Ahmet Gurdal

Coronary flow reserve is impaired in patients with nonalcoholic fatty liver disease: Association with liver fibrosis

BACKGROUND Nonalcoholic fatty liver disease (NAFLD) is associated with an increased risk of cardiovascular disease. Coronary flow reserve (CFR) is widely used to examine the integrity of coronary microvascular circulation. We evaluated the prevalence of impaired CFR in patients with biopsy-proven NAFLD. We also investigated the independent clinical, biochemical, and liver histology predictors of CFR in the setting of NAFLD. METHODS Fifty-nine consecutive patients with NAFLD and 77 age- and gender-matched controls were evaluated. CFR recordings were performed by transthoracic Doppler harmonic echocardiography. CFR>or=2.0 was considered normal. RESULTS CFR was significantly lower in patients with NAFLD than in controls (2.11+/-0.45 vs. 2.52+/-0.62, P<0.001). An impaired CFR (i.e. <2) was found in 25 NAFLD patients (42.4%) whereas all controls had normal CFR values (P<0.001). A stepwise linear regression analysis in NAFLD patients identified liver fibrosis scores as the only independent predictor of CFR values (beta=-0.60; t=-2.44, P=0.021). CONCLUSION Our findings indicate that in patients with biopsy-proven NAFLD: (a) an abnormal CFR is found in approximately 42.4% of cases, and (b) liver fibrosis scores are an independent predictor of depressed CFR.

Circulating vaspin levels and epicardial adipose tissue thickness are associated with impaired coronary flow reserve in patients with nonalcoholic fatty liver disease

BACKGROUND Patients with nonalcoholic fatty liver disease (NAFLD) have a reduced coronary flow reserve (CFR) and an increased risk of cardiovascular disease. The fat cells that surround coronary arteries may play a central and underrecognized role in development of cardiovascular disease through the systemic secretion of adipokines. We therefore evaluated the relation of epicardial fat thickness, serum levels of epicardial fat-related adipokines (chemerin and vaspin), and CFR in patients with NAFLD. METHODS We investigated 54 patients with biopsy-proven NAFLD and 56 age- and sex-matched controls. CFR and epicardial fat thickness (EFT) were measured by transthoracic echocardiography. Serum levels of chemerin and vaspin were measured by ELISA. RESULTS EFT was significantly higher (0.64 ± 0.13 vs. 0.54 ± 0.10 cm, P<0.001) and CFR significantly lower (2.11 ± 0.45 vs. 2.52 ± 0.62, P < 0.001) in patients with NAFLD than in controls. Serum levels of vaspin and chemerin were both significantly increased in patients with NAFLD compared with controls. Stepwise regression analysis showed that EFT (β=-0.53, t=-3.7, P<0.001), serum vaspin levels (β=-0.30, t=-2.5, P=0.014), and liver fibrosis (β=-0.31, t=-2.11, P=0.041), in the order they entered into the model, were independent predictors of CFR in NAFLD patients. CONCLUSION Our data suggest the presence of a complex interplay between EFT, serum vaspin, and liver histology in promoting an impaired hyperemic stimulation of coronary blood flow in patients with NAFLD.

Assessment of myocardial damage by cardiac MRI in patients with anorexia nervosa

OBJECTIVE Cardiac damage is a major complication of anorexia nervosa (AN). The present study evaluated the prevalence of myocardial damage in patients with AN by cardiac magnetic resonance imaging (CMR). METHOD This study was cross-sectional and observational. Forty consecutive female patients with a diagnosis of AN and 28 healthy female subjects were evaluated from January 2007 to 2011 at the Department of Psychiatry (University of Istanbul, Istanbul, Turkey). Following enrollment in the study, participants underwent a cardiac evaluation, a physical examination, a standard electrocardiogram (ECG), an echocardiography and a CMR. RESULTS Body weight, body mass index and heart rate values were lower in patients with AN than in the control group. When compared with control groups, patients with AN showed reduced left ventricular mass with normal systolic function. Compared to control subjects, patients with AN had higher prevalence of pericardial effusion (30% in the AN group, 4% in the control group, p = .005) and mitral valve prolapses (23% in the AN group, 4% in the control group, p = .03). Myocardial fibrosis (detected as late gadolinium enhancement on CMR) was found in 23% of patients with AN. Myocardial fibrosis was not detected in any control subject (p = .007). CONCLUSION A strong association was found between myocardial fibrosis and AN. Cardiac damage of myocardial fibrosis in asymptomatic patients with AN can be found by CMR examination.

There is an increased risk of atherosclerosis in hereditary angioedema.

BACKGROUND Hereditary angioedema is associated either with a deficiency in the amount or in the function of the C1 inhibitor (C1 INH). OBJECTIVE In this study the endothelial function of HAE patients was investigated to evaluate the impact of hereditary C1-INH deficiency on atherosclerosis, which has not yet been established before. METHODS A total of 26 patients (14 female, 12 male. Mean age: 38±13) diagnosed with HAE and 30 healthy controls were enrolled in the study. Measurement of coronary flow reserve (CFR) in the left anterior descending coronary artery was performed using transthoracic doppler harmonic echocardiography at baseline and following dipyridamol infusion. The intima-media thickness (IMT) in the carotid artery was measured using an echocardiographic system equipped with 10 MHz linear transducer (Vingmed System Five). RESULTS The mean CFR value for the HAE patient group was significantly lower than that of the control group (p<0.001). The mean IMT was not found to be significantly different between the two groups, although it was slightly higher in the HAE patient group. No correlation was found between the CFR and the disease severity scores, nor was it shown between the CFR values and the duration of danazol treatment. CONCLUSION Our results indicate that there is a microvascular endothelial dysfunction in HAE patients. Although carotid intima media thickness of these patients was not significantly increased, the presence of microvascular endothelial dysfunction might be regarded as an early indicator of a premature atherosclerosis.

Impact of diabetes and diastolic dysfunction on exercise capacity in normotensive patients without coronary artery disease

Objective: The aim of this study was to determine the impact of diabetes and diastolic dysfunction on exercise capacity in asymptomatic, normotensive patients with type 2 diabetes without coronary artery disease. Methods: A total of 43 type 2 diabetes patients (age: 50 ± 5 years) and 20 healthy controls (age: 48 ± 4 years) were enrolled. Diastolic function was investigated by conventional pulsed-wave (PW) Doppler and tissue Doppler imaging (TDI). Exercise capacity was evaluated with cardiopulmonary exercise testing (CPET). Results: In patients with type 2 diabetes, increase in resting heart rate (HR-rest) (p = 0.013), decrease in maximum heart rate during exercise (HR-max) (p < 0.001) and exercise time (p < 0.001) compared with controls were significant. Patients had significantly increased minute ventilation volume (VE)/maximum carbon dioxide discharge (VCO2) ratio (p < 0.001), decreased maximum oxygen consumption (VO2-max) (p < 0.001), oxygen consumption at anaerobic threshold (VO2-an) (p < 0.001) and maximum carbon dioxide discharge (VCO2) (p < 0.001) compared to controls indicating significantly reduced exercise capacity. HbA1c was inversely correlated with VO2-max (r = −0.456, p < 0.01) independent of the absence or presence of mild diastolic dysfunction. Conclusion: Exercise capacity was found to be significantly decreased in normotensive patients with type 2 diabetes without coronary artery disease, and this decrease was independent of diastolic dysfunction.