An asymptomatic case with single atrium.
Single atrium or common atrium is a rare, isolated defect. We report here an adult patient with single atrium detected by transthoracic echocardiography.
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Biomedical subjects
H Asuman Kaftan
Publications and source records attributed to H Asuman Kaftan.
Cigarette smoking induced oxidative stress may impair endothelial function and coronary blood flow in angiographically normal coronary arteries.
BACKGROUND: 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. MATERIALS AND RESULTS: 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. CONCLUSION: Smoking induced oxidative stress deteriorates coronary blood flow by disturbing endothelial function.
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Effect of insulin resistance on left ventricular structural changes in hypertensive patients.
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.
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Improved endothelium dependent vasodilation in endurance athletes and its relation with ACE I/D polymorphism.
BACKGROUND: Aerobic exercise enhances endothelium-dependent vasodilation in healthy individuals. It is thought that exercise increases nitric oxide (NO) production and decreases NO inactivation, leading to an increase in NO bioavailability. Angiotensin II and NO have important roles in maintaining vascular tone. There are polymorphisms of the angiotensin converting enzyme (ACE) gene and the presence of the deletion (D) allele has been associated with higher concentrations of circulating and tissue ACE. In this study, the relationship between endothelial function and ACE gene polymorphisms was investigated in athletes and sedentary subjects. METHODS AND RESULTS: The study group comprised 56 endurance athletes and 46 sedentary subjects who underwent brachial artery ultrasonographic examination. ACE insertion (I) and D allele frequencies were analyzed in all patients. Baseline brachial artery diameter and resting blood flow were similar in athletes and controls (p > 0.05). The flow-mediated dilation (FMD) was 8.48+/-3.65% in athletes and 5.16+/-2.5% in controls (p = 0.0001). FMD was significantly different between ACE genotypes in the athletes (p < 0.0001): it was higher in ACE II (10.5+/-1.6%) subjects than in the DI (8.4+/-2.3%) or DD (7+/-1.2%) subgroups. CONCLUSION: Regular isotonic exercise can improve endothelium-dependent vasodilation especially in those with the ACE II genotype.
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Angiotensin-converting enzyme polymorphism in healthy young subjects: relationship to left ventricular mass and functions.
OBJECTIVES: Angiotensin-converting enzyme (ACE) is a key enzyme in the production of angiotensin II and thus may participate in the modulation of cardiac growth. 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. The aim of the study is to analyse the ACE gene I/D polymorphisms in healthy young subjects and to evaluate its relationship to left ventricular mass and functions. METHODS: 38 women and 40 men (mean age 21.1 +/- 1.7 and 21.4 +/- 1.7 years) were studied. They underwent complete echocardiographic assessment and analysis of ACE insertion (I) and deletion (D) allele frequencies in peripheral blood by polymerase chain reaction. Thickness of interventricular septum (IVS) and posterior wall (LVPW) and left ventricular mass (LVM) and LVM index (LVMI) were measured by M-mode. Left ventricular ejection fraction (LVEF) was calculated by Simpson's method. RESULTS: There was no statistically significant difference among the DD, DI and II genotypes, concerning age, body mass index, heart rate, systolic and diastolic blood pressures.The thickness of IVS (9.5 mm), LVPW (9.0 mm), LVM (204.5 g) and LVMI (105.5 g/m2) in DD genotypes were higher than both DI (8.3 mm; 8.1 mm; 168.1 g; 90.9 g/m2) and II genotypes (8.2 mm; 7.0 mm; 141.7 g; 77.8 g/m2) in men, but not in women. LVEF among the 3 genotypes were not statistically different. CONCLUSION: Our findings suggest that left ventricular hypertrophy is partially determined by genetic disposition especially in men but not in women.
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QT dispersion and left ventricular hypertrophy in athletes: relationship with angiotensin-converting enzyme I/D polymorphism.
BACKGROUND: 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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.
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