Exercise and oxidative stress.
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Cardiovascular Diseases↗
Biomedical subjects
Dilek Ciçek
Publications and source records attributed to Dilek Ciçek.
Coronary angioplasty induced oxidative stress and its relation with metoprolol use and plasma homocysteine levels.
OBJECTIVE: Short episodes of myocardial ischemia during coronary angioplasty may induce oxidative stress and increase lipid peroxidation. The aim of this study was to determine the effect of metoprolol on lipid peroxidation by measurements of malondialdehyde (MDA) and total antioxidant capacity (TRAP) in patients undergoing angioplasty. The relations between homocysteine level and lipid peroxidation were also studied. METHODS: Forty-six patients (mean age 57 years, 37 males) undergoing elective angioplasty were enrolled. Metoprolol treatment was initiated in 27 patients (group 1), meanwhile 19 patients could not take metoprolol due to diverse contraindications (group 2). RESULTS: Following angioplasty, while venous MDA levels decreased in group 1 (0.188+/-0.021 vs. 0.159+/-0.020 nmol/ml, p=0.05), an increase was detected in group 2 (0.203+/-0.025 vs. 0.229+/-0.024 nmol/ml, p=0.045) as compared with baseline levels. In group 1, TRAP levels markedly increased after angioplasty in venous samples (1.201+/-0.036 vs. 1.478+/-0.044 mmol/L, p=0.0001). However, small increase was observed for TRAP in group 2 (1.274+/-0.043 vs. 1.363+/-0.053 mmol/L, p=0.05). There was no significant change in plasma homocysteine levels with angioplasty. There was no significant correlation between homocysteine, changes in MDA and TRAP levels either. CONCLUSION: Administration of metoprolol may cause a reduction in the oxidative stress and an increase in the antioxidant activity in patients undergoing elective angioplasty.
Adrenergic beta-Antagonists↗
Apolipoprotein E polymorphism in diabetic and non-diabetic patients: does it really contribute to atherosclerosis?
OBJECTIVE: The exact mechanism of the increased cardiovascular morbidity and mortality in type-2 diabetes is still undefined. The aim of our study was to assess the impact of apolipoprotein E (apo E) polymorphism and other factors on atherosclerotic vascular disease in type-2 diabetic patients. We also examined the association between apo E polymorphism and lipid profile in diabetic patients. METHODS AND RESULTS: We assessed the apo E polymorphism in 295 atherosclerotic patients (124 of them had diabetes (according to WHO criteria) and 171 of them had coronary artery narrowing > 50). The detection of apo E polymorphism was made by Real-Time PCR using a Light-Cycler (Roche diagnostics, GmbH, Mannheim, Germany). Serum triglycerides (TG), total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), lipoprotein (a) [Lp(a)], apolipoprotein A (Apo A) and apolipoprotein B (Apo B) levels were determined by biochemical analyser. Genotypic distribution of apo E polymorphism did not differ between diabetic and non-diabetic atherosclerotic patients. The distributions of apo E2/2, E2/3, E2/4, E3/3, E3/4 and E4/4 genotypes in diabetic and non-diabetic atherosclerotic patients were 7.3%: 8.2%, 15.3%: 15.8%, 4.0%: 5.3%, 50.8%: 56.7%, 16.9%: 11.1% and 5.6%: 2.9%, respectively. Participants were grouped as apo E2 (E2/2 or E2/3), apo E3 (E3/3), or apo E4 (E4/4 or E4/3). The distributions of apo E2, E3 and E4 alleles were 23.5%, 52.9%, 23.5%, for diabetic patients, and 25.3%, 59.9%, 14.8% for non-diabetic patients, respectively. The apolipoprotein E genotype was not associated with the lipid levels in diabetic patients. CONCLUSIONS: Our findings imply that apo E polymorphism is not related to the development of atherosclerosis in patients with type-2 diabetes.
Alleles↗
Glutathione S-transferase gene polymorphism as a susceptibility factor in smoking-related coronary artery disease.
Coronary artery disease (CAD) is the leading cause of morbidity and mortality in the world, and cigarette smoking is a major contributing factor to the disease. Glutathione S-transferase (GST) enzyme is implicated in the detoxification of carcinogens present in tobacco smoke and consequent polymorphisms in this gene may confer susceptibility to cardiovascular disease if DNA damage is important in CAD. Therefore, we examined this question in a case-control study of subjects having coronary atheroma by angiography and with a past history of myocardial infarction (MI). The study population consists of 247 healthy controls and 148 consecutive patients who had undergone coronary angiography for suspicion of coronary artery disease. DNA was extracted from whole blood, and the GSTM1 and GSTT1 polymorphisms were determined using a real-time polymerase chain reaction (PCR). We found that the null GSTM1 and GSTT1 genotypes were associated with an increase in the risk of developing coronary heart disease (OR = 1.14; 95% CI: 0.71 - 1.82; OR = 1.38; 95% CI: 0.82 - 2.32), respectively, but this increase was not significant. Patients who smoke having the null genotypes of GSTM1 (OR: 1.63 (1.10 - 2.63)) and GSTT1 (2.66 (1.50 - 4.72)) and both (3.20 (1.37 - 7.45)) were at a higher risk for developing coronary heart disease. In conclusion, the finding of a significant association between GSTM1 and T1 with smoking status may influence cardiovascular disease via DNA damage.
Case-Control Studies↗
Early and late angiographic and clinical outcome following helistent stent implantation.
There is still a lack of data on the influence of different stent designs on long-term restenosis rates and major adverse cardiac events (MACE) with the use of new antithrombotic regimens. We evaluated the midterm (6 months) clinical and angiographic and lateterm (2 years) clinical outcome of Helistent stent implantation. The study population consisted of 150 patients with high risk factor rates who had single or multivessel disease and had undergone coronary Helistent stent implantation with new antiplatelet regimens. The control coronary angiographies were done at 6 months and they were followed clinically to the end of 2 years. In 150 patients, 236 Helistent stents were implanted for 224 lesions. Helistent stent implantation was associated with a very high success rate (99%). The angiographic re-stenosis rate was 11.3% at 6 months. Only 16% of the patients experienced target lesion revascularization, 20% of the patients experienced MACE and of them, only 3.3% died at the end of two year follow-up period. The results demonstrate that the Helistent stent can be implanted with a high success rate with encouraging 6 month angiographic and late clinical outcomes.
Adult↗
Endothelin-1 and nitric oxide levels in patients with mitral annulus calcification.
Mitral annulus calcification (MAC) is a chronic degenerative noninflammatory process. The goal of this study was to determine endothelin-1 (ET-1) and nitric oxide (NOx) levels in patients with MAC and compare them with those in normal subjects. The study group included 39 patients [26 females (66%), age, 63 +/- 8 years] with MAC and 20 [11 females (55%), age, 61 +/- 7 years] healthy subjects. The patients were divided into two subgroups, group A with severe MAC and group B with mild MAC, according to the severity of the MAC. Plasma ET-1 levels were higher and NOx levels were lower in patients than controls [(6.5 +/- 5.6 pg/mL vs 3.7 +/- 2.9 pg/mL for ET-1 and 35.0 +/- 10.6 micromol/L vs 42.3 +/- 9.9 micromol/L for NOx; P < 0.05 for both)]. In the subgroups, ET-1 levels were higher in group A than group B (8.65 +/- 6.84 pg/mL vs 4.74 +/- 3.45 pg/mL, P < 0.05) and the control group (8.65 +/- 6.84 pg/mL vs 3.70 +/- 2.88 pg/mL, P < 0.05). There was no difference between group B and the control group. Plasma NOx levels were significantly decreased in group A compared to controls (32.22 +/- 11.88 micromol/L vs 42.25 +/- 9.99 micromol/L, P < 0.05). However, no significant difference was observed between group B (37.38 +/- 9.06 micromol/L) and the other groups. Diabetes mellitus, coronary artery disease, and dyslipidemia were significantly associated with ET-1 levels. However, this association was not observed for NOx. In conclusion, patients with MAC have increased ET-1 and decreased NOx levels. This seems to be more prominent in patients with severe MAC.
Aged↗
Slow coronary flow may be a sign of diffuse atherosclerosis. Contribution of FFR and IVUS.
OBJECTIVE: Slow coronary flow (SCF) is a phenomenon characterized by delayed opacification of coronary arteries in the absence of epicardial occlusive disease, in which many aetiological factors such as microvascular and endothelial dysfunction, and small vessel disease have been implicated. We aimed to investigate the epicardial resistance in relation with SCF by using fractional flow reserve (FFR) and intravascular ultrasound (IVUS). Both have been combined to disclose the related epicardial flow resistance and the arterial anatomy. METHODS AND RESULTS: Coronary pressure and FFR measurement were performed in 19 (8 (42.1%) men, 11 (57.9%) women; age = 55.9 +/- 9.4 years) patients with SCF. All patients underwent subsequent IVUS investigation at the same setting. As compared with expected normal values, FFR values were significantly lower (1.0 vs. 0.83 +/- 0.13, p < 0.0001). In patients with SCF, a strong negative correlation was seen between TIMI frame count and FFR (r = -0.551, p < 0.05). Upon IVUS investigation, the common finding was longitudinally extended massive calcification throughout the epicardial arteries and increased intimal thickness (0.59 +/- 0.18 mm). A negative correlation between intimal thickness and FFR was determined (r = -467, p < 0.05). CONCLUSION: We have demonstrated the decreased FFR in the patients with SCF. Decreased FFR levels have been attributed to increased resistance in the epicardial coronary arteries due to diffuse atherosclerotic disease which has been demonstrated by IVUS.
Aged↗
Effects of atrial pacing on coronary sinus endothelin-1 and nitric oxide levels in patients with myocardial bridging.
Myocardial bridging (MB) is associated with clinical and metabolic evidence of ischaemia. In the present study, we aimed to evaluate the extent of atherosclerosis and endothelial dysfunction in patients with MB. The study population consisted of 15 patients with MB [9 women (60%), aged 56 +/- 9 years] and 14 control subjects [8 women (57%), aged 54 +/- 10 years]. All patients underwent coronary angiography. The femoral artery and coronary sinus endothelin-1 (ET-1) and nitric oxide (NOx) plasma levels were measured before and after right atrial pacing in all subjects. Also, intravascular ultrasonography was performed in 13 patients with MB. With right atrial pacing, coronary sinus ET-1 levels increased significantly in patients with MB compared with baseline levels (5.77 +/- 6.76 versus 11.32 +/- 9.40 pg/ml, p < 0.05). The coronary sinus ET-1 levels remained unchanged in controls with pacing (3.99 +/- 4.00 versus 4.19 +/- 7.15 pg/ml, p > 0.05). There was no significant difference between the two groups according to the increase in NOx levels with atrial pacing. Ten (77%) of the 13 patients had plaque formation in the segments proximal to the bridge with an area stenosis of 37 +/- 21% (12% to 75%). In patients with MB, post-pacing levels of coronary sinus ET-1 correlated significantly with the cross-sectional area of the plaque (r = 0.65, p = 0,04). Increased ET-1 levels and the pathological data of intravascular ultrasonography may be associated with endothelial dysfunction and atherosclerosis development in patients with MB. The presence of atherosclerosis in the proximal segments to the bridge may contribute to the myocardial ischaemia detected in these patients.
Case-Control Studies↗
[Femoral vascular complications after percutaneous coronary interventions].
OBJECTIVE: We aimed to investigate peripheral vascular complications and their relation with treatment and clinical parameters in percutaneous transluminal coronary angioplasty (PTCA) patients. METHODS: We included into the study 321 patients (aged 57+/-11 years) underwent PTCA between November 2001-August 2002. The age, gender, glycoprotein 2b/3a use, thrombolytic use, intraaortic balloon treatment, transient pacemaker treatment, reintervention history, hypertension, diabetes mellitus, smoking status, family history and the correlations of these parameters with local vascular complications were assessed in all patients. RESULTS: Pseudoaneurysm incidence was significantly correlated with; age [(n=13, 68.0%) p=0.0001, OR 8.38], female gender [(n=12, 63.1%) p<0.015, OR 0.32], reintervention [(n=10, 52.1%) p<0.004, OR 3.6], venous sheath usage [(n=12, 63%) p<0.0001, OR 9.07], thrombolytic treatment [(n=5, 26.3%) p<0.0001, OR 7.9], and intraaortic balloon adjustment [(n=6, 31.5%) p<0.0001, OR 7.2]. No correlation was found between pseudoaneurysm incidence and glycoprotein 2b/3a treatment, smoking, diabetes mellitus, hypertension and family history. CONCLUSION: The present study showed that patients of female gender, with reintervention, thrombolytic treatment, venous sheath use and intraaortic balloon adjustment are at high risk for serious femoral vascular complications, especially when they are aged. Additionally, glycoprotein 2b/3a agents can be used without increased risk of peripheral vascular complications.
Age Factors↗
Metoprolol, a beta-1 selective blocker, can be used safely in coronary artery disease patients with chronic obstructive pulmonary disease.
The coexistence of coronary artery disease (CAD) and chronic obstructive pulmonary disease (COPD) is frequent because of common etiological factors. Beta-blockers remain underutilized in patients with CAD who also have COPD. This study was performed to evaluate the safety of beta-1 selective blocker agents in CAD patients with COPD. Fifty patients (aged 57.3 +/- 10.1 years) were enrolled in this study; 27 patients received metoprolol CR (controlled release), and 23 received metoprolol (conventional). The patients were stratified according to the severity of COPD (21 severe, 21 moderate, and 8 mild), started on metoprolol CR or conventional metoprolol, and titrated up to the maximum tolerated dose. The clinical controls were done during the first week and then at the first and third month. Patients received a mean total daily dose of 92.5 +/- 18 mg of metoprolol CR or 189 +/- 36.7 mg of metoprolol. Seven patients could not receive the maximum dose. There was no significant decrease in forced expiratory volume in 1 s (FEV(1)) in either group (basal vs last FEV(1): 54.5% +/- 13.4% vs 54.3% +/- 13% in the metoprolol CR group and 49.6% +/- 14.5% vs 53.2% +/- 12.8% in the metoprolol group). No adverse event was experienced. Metoprolol, a beta-1 selective blocker, can be used safely at the maximum dose in CAD patients with COPD.
Adrenergic beta-1 Receptor Antagonists↗
Predictive value of P-wave signal-averaged electrocardiogram for atrial fibrillation in acute myocardial infarction.
BACKGROUND: Atrial fibrillation (AF) is a common complication of acute myocardial infarction (AMI) with a reported incidence of 7-18%. Recently, P-wave signal-averaged electrocardiogram (P-SAECG) has been used to assess the risk of paroxysmal AF attacks in some diseases. The aim of this study was to determine prospectively whether patients with AMI at risk for paroxysmal AF would be identified by P-SAECG and other clinical variables. METHODS: A total of 100 patients (mean age: 59+/-12, 77 male, 23 female) with ST segment elevation AMI were enrolled in this study. Patients with chronic AF were excluded. At entry, all patients underwent standard 12-lead ECG and in the first 24 hours, P-SAECG was taken, and echocardiography and coronary angiography were performed on the patients. Patients are followed for a month in terms of paroxysmal AF attacks and mortality. RESULTS: AF was determined in 19 patients (19%). In patients with AF, abnormal P-SAECG more frequently occurred than in patients without AF (37% vs 15%, P<0.05). Patients with AF were older (70+/-14 vs 56+/-10, P<0.001) and had lower left ventricular ejection fraction (42%+/-8 vs 49%+/-11, P<0.05). AF was less common in thrombolysis-treated patients (47% vs 74%, P<0.05). Thirty-day mortality was higher in patients with AF (16% vs 2%, P=0.05). CONCLUSIONS: An abnormal P-SAECG may be a predictor of paroxysmal AF in patients with AMI. Advanced age and systolic heart failure were detected as two important clinical risk factors for the development of AF.
Adrenergic beta-Antagonists↗
Diffuse intimal thickening of coronary arteries in slow coronary flow.
Intravascular ultrasound imaging can detect intimal thickening and is suitable for detection of early atherosclerosis, which cannot be detected by conventional angiography. The aim of the present study was to investigate the epicardial coronary morphology and intracoronary pressure in relation to slow coronary flow (SCF). The study population consisted of 19 patients with SCF [11 (57.9%) females; 55.95 +/- 9.42 years]. Proximal, middle, distal and mean total vessel area, lumen area, intima + media area (IMA), percent IMA, and maximal intima + media (I + M) thickness were calculated and compared to healthy subjects. Proximal, middle, distal and mean I + M thickness, IMA, and % IMA of patients with SCF were found to be significantly higher than those of control subjects. Longitudinally extended massive calcification throughout the epicardial arteries was found in 13 (68.49%) patients with SCF and regional calcification was found in 6 (31.6%) patients with SCF. Proximal and distal pressure gradients of patients with SCF were determined to be 15.84 +/- 12.11 mmHg in the intracoronary pressure measurements. Fractional flow reserve values were significantly lower than the normal population (0.83 +/- 0.13, P < 0.0001). This study indicates that patients with SCF have diffuse intimal thickening, widespread calcification along the vessel wall and atheroma which does not cause luminal irregularities in coronary angiography, and a pressure gradient between proximal and distal segments of epicardial coronary arteries with SCF. Based on these results, we believe that SCF may be a form of diffuse atherosclerosis involving both the microvascular system and epicardial coronary arteries.
Aged↗