection fraction (HFrEF). A total of 40 patients with New York Heart Association 2 and 3 HF with left ventricular ejection fraction (LVEF) <35%, and 40 subjects without HF as control group were included in the study. Patients with HFrEF were given additional ozone therapy of major and minor administrations along with conventional HF treatment for 5 weeks. Before and after ozone therapy, left ventricular end-systolic and end-diastolic volumes (LVESV, LVEDV) and the 6 minute walk distance (6MWD) and blood levels of the superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GSHPx), malondialdehyde (MDA), nitric oxide (NO) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured. Ozone therapy significantly reduced the serum levels of NO and MDA (p < 0.001, respectively) and significantly increased the levels of SOD, CAT, GSH and GSHPx (p < 0.001, respectively). LVEDV and LVESV were found to be significantly reduced; however, LVEF was not found to be significantly increased (p = 0.567). As the biochemical improvement marker of HF, NT-proBNP was significantly reduced (p < 0.001). The clinical HF improvement marker of 6 minute walk distance was also modestly increased (p < 0.001). Ozone therapy might be beneficial in terms of activating antioxidant system and merit further therapeutic potential to conventional HF treatment in patients with HFrEF.

Neutrophil-to-lymphocyte ratio as a possible indicator of epicardial adipose tissue in patients undergoing hemodialysis.

INTRODUCTION: Chronic inflammation is a major risk factor in the pathogenesis of cardiovascular disease in end-stage renal disease (ESRD) patients. Epicardial adipose tissue (EAT) is the true visceral fat depot of the heart. The relationship between coronary artery disease and EAT was shown in healthy subjects and ESRD patients. In the present study we aimed to investigate the relationship between EAT and inflammation parameters including neutrophil-to-lymphocyte ratio (NLR) in hemodialysis (HD) patients. MATERIAL AND METHODS: Forty-three HD patients (25 females, 18 males; mean age: 64.1 ±11.9 years) receiving HD and 30 healthy subjects (15 females, 15 males; mean age: 59.1 ±10.8 years) were enrolled in the study. Epicardial adipose tissue measurements were performed by echocardiography. RESULTS: Neutrophil-to-lymphocyte ratio levels were significantly higher in HD patients than in the healthy control group. Hemodialysis patients were separated into two groups according to their median value of NLR (group 1, NLR < 3.07 (n = 21) and group 2, NLR ≥ 3.07 (n = 22)). Group 2 patients had significantly higher EAT, C-reactive protein and ferritin levels, while albumin levels were significantly lower in this group. In the bivariate correlation analysis, EAT was positively correlated with NLR (r = 0.600, p < 0.001) and ferritin (r = 0.485, p = 0.001) levels. CONCLUSIONS: Neutrophil-to-lymphocyte ratio was found to be an independent predictor of EAT in HD patients (odds ratio = 3.178; p = 0.008). We concluded that this relationship might be attributed to increased inflammation in uremic patients.

The effect of moxonidine on endothelial dysfunction in metabolic syndrome.

BACKGROUND: Endothelial dysfunction has been reported in patients with type 2 diabetes mellitus and even in healthy obese individuals with a normal metabolic profile. Sympathetic activity commonly is increased in obese hypertensive patients, and moxonidine is effective in lowering BP and improving insulin sensitivity. OBJECTIVE: To evaluate the effect of moxonidine on endothelial dysfunction in patients with metabolic syndrome. METHODS: Twenty-six patients with mild hypertension were treated with moxonidine and a hypocaloric diet for 3 months, while a second normotensive group (n = 26) were followed-up with calorie restriction alone. Anthropometric (body mass index, waist and hip circumferences, and waist-to-hip ratio) and metabolic features (fasting plasma glucose and insulin, aminotransferases, gamma-glutamyl transpeptidase, triglycerides, and cholesterol levels) and flow-mediated dilatation (FMD) were evaluated. Insulin resistance was calculated by using the homeostasis model assessment formula. Insulin sensitivity was calculated according to the quantitative insulin-sensitivity check index (QUICKI). RESULTS: SBP and DBP (both p < 0.001) and waist circumference (p = 0.02) were higher, and QUICKI (p = 0.043) and FMD (p = 0.01) were lower in the hypertensive group at baseline. After 3 months, nearly all the study parameters improved in both treatment groups. The decrease in BP, increase in FMD, and improvements in metabolic and anthropometric parameters were significantly greater in the moxonidine-treated group than in those treated with diet alone. CONCLUSION: Moxonidine is proposed as a valuable option for treating mild-to-moderate hypertension in obese and insulin-resistant patients with metabolic syndrome as it appears to improve endothelial dysfunction in these patients.

Impact of coronary collateral circulation on QT dispersion in patients with coronary artery disease.

OBJECTIVE: The aim of this study was to assess the effect of coronary collateral circulation (CCC) on QT dispersion (QTD) in coronary artery disease. BACKGROUND: A prolonged QTD has been linked to increased heterogeneity of ventricular repolarization implicated in the genesis of ventricular arrhythmias and has been associated with an adverse prognosis in patients with coronary artery disease. METHOD: CCC and corrected QTD (QTcD) were established in patients who had at least 85% stenosis in the left anterior descending coronary artery or in proximal part or in the body of the right coronary artery. Furthermore, left ventricular function score was determined for all the patients. RESULTS: While CCC was not present (CCC grade 0) in 32 patients, 68 patients were observed with CCC (CCC grade > or =1). Mean QTcD was higher in patients who had CCC grade > or =1 than in patients with grade 0 (64.3+/-3.5 and 46.8+/-2.7, respectively, P=0.002). We detected a significant correlation between the collateral score and QTcD (r=0.354, P=0.001). CCC grade > or =1 patients had higher mean left ventricular function scores than grade 0 patients (P=0.048). Left ventricular function score and QTcD were observed to be correlated (r=0.200, P=0.046). CONCLUSION: CCC in chronic coronary artery disease was not established to have a positive decreasing effect on QTcD. On the contrary, QTcD values were observed to be even higher in patients with well developed CCC. Further research including larger series and long-term follow-up is required to investigate this issue.

Comparison of direct stenting versus conventional stent implantation on blood flow in patients with ST-segment elevation myocardial infarction.

As compared with balloon angioplasty, stent implantation in treatment of acute myocardial infarction (AMI) reduces abrupt vessel closure, restenosis, and reocclusion rate. However, a few studies have demonstrated the safety and feasibility of direct stenting compared to conventional stent implantation technique. This study was designed to compare possible advantages of direct stenting with conventional stent implantation on immediate coronary blood flow and short-term clinical benefits in patients with AMI. Fifty patients with AMI who underwent mechanical revascularization were eligible for the study. The patients were randomly assigned to undergo either direct stenting (n = 25) or conventional stent implantation (n = 25). Before and after the procedure thrombolysis in myocardial infarction (TIMI) flow and postprocedural corrected TIMI frame count (cTFC) of the infarct-related artery were measured. There was no difference in TIMI flow distribution at baseline between the 2 groups. TIMI 3 flow rate significantly increased after procedure in both groups compared to baseline (p < 0.05). Postprocedural cTFC was found significantly lower in the direct stent arm compared to conventional stenting (p < 0.001). Both during and after the procedure the complication rate and procedural time were lower in the direct stenting arm. Direct stenting provides better immediate coronary blood flow and is a safe and feasible method compared with conventional stenting in patients with AMI. Improvement in coronary blood flow measured by the corrected TIMI frame count method may suggests a significant reduction of microvascular injury.

Contribution of plasma lipid disturbances to vascular endothelial function in patients with slow coronary flow.

Previous studies have suggested that microcirculatory abnormalities cause slow coronary flow (SCF). However, the underlying mechanism of this phenomenon has not yet been well documented. Therefore, the aim of this study was to determine the role of plasma lipid disturbances in pathogenesis of slow coronary flow (SCF). Forty patients with SCF (group I) and 37 subjects with normal coronary arteries (group II) were included in the study. In each subject plasma lipid concentrations (total cholesterol [TC], low-density lipoprotein cholesterol [LDL-C], high-density lipoprotein cholesterol [HDL-C], and triglyceride [TG]) and brachial artery flow-mediated dilatation (FMD) and nitroglycerin (NTG)-induced dilatation were measured. Total cholesterol level was found to be similar in the 2 groups. In group I, HDL-C level was lower than in group II (34 +/-3 vs 40 +/-4 mg/dL, p=0.0001). In group I, TG level was higher than in group II (213 +/-29 vs 198 +/-24 mg/dL p=0.002). In group I, FMD was smaller than that of group II (3.48 +/-3.1% vs 10.4 +/-5.6%, p=0.0001). The percent NTG-induced dilatation was not different between the groups (15.5 +/-5.3% vs 17.3 +/-6.9%, p=0.27). On regression analysis; there was a significant relationship between percent of FMD and HDL-C (r =0.65, p=0.0001). When the 2 groups were analyzed separately, HDL-C was still related to percent of FMD in both groups (r =0.47 p=0.002 and r =0.45 p=0.005, respectively). Multivariate regression analysis showed that only plasma HDL-C was independently related to FMD (F=7.5 p=0.0001). In patients with SCF, reduced flow-mediated dilatation was detected and was found to be associated with plasma lipid disturbances, principally low HDL and high TG levels.

Tissue Doppler velocities of the right and left ventricles and their association with C-reactive protein and homocysteine levels in Behcet's disease.

In the present study, we aimed to investigate whether tissue Doppler imaging could provide more information than standard echocardiography about left and right ventricular functions and their relations to homocysteine and C-reactive protein (CRP) levels in the course of Behcet's disease (BD). In the right ventricle, patients with BD had lower early diastolic tricuspid annular velocity and early diastolic/late diastolic tricuspid annular velocity ratios than the control group. Mitral and tricuspid annular systolic velocities did not significantly differ; however, diastolic velocities were correlated with duration of the disease. In addition, early/late diastolic mitral annular velocity ratio and early/late diastolic tricuspid annular velocity ratios showed an inverse relation with ocular involvement, serum homocysteine, and CRP levels in patients with BD.

Increased aortic stiffness in patients with coronary artery ectasia.

OBJECTIVE: Alterations in aortic stiffness may reflect the elastic properties of the larger arteries. In many diseases, aortic elastic properties have been investigated to show whether the larger arteries are involved. The elastic properties of aorta in patients with coronary artery ectasia, however, have not been studied yet. We aimed to investigate aortic stiffness parameters in patients with coronary artery ectasia and to compare patients with coronary artery ectasia and coronary artery disease with the control group. METHOD: Thirty-three patients with coronary artery ectasia, 31 patients with coronary artery disease and 30 patients with angiographically normal coronary arteries were included in this study. Aortic diameters were measured on the M-mode tracing obtained at a level 3 cm beyond the aortic valve at parasternal long-axis view. Aortic diameter change, aortic strain, aortic distensibility and stiffness parameters were measured as aortic stiffness parameters. RESULTS: Aortic diameter changes were fewer in the coronary artery ectasia and coronary artery disease group than in the control group (0.4 +/- 0.1 and 0.3 +/- 0.1 vs. 0.8 +/- 0.2; P < 0.001). Aortic distensibility and aortic strain were significantly lower in patients with coronary artery ectasia and coronary artery disease than in the controls (for aortic distensibility P < 0.001 and for aortic strain P < 0.001, < 0.001, respectively). In contrast, a significantly higher aortic stiffness index was observed in patients with coronary artery ectasia and coronary artery disease than in the control group (14.2+/-2.6 and 18.1 +/- 2.9 vs. 5.9 +/- 1.8; P < 0.001, respectively). CONCLUSIONS: The impairment in aortic elastic properties in patients with coronary artery ectasia indicates that this disease is a generalized disease rather than a localized disease of the coronary arteries.

Aortic valve calcification: association with bone mineral density and cardiovascular risk factors.

BACKGROUND: Cardiovascular risk factors are reported to increase the incidence of aortic valve calcification. Among older women, low bone mineral density appears to be associated with increased prevalence of aortic calcification. We aimed to assess and compare cardiovascular risk factors and bone mineral density of patients with and without aortic valve calcification. MATERIALS AND METHODS: Cardiovascular risk factors and bone mineral density measurements have been assessed in 49 patients with aortic valve calcification and in 65 patients without aortic valve calcification. All patients were subsequently referred to the nuclear medicine department to measure bone mineral density after echocardiographic evaluation. RESULTS: No statistically significant differences were observed between the two groups with respect to sex, body mass index, history of coronary artery disease, diabetes mellitus, hypercholesterolemia, and smoking status. Although height and weight of the patients with aortic valve calcification were significantly lower than those of patients without aortic valve calcification, they were not independent risk factors. Age and hypertension were found to be independent positive risk factors for aortic valve calcification, whereas T score was found to be negatively associated with aortic valve calcification. CONCLUSION: We have shown that aortic valve calcification is positively associated with age and hypertension, whereas bone mineral density is negatively associated with aortic valve calcification. The mechanism underlying the association between decreased bone mineral density and aortic valve calcification remains to be clarified in further studies.

Elevated plasma homocysteine level in slow coronary flow.

BACKGROUND: Slow flow velocity of dye in coronary arteries is not an infrequent finding during routine coronary angiography and its precise mechanism is unknown. In this study, we measured the plasma homocysteine level in patients with slow coronary flow (SCF) in comparison with subjects having normal coronary flow (NCF). METHOD: The study consisted 39 patients (mean age, 47+/-8 years) with angiographically diagnosed SCF. SCF was defined according to TIMI frame count (TFC) method. Thirty subjects (mean age 46+/-8 years) with NCF served as control group. Plasma homocysteine levels were measured after 12 h fasting period in each subject. RESULTS: Baseline demographic properties were similar in both groups. In patients with SCF, TFC was significantly higher than those with NCF. Similarly, in patients with SCF plasma homocysteine level was significantly higher than that of control group (14.1+/-2.2 vs. 5.5+/-1.3 micromol/l, respectively p < 0.001). CONCLUSION: Elevated plasma homocysteine level supports the hypothesis that endothelial function is impaired in slow coronary flow.