Hakan Tikiz

QT Dispersion in Single Coronary Artery Disease: Is There a Relation Between QT Dispersion and Diseased Coronary Artery or Lesion Localization?

It has been shown that QT dispersion (QTD) increases during episodes of myocardial ischemia or infarction. However, no extensive data on the relation between the diseased coronary artery or the localization of stenosis and the QTD are available. The aim of the study was to examine the relation between QTD and diseased coronary artery and lesion localization during exercise stress test in patients with single coronary artery disease without prior myocardial infarction. One hundred nineteen patients with single coronary artery disease and 53 patients with normal coronary arteries were enrolled in study. All patients underwent exercise stress test with modified Bruce protocol, and QT interval parameters were measured at rest and at minute 2 of the recovery (rec-2) period. QT dispersion at rest was found higher in all single-vessel disease groups compared with that in the control group, and corrected QT dispersion at rec-2 period was also markedly higher in left anterior descending, circumflex, and right coronary artery groups compared with that in the control group. No relation was found between QT dispersion and diseased coronary artery or the lesion localization. In conclusion, no qualitative difference was found between QT dispersion and diseased coronary artery or proximal or distal lesion localization. However, it was observed that patients with single-vessel disease had wider baseline QT dispersion as compared with that in the control group, which further increased significantly with exercise. This finding supports the idea that severity of localized ischemia rather than extent of coronary artery disease would be expected to have a greater effect on inducible QT dispersion.

Endothelıal dysfunctıon ın patıents wıth prımary Sjögren’s syndrome

The aim of this study was to determine the endothelial function in patients with primary Sjögren’s syndrome (SS). We also aimed to determine whether endothelial (dys)function correlates with extraglandular manifestations, specific autoantibodies and the severity of salivary gland involvement of SS. Endothelium-dependent vasodilation and endothelium-independent vasodilation of the brachial artery were assessed by a high-resolution ultrasound on 25 patients with primary SS and on 29 healthy controls. Patients with primary SS had significantly less mean endothelium-dependent vasodilation than did controls (3.0±0.4% vs 4.2±0.3%; p=0.012). Endothelium-independent vasodilation induced by sublingual glycerol trinitrate was not different between the two groups (12.9±1.4% vs 14.1±1.2%; p=0.86;). We concluded that endothelium-dependent vasodilation was impaired in primary SS patients, in particular those presenting with Raynaud’s phenomenon, when compared with the healthy controls and this impairment was not associated with the presence of RF, ANA, anti-Ro/SS-A, anti-La/SS-B and with the other extraglandular manifestations of the disease.

Increased serum leptin concentrations in patients with chronic stable angina pectoris and ST-elevated myocardial infarction.

Leptin is an adipocytokine that is produced mainly by adipose tissue; it is also identified in atherosclerotic lesions in human coronary atherosclerosis. However, the relation of serum leptin concentrations to ischemic heart disease (IHD) is still obscure. The aims of the present study were to investigate serum leptin concentrations in patients with ST-elevated myocardial infarction (STEMI) and with chronic stable angina pectoris (CSAP) and to evaluate the possible correlations of leptin to other atherosclerotic risk factors; including serum high sensitive C-reactive protein (Hs-CRP), serum homocysteine, and fibrinogen concentrations. For this purpose, 35 patients with CSAP, 40 with acute STEMI, and 30 control subjects with normal findings from coronary angiography were taken into the study prospectively. Serum leptin concentrations were significantly higher in patients with CSAP and STEMI compared to the control group (7.74 ±1.34 vs 6.37 ±1.85 ng/mL, p=0.021 and 8.22 ±3.13 vs 6.37 ±1.85 ng/mL, p=0.023, respectively). In addition, serum homocysteine concentrations were significantly increased in patients with CSAP (15.23 ±5.96 vs 11.40 ±2.11 μmol/L, p=0.025) and patients with STEMI (15.90 ±5.02 vs 11.40 ±2.11 μmol/L, p=0.012) compared to the control group. Serum fibrinogen concentrations were significantly increased only in the CSAP group as compared to controls (4.15 ±1.39 vs 3.45 ±1.19 g/L, p=0.025). No significant correlation was found between leptin levels and selected risk factors. In conclusion, serum leptin concentrations were significantly higher in both the CSAP and STEMI groups. However, owing to the lack of correlation between the leptin levels and selected classical coronary risk factors, it may be considered that leptin can be evaluated as one of the independent risk factors for IHD. Further randomized and controlled studies will be required to determine the pathophysiological meaning of the increased leptin levels and the central role between adipocyte function and atherosclerosis.

Left ventricular aneurysm formation after anterior myocardial infarction: clinical and angiographic determinants in 809 patients.

BACKGROUND Previous studies have reported controversial results regarding the clinical and angiographic factors involved in the left ventricular aneurysm (LVA) formation after myocardial infarction (MI). OBJECTIVE This study was performed to determine the clinical and angiographic factors that are priori predictors of LVA following anterior myocardial infarction and so to provide a paradigm which may identify patients who were candidates for aneurysm formation. METHODS Of the patients who underwent coronary angiography during the interval between 1995 and 2000 in our clinic, 809 were found to have anterior MI and LVA (aneurysm group) (677 men, 132 women, mean age 53.3+/-11.4 years). The clinical and the angiographic data of these patients were compared with those of 446 patients (399 men, 47 women, mean age 55.2+/-10.5 years) with previous anterior MI and without LVA (control group). RESULTS LVA was found to occur more frequently in females (16.3% in women and 10.4%, in men, P=0.03) and in patients without previous angina (23.5 vs. 8.2%, P<0.0001). Major cardiovascular risk factors, previous anti-anginal medication and thrombolytic therapy did not show a significant difference between the two groups. Angiographic examination revealed that single-vessel disease, proximal left anterior descending artery (LAD) stenosis, total LAD occlusion, mean stenosis in LAD artery, end-diastolic pressure and left ventricular score were all higher in the aneurysm group compared to control group. After adjustment for other clinical and angiographic variables, single-vessel disease [odds ratio (OR) 5.89, 95% confidence interval (CI)=3.68-9.28, P<0.0001), absence of previous angina (OR=4.21, 95% CI=2.1-7.48, P=0.0003), total LAD occlusion (OR=2.63, 95% CI=1.97-3.53, P<0.0017) and female gender (OR=1.60, 95% CI=1.20-2.28, P=0.043) remained the independent determinants of LVA formation after anterior MI. CONCLUSION In patients with LVA, logistic regression analysis revealed that (1) single-vessel disease, (2) absence of previous angina, (3) total LAD occlusion and (4) female gender were independent determinants in the formation of LVA after anterior MI. Coronary collateral status and risk factors, such as hypertension, diabetes mellitus, hypercholesterolemia, smoking and family history of CAD were not found to be important determinants in the aneurysm formation.

The effect of simvastatin on serum cytokine levels and bone metabolism in postmenopausal subjects: negative correlation between TNF-α and anabolic bone parameters

In this prospective study, we aimed to evaluate the effect of simvastatin on bone metabolism and the correlation between changes in bone turnover parameters and serum cytokine levels. For this purpose, 38 postmenopausal subjects with hypercholesterolemia (>240 mg/dl), not on osteoporosis treatment, were studied. Simvastatin was started at a dose of 20 mg daily and continued for 3 months. Six patients were excluded from the study during the follow-up period. Pre- and post-treatment samples were analyzed for bone alkaline phosphatase (BAP) and osteocalcin (OCL), as markers of bone formation; for carboxyterminal telopeptide of collagen I (CTX), as a marker of bone resorption; and for interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) cytokine levels. Total cholesterol level was decreased from 262.1 ± 30.9 to 210.2 ± 35.6 mg/dl after simvastatin treatment (P < 0.0001). While no significant change was observed in serum CTX level, BAP and OCL levels were significantly increased (from 120.8 ± 56.6 to 149.5 ± 57.6 IU/l [P = 0.008], and from 20.8 ± 12.6 to 34.7 ± 18.4 µg/l [P = 0.015], respectively). In the analysis of cytokines, while no significant change was observed in IL-6 levels, the TNF-α level was found to be significantly decreased after simvastatin treatment (from 77.9 ± 31.6 pg/ml to 23.5 ± 12.6 pg/ml [P = 0.021]). Individual changes in TNF-α levels showed a moderate negative correlation with the individual changes in BAP and OCL levels (r = −0.550 [P = 0.001], and r = −0.497 [P = 0.004], respectively). In conclusion; 20-mg daily simvastatin treatment for 3 months significantly increased BAP and OCL levels (markers of bone formation) in hypercholesterolemic postmenopausal subjects, without affecting bone resorption. These findings support the idea that simvastatin has an anabolic effect on bone formation. Additionally, the presence of a negative correlation between TNF-α levels and the anabolic bone parameters suggests that a cytokine-lowering effect of simvastatin may also be involved in the remodeling process and could exert some additive beneficial effect on bone metabolism.

Standard dose of inhaled albuterol significantly increases QT dispersion compared to low dose of albuterol plus ipratropium bromide therapy in moderate to severe acute asthma attacks in children

Abstract Background : Beta‐2 agonist therapy has previously shown to increase the QT dispersion (QTd) in asthmatic patients and increased QTd has been well documented in association with cardiac arrhythmias and sudden death. However, the data concerning the effect of low doses of beta‐2 agonist therapy in combination with the anticholinergic agents to potentiate bronchodilatation on QTd in asthmatic children are limited. The objectives of this study was to investigate the changes on QTd during both the standard dose of nebulized albuterol therapy and low dose nebulized albuterol plus inhaled ipratropium therapyn to assess the potential arrhytmogenic risk of these two treatment strategies in children with acute asthmatic attacks.

The effect of anti-tumor necrosis factor (TNF)-alpha therapy with etanercept on endothelial functions in patients with rheumatoid arthritis.

OBJECTIVE To investigate the effects of tumor necrosis factor (TNF)- alpha antagonism with etanercept (ENC) on endothelial functions in patients with active rheumatoid arthritis (RA). METHODS A total of 21 patients with RA were enrolled in this prospective study. Eleven of them (8 women, 3 men mean age 47.0+/-10.1 years) with high disease activity despite the conventional treatment were assigned to Group 1 and were given ENC treatment twice a week (25 mg SC injection) for 12 weeks. Ten patients with RA (8 women, 2 men mean age 55.0+/-6.4 years) under conventional methotrexate and prednisone therapy were assigned as Control group (Group 2). Endothelium-dependent and -independent vasodilator responses of the brachial artery were assessed by high-resolution ultrasound. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were also measured at baseline and at the post treatment period. Mann-Whitney U and Wilcoxon tests were used to compare the data and correlation analysis was performed using Pearson correlation test. RESULTS Endothelium-dependent vasodilatation improved from 5.2+/-0.8% to 7.9+/-1.3% (p=0.04) in ENC group, while no significant change was observed in the control group (from 6.6+/-1.1% to 7.0+/-1.8% p=0.67). No significant changes were found in endothelium-independent vasodilatation and baseline brachial artery diameters in both groups. A significant reduction in ESR and CRP were observed in patients receiving ENC (from 16.2+/-6.8 to 9.2+/-5.1 mm/h, p=0.003 and from 14.68+/-3.4 to 9.25+/-3.7 mg/L, p=0.003, respectively). CONCLUSION Treatment with ENC for 12 weeks significantly improved endothelial function in patients with active RA compared to those under conventional therapy. The findings of the present study support the hypothesis that the use of TNF-alpha blockers in patients with active RA may reduce the high incidence of cardiovascular complications.

The effect of long-term continuous positive airway pressure treatment on systolic and diastolic function in patients with obstructive sleep apnoea syndrome: a five year observational study.

OBJECTIVE Evaluation of the long-term effects of continuous positive airway presure (CPAP) on mean heart rate and left ventricular systolic and diastolic parameters in obstructive sleep apnea syndrome (OSAS) using conventional and tissue Doppler techniques. METHODS This prospective cohort study is designed to evaluate the long-term effects of CPAP treatments in normotensive OSAS patients. Initially 40 patients aged from eighteen to fifty five with documented OSAS syndrome were evaluated within one month of CPAP treatment. All had high self-reported compliance with treatment. From the latter, 21 patients with uninterrupted CPAP therapy (for at least 5 years, 5 hours per day) were included in the study and further evaluated with treatment. The left ventricular systolic function was assessed on apical four- chamber view using modified Simpson method and diastolic function was evaluated with classic transmitral pulsed and tissue Doppler techniques. Paired t test and Wilcoxon signed rank test had been used to compare the clinical and echocardiography data before and after treatment period. RESULTS A comparison of values assessed after one month and after 5 years of CPAP therapy, revealed a significant increase in the acceleration time(AT) Em/Am ratio and ejection time (ET) (AT: p=0.04; Em/Am ratio p=0.03 ET: p=0.04) while a significant decrease was observed on deceleration time (DT), isovolumetric relaxation time (IRT), myocardial performance index (MPI), mitral regurgitation (MR) and 24 hour mean heart rate (HR) in all subjects (DT: p=0.02; IVRT: p=0,04; MPI: p=0,01; MR: p≤0.001; HR: p=0.004). CONCLUSION We observed a significant improvement in the left ventricular systolic and diastolic function and a significant decrease of 24-hour heart rate and mitral regurgitation with unchanged ejection fraction of the left ventricle with long-term CPAP treatment similar to short-term treatment studies. The long-term maintenance of the beneficial effect of CPAP throughout the 5 year long-term treatment can be one of the pathophysiologic mechanisms that may explain the decrease of cardiovascular mortality observed with long-term CPAP therapy in OSAS patients.

Giant Unruptured Noncoronary Sinus of Valsalva Aneurysm

A 66-year-old woman presented with dyspnea on exertion (NYHA class II), which she had been experiencing for 2 years. An examination revealed normal systolic and diastolic blood pressures and a grade 2/6 continuous murmur on the left side of the sternum. The transthoracic echocardiogram showed serious aortic regurgitation and …

Effects of atrial pacing on QT dispersion in patients with coronary artery disease without angina pectoris and ST segment depression.

The aim of this study was to investigate QT dispersion during atrial pacing in patients with coronary artery disease (CAD) without clinical ischemia, such as angina pectoris and ST segment depression. Thirteen patients with normal coronary arteries and 42 patients with CAD (12 with single-vessel, 16 with two-vessel and 14 with three-vessel disease) having no angina pectoris or ST segment depression during atrial pacing with maximum rate of 120/minute were enrolled in the study. Twelve-lead surface ECGs were recorded at 100 mm/second paper speed before pacing, at maximum pacing rate, and during the recovery period for measurement of QT interval parameters. Corrected QTd (QTcd) increased from 43.4 ±8.1 to 49.3 ±9.5 ms (p<0.05) in the control group, from 46.1 ±8.1 to 74.3 ±7.7 ms (p < 0.000 1) in the single-vessel disease group, from 48.5 ±10.4 to 93.8 ±22.1 ms in the two-vessel disease group (p< 0.0001), and from 49.7 ±13.6 to 128.5 ±31 ms (p<0.0001) in the three-vessel disease group at peak atrial pacing period. A positive correlation was found between the severity of CAD and QTcd (r=0.49, p<0.0001). It was found that pacing-induced QTc dispersion identifies coronary disease extent, even when there is no ST depression or T wave inversion during pacing.