Epicardial adipose tissue is associated with cardiorespiratory fitness and hemodynamics among Japanese individuals of various ages and of both sexes.

Epicardial adipose tissue may affect hemodynamics and cardiorespiratory fitness as it is a metabolically active visceral adipose tissue and a source of inflammatory bioactive substances that can substantially modulate cardiovascular morphology and function. However, the associations between epicardial adipose tissue and hemodynamics and cardiorespiratory fitness remain unclear. This cross-sectional study aimed to examine the association between epicardial adipose tissue volume and hemodynamics, and cardiorespiratory fitness among Japanese individuals of various ages and of both sexes. Epicardial adipose tissue volume was measured in 120 participants (age, 21-85 years) by cardiac magnetic resonance imaging. To evaluate cardiorespiratory fitness, peak oxygen uptake was measured by cardiopulmonary exercise testing. Peak cardiac output and arteriovenous oxygen difference were calculated by impedance cardiography. The epicardial adipose tissue volume was significantly increased in middle-aged and older women. The epicardial adipose tissue volume was significantly and negatively correlated to peak cardiac output and peak oxygen uptake, regardless of age and sex; furthermore, epicardial adipose tissue showed a strong negative correlation with peak heart rate. Epicardial adipose tissue and peak cardiac output were significantly associated (ß = -0.359, 95% confidence interval, -0.119 to -0.049, p < 0.001), even after multivariate adjustment (R2 = 0.778). However, in the multiple regression analysis with peak oxygen uptake as a dependent variable, the epicardial adipose tissue volume was not an independent predictor. These data suggest that increased epicardial adipose tissue volume may be correlated with decreased peak oxygen uptake, which might have mediated the abnormal hemodynamics among Japanese people of various ages and of both sexes. Interventions targeting epicardial adipose tissue could potentially improve hemodynamics and cardiorespiratory fitness.

Epicardial adipose tissue is tightly associated with exercise intolerance in patients with type 2 diabetes mellitus with asymptomatic left ventricular structural and functional abnormalities.

AIMS: This study aimed to elucidate whether the volume of epicardial adipose tissue (EAT) is associated with left ventricular (LV) structural and functional abnormalities and exercise capacity in patients with type 2 diabetes mellitus (T2DM). METHODS: EAT thickness and LV structural and functional abnormality components (e.g., global longitudinal strain, E/e', LV mass index, relative wall thickness) were measured using echocardiography in 176 patients with asymptomatic stage A and B heart failure (SAHF and SBHF, respectively) and 62 healthy controls (HC). Peak oxygen uptake (peakVO2) was measured by using cardiopulmonary exercise testing. RESULTS: Even when matching study participants for age, sex, and body mass index, the EAT was thicker (HCs 5.5 ±â€¯1.2 versus SAHF 6.4 ±â€¯1.0 and SBHF 9.3 ±â€¯1.7 mm) and peakVO2 was lower (HC 24.1 ±â€¯3.3 versus SAHF 19.1 ±â€¯2.0 and SBHF 16.9 ±â€¯3.1 ml/kg/min) in the heart failure (HF) group than in the HC group (p < 0.001). EAT thickness (ß = -0.189, p < 0.001) and peakVO2 were significantly associated, even after adjusting for multivariates (R2 = 0.457). CONCLUSIONS: In T2DM patients with asymptomatic HF, EAT may be associated with LV structural and functional abnormalities and exercise intolerance.

Effectiveness of nocturnal home oxygen therapy to improve exercise capacity, cardiac function and cardiac sympathetic nerve activity in patients with chronic heart failure and central sleep apnea.

BACKGROUND: Central sleep apnea, often found in patients with chronic heart failure (CHF), has a high risk of poor prognosis. METHODS AND RESULTS: This study involved 20 patients with CHF (left ventricular ejection fraction (LVEF) <45%, M/F =19/1, age 65+/-10 years) and an apnea-hypopnea index (AHI) >5 times/h who were divided into 2 groups: 10 patients treated with nocturnal home oxygen therapy (HOT) and 10 patients without HOT (non-HOT). All patients had dilated cardiomyopathy and underwent overnight polysomnography, cardiopulmonary exercise testing, and nuclear cardiac examinations to evaluate AHI, exercise capacity according to the specific activity scale and oxygen uptake at anaerobic threshold and peak exercise (peak VO(2)). Cardiac function according to (99m)Tc-MIBI QGS, and the total defect score (TDS), H/M ratio and the washout rate (WR) on (123)I-metaiodobenzylguanidine (MIBG) imaging were calculated for all patients. As compared with the non-HOT group, the HOT group demonstrated a greater reduction in AHI (26.1+/-9.1 to 5.1+/-3.4), (123)I-MIBG TDS (31+/-8 to 25+/-9), and (123)I-MIBG WR (48+/-8% to 41+/-5%) and a greater increase in the specific activity scale (4.0+/-0.9 to 5.8+/-1.2 Mets), peak VO(2) (16.0+/-3.8 to 18.3+/-4.7 ml . min(-1) . kg(-1)), and LVEF (27+/-9% to 37+/-10%). CONCLUSIONS: HOT improves exercise capacity, cardiac function, and cardiac sympathetic nerve activity in patients with CHF and central sleep apnea.

Nitric oxide exhalation correlates with ventilatory response to exercise in patients with heart disease.

AIMS: It is controversial whether or not pulmonary nitric oxide (NO) production, reflected in the end-tidal alveolar NO concentration, is diminished in patients with heart failure. Since pulmonary perfusion is regulated by NO production, decreased NO production in the pulmonary vasculature is assumed to result in diminished lung perfusion and further increases in ventilation-perfusion mismatch. The aim of this study is to investigate whether exhaled NO correlates with both exercise-induced hyperpnea and exercise tolerance in patients with heart disease. METHODS AND RESULTS: Forty-two patients with heart disease were enrolled (history of prior myocardial infarction (n=19), dilated cardiomyopathy (n=2), hypertensive heart disease (n=5) and prior open-heart surgery (n=16)). During cardiopulmonary exercise testing, exhaled air was collected and end-tidal NO (ETNO) was measured using a chemiluminescent method. Peak ETNO was found to correlate positively with both ventilatory anaerobic threshold (r=0.468) and peak VO(2) (r=0.562). The VE-CO(2) slope, which reflects the ventilatory response to exercise, correlated negatively with peak ETNO (r=-0.588). CONCLUSION: These data indicate that NO exhalation correlates, inversely, with the ventilatory response to exercise and directly with exercise intolerance, although the weakness of the correlation coefficient suggests there may be other possible mechanisms.

Impedance cardiography and quantitative tissue Doppler echocardiography for evaluating the effect of cardiac resynchronization therapy: a case report.

An 83-year-old woman presented with dilated cardiomyopathy. Cardiac resynchronization therapy was performed. Two weeks later, cardiac output and ventricular wall motion were estimated using impedance cardiography and tissue Doppler echocardiography with and without pacing. Cardiac output increased from 3.5 to 4.5 l/min during biventricular pacing with a 120 msec atrioventricular interval. Intraventricular phase difference for contraction decreased from 190 to 150 msec. When the atrioventricular interval was 180 msec, cardiac output and phase difference became 4.6 l/min and 170 msec. These assessments were performed rapidly and non-invasively. New impedance cardiography and tissue Doppler echocardiography are useful to evaluate the effect of cardiac resynchronization therapy.

Left ventricular regional variations in myosin isoform shift in Dahl salt-sensitive hypertensive rats.

To evaluate the effects of chronic pressure overload on different parts of the left ventricle (LV), we examined a myosin isoform shift from V1 to V3 as a biochemical marker of LV hypertrophy in Dahl salt-sensitive (DS) rats. Six-week-old DS rats were fed an 8% (high salt, HS; n = 24) or a 0.3% (low salt, LS; n = 12) NaCl diet. After 2 or 4 weeks, the hearts were dissected and the LVs were separated into four parts (the base and mid-portion of the interventricular septum (IVS), and the base and mid-portion of the LV free wall) for isomyosin analysis. The myosin isoform shift was analyzed by pyrophosphate gel electrophoresis. Both blood pressure and LV/body weight ratio were clearly increased in the HS group. The myosin isoform shift from V1 to V3, which was measured as a decrease in the percentage of V1 isomyosin, was demonstrated only in the base of LV, with significant predominance in the IVS at 2 weeks and in all four parts at 4 weeks in the HS group. In the LS group, a myosin isoform shift was demonstrated only in the basal portion of the LV at 4 weeks. We concluded that, in rats with salt-induced hypertension, the myosin isoform shift from V1 to V3 starts at the base of the LV, and particularly at the base of the IVS, and then spreads across the entire LV. These results suggest that pressure overload from hypertension may be strongest at the base of the IVS, and that LV hypertrophy may originate at the IVS base.