Browsing by Author "Güntekin, Ü"

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Effect of Blood Pressure Reduction on Abnormal Left Atrial Appendage Function in Untreated Systemic Hypertensive Patients With Sinus Rhythm
(Sage Publications inc, 2001) Bilge, M; Güler, N; Eryonucu, B; Güntekin, Ü
To investigate whether reduction in blood pressure has a beneficial effect on left atrial appendage (LAA) function, the authors evaluated 24 untreated systemic hypertensive patients with normal left ventricular systolic function in sinus rhythm at baseline and at 3 months after initiation of anti hypertensive therapy. They performed transthoracic and transesophageal echocardiographic examinations in hypertensive patients before and after treatment of hypertension. Three of the 24 patients had blood pressure that failed to respond to the regimen of antihypertensive therapy and were removed from the analysis. Of the remaining 21 patients, mean systolic and diastolic blood pressures at baseline were 170 +/- 18 and 104 +/-6 mm Hg, respectively, and fell significantly at 3 months to 141 +/- 10 and 90 +/-5 mm Hg, respectively, (p <0.001) after initiation of antihypertensive therapy. There was no significant change in heart rate with treatment (baseline 81 +/-8 and at 3 months 84 +/-9 beats/min). There was no significant change in left ventricular end-diastolic diameter, left ventricular ejection fraction, left ventricular wall thickness, or left atrial diameter from baseline (49 +/-4 mm, 58 +/-5%, 12 +/-1 mm, and 41 +/-4 mm, respectively) at 3 months (48 +/-5 mm, 59 +/-4%,12 +/-1 mm, and 40 +/-3 mm). The treatment caused a significant reduction in maximal LAA areas (6.3 +/- 13 cm(2) at baseline, 4.6 +/-0.7 cm(2) at 3 months, p <0.001), with a concomitant increase in LAA emptying velocity (44 +/-7 cm/sec at baseline, 60 +/-9 cm/sec at 3 months, p <0.001). In conclusion, these findings suggest that reduction in blood pressure with antihypertensive therapy could improve LAA function in hypertensive patients with normal left ventricular systolic function in sinus rhythm.
Effects of Trimetazidine on Submaximal Exercise Test in Patients With Acute Myocardial Infarction
(Springer, 2003) Güler, N; Eryonucu, B; Günes, A; Güntekin, Ü; Tuncer, M; Özbek, H
Background: It was demonstrated that the novel metabolic agent, trimetazidine, could lessen the incidence and severity of angina, whether used in monotherapy or combination. Although the animal studies demonstrated that trimetazidine reduces myocardial infarct size and improves recovery of mechanic function after ischemia, little is known on the potential benefits of trimetazidine in patients with acute myocardial infarction (AMI). The aim of this study was to evaluate the efficacy of trimetazidine on AMI by sub-maximal exercise test. Methods: A double-blind crossover trimetazidine versus placebo trial was carried out in 44 patients with AMI. Patients were randomly allotted into trimetazidine (23 patients) or placebo (21 patients) for 5 days and underwent an initial sub-maximal exercise test. Exercise tests according to the modified Bruce protocol were performed. Exercise end points included completion of stage II or 75% of maximum predicted heart rate whichever came first. An averaged 12-lead ECG was obtained at rest, every minute during exercise, at the onset of anginal symptoms, at the onset of 1-mm ST segment depression, at peak exercise and every 2-minute during recovery. After the initial exercise tests, study groups resumed the drugs in the opposite order for 4 to 5 days and underwent a second sub-maximal exercise test. Results: Exercise induced ST segment depression was noted in 17 patients (38.6%) receiving placebo. However, exercise induced ST-segment depression was observed in 8 patients (18.1%) taking TMZ. Positive exercise test results were significantly higher in placebo group than TMZ group (p=0.018). Additionally, trimetazidine prolonged the time to 1-mm ST-segment depression (6.1+/-0.5 vs 4.9+/-0.4, p<0.031) and exercise duration (7.2 +/- 0.9 vs 5.8 +/- 0.9, p<0.025). Conclusion: Trimetazidine therapy improves the exercise capacity and reduces evidence of ischemia derived from sub-maximal post-infarction exercise testing.