Mustafa Kilic

Pamukkale University, Denisli, Denizli, Turkey

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Publications (34)58.14 Total impact


  • No preview · Article · Apr 2012 · Cardiology in the Young
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    ABSTRACT: Although hypertension has been shown to be one of the most important risk factors for atherosclerosis, data about the presence of subclinical atherosclerosis in normotensive offspring with parental history of hypertension are scarce. Accordingly, the current study was designated to evaluate flow-mediated dilatation and aortic stiffness, which are early signs of atherosclerosis in young subjects with parental history of hypertension. A total of 102 healthy, non-obese subjects in the age group of 18-22 years were included in this study and divided into two groups. The first group included 70 offspring of hypertensive parents and the second group included 70 offspring of normotensive parents as controls. In all subjects, endothelium-dependent and endothelium-independent vasodilatation of the brachial artery and aortic elastic parameters were investigated using high-resolution Doppler echocardiography. Offspring of hypertensive parents demonstrated higher values of aortic stiffness (7.1 plus or minus 1.88 and 6.42 plus or minus 1.56, respectively) but lower distensibility (9.47 plus or minus 1.33 and 11.8 plus or minus 3.36 square centimetres per dyne per 106) and flow-mediated dilatation (4.57 plus or minus 1.3 versus 6.34 plus or minus 0.83 percent, p equals 0.0001, respectively) than offspring of hypertensive parents. We observed blunted endothelium-dependent dilatation and aortic stiffness in offspring of hypertensive parents compared with offspring of hypertensive parents. This is evident in the absence of overt hypertension and other diseases, suggesting that parental history of hypertension is a risk for subclinical atherosclerosis and it may contribute to the progression to hypertension and overt atherosclerosis in later life.
    No preview · Article · Feb 2012 · Cardiology in the Young
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    ABSTRACT: Cheyne Stokes respiration (CSR) is frequently seen in the patients with heart failure (HF) and it increases mortality. In the present study, we aimed to evaluate acute effects of adaptive servo ventilation (ASV) on CSR and neurohormones in the patients with HF. Nineteen males and 1 female patients with HF in the functional capacity of NYHA II-III were included into the study prospectively. One night polysomnography (PSG) was performed to all patients. In addition to medical treatment, 10 patients having CSR were applied ASV in another night together with PSG.. Arterial blood gases, plasma epinephrine and norepinephrine, serum N-terminal -pro-B type brain natriuretic peptide (NT-pro-BNP) were studied in the first night and after ASV treatment. A Wilcoxon test was used for comparison of parameters before and after treatment;and Mann-Whitney-U test was used for comparison of parameters between the patients with CSR and without CSR. Mean age of 10 patients with CSR was 62.2+/-11.1 years. Their etiologies were ischemic in 9 patients and idiopathic dilated cardiomyopathy in 1 patient. While there were no significant differences in the levels of PaCO2, HCO3, PH, before and after treatment; PaO2 (75.3 mmHg) and SatO2 (94.7%) significantly increased after the therapy (84.7 mmHg, 96.5% and p=0.007 and p=0.008 respectively). While NT-proBNP (3029.6+/-1450.5 pg/ml), norepinephrine (625.4+/-304.7 pg/ml) and epinephrine (65.4+/-24.1 pg/ml) were higher than normal before ASV treatment, all of them showed significant reductions after treatment (1694.0+/-925.9 pg/ml, 333.9+/-165.4 pg/ml and 45.0+/-20.5 pg/ml; p=0.005, p=0.005 and p=0.02, respectively). One night ASV treatment improves CSR, partial pressure of oxygen in arterial blood, and oxygen saturation and provides significant reductions in plasma catecholamines and NT-proBNP levels in the patients with HF and CSR. Prospective studies are needed to evaluate long-term effects of ASV treatment on morbidity and mortality in the patients with HF.
    No preview · Article · Jul 2009 · Anadolu kardiyoloji dergisi: AKD = the Anatolian journal of cardiology
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    ABSTRACT: Endothelial dysfunction is an early marker of atherosclerosis. Angiotensin II and nitric oxide have important roles in maintaining the vascular tone. The existence of the angiotensin converting enzyme (ACE) gene polymorphisms has been known, and deletion (D) of the allele has been associated with coronary artery disease. As ACE genotype affects endothelial functions in the patients with risk factors for coronary artery disease, it may also be a determinant of atherosclerosis. In this study, the relationship between endothelial function and ACE gene polymorphisms was investigated in healthy young subjects. Forty-six healthy young subjects were included in this cross-sectional, randomized study. Participants were further divided into three groups according with ACE genotypes: DD genotype--24 subjects, DI genotype--13 subjects and II genotype--9 subjects. All patients underwent brachial artery ultrasonographic examination. We analyzed ACE insertion (I) and D allele frequencies in all subjects. Kruskal-Wallis test was used to compare continuous variables, and the Chi-square test was used to compare proportions among groups. Demographic features were similar except gender between the groups according to the ACE genotypes. Total cholesterol levels were lower in the DD genotype comparing with the others (p<0.05). High-density lipoprotein cholesterol levels, baseline brachial artery diameter, baseline blood flow and the increase in the blood flow during the reactive hyperemia were also similar. The changes in flow-mediated dilatation (endothelium dependent) were 4.9+/-1.3% in DD genotype, 5.5+/-1.7% in DI genotype and 5.5+/-1.9% in II genotype groups. Flow mediated dilatation was lower in DD genotype group as compared with ID and II genotype groups, however, this result did not reach statistical significance (p>0.05). Endothelium independent dilatations were similar among different ACE genotypes. Our data showed that ACE genotype has no effect on endothelial functions in patients without risk factors for coronary artery disease.
    No preview · Article · Mar 2008 · Anadolu kardiyoloji dergisi: AKD = the Anatolian journal of cardiology
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    ABSTRACT: Elevation of plasma homocysteine (Hcy) level has been implicated in the pathogenesis of slow coronary flow (SCF) as it can severely disturb vascular endothelial function. Helicobacter pylori chronically infect the human stomach and causes malabsorption of vitamin B(12) and folate in food, leading ultimately to an increase in circulating Hcy levels. Forty-three patients with angiographically proven SCF (group I) were enrolled in this study; 43 cases with normal coronary flow pattern (group II) served as controls. Fasting plasma levels of Hcy, vitamin B(12), and folate were measured in all subjects. Presence of H. pylori infection was defined as positive 14 C urea breath test. Coronary flow patterns for each major epicardial coronary artery were determined with the Thrombolysis in Myocardial Infarction (TIMI) frame count method. Mean TIMI frame count was 46.3 +/- 8.7 in group I and 24.3 +/- 2.9 in Group II (p = .0001). Vitamin B(12) levels were similar, whereas folate levels were dramatically reduced in group I compared to group II (13.2 +/- 4.3 vs. 17.1 +/- 5.2, p = .0001). Plasma Hcy levels were significantly higher in group I compared to group II (13.4 +/- 5.6 vs. 7.9 +/- 2.5, p = .0001) as was the prevalence of H. pylori infection (90.7% in group I vs. 58.1% in group II, p = .001). Hcy levels were elevated (11.7 +/- 5.3 vs. 7.5 +/- 2.7, p = .0001) and folate levels were reduced (13.9 +/- 4.7 vs. 18.6 +/- 4.9, p = .0001) in patients with H. pylori infection, while vitamin B(12) levels were similar in patients with and without H. pylori infection. Correlation analysis revealed a significant negative correlation between plasma folate and Hcy levels and also between folate levels and mean TIMI frame counts (r = -.33, p = .002 vs. r = -.33, p = .003). Moreover, there was a significant positive correlation between plasma Hcy levels and mean TIMI frame counts (r = .66, p = .0001). In addition, the folate level was the only significant determinant of the variance of Hcy in multiple regression analysis (r = -.21, p = .03). Our data showed that plasma folate levels were decreased and plasma Hcy levels were increased in patients with SCF compared to controls. Also, the prevalence of H. pylori infection was increased in patients with SCF. These findings suggest that elevated levels of plasma Hcy, possibly caused by H. pylori infection, and/or a possible disturbance in its metabolism may play a role in the pathogenesis of SCF.
    No preview · Article · Sep 2007 · Helicobacter

  • No preview · Article · Jul 2007 · Journal of Electrocardiology
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    ABSTRACT: The slow coronary flow (SCF) phenomenon is an angiographic observation and a well-recognized clinical entity characterized by delayed opacification of vessels in a normal coronary angiogram due to reasons yet unclear. Thyroid hormones exert significant effects on plasma homocysteine (Hcy) levels and microvascular resistance. Recently, several investigators have consistently reported that elevation of the plasma Hcy level can severely disturb vascular endothelial function and play a role in the pathogenesis of SCF. Accordingly, we investigated the levels of plasma Hcy and thyroid hormones and their relationship in patients with SCF. Forty-four patients with angiographically proven SCF (Group I) (mean age 55.5 +/- 10.4 years, 26 males) and 44 cases with normal coronary flow (NCF) pattern (Group II) (mean age 53.9 +/- 11 years, 22 males) with similar risk profiles were enrolled in the study. Coronary flow patterns of the cases were determined by the thrombolysis in myocardial infarction (TIMI) frame count method. The coronary TIMI frame counts were calculated separately for each coronary artery and their average was determined as the mean TIMI frame count for each subject. Serum levels of free tri-iodothyronine (fT3), free thyroxine (fT4), thyroid stimulating hormone (TSH) and Hcy were measured. Patients with thyroid disease or on medications with a potential to affect thyroid functions were excluded. There were no statistically significant differences between the groups concerning the demographic characteristics and major cardiovascular risk factors. Mean TIMI frame counts of SCF and NCF groups were 45.9 +/- 12 and 23.3 +/- 3.7, respectively. fT4 (ng/dl) and TSH (microIU/ml) levels of the two groups were similar (p > 0.05). The level of fT3, the active metabolite of the thyroid hormone family, was dramatically reduced in the SCF group when compared to the NCF group (2.3 +/- 0.2 vs. 3.0 +/- 0.3, p = 0.0001, respectively). Plasma Hcy levels of patients with SCF were found to be significantly higher than controls (12.2 +/- 4.9 vs. 8.5 +/- 2.9, p = 0.0001, respectively). Correlation analysis showed a significant negative correlation between the plasma fT3 and Hcy levels and the mean TIMI frame counts (r = -0.31, p = 0.003 vs. r = -0.66, p = 0.0001). Moreover, there was a significant positive correlation between the plasma Hcy levels and the mean TIMI frame counts (r = 0.58, p = 0.0001). Also, fT3 was the only significant determinant of the variance of Hcy in multiple regression analysis (r = -0.30, p = 0.005). fT3 levels were decreased and plasma Hcy levels were increased significantly in patients with SCF as compared to controls. This finding suggests that thyroid hormones and/or (?) a possible disturbance in their metabolism may be responsible for the elevated levels of plasma Hcy in patients with SCF and may play a role in the pathogenesis of the SCF phenomenon.
    No preview · Article · Feb 2007 · Cardiology
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    ABSTRACT: Objectives: We investigated the effect of nasal continuous positive airway pressure (CPAP) on blood pressure (BP) and left ventricular structure in male patients with severe obstructive sleep apnea (OSA). Study design: Thirty-three male patients with severe OSA underwent CPAP treatment for six months. Compliance was defined as the use of CPAP for at least 3.5 hours per night during treatment; thus, 25 patients (mean age 47.9±8.2 years) were compliant with a mean of 5.3±1.9 hours, and eight patients (mean age 48.6±8.4 years) were noncompliant with a mean of 1.0±0.8 hours. Before and after CPAP, echocardiographic assessments were made to determine left ventricular structure (interventricular septum thickness, left ventricular posterior wall thickness, left ventricular mass, and left ventricular mass index) and function (E/A ratio, isovolumic relaxation time, mitral deceleration time, and velocity of mitral flow propagation), and systolic and diastolic blood pressures were measured. In the compliant group, 20 patients had hypertension, 22 patients had diastolic dysfunction, and 16 patients had left ventricular hypertrophy (LVH). All noncompliant patients were hypertensive, four had diastolic dysfunction, and four had LVH. Results: Systolic and diastolic BPs significantly decreased after CPAP treatment, the decreases being more pronounced in the compliant group (p<0.001 vs p<0.01). Parameters of left ventricular structure and diastolic function significantly improved in compliant patients following CPAP. Left ventricular hypertrophy improved in nine patients (56.3%, p<0.0001) and diastolic dysfunction improved in 11 patients (50%, p<0.001). However, in the noncompliant group, parameters of left ventricular structure and diastolic functions did not differ significantly and the number of patients having LVH or diastolic dysfunction did not change. Conclusion: In severe OSA, CPAP treatment significantly decreases BP and left ventricular wall thickness, and improves left ventricular diastolic function.
    No preview · Article · Dec 2006
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    ABSTRACT: Obstructive sleep apnea (OSA) has a critical association with cardiovascular mortality and morbidity. Carotid intima-media thickness (IMT), flow-mediated dilatation (FMD) and aortic stiffness are early signs of atherosclerosis. The presence of subclinical atherosclerosis was assessed in OSA patients using these parameters. 40 patients with OSA showing an apnea-hypopnea index (AHI) > or =5 (mean age 51.3 +/- 9 years, 32 males) and 24 controls (AHI < 5, mean age 51.9 +/- 5.2 years, 19 males) were enrolled in the study. In all subjects, polysomnographic examination and recordings were performed during sleep. IMT of the carotid artery, endothelium-dependent/-independent vasodilation of the brachial artery and aortic elastic parameters were investigated using high-resolution Doppler echocardiography. The demographic data of the patients with OSA and controls were not significantly different. Subjects with OSA demonstrated higher values of aortic stiffness (7.1 +/- 1.88 vs. 6.42 +/- 1.56, respectively) and IMT (0.85 +/- 0.13 vs. 0.63 +/- 0.11 mm, p = 0.0001, respectively) but lower distensibility (9.47 +/- 1.33 vs. 11.8 +/- 3.36 cm(2)/dyn/10(6)) and FMD (4.57 +/- 1.3 vs. 6.34 +/- 0.83%, p = 0.0001, respectively) than the controls. The respiratory disturbance index correlated positively with aortic stiffness and IMT and negatively with distensibility and FMD. We observed blunted endothelium-dependent dilatation, increased carotid IMT and aortic stiffness in patients with OSA compared with matched control subjects. This is evident in the absence of other diseases, suggesting that OSA is an independent cause of atherosclerosis. These simple and non-invasive methods help to detect subclinical atherosclerosis in OSA.
    No preview · Article · Nov 2006 · Respiration
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    ABSTRACT: Coronary slow-flow phenomenon is characterized by delayed opacification of coronary vessels in a normal coronary angiogram. Although clinical and pathological features have been previously described, the underlying pathophysiology has not been fully elucidated. Thus, it still remains to be determined whether either microvascular or epicardial diffuse atherosclerotic disease is related to slow flow. In this study, we aimed to determine the carotid artery intima-media thickness, which is a marker of atherosclerosis in patients with coronary slow flow, and its possible relationship with the total homocysteine level. The study population consisted of 88 patients who underwent coronary angiography because of typical and quasi-typical symptoms of angina. Forty-four patients with angiographically proven coronary slow flow and 44 individuals with normal coronary flow pattern with similar risk profiles were enrolled in the study. Coronary flow patterns of the latter were determined by the thrombolysis in myocardial infarction frame count method. Intima-media thickness was measured by recording ultrasonographic images of both the left and the right common carotid artery with a 12-MHz linear array transducer. Plasma homocysteine, folate and B12 levels were measured from blood samples. Plasma homocysteine levels (mumol/l) and carotid intima-media thickness (mm) of patients with coronary slow flow were found to be significantly higher than that of controls (12.4+/-4.9 vs. 8.5+/-2.8, P=0.0001; 0.75+/-0.08 vs. 0.69+/-0.06, P=0.0001, respectively). The plasma folate level (ng/ml) was lower in coronary slow-flow patients than in controls (13.8+/-4.4 vs. 16.5+/-5.6, P=0.014). The plasma homocysteine level was significantly positively correlated with the mean thrombolysis in myocardial infarction frame count and intima-media thickness of the carotid artery in correlation analysis (r=0.58, P=0.0001; r=0.41, P=0.0001; respectively). Homocysteine levels and carotid intima-media thickness increased but folate levels decreased in patients with coronary slow flow. The present findings allow us to conclude that the possible disturbance in the metabolism of homocysteine in patients with coronary slow flow may have a role in the etiopathogenesis of this phenomenon by causing generalized atherosclerosis.
    No preview · Article · Jun 2006 · Coronary Artery Disease
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    ABSTRACT: Smoking contributes to the progression of atherosclerotic heart disease by causing endothelial dysfunction. In the present study the effect of smoking on endothelial functions and coronary flow was investigated, as well as the relationship of these factors with oxidative stress parameters, in subjects with normal coronary arteries. The study group comprised 87 patients with angiographically normal coronary arteries (36 smokers, 51 nonsmokers). Coronary flow patterns were determined by the Thrombolysis In Myocardial Infarction (TIMI) frame count method. Endothelial function was evaluated by high-frequency ultrasound imaging of the brachial artery. Superoxide dismutase (SOD) and reduced glutathione (GSH) and reduction of oxidative material in the body and the endproduct of lipid peroxidation, malondialdehyde (MDA), were measured as oxidative stress markers. Mean TIMI frame count was significantly higher in smokers than nonsmokers (42.2 +/- 16 vs 29.5 +/- 9.5, p = 0.0001). Endothelium-dependent flow-mediated dilatation was 6.81+/-1.95% in nonsmokers and 5.7 +/- 2.2% in smokers (p = 0.0001). The smokers had dramatically higher levels of SOD and MDA and lower levels of GSH than the nonsmoker group. Smoking induced oxidative stress deteriorates coronary blood flow by disturbing endothelial function.
    No preview · Article · Jun 2006 · Circulation Journal
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    ABSTRACT: Both left ventricular (LV) hypertrophy and insulin resistance (IR) have often been demonstrated in patients with essential hypertension (EH). Insulin may exert a direct growth promoting effect on cardiomyocytes rather than affecting the LV internal diameter. The purpose of this study was to examine the effect of IR on LV geometry. We enrolled 105 patients (71 females, mean age, 49.2 +/- 13.6 years) with recently diagnosed and untreated hypertension (blood pressure > 140 and/or 90 mmHg, fasting glucose < 110 mg/dL), and grouped them as normal (N) (39 patients, 26 females, mean age, 48.5 +/- 14.7 years) if all M-mode echocardiographic measurements were within normal limits, concentric remodeling (CR) (22 patients, 15 females, mean age, 50.5 +/- 14.8 years) if relative wall thickness was increased but left ventricular mass index (LVMI) was normal, concentric hypertrophy (CH) (13 patients, 9 females, mean age, 50.3 +/- 10.8 years) if both ventricular thicknesses and the LVMI were increased, and eccentric hypertrophy (EH) (31 patients, 21 females, mean age, 48.6 +/- 12.9 years) if ventricular thicknesses were normal, but LVMI was increased. Transthoracic echocardiography was performed in all subjects, and interventricular septal thickness (IVS), posterior wall thickness (PWT), sum of wall thickness (SWT), left ventricular end-diastolic internal diameter (LVED), relative wall thickness (RWT), and LVMI were recorded. Blood samples for routine biochemical examination and fasting insulin levels were obtained and then the homeostasis model assessment (HOMA) index was calculated by the formula: HOMA Index = Fasting Blood Glucose (mg/dL) x Immunoreactive Insulin (microU/mL)/405, for the assessment of IR. There were no significant differences among the groups with respect to age, blood pressure (BP) levels, fasting blood glucose (FBG), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C), total cholesterol (TC), or triglyceride (TG) levels. Insulin levels were significantly higher in the CR and CH groups in comparison with the N group (P = 0.004), and the HOMA index was higher in the CH group compared to the N group (P = 0.024). In Pearson's correlation analysis, insulin was found to be directly correlated with IVS (r = 0.29, P = 0.002), SWT (r = 0.25, P = 0.009), and RWT (r = 0.33, P = 0.0001). The HOMA index was also directly correlated with IVS (r = 0.33, P = 0.001), SWT (r = 0.29, P = 0.002), and RWT (r = 0.29, P = 0.003). Cardiac changes in hypertensive patients include increased LVMI and altered LV geometry. The concentric LV geometry seen in hypertensive patients might be mediated, at least in part, by increased insulin levels and the HOMA index.
    No preview · Article · Jun 2006 · International Heart Journal
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    ABSTRACT: Metabolic syndrome (MS) is a condition, which is recognized as raising the risk of cardiovascular disease. The aim of our study is to estimate the left ventricular functions by atrioventricular plane displacement (AVPD), myocardial performance index (MPI) and conventional methods in patients with MS who were diagnosed according to NCEP (ATP III) criteria. Fifty-three female patients with MS (mean age 53.1+/-6.9 years) and 30 healthy female subjects (mean age 52.8+/-6.3 years, p>0.05) underwent complete echocardiographic assessment. All of the subjects had no heart and pulmonary diseases. The systolic mitral AVPD was recorded at 4 sites (septal, lateral, anterior, and posterior) by M-mode echocardiography and left ventricle ejection fraction (LVEF) was calculated from the AVPD-mean (EF-AVPD). The LVEF was also established by biplane Simpson's (EF-2D) and Teichholz's methods (EF-T). Left ventricular MPI was calculated as (isovolumic contraction time + isovolumic relaxation time) / aortic ejection time by Doppler echocardiography. Patients with MS showed mild left ventricular diastolic dysfunction (DD) in comparison to healthy subjects. The EF-2D and EF-T in patients with MS and healthy subjects were not different significantly and were within normal limits. Patients with MS showed LV global dysfunctions compared to healthy subjects (MPI: 0.56+/-0.12 and 0.46+/-0.11 respectively, p<0.01). Both the septal, anterior, lateral and posterior part of the atrioventricular plane values and also AVPD-mean during systole were statistically lower in patients with MS (12.85+/-1.76 mm) as compared with controls (14.65+/-2.19 mm, p<0.05). The EF-AVPD in patients with MS was statistically lower (65.58+/-11.95%) as compared with healthy subjects (74.45+/-11.07%, p<0.01). Female patients with MS had both left ventricular DD and a global dysfunction with an increased MPI. The EF-2D and EF-T were not different significantly between patients and controls, but patients with MS had a relatively reduced EF-AVPD. The AVPD method may indicate a systolic dysfunction with a relatively lower AVPD-mean and relatively lower EF-AVPD. The presence of global dysfunction in patients with MS may lead to heart failure.
    No preview · Article · Dec 2005 · Anadolu kardiyoloji dergisi: AKD = the Anatolian journal of cardiology
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    ABSTRACT: Angiotensin converting enzyme (ACE) is a key enzyme in angiotensin II production which causes myocardial hypertrophy and hyperplasia. In this study we aimed to investigate the relation between ACE I/D gene polymorphism and left ventricular mass (LVM), dimensions and systolic functions calculated by mitral annular motion (MAM) in young healthy male subjects. Complete echocardiographic examination was performed in 49 male healthy subjects (mean age 22.9+/-2.1 years) consisting of 18 ACE DD, 18 ACE DI and 13 ACE II genotypes. We calculated LVM and mass index (LVMI) by M-Mode echocardiography. The systolic MAM was recorded at 4 sites (septal, lateral, anterior, and posterior) by M-mode echocardiography and the MAM-ejection fraction (EF) was calculated from above four sites. Ejection fraction was also calculated by Simpson's method. There was no significant difference among the three genotypes according to age, body mass index, systolic and diastolic blood pressure and heart rate. Interventricular septum (IVS) and left ventricular posterior wall (LVPW) diastolic thickness, LVM and LVMI were found significantly different among 3 ACE genotypes. Those measurements were higher in DD genotype in comparison to the DI and II genotypes. There was no significant difference among the three genotypes according to EF-MAM and EF by Simpson's method. In young healthy male subjects having ACE DD genotype, even though LVM and LVMI were within normal limits, their measurements were found to be higher than in subjects with ACE DI and II genotypes respectively. There was no difference among the three genotypes according to left ventricular systolic functions.
    No preview · Article · Oct 2005 · Anadolu kardiyoloji dergisi: AKD = the Anatolian journal of cardiology
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    ABSTRACT: Preinfarction angina (PA) and early reperfusion of infarct-related arteries have been shown to reduce infarct size in patients with acute myocardial infarction (AMI). The beneficial effects of PA on infarct size have been attributed to the development of ischemic preconditioning and faster coronary recanalization in patients treated with thrombolytic therapy (TT). To evaluate the effect of PA on clinical coronary reperfusion time in patients with AMI receiving successful TT. Seventy-five patients presenting with AMI (within 6 h after the initial onset of symptoms) were studied. All patients received TT and were evaluated with coronary angiography (CA) at predischarge. The patients were divided into two groups: group 1 (PA-positive) comprised those who experienced a new onset of prodromal angina within 72 h before the onset of AMI. Group 2 (PA-negative) comprised those who had a sudden onset of AMI without the preceding angina. The successful myocardial reperfusion criteria after TT were ST segment resolution of 50% or greater, the appearance of reperfusion arrhythmias and the resolution of chest pain. The time of reperfusion criteria was recorded after TT. CA was performed in all patients at predischarge. Patients with no patent infarct-related arteries on CA and clinical failure of reperfusion were excluded from the study. Clinical characteristics, risk factors and angiographic findings did not differ significantly between the groups. The time interval from the start of continuous chest pain to TT was also similar between the groups. The left ventricular ejection fraction was higher and there were less frequent ventricular arrhythmias in patients with PA than in those without PA (47.9+/-7.4 versus 44.4+/-8.1, P=0.041, and 17.1% versus 37.5%, P=0.043, respectively). The clinical reperfusion time was significantly shorter in the patients with PA than in those without PA (68.2+/-24.5 min versus 81.4+/-19.3, P=0.012). The clinical reperfusion time was positively correlated with age and the time interval from the start of continuous chest pain to TT but inversely related to the presence of PA. In patients with AMI preceded by PA, TT resulted in more rapid clinical reperfusion than in patients without PA. Thus, earlier myocardial reperfusion may account for smaller infarct size and better prognosis in patients with PA.
    No preview · Article · Oct 2005 · The Canadian journal of cardiology
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    ABSTRACT: Obstructive sleep apnoea syndrome (OSAS) might be a cause of heart failure. The present study aimed to assess left ventricular mass and myocardial performance index (MPI) in OSAS patients. A total of 67 subjects without any cardiac or pulmonary disease, referred for evaluation of OSAS, had overnight polysomnography and echocardiography. According to apnoea-hypopnoea index (AHI), subjects were classified into three groups: mild OSAS (AHI: 5-14; n = 16), moderate OSAS (AHI: 15-29; n = 18), and severe OSAS (AHI: > or = 30; n = 33). Thickness of interventricular septum (IVS) and posterior wall (LVPW) were measured by M-mode, along with left ventricular mass (LVM) and LVM index (LVMI). Left ventricular MPI was calculated as (isovolumic contraction time+isovolumic relaxation time)/aortic ejection time by Döppler echocardiography. There were no differences in age or body mass index among the groups, but blood pressures were higher in severe OSAS compared with moderate and mild OSAS. In severe OSAS, thickness of IVS (11.2+/-1.1 mm), LVPW (11.4+/-0.9 mm), LVM (298.8+/-83.1 g) and LVMI (144.7+/-39.8 g x m(-2)) were higher than in moderate OSAS (10.9+/-1.3 mm; 10.8+/-0.9 mm; 287.3+/-74.6 g; 126.5+/-41.2 g x m(-2), respectively) and mild OSAS (9.9+/-0.9 mm; 9.8+/-0.8 mm; 225.6+/-84.3 g; 100.5+/-42.3 g x m(-2), respectively). In severe OSAS, MPI (0.64+/-0.14) was significantly higher than in mild OSAS (0.50+/-0.09), but not significantly higher than moderate OSAS (0.60+/-0.10). In conclusion, severe and moderate obstructive sleep apnoea syndrome patients had higher left ventricular mass and left ventricular mass index, and also left ventricular global dysfunction.
    No preview · Article · Sep 2005 · European Respiratory Journal
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    ABSTRACT: Physiologic adaptations in an athlete's heart include increased left and right ventricular chamber size, left ventricular wall thickness and mass. Angiotensin-converting enzyme (ACE) is a key enzyme in angiotensin II production causing cardiac hypertrophy. The cloning of the ACE gene has made it possible to identify a deletion (D)-insertion (I) polymorphism that appears to affect the level of serum ACE activity. Therefore, the ACE genes, which have been shown to be polymorphic, could be candidate genes for large-artery stiffness. 56 endurance athletes and 46 sedentary subjects were included in this study, and they underwent both complete echocardiographic examination, and analysis of ACE insertion (I) and deletion (D) allele frequencies in peripheral blood. The aortic diameter was recorded by M-mode echocardiography at a level 3 cm above the aortic valve. Aortic systolic diameter was measured at the time of full opening of the aortic valve, and diastolic diameter was measured at the peak of QRS. Aortic strain, stiffness index and distensibility were calculated. Left ventricular mass index and left ventricular ejection fraction were significantly higher in athletes than controls (p < 0.001). The aortic distensibility index and strain were significantly greater in athletes compared with controls (respectively: 5.8 +/- 2.7 vs. 4.7 +/- 1.8 cm(-2) dyn(-1) 10(-6), p = 0.017; 12.3 +/- 2.4 vs. 9.3 +/- 3.1, p < 0.001). The aortic stiffness index was significantly lower in athletes than in controls (4.8 +/- 1.9 vs. 6.1 +/- 2.1, p < 0.001). The aortic distensibility index and strain were statistically different in ACE DD vs. DI groups and DD vs. II groups of athletes. The aortic stiffness index was statistically different in ACE DD vs. II groups of athletes. Aortic parameters were similar according to ACE genotypes in controls. The results of this study indicate that aortic distensibility was increased by prolonged training in endurance athletes, particularly in those with the ACE II genotype. This effect represents an extracardiac adaptation to chronic prolonged training in athletes.
    No preview · Article · Sep 2005 · Cardiology

  • No preview · Article · Aug 2005 · Acta cardiologica
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    ABSTRACT: QT dispersion (QTd) is a measure of inhomogeneous repolarization of myocardium and is used as an indicator of arrhythmogenicity. QTd is increased in myocardial hypertrophy secondary to systemic hypertension. The relation between left ventricular (LV) enlargement in endurance trained subjects and QTd is unknown. The cloning of the angiotensin-converting enzyme (ACE) gene has made it possible to identify a deletion (D)-insertion (I) polymorphism that appears to affect the level of serum ACE activity. The aim of this study was to assess whether physiologic left ventricular hypertrophy as a result of physical training is associated with an increased QT length or dispersion depending on ACE I/D polymorphism. 56 endurance athletes and 46 sedentary subjects were included in this study, and they underwent both complete echocardiographic and electrocardiographic examination, the QT interval was measured manually as an average based on a 12-lead ECG. We also analysed ACE I and D allele frequencies in all patients. Athletes had a significantly increased LV mass (235.1 +/- 68.5 g vs. 144.9 +/- 44.5 g, p < 0.001) and corrected QTd (QTcd) (55.5 +/- 18.1 ms vs. 42.9 +/- 17.2 ms, p < 0.001) in comparison to control subjects. There was a positive correlation between left ventricular mass index and QTcd in athletes (r = 0.3, p = 0.024). Left ventricular mass and mass index in ACE DD, DI and II genotypes were significantly different (p < 0.001). QTcd was significantly different between ACE DD (63.2 +/- 12.8 ms) and ACE II (44.9 +/- 17.6 ms) genotypes in athletes (p < 0.05). These data show that myocardial hypertrophy induced by exercise training might be associated with increased QTd as observed in systemic hypertension and might be affected by ACE I/D polymorphism.
    No preview · Article · Aug 2005 · Acta cardiologica
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    ABSTRACT: Changes in lipid profiles, Lp(a) lipoprotein, and acute phase reactants are associated with early atherosclerosis in rheumatoid arthritis (RA). The associations of Lp(a) levels with atherosclerotic disorders, diabetes, RA, and renal diseases suggest that Lp(a) might be involved in autoimmune reactions. Eighty-seven women with RA diagnosed according to American Rheumatism Association criteria (mean age 45.4+/-9.4 years) were recruited and 50 healthy women (mean age 44+/-10.7 years) included as a control group. Serum Lp(a), total cholesterol (TC), triglyceride (TG), LDL cholesterol (LDL-C), HDL cholesterol (HDL-C), and C-reactive protein levels were analyzed. In the RA and C groups, serum Lp(a) levels were 39.2+/-20.6 mg/dl and 14.8+/-9.7 mg/dl, respectively (P<0.001). The TC levels were 188.4+/-41.8 mg/dl and 185.3+/-19.3 mg/dl (P>0.05), TG levels were 124.5+/-50.1 mg/dl and 94.6+/-24.9 mg/dl (P<0.01), HDL-C levels were 40.0+/-7.4 mg/dl and 52.8+/-4.8 mg/dl (P<0.01), and LDL-C levels were 123.4+/-24.6 mg/dl and 113.3+/-21.1 mg/dl (P>0.05). While serum CRP levels showed a positive correlation with Lp(a), they correlated negatively with HDL-C levels (r=0.83 and P<0.0001, r=-0.49 and P<0.0001, respectively). It was meaningful that Lp(a) correlated negatively with serum HDL-C level (r=-0.36, P<0.001). It is suggested that higher serum Lp(a), lower HDL-C, higher TG level, and a high ratio of TC/HDL-C might show high risk of atherosclerosis. Inflammation in RA may cause changes in HDL-C and Lp(a) metabolisms.
    No preview · Article · Jun 2005 · Rheumatology International