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Yücel Balbay

Publications and source records attributed to Yücel Balbay.

6 recordsLinked to original sources

[Thrombotic, fibrinolytic and proliferative activities of pulmonary vascular bed in secondary pulmonary hypertension].

OBJECTIVE: To determine whether pulmonary vascular bed contributes to the development of in situ thrombosis and vascular remodelling in secondary pulmonary hypertension (SPH) via changes in its local secretory activities. METHODS: Seventy-one patients with the diagnosis of secondary pulmonary hypertension (38 females, mean age 40.36+/-1.05 years) were included in the study. Selective right and left heart catheterization was performed to each patient for diagnostic purposes. Blood samples obtained from left ventricle (LV) and pulmonary artery (PA) of each patient were analyzed for levels of plasminogen activator inhibitor-1 (PAI-1), platelet derived growth factor (PDGF), vascular endothelial growth factor (VEGF), D-dimer, von Willebrand factor (vWF), protein-C, antithrombin-III, fibrinogen, and plasminogen. Results were compared between LV and PA. Correlation analysis between each parameter and mean pulmonary artery pressure (MPAP) was performed. RESULTS: Although mean level of VEGF in LV and PA were found to be in normal range, it was significantly higher in LV than in PA (p<0.001). Mean PDGF and D-dimer levels, which remained in normal range were also higher in LV (p<0.001 and p<0.001, respectively) than in PA;.vWF showed similar degree of elevation in both LV and PA. Only one parameter, PAI-1, was found to be significantly higher in PA than in LV (p=0.012). Antithrombin-III, protein C, plasminogen, and fibrinogen levels showed no significant differences between two chambers. They also remained in normal range, except for fibrinogen, which was slightly elevated in both LV and PA. Correlation analysis revealed strong positive correlation between D-dimer level in both LV and PA and MPAP (r=0.775, p<0.001 and r=0.649, p<0.001, respectively). CONCLUSION: In SPH, pulmonary vascular bed shows increased thrombotic, hypofibrinolytic, and proliferative activities, which are partially related to the severity of illness.

Adult↗

Do collaterals affect heart rate variability in patients with acute myocardial infarction?

BACKGROUND: The protective effects and the prognostic importance of collaterals during and after acute myocardial infarction (MI) are under debate and heart rate variability (HRV) is a strong predictor of risk of mortality and arrhythmic events after acute MI. We aimed to examine the effects of collateral circulation on HRV in the early period after acute MI. METHODS: Sixty-four patients admitted to our clinics who were diagnosed with acute anterior MI and underwent thrombolytic therapy were enrolled in this study. We applied 24 h Holter monitoring for HRV analysis to all patients and compared the patients with and without collaterals to the infarct-related artery. RESULTS: Mean heart rate, low frequency (LF) (day, night and 24 h) and LF/high frequency (HF) (day, night and 24 h) were higher, SD of all NN intervals (SDNN), root mean square of successive differences (RMSSD), number of NN intervals that differed by more than 50 ms from the adjacent interval divided by the total number of all NN intervals (PNN50) and HF night values were lower in patients without collaterals than in those with collaterals. SDNN was negatively correlated with left anterior descending coronary artery (LAD) stenosis, ventricle score indices and left ventricular ejection fraction (LVEF); LF/HF ratio was positively correlated with ventricle score indices and negatively correlated with LVEF and Thrombolysis in Myocardial Infarction flow grade. Linear regression analysis showed that ventricle score index and coronary collaterals affect HRV and LAD stenosis, ventricle score, LVEF and coronary collaterals affect LF/HF ratio. A SDNN <80 ms increased the development of ventricular arrhythmias in the early period by 4.7 fold, a LF/HF ratio >2.7 increased it by 9.8 fold and a LVEF <35% increased it by 12.8 fold, whereas the presence of well-developed collaterals decreased the arrhythmia development by 2.5 fold. CONCLUSIONS: The collaterals to the infarct-related artery have great impact on HRV, autonomic nervous system activity and the development of ventricular arrhythmias in patients with acute anterior MI. Our results suggest a protective role of collaterals on myocardial electrophysiology in the early period after acute MI.

Collateral Circulation↗

[Aspirin resistance].

Aspirin is an effective antithrombotic agent for many patients. However, patients taking aspirin might exhibit variable responses to in vitro tests for platelet aggregation and might experience breakthrough thromboembolic events. Although this phenomenon has been called aspirin resistance, the lack of an uniform definition or agreement on diagnostic criteria precludes definitive recommendations at this time. Aspirin resistance has been defined in patients with cardiovascular, cerebrovascular, and peripheral vascular disease. In this article, mechanisms related with aspirin resistance and clinical background in which resistance is defined, are reviewed.

Aspirin↗

Determinants of persistent atrial fibrillation in patients with DDD pacemaker implantation.

Occurrence of AF in a pacemaker implanted patient is a significant cause of morbidity and mortality. The aim of this study was to prospectively investigate the clinical, echocardiographic, and electrocardiographic determinants of persistent AF in patients with DDD pacemakers. A 101 consecutive patients were followed for an average of 19.8 +/- 11.8 months. Persistent AF was documented in 21 (20.8%) patients and 80 (79.2%) patients were in sinus or physiologically paced rhythm. In patients with persistent AF, previous AF attacks were observed more frequently (P < 0.03) and left atrial dimension was higher (3.5 +/- 0.6 vs 3.0 +/- 0.5 cm, P < 0.001). Average P maximum and P wave dispersion (PWD) values calculated in a 12-lead surface electrocardiogram were also found to be significantly higher in patients with persistent AF (P < 0.001). Cox regression analysis demonstrated that the presence of previous AF attacks (RR 8.95, P < 0.001), increased left atrial dimension (RR 2.1, P < 0.02), P maximum duration 120 ms (RR 6.1, P < 0.001), and PWD 40 ms (RR 12.2, P < 0.001) were associated with an increased risk of persistent AF. Cut-off points were 120 ms for P maximum and 40 ms for PWD. Sensitivity, specificity, and positive and negative predictive values were calculated as 76.2, 82.5, 53.3, and 92.9 for P maximum and as 85.7, 87.5, 64.3, and 95.9 for PWD, respectively. In patients with DDD pacemakers, previous AF attacks, increased left atrial dimension, P maximum value of 120 ms, and a PWD value of 40 ms were associated with a significantly increased risk of persistent AF. These patients must further be managed with other treatment modalities to prevent the development of persistent AF.

Aged↗

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.

Adult↗

Diabetes mellitus adversely affects the outcomes of thrombolytic therapy in patients with acute myocardial infarction.

This study was performed to evaluate whether coexistent diabetes mellitus has any adverse effect on the outcomes of thrombolytic therapy in patients with acute myocardial infarction. Although the early reperfusion rates were similar between the two groups of patients who had acute myocardial infarction with and without diabetes mellitus (42% vs 45.4%, p > 0.05), the results of late angiographic examination showed a significantly lower rate of patency in infarct-related coronary artery (defined as TIMI 3 flow) in diabetics compared to nondiabetics (28.9% vs 41.3%, p < 0.001). The global left ventricular function was also poorer in diabetics (left ventricular wall motion score was 18.6 +/- 7.3 in diabetics and 14.1 +/- 4.6 in nondiabetics, p < 0.01).

Cardiomyopathies↗