[Effect of overweight on cardiac function in children]. / Çocuklarda kilo fazlaliginin kalp fonksiyonlarina etkisi.

OBJECTIVES: It is known that obesity is related to heart failure. Asymptomatic left ventricular diastolic dysfunction (LVDD) is associated with the development of heart failure. The relationship between subclinical LVDD and overweight in children is not clear. The purpose of this study was to evaluate the effect of body mass index (BMI) and waist circumference on left ventricular mass index (LVMI) and LVDD in overweight children. STUDY DESIGN: A total of 153 children were enrolled in the study. Of these, 91 were normal weight (age-adjusted BMI: 15-85 percentile), and 62 were overweight (age-adjusted BMI: 85-95 percentile). After measuring two-dimensional and M-mode echocardiographic variables, left and right ventricle diastolic functions were assessed by conventional and tissue Doppler imaging. RESULTS: Compared to controls, overweight children had increased left atrium, aortic and left ventricular diameters, left ventricular wall thickness, LVM and LVMI, and septal mitral annulus e', septal e'/a', lateral e', lateral e'/a', lateral tricuspid annulus e', and e'/a' values. There were negative correlations between tissue Doppler diastolic parameters (septal mitral annulus e', lateral mitral annulus e', lateral tricuspid annulus e', septal mitral annulus e'/a', lateral mitral annulus e'/a', and lateral tricuspid annulus e'/a') and BMI, waist circumference, insulin, HOMA index, as well as systolic and diastolic blood pressure. Positive correlations were found between LVMI and BMI and between LVMI and waist circumference. BMI was found to be the predictor of decreased mitral anulus septal e', septal e'/a', lateral e', lateral e'/a'. CONCLUSION: Compared with normal-weight children, overweight children have decreased LV diastolic function. BMI is associated with a reduction in LV diastolic function in overweight children.

Effects of idiopathic erythrocytosis on the left ventricular diastolic functions and the spectrum of genetic mutations: A case control study.

BACKGROUND: We have aimed at exposing left ventricular diastolic functions and the presence of known genetic mutations for familial erythrocytosis, in patients who exhibit idiopathic erythrocytosis. METHODS: Sixty-four patients with idiopathic erythrocytosis (mean age, 46.4 ± 2.7 years) and 30 age-matched healthy subjects were prospectively evaluated. The regions of interest of the erythropoietin receptor, hemoglobin beta-globin, von Hippel-Lindau, hypoxia-inducible factor 2 alpha, and Egl-9 family hypoxia-inducible factor genes were amplified by PCR. Left ventricular (LV) mass was measured by M-mode and 2-dimensional echocardiography. LV diastolic functions were assessed by conventional echocardiography and tissue Doppler imaging. RESULTS: As a result of genetic analyses, genetic mutations for familial erythrocytosis were detected in 5 patients. It has been observed in our study that the risk of cardiovascular disorders is higher in patients. Interventricular septum thickness, left atrial diameter, and some diastolic function parameters such as deceleration time and isovolumetric relaxation time have been found to be significantly higher in idiopathic erythrocytosis group than in the controls. CONCLUSION: This study has shown that LV diastolic functions were impaired in patients with idiopathic erythrocytosis. In this patient group with increased risk of cardiovascular disorders, the frequent genetic mutations have been detected in 5 patients only. Therefore, further clinical investigations are needed as novel genetic mutations may be discovered in patients with idiopathic erythrocytosis because of cardiovascular risk.

Rosuvastatin Decreases Mean Platelet Volume in Patients With Diabetes Mellitus.

Statins have multiple effects (also known as pleiotropic effects) on inflammation, plaque stabilization, endothelial function, and hemostasis. We evaluated the effects of rosuvastatin on mean platelet volume (MPV)--a marker for platelet activity--in patients with diabetes mellitus (DM) on rosuvastatin medication. Patients (n = 178) who were to be prescribed high-intensity rosuvastatin were retrospectively enrolled according to their medical records. Baseline and 6-month biochemical tests, automated blood count, cell-volume analysis, and their cardiovascular risk factors were recorded. Rosuvastatin significantly reduced the MPV and the lipid parameters including total cholesterol, triglyceride, and low-density lipoprotein cholesterol (LDL-C). However, there was no correlation between MPV and LDL-C before (r = -.66; P = .383) and after (r = -.112; P = .135) rosuvastatin treatment or between ΔMPV and ΔLDL-C after 40 mg rosuvastatin daily therapy (r = -.155; P = .073). Rosuvastatin significantly decreases the MPV as well as cholesterol levels. The antiplatelet activation properties of high-dose rosuvastatin treatment in patients with DM are not lipid dependent.

Atrial Fibrillation Is Associated With Increased Mean Platelet Volume and Apnea Hypopnea Index in Patients With Obstructive Sleep Apnea.

This study investigated whether there is a relationship between atrial fibrillation (AF), mean platelet volume (MPV), and apnea hypopnea index (AHI) in patients who have obstructive sleep apnea syndrome (OSAS). We enrolled patients who had OSAS with either AF or normal sinus rhythm (NSR). We divided 90 patients (aged 50-80 years) into 2 groups: group 1 consisted of 40 patients with OSAS having AF and group 2 of 50 patients with OSAS having NSR. Mean platelet volume was higher in patients with AF than in those with NSR (9.8 ± 0.6 vs 8.4 ± 0.6 fL; P < .001). The MPV and AHI were substantial variables associated with AF (odds ratio [OR] = 2.41; 95% confidence interval [CI], 1.36-5.26; P < .004 and OR = 1.91; 95% CI, 1.26-3.32; P = .02). Elevated MPV value of ≥9.4 fL is associated with AF (70% sensitivity and 63% specificity). More research is needed to establish the clinical relevance of this association.

Plasma urotensin II and neurokinin B levels in acute myocardial infarction and stable coronary artery disease.

OBJECTIVE: This aim of the study is to investigate whether there are possible plasma urotensin-II (U-II) and neurokinin B (NKB) level changes in patients with acute myocardial infarction (AMI) or not and plasma urotensin-II (U-II) and neurokinin B (NKB) level changes in patients with acute myocardial infarction (AMI) and stable coronary artery disease (CAD) and to evaluate whether there is any relationship between these changes and the pathogenesis of these diseases. METHODS: This is a prospective case-control study. Three groups were formed from randomly admitted patients with AMI, stable CAD, and controls. Biochemical parameters and U-II and NKB levels were measured. Patients with congestive heart failure, chronic hepatic and renal failure, severe cardiac valve disease, and severe pulmonary hypertension were excluded from the study. The normality of the data was evaluated using the Kolmogorov-Smirnov test. We compared the three groups with one-way ANOVA and Tukey test (Kruskal-Wallis test and Mann-Whitney U test). RESULTS: Compared with controls (n=31) and CAD patients (n=32), AMI patients (n=32) had lower U-II and NKB levels. In cases of stable CAD, U-II and NKB levels were similar. A positive correlation was found between U-II and NKB (r=0.720; p=0.000). U-II and NKB were poorly correlated with left ventricle ejection fraction but not with C-reactive protein. CONCLUSION: We found that U-II and NKB levels were lower in patients with AMI in than those with CAD or the control group. According to our findings, the decreased U-II and NKB levels were related to complicated atherosclerotic events.

Mean platelet volume in patients with obstructive sleep apnea and its relationship with simpler heart rate derivatives.

Some studies show increased mean platelet volume (MPV) in obstructive sleep apnea (OSA). The aim of this study was to evaluate MPV in OSA patients without cardiovascular risk factors and the possible association of heart rate derivatives with MPV. A total of 82 patients (aged 30-70 years) were divided into 2 groups according to the presence of either OSA or non-OSA as the control group. The OSA group consisted of 52 patients and the control group consisted of 30 subjects. Neither group was significantly different in terms of MPV values as well as heart rate (HR) derivatives such as minimum HR, maximum HR, the difference between maximum HR and minimum HR, mean HR, and heart rate performance index (HRPI) [(HR max. - HR min.)/HR mean] (P > 0.05 for all variables). In multivariate analysis, platelet count and percentages of recording time spent at arterial oxygen saturation < 90% significant variables are associated with MPV (ß ± SE: -0.004 ± 0.002, 95% CI, -0.008 to -0.001; P = 0.034) and (ß ± SE: 2.93 ± 1.93, 95% CI, 0.167 to 5.69; P = 0.038). Consequently, our findings predominantly suggest that there is a casual and reciprocal interaction between MPV and autonomic activation.

Heart rate recovery may predict the presence of coronary artery disease.

OBJECTIVE: We investigated whether post-exercise first minute abnormal heart rate recovery (HRR1) helps to predict the presence and severity of CAD, because of some confounding data. METHODS: A cross-sectional, retrospective study was performed. Two hundred individuals were included. Gensini scores and the number of coronary artery involvements were used to evaluate the severity of CAD. Student's t-test, Mann-Whitney U test and chi-square test were used for the analysis continuous and categorical data. Spearman's correlation analysis was used to determine whether there is correlation between Gensini scoring and HRR1. Univariate and multivariate logistic regression were used to determine predictors for abnormal HRR1. ROC curve analysis was performed to detect the best sensitivity and specificity value of HRR1 in predicting CAD presence. RESULTS: Seventy subjects (35%) did not have CAD, and CAD was present in 130 patients (65%). HRR1 ≤21 beats with ROC analysis was determined to be the best cut off point. After adjustment between the two groups in terms of age, gender, diabetes, hypertension, dyslipidemia or smoking (all p>0.05), there was relationship CAD presence and abnormal HRR1 (OR=2.1, 95% CI: 1.1-3.9, p=0.02), but not between CAD severity and HRR1 (r=-0.13, p=0.112). The sensitivity, specificity, and the positive and negative predictive values of abnormal HRR1 ≤21 beats at first minute for predicting CAD presence were 76.1%, 41.3% (AUC=0.588, CI 95%: 0.517-0,657, p=0.039), 70.7% and 48.3%, respectively. CONCLUSION: In the study abnormal HRR1 predicted the presence of CAD, but not the severity of it.

Serum fetuin-A levels are associated with carotid intima-media thickness in patients with normotensive chronic obstructive pulmonary disease.

BACKGROUND: There are contradictory reports about the relationship between fetuin-A and atherosclerotic process. Coronary artery disease is the most important cause of mortality in patients with chronic obstructive pulmonary disease (COPD). We aimed to investigate the association of serum fetuin-A level with mean carotid intima-media thickness (cIMT) and ankle-brachial index (ABI) in COPD. METHODS: We evaluated the association of serum fetuin-A level, mean cIMT and ABI in normotensive subjects with COPD (n = 65) and with non-COPD (n = 50). RESULTS: Fetuin-A level was significantly lower (63.5 ± 19.8 ng/mL, 72.9 ± 16.2 ng/mL, p = 0.035) and C-reactive protein level higher (4 [1-10] vs. 3 [1-12] mg/dL, p = 0.034) in COPD patients than the control group. Compared to controls, fetuin-A level was significantly lower (63.5 ± 19.8 ng/mL, 72.9 ± 16.2 ng/mL, p = 0.035) and mean cIMT higher (0.69 [0.50-0.98] vs. 0.62 [0.44-0.98] mm, p = 0.034, respectively) in the COPD group. There was a significant negative correlation between mean cIMT and fetuin-A levels (r = -0.320, p = 0.032). Age (b ± SE: 0.002 ± 0.001, p = 0.008) and fetuin-A (b ± SE: -0.002 ± 0.001, p = 0.035) were decisive for the mean cIMT. CONCLUSIONS: There are increased cIMT values, decreased fetuin-A levels, but unchanged ABI values in patients with normotensive COPD. Age and fetuin-A were predictors for cIMT, while fetuin-A was negatively correlated with cIMT.

Maximal Exercise-Corrected QT as a Predictor of Coronary Artery Disease: Comparison of Simpler Heart Rate Corrections.

BACKGROUND AND OBJECTIVES: The relationship between QT prolongation and myocardial ischemia is widely known. Due to the limited value of ST depression, we aimed to evaluate, by using four simpler heart rate corrections (Bazett, Framingham, Fridericia and Hodges), the value of maximal exercise-QTc prolongation in the diagnosis of coronary artery disease (CAD) presence and severity. SUBJECTS AND METHODS: We enrolled 234 subjects (mean age 57.3±9 years, 143 men) who had undergone exercise testing and coronary angiography due to a suspicion of CAD in the study. Evaluating CAD severity with Gensini scoring, the CAD group (n=122) and controls with non-CAD were compared in terms of corrected QT duration at maximal exercise. RESULTS: Age, gender, hypertension, dyslipidemia, smoking, exercise duration, resting, and peak heart rate were similar between the two groups (all p>0.05). The CAD group had higher raw QT values than the controls {268 (169-438) vs. 240 (168-348), p<0.001}. Although Framingham QTc of ≥350 ms and Fridericia QTc of ≥340 ms were seen to be useful for the diagnosis of CAD, there was no additive diagnostic value of exercise QTc in addition to ST depression. Maximal exercise-QTc Bazett (r=0.163, p=0.01), Framingham (r=0.239, p=0.001), and Fridericia (r=0.206, p=0.001) equations were weakly positively correlated with Gensini scoring. CONCLUSION: The patients with CAD have longer QTc intervals at peak heart rates during exercise. This finding provides insufficient evidence to support routine incorporation of QTc at peak heart rates into exercise test interpretation.

Effect of lifestyle modifications on diastolic functions and aortic stiffness in prehypertensive subjects: a prospective cohort study.

OBJECTIVE: Prehypertension is one of the primary causes of major cardiovascular events independent from other cardiovascular risk factors. The aim of the study was to evaluate the effect of therapeutic lifestyle modifications (LSMs) on cardiac diastolic function and aortic stiffness in prehypertensive subjects. METHODS: This study designed as a prospective cohort study. Sixty-one prehypertensive adults were included in this study. The goals of LMS were weight loss of at least 5 kg in subjects with a BMI ≥25 kg/m² and moderate-intensity physical activity at least 180 minutes per week. We evaluated left ventricular (LV) diastolic function and aortic stiffness parameters at baseline and after 6 months by conventional and tissue Doppler imaging (TDI) echocardiography. Statistical analyses were performed using Wilcoxon-signed rank test and the paired sample t test. RESULTS: Transmitral early velocity (E), the ratio of E to transmitral late velocity (E/A), TDI diastolic early septal velocity (septal E), TDI systolic septal velocity (septal S), TDI early lateral velocity (lateral E), the ratio of septal E to TDI late septal (septal A) velocity (septal E/A) and the ratio of lateral E to late lateral (lateral A) velocity (lateral E/A) were found to be significantly increased after the LSMs (p<0.05 for all). The beta stiffness index was decreased (12.07 vs. 6.33; p<0.001) and the aortic compliance (0.02 cm/mmHg vs. 0.05 cm/mmHg; p<0.001) and the aortic strain (3.28% vs. 7.02%; p<0.001) were increased significantly after the LSMs. CONCLUSION: LSMs improve conventional and TDI echocardiographic parameters and aortic stiffness measurements in subjects with prehypertension.