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Figen Ciloglu

Publications and source records attributed to Figen Ciloglu.

7 recordsLinked to original sources

The relationship between endothelial nitric oxide synthase gene polymorphism (T-786 C) and coronary artery disease in the Turkish population.

Previous studies revealed that there were various mutations on endothelial nitric oxide synthase (eNOS) gene and these mutations might be a risk factor for coronary artery disease (CAD), myocardial infarction (MI), and hypertension (HT). In this study, we aimed to investigate the relationship between eNOS gene polymorphism (T-786 C) and coronary artery disease in the Turkish population. Two hundred and eleven unrelated individuals (152 male, 59 female, mean age 59 years, range 27-85) whose angiographic examinations were performed in our hospital were enrolled into the study; 159 of these had angiographically determined coronary artery lesions (>or=50% stenosis at least in one vessel). Fifty-two individuals were free of coronary artery disease on their coronary angiography. The Gensini scoring system was used to determine the severity of the CAD. The polymerase chain reaction (PCR) method was used for genotyping the individuals. To determine the independent risk factors for coronary artery disease, multivariate logistic regression analysis was used. The variant distribution of the T-786 C polymorphism was as follows. For all individuals: TT 94 (44.5%), TC 88 (41.7%), CC 29 (13.8%); in CAD patients: TT 63 (39.6%), TC 73 (45.9%), CC 23 (14.5%); and in normal individuals: TT 31 (59.6%), TC 15 (28.8%), CC 6 (11.5%). There was a statistically significant difference in the variant distribution between CAD and normal individuals (P<0.05). On the other hand, when we compared the frequency of the at-least-one-C-allele carriers (CC+TC, dominant model) and TT homozygous, those with at least one C allele were more prevalent in CAD patients. The results were as follows. In coronary artery disease patients: CC+TC 96 (60.4%), TT 63 (39.6%); in normals: TC+CC 21 (40.4%), TT 31 (59.6%) (P<0.01). When we compared the allele distribution (T vs C, additive model) between CAD patients and normal controls, the results were as follows: T 0.625 vs 0.740, C 0.375 vs 0.260; there was also a statistically significant association between CAD and C allele (P<0.05). When we compared the means of the Gensini scores between each genotype of the T-786 C mutation, there was a statistically significant difference. The results were TT (48.6+/-37.3, median 43.0), TC (55.4+/-41.2, median 41.0), CC (77+/-43.6, median 80.0) (P<0.05). Multivariate logistic regression analysis revealed that C-dominant (CC+TC) individuals had 2.9-fold more likelihood to suffer from CAD (odds ratio: 2.902; confidence interval: 1.272-6.622) (P<0.05). We conclude that the T-786 C polymorphism of eNOS gene might be a risk factor for coronary artery disease in the Turkish population.

Adult↗

Single high-dose bolus tirofiban with high-loading-dose clopidogrel in primary coronary angioplasty.

Glycoprotein IIb/IIIa inhibitor therapy during primary percutaneous coronary intervention (PCI) decreases the incidence of major adverse cardiac events. These effects directly result from the level of platelet inhibition. It was shown that standard dosing of tirofiban is insufficient for optimal platelet inhibition. We sought to determine the efficacy and safety of single high-dose bolus (HDB) tirofiban with high-dose clopidogrel loading in primary PCI in acute ST elevation myocardial infarction. A total of 100 patients (mean age 55.2 +/- 9.9 years, male/female = 86/14) undergoing primary PCI, pretreated with clopidogrel (450 mg) and aspirin (325 mg), were consecutively randomized into two groups. Group I (n = 50) received a standard dose bolus of tirofiban (10 microg/kg/3 min) with 24-h infusion at a rate of 0.15 microg/kg/min. Group II received single HDB tirofiban (25 microg/kg/3 min). The assessed angiographic, clinical, and echocardiographic endpoints were: initial and final Thrombolysis in Myocardial Infarction (TIMI) grade flow (TGF), corrected TIMI frame count (CTFC), ST-segment resolution (STR) at 90 min, in-hospital bleeding complications, echocardiographic left ventricular ejection fraction (LVEF), death, reinfarction, and repeat target vessel revascularization at 1 month. Platelet function inhibition was measured using PFA-100 (Behring-Dade, Liederbach, Germany) with a test cartridge unit containing a membrane coated with 2 microg of equine Type I collagen and 50 microg adenosine diphosphate before, and 10 min, 2, 4, 6, 12, and 24 h after the bolus of the tirofiban in the first 10 cases of each group. There were no significant differences in baseline characteristics between groups. Initial TGF III was more frequent (24% vs 8%, P = 0.029) and the value of CTFC was lower (75 +/- 34 vs 89 +/- 25, P = 0.03) in group II. Postprocedural TGF, CTFC, STR, bleeding complications, and LVEF at 1 month were not different between the two groups. There was a higher rate of reinfarction in group II (8%) compared with group I (2%), but this difference was not statistically significant (P > 0.05). The results of platelet function analyses showed that group II patients had significantly prolonged platelet function assay closure times (299 +/- 6 s) compared with group patients (236 +/- 97 s) at 10 min after the bolus dose (P = 0.04). However, after the first dose between 2 and 24 h, PFA closure times were significantly prolonged in patients with tirofiban infusion. High-dose bolus of tirofiban seems to be safe and more effective than conventional dose at the periprocedural time, whereas continuous infusion of tirofiban may be necessary in the first 24 h before stable and safe antiplatelet status is reached with clopidogrel. However, safety and efficacy of HDB tirofiban and high-loading-dose clopidogrel together with tirofiban infusion requires further studies with a larger population.

Angioplasty, Balloon, Coronary↗

Effects of exercise on visual evoked potentials.

The aim of this study was to investigate the effects of acute or habitual exercise on visual evoked potentials (VEP). The study group consisted of 9 female and 7 male volleyball players and the control group contained 9 female and 7 male students who were not involved in any sportive activity. The N75, P100, and N145 latency and amplitudes were measured before and after exercise. Intragroup comparison was made to evaluate the acute effects and intergroup comparison for the chronic effects of exercise. Significant differences were noted between athletes and the sedentary subjects in terms of pre-exercise left-N145 latencies and amplitudes and left -P100 amplitudes. Right-eye N145 latencies of inactive female subjects obtained before and after exercise were also statistically different. The results suggest that acute and habitual exercise affects the VEP responses independent from the body temperature and other physiological parameters. Small sized pre-exercise P100 amplitudes in the athletes can be attributed to the effect of rapid visual-activity-demanding sports on the central nervous system. Visual evoked potentials maybe used as neurophysiological criteria in defining the performance of an athlete.

Adult↗

Influence of angiotensin converting enzyme insertion/deletion polymorphism on long-term total graft occlusion after coronary artery bypass surgery.

BACKGROUND: The renin-angiotensin system has a very important role in coronary thrombosis and restenosis. Plasma angiotensin converting enzyme (ACE) activity is associated with an insertion/deletion polymorphism in the gene coding for ACE. It is known that there is a strong correlation between ACE DD and atherosclerosis. However, little has been documented about its role in venous graft failure. The objective of this study was to investigate the relationships among the ACE gen polymorphism and long-term vein graft occlusion. METHODS: The study population consisted of 87 consecutive white patients with symptomatic coronary artery disease in the previous month, who had had aorto-coronary bypass surgery (ACBS) more than 5 years back and who underwent coronary angiography for diagnostic purposes. On the same day of angiography, 10 mL whole blood was taken for ACE gene insertion/deletion (I/D) polymorphism. RESULTS: Mean age of the patients was 64.4 +/- 8.6 years, and 71 (82%) of the patients were men. The average ACBS time was 7.9 +/- 1.9 years. The ACE genotype was II in 15 patients (17.2%), ID in 47 patients (54.0%), and DD in 25 patients (28.7%). Thus, D allele frequency was .82. There was no significant difference between the cases with regard to age, body mass index, blood pressure status, plasma glucose level, plasma lipid profile, smoking status, average of ACBS time or family history of coronary heart disease. In ACE II group 5 patients had total venous graft occlusion, in ACE ID group 27 patients had total occlusion and in ACE DD group 20 patients had at least one graft total occlusion. The frequency of the venous graft occlusion about total venous grafts is 36% in the ACE II group, 49% in the ACE ID group, and 80% in the ACE DD group (P = .01). CONCLUSION: The ACE I/D gene polymorphism is associated with long-term survival of venous conduit. The ACE DD genotype or D allele influences the angiographic outcome of patients post-ACBS. These data suggest that routine determination of the ACE genotype may help identify patients who are at higher risk of venous graft failure after ACBS.

Aged↗

Long-term combined therapy with losartan and an angiotensin-converting enzyme inhibitor improves functional capacity in patients with left ventricular dysfunction.

OBJECTIVE: The efficacy of angiotensin-converting enzyme (ACE) inhibitors in the treatment of heart failure (HF) is well documented. However, ACE inhibitors may provide incomplete blockade of the renin-angiotensin-aldosterone system due to the alternative pathways for the production of angiotensin II (Ang II). The aim of this study was to evaluate the efficacy of combined therapy of an ACE inhibitor and the Ang II receptor blocker losartan in patients with HF by using cardiopulmonary exercise testing (CPET) on a treadmill. METHODS AND RESULTS: Seventeen patients (ejection fraction < or = 40%) were included in the study group. At the start of the study, all participants were on chronic ACE inhibitors therapy. Fifty mg losartan was added to the treatment and CPET was performed before and 6-8 months after starting losartan therapy. Sixteen patients with HF were included in the control group. CPET was performed once at the beginning and repeated 6-8 months later without any change in the treatment protocol. The change in CPET values (walk-time (WT), peakVO2, anaerobic threshold (AT), minute ventilation (VE), VE/VO2, peak heart rate (HR),VO2/HR) was investigated. In the losartan-treated group a significant increase was noted in WT (393 +/- 157 vs. 507 +/- 155 sec, p < 0.01); peak VO2 (1205 +/- 240 vs. 1330 +/- 253 ml/min, p < 0.05); and AT (794 +/- 131 vs. 895 +/- 177 ml/min, p < 0.05). In the control group exercise parameters did not change significantly. The change from baseline to follow-up between the two groups is statistically significant for WT and peak VO2 (114 +/- 94 vs. -58 +/- 134 sec, p < 0.0 1 and 125 +/-183 vs. -116 +/- 221 ml/min, p <0.01). CONCLUSIONS: Addition of losartan to the ACE inhibitor therapy in patients with HF improves functional capacity in the long run.

Angiotensin II Type 1 Receptor Blockers↗

Exercise intensity and its effects on thyroid hormones.

BACKGROUND: Physical activity influences energy metabolism in human subjects by increasing activity-induced energy expenditure and resting metabolic rate for several hours after exercise. Effects of exercise on circulating thyroid hormone values remain controversial. We have investigated the effect of acute aerobic exercise on thyroid hormone values. MATERIALS/METHODS: The effect of different intensity levels of acute aerobic exercise on thyroid hormones was investigated in 60 male well-trained athletes by performing bicycle ergometer at 45% (low intensity), 70% (moderate intensity), and 90% (high intensity). These intensities were selected according to their maximum heart rate (MHR). At each intensity level, heart rate, blood lactic acid, serum total thyroxine (T4), free thyroxine (fT4), total triiodothyronine (T3), free triiodothyronine (fT3) and thyroid stimulating hormone (TSH) values were measured. RESULTS: The results of this study show that exercise performed at the anaerobic threshold (70% of maximum heart rate, lactate level 4.59 +/- 1.75 mmol/l) caused the most prominent changes in the amount of any hormone values. While the rate of T4, fT4, and TSH continued to rise at 90% of maximum heart rate, the rate of T3 and fT3 started to fall. CONCLUSIONS: Maximal aerobic exercise greatly affects the level of circulating thyroid hormones.

Adult↗

Angiotensin-converting enzyme gene polymorphism, left ventricular remodeling, and exercise capacity in strength-trained athletes.

The mechanisms that regulate the development of human physiological cardiac hypertrophy remain poorly understood. The renin-angiotensin system, which is modulated by genetic polymorphism, plays an important role in the regulation of vascular tone and myocardial hypertrophy. Although a few studies have analyzed the association of angiotensin-converting enzyme (ACE) polymorphism and left ventricular (LV) hypertrophy in isotonic exercise-trained subjects who developed eccentric cardiac hypertrophy, there has been no research done in power athletes who developed concentric cardiac hypertrophy. We have hypothesized that ACE genotypic modulation characteristics may affect LV mass in power athletes. This study included 29 elite Caucasian wrestlers (mean age, 22.6 years) and 51 age-matched sedentary subjects. According to the absence or presence of the insertion segment in the polymerase chain reaction (PCR) product, the subjects were classified as homozygous deletion-deletion (DD), insertion-insertion (II), or heterozygous insertion-deletion (ID). The association of LV hypertrophy with ACE gene insertion/deletion (I/D) polymorphism was analyzed. Left ventricular mass and index were determined by echocardiography. Angiotensin-converting enzyme genotyping was performed on peripheral leukocytes using the polymerase chain reaction technique. The study and control group subjects were similar in height and weight. Left ventricular hypertrophy in the athletes was more apparent than in the controls. Angiotensin-converting enzyme genotype II frequency was 17.2% (5) in the athletes, 17.6% (9) in the controls; ID frequency was 51.7% (15) in the athletes, 56.8% (29) in the controls; and the DD frequency was 31% (9) in the athletes and 25.4% (13) in the controls. Left ventricular mass and mass index were found to be higher in genotype DD (126.2 +/- 2.9g/m2) than genotype II (85.5 +/- 4.0g/m2) or genotype ID (110.1 +/- 2.3g/m2) in the athletes (P < 0.001). Furthermore, maximal oxygen consumption in genotype DD was found to be higher than in II and ID. An association was found between ACE gene I/D polymorphism and LV hypertrophy in strength-trained athletes.

Adult↗