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We studied the ECGs of patients with single vessel disease before and after (long term) coronary stent implantation. The interlead variability of the QT interval, known as QT dispersion (QTd), is believed to reflect the regional variations in ventricular repolarization and, thus, may provide an indirect marker of arrhythmogenicity. There are no reliable noninvasive markers of significant restenosis after stent implantation. The effect of coronary revascularization on QTd in patients who underwent coronary stenting has not been investigated extensively. The aim of this study was to evaluate the value of QTd in predicting restenosis after intracoronary stent implantation. QTd with 12 lead surface ECG was measured in 48 patients (21 with restenosis and 27 without restenosis; 33 male; mean age, 58 +/- 10.8 years) before the procedure and after long-term follow-up (mean, 6.8 +/- 3.2 months). All patients had coronary angiographic control at the end of the follow-up period. QTd (as the difference between the maximum and minimum QT interval measured from 12 lead EGG) and rate-corrected QT (QTcd) were evaluated at rest. In 27 patients without restenosis, QTd and QTcd decreased from 58 +/- 14.4 and 62.8 +/- 20.4 ms to 26.3 +/- 9.2 and 29.6 +/- 10.6 ms in the long term follow-up, respectively (P < 0.001). However, in 21 patients with restenosis, there was no significant change in QTd and QTcd intervals and they were still increased at the end of the long-term follow-up (P > 0.05). In conclusion, increased QT interval dispersion may be an inexpensive and simple marker of restenosis after intracoronary stent implantation. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.

OBJECTIVE: The role of coagulation parameters left atrial thrombus formation in atrial fibrillation has not been investigated before. We aimed to investigate the association between the beta-fibrinogen gene polymorphism or glycoprotein IIIa gene polymorphism and presence of left atrial (LA) thrombus or spontaneous echo contrast (SEC) in patients with atrial fibrillation (AF). METHODS: Forty-seven patients with AF, in whom transesophageal echocardiography was performed, were included to this cross-sectional observational study. Patients were divided in two groups; those with LA thrombus (n=24) were assigned to group 1 and those without thrombus in group 2 (n=23). DNA analysis was conducted to determine gene polymorphism in all patients. Mann-Whitney U test or Chi-square tests were used for statistical analysis. RESULTS: There were no significant differences between groups regarding to demographic and clinical characteristics. The frequency of beta-fibrinogen 455 G/A polymorphism was higher (37.5%) in group 1 as compared to group 2 (15.1%) but it did not reach statistical difference (p=0.23). When we added patients with severe SEC in the study group (patients with severe SEC and/or thrombus n=27) the difference (44.40%-10%) reached the statistical difference (p=0.01). Glycoprotein IIIa Pl A1/A2 polymorphism was not different between groups with (p=0.82) or without SEC (p=0.73). CONCLUSION: In patients with atrial fibrillation, beta-fibrinogen 455 G/A gene polymorphism is associated with the presence of left atrial thrombus and severe SEC. Beta-fibrinogen 455 G/A gene polymorphism may be a promising marker for the prediction of thromboembolism risk in patients with atrial fibrillation.

The aim of this study was investigate the effects of carvedilol therapy on ventricular repolarization characteristics as assessed by QT dispersion (QTd) and heart rate variability (HRV) in patients with heart failure. Thirty-one patients with heart failure (mean age, 63.9 years) were included in the study. Carvedilol was administered in addition to standard therapy for CHF at a dose of 6.25 mg/day and uptitrated to the maximum tolerated dose. Control group consisted of 14 patients with heart failure (mean age, 69.4 years) who could not take carvedilol due to several reasons. All patients were followed-up 6 months. QT dispersion (QTd), and corrected QTd (QTcd) values were calculated at baseline and at the end of follow-up. Time domain and frequency domain heart rate variability analysis were performed with ambulatory Holter ECG. Mean carvedilol dose was 23.9 +/- 13.9 mg. Significant reductions were observed in the QTd (P = 0.016) and QTcd (P = 0.001) with carvedilol therapy, whereas QTd (P = 0.47) and QTcd (P = 0.43) did not change significantly in the control group. The QT maximum value did not change significantly but the QT minimum value (P = 0.03) was significantly increased after carvedilol therapy. Although the mean SDANN value was improved (P = 0.039), other HRV parameters such as mean SDNN (P = 0.32), rMSSD (P = 0.74), and the LF/HF ratio (P = 0.35) did not change significantly after carvedilol therapy. This prospective controlled study shows that carvedilol therapy decreased QT dispersion and improved ventricular repolarization characteristics but did not change autonomic dysfunction in patients with heart failure.

Restoration of sinus rhythm by electrical cardioversion is a therapeutic option in appropriately selected patients with atrial fibrillation. It is important to determine predictors of electrical cardioversion outcome in patients with atrial fibrillation. Predictive value of clinical and conventional echocardiographic parameters for predicting cardioversion outcome is limited. The role of left atrial appendage (LAA) function, which may reflect left atrial contractile function, for prediction of cardioversion outcome remains unclear. We conducted a single center prospective study to evaluate the role of LAA function for prediction of cardioversion success in patients with atrial fibrillation. One hundred sixty three patients with atrial fibrillation underwent transthoracic and transesophageal echocardiography (TEE) before electrical cardioversion. LAA functions, including LAA peak flow velocity, LAA area and LAA ejection fraction, were examined. Cardioversion was successful in 133 patients and unsuccessful in 30 patients. Mean LAA peak emptying flow velocity was significantly higher in the patients with successful cardioversion than in those with unsuccessful cardioversion (0.34 +/- 0.14 vs 0.27 +/- 0.1 m/sec; p = 0.013). At multivariate logistic regression analysis, only LAA flow velocity (> 0.28 m/sec, odds ratio = 2.8 ; p = 0.03) proved to be an independent predictor of cardioversion success. LAA area (p = 0.18) and LAA ejection fraction (p = 0.52) were not different between successful and unsuccessful cardioversion groups. Therefore, measurement of LAA flow velocity provides valuable information for prediction of cardioversion outcome in patients with atrial fibrillation before TEE guided cardioversion.

CD40-CD40 ligand interaction is involved in the inflammatory pathogenesis of atherosclerosis but clinical data about its role in stent restenosis are still limited. We investigated the effect of preprocedural CD40 ligand (sCD40L) on stent restenosis. We enrolled 36 patients (mean age 61.4 +/- 8.5 years) with stable angina who underwent successful stent implantation. Control angiograms were performed in all patients after 6 months. Plasma sCD40L and high-sensitive C-reactive protein levels were measured before stent implantation and at 1 and 6 months after the procedure. Angiographically proven restenosis rate was 27.8%. Plasma sCD40L levels were significantly higher (preprocedural 0.74 +/- 0.79) and more prolonged in patients with stent restenosis compared with patients without stent restenosis (0.02 +/- 0.22 ng/ml, p 0.41 ng/ml was the best distinguished parameter between patients with and without restenosis. At the multivariate logistic regression analysis, preprocedural sCD40L was an independent predictor (RR 39.4, 95% confidence interval 4.05 to 383.8, p = 0.002) of stent restenosis after adjusting for confounding variables, including diabetes, reference vessel diameter, lesion length, stent diameter, stent length, and baseline high-sensitive C-reactive protein. Sensitivity, specificity, and positive and negative predictive values and likelihood ratio of preprocedural sCD40L levels in stent restenosis were 78%, 92%, 78%, 92%, and 9.37%, respectively. In conclusion, enhanced inflammation of plaque (increased sCD40L) before percutaneous coronary intervention may increase the rate of stent restenosis. Increased preprocedural sCD40L level is an independent predictor of stent restenosis. We can use this marker for the assessment of risk stratification before planning stent implantation. (C) 2006 Elsevier Inc. All rights reserved.

Background : Transesophageal echocardiography (TEE) guided cardioversion to restoration of sinus rhythm is a therapeutic option in patients with atrial fibrillation (AF). Anticoagulation at the time of and after cardioversion is necessary to prevent formation of new thrombus during atrial stunning period. We aimed to evaluate the efficacy and safety to TEE guided cardioversion with low molecular weight heparin (LMWH) in patients with atrial fibrillation Methods : We followed up 208 patients with persistent AF (mean age: 65.5±10.2 years) who were attempted TEE guided cardioversion. LMWH were used as an anticoagulant and warfarin therapy was continued. Results : Cardioversion were performed in 183 patients. Sinus rhythm restored in 144 patients (78.7%). Mean follow up duration was 155 days. No cardiac death occurred. In the early follow up period (within 30 day) one thromboembolic event (0.54%) occurred in a petient who was cardioverted. Two patients who had not been cardioverted because of left atrial thrombus presented embolic stroke, one in early and another in late follow up period. All embolic complications occurred in patients who had been taking warfarin and whose INR level was subtherapeutic at the time of stroke. Sinus rhythm was maintained in 64% and total hemorrhagic complications occurred in 4.8% of the patients in long-term follow-up. Conclusion : TEE guided cardioversion with a short-term anticoagulation protocol using low molecular weight heparin is a safe and effective method in restoring and maintaining sinus rhythm and enables us to make earlier cardioversion in atrial fibrillation.

Previous studies have demonstrated increased serum copper and iron levels and decreased selenium and zinc levels in patients with myocardial infarction. Furthermore, the prognostic value of the levels of trace elements in myocardial infarction has been stressed. We examined serum levels of Cu, Fe, Zn and Se, as well as glutathione peroxidase (GPx), a selenoenzyme with antioxidant properties, and C-reactive protein (CRP), a marker of inflammation, in acute coronary syndromes (ACS) regarding their relationship to cardiac troponins and creatine kinase-MB mass (CK-MBm), important prognostic markers. Serum trace elements, GPx activity and CRP were determined in 70 patients with ACS who were admitted within 12h after the onset. Differences in these parameters were evaluated in three groups of patients divided according to the levels of cardiac markers: group III consisted of patients with high increases in cTnT, cTnI and CK-MBm (>= 0.9 ng/mL, >= 1.0 ng/mL, >= 30 ng/mL, respectively), patients with milder increases in these markers were included in groups II and I consisted of patients with values just above the upper reference limits. Serum Fe levels increased significantly in group II and even more prominently in group III compared to group I (p = 0.04,0.002, respectively). There was no significant difference between groups II and III. The increase in serum Cu was significant in group III compared to both groups II and I (p = 0.04, 0.001, respectively). There was no significant difference between groups I and II regarding Cu and Zn. The decrease in serum Se and GPx levels was significant only between groups III and I (p = 0.004 for Se and p = 0.0001 for GPx). CRP levels showed a significant increase in group III compared to groups II and I (p = 0.03 and 0.001). CRP showed a significant positive and GPx a significant negative correlation to the cardiac markers cTnT, cTnI and CK-MBm. Cu was positively correlated to all cardiac markers, while the positive correlation between Fe and cardiac markers was significant only for cTnI. Both Zn and Se were negatively correlated to cTnT, and Se was also to cTnI. In conclusion, the increase in serum levels of Cu and Fe and the decrease in serum levels of Zn and Se in patients with higher levels of troponins and CK-MBm imply that trace element levels are related to the degree of myocardial damage and thus may play a role in the pathogenesis of ischemic heart disease. The strong correlations between cardiac markers and both CRP and GPx suggest that these parameters are promising prognostic factors in acute coronary syndromes. (c) 2005 Elsevier GmbH. All rights reserved.

The effects of captopril on serum digoxin concentrations were studied in 8 patients with severe (NYHA Class IV) congestive heart failure. Serum digoxin concentrations were determined before and after the administration of captopril for 1 week in patients on chronic digoxin therapy, Each patient who was taking 0.25 mg of digoxin PO q.d., was administered 12.5 mg of captopril PO t.i.d. for 7 days. The peak serum concentration of digoxin (C-max) before and after (on Days 0 and 7) captopril administration was 1.7 +/- 0.2 ng/ml and 2.7 +/- 0.2 ng/ml, the time to peak (t(max)) was 2.4 +/- 0.5 h and 1.3 +/- 0.2 h, and the area under the 24-hour digoxin concentration-time curve (AUC(0-24h)) was 30.0 +/- 1.5 ngxh/ml and 41.7 +/- 3.4 ngxh/ml, respectively. While captopril caused a significant increase in peak serum concentration and the area under the digoxin concentration-time curve, it decreased the time to digoxin peak (p = 0.01, p = 0.04, p = 0.01, respectively). No patient developed evidence of digoxin toxicity. Concomitant administration of captopril with digoxin increases serum digoxin concentration in patients with severe congestive heart failure.