Association of Geomagnetic Disturbances and Suicide Attempts in Taiwan, 1997-2013: A Cross-Sectional Study.

BACKGROUND: A previous study in Japan found that monthly mean K index values were related to the monthly number of male, but not female, suicides. Correlations between geomagnetic disturbances and suicide/depression have also been reported in countries such as Canada, South Africa, Finland, Australia, Russia, and Japan. We have previously shown that stronger geomagnetism is linked to a higher standardized mortality ratio for suicide. To date, however, no published studies have reported the correlation between geomagnetic disturbances and suicide attempts in Taiwan. METHODS: Data on the monthly number of suicide attempts in Taiwan from January 1997 to December 2013 were obtained. We performed a multivariable analysis, with the number of suicide attempts as the response variable and monthly Kp10 index, F10.7 index, sulfur dioxide, carbon monoxide, ozone, fine particulate matter (PM2.5), temperature, humidity, unemployment rate, and cosmic rays as the explanatory variables. RESULTS: The multivariable analysis showed that Kp10 index, temperature, humidity, unemployment rate, and cosmic rays were associated with the number of male suicide attempts and that Kp10 index, F10.7 index, carbon monoxide, temperature, humidity, and unemployment rate were associated with the number of female suicide attempts. CONCLUSION: This is the first article reporting statistically significant relationships between the monthly number of male and female suicide attempts and the monthly mean Kp10 value in Taiwan.

Regulation of the circadian rhythmic expression of Sglt1 in the mouse small intestine through histone acetylation and the mRNA elongation factor, BRD4-P-TEFb.

Jejunal sodium/glucose co-transporter (Sglt1) displays circadian expression. The jejunum was collected every 4 h from mice, and we examined histone acetylation and binding of bromodomain-containing protein-4 (BRD4) around of the gene. Histone acetylation increased in the transcribed region of Sglt1 prior to induction of the gene. Furthermore, the binding of mRNA elongation factor around the gene showed circadian rhythm.

Decline in estimated glomerular filtration rate is associated with risk of end-stage renal disease in type 2 diabetes with macroalbuminuria: an observational study from JDNCS.

BACKGROUND: There is increased interest in surrogate endpoints for clinical trials of chronic kidney disease. METHODS: In this nationwide observational study of 456 patients with type 2 diabetes and clinically suspected diabetic nephropathy followed for a median of 4.2 years, we evaluated the association between estimated glomerular filtration rate (eGFR) and albuminuria at baseline or during follow-up and risk of ESRD. RESULTS: Low eGFR (<60 mL/min/1.73 m2) and macroalbuminuria at enrollment were independently associated with risk of ESRD. In patients with macroalbuminuria, both ≤-50% change and -50 to -30% change in eGFR over 1 and 2 years were predictive of ESRD. The higher cut point (≥50% decline in eGFR) was more strongly predictive but less common. Remission of macroalbuminuria to normo-/microalbuminuria at 1 and 2 years was associated with a lower incidence of ESRD than no remission; however, it was not a determinant for ESRD independently of initial eGFR and initial protein-to-creatinine ratio. CONCLUSION: These results suggest that a ≥30% decline in eGFR over 1 or 2 years adds prognostic information about risk for ESRD in patients with type 2 diabetes and macroalbuminuria, supporting the consideration of percentage decline in eGFR as a surrogate endpoint among macroalbuminuric cases in type 2 diabetes. On the other hand, our study suggests that additional analyses on the relationship between remission of macroalbuminuria and risk of ESRD are needed in type 2 diabetes.

Mitochondrial-Targeted Antioxidant Maintains Blood Flow, Mitochondrial Function, and Redox Balance in Old Mice Following Prolonged Limb Ischemia.

Aging is a major factor in the decline of limb blood flow with ischemia. However, the underlying mechanism remains unclear. We investigated the role of mitochondrial reactive oxygen species (ROS) with regard to limb perfusion recovery in aging during ischemia. We performed femoral artery ligation in young and old mice with or without treatment with a scavenger of mitochondrial superoxide, MitoTEMPO (180 µg/kg/day, from pre-operative day 7 to post-operative day (POD) 21) infusion using an implanted mini-pump. The recoveries of cutaneous blood flow in the ischemic hind limb were lower in old mice than in young mice but were improved in MitoTEMPO-treated old mice. Mitochondrial DNA damage appeared in ischemic aged muscles but was eliminated by MitoTEMPO treatment. For POD 2, MitoTEMPO treatment suppressed the expression of p53 and the ratio of Bax/Bcl2 and upregulated the expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in ischemic aged skeletal muscles. For POD 21, MitoTEMPO treatment preserved the expression of PGC-1α in ischemic aged skeletal muscle. The ischemic soleus of old mice showed a lower mitochondrial respiratory control ratio in POD 21 compared to young mice, which was recovered in MitoTEMPO-treated old mice. Scavenging of mitochondrial superoxide attenuated mitochondrial DNA damage and preserved the mitochondrial respiration, in addition to suppression of the expression of p53 and preservation of the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) in ischemic skeletal muscles with aging. Resolution of excessive mitochondrial superoxide could be an effective therapy to recover blood flow of skeletal muscle during ischemia in senescence.

Statistical Evaluations of Variations in Dairy Cows' Milk Yields as a Precursor of Earthquakes.

Previous studies have provided quantitative data regarding unusual animal behavior prior to earthquakes; however, few studies include long-term, observational data. Our previous study revealed that the milk yields of dairy cows decreased prior to an extremely large earthquake. To clarify whether the milk yields decrease prior to earthquakes, we examined the relationship between earthquakes of various magnitudes and daily milk yields. The observation period was one year. In the results, cross-correlation analyses revealed a significant negative correlation between earthquake occurrence and milk yields approximately three weeks beforehand. Approximately a week and a half beforehand, a positive correlation was revealed, and the correlation gradually receded to zero as the day of the earthquake approached. Future studies that use data from a longer observation period are needed because this study only considered ten earthquakes and therefore does not have strong statistical power. Additionally, we compared the milk yields with the subionospheric very low frequency/low frequency (VLF/LF) propagation data indicating ionospheric perturbations. The results showed that anomalies of VLF/LF propagation data emerged prior to all of the earthquakes following decreases in milk yields; the milk yields decreased earlier than propagation anomalies. We mention how ultralow frequency magnetic fields are a stimulus that could reduce milk yields. This study suggests that dairy cow milk yields decrease prior to earthquakes, and that they might respond to stimuli emerging earlier than ionospheric perturbations.

Resolution of mitochondrial oxidant stress improves aged-cardiovascular performance.

BACKGROUND: Senescence is a major factor that increases oxidative stress in mitochondria, which contributes toward the pathogenesis of heart disease. However, the effect of antioxidant therapy on cardiac mitochondria in aged-cardiac performance remains elusive. OBJECTIVES: We postulated that the mitochondrial targeting of superoxide scavenging would have benefits in the aged heart. METHODS AND RESULTS: Generation of superoxide in the mitochondria and nicotinamide adenine dinucleotide phosphate oxidase activity increased in the heart of old mice compared with that in young mice. In old mice treated with a mitochondria-targeted antioxidant MitoTEMPO (180 µg/kg/day, 28 days) co-infusion using a subcutaneously implanted minipump, levels of superoxide in the mitochondria and nicotinamide adenine dinucleotide phosphate oxidase activity as well as hydrogen peroxide decreased markedly in cardiomyocytes. Treatment with MitoTEMPO in old mice improved the systolic and diastolic function assessed by echocardiography. Endothelium-dependent vasodilation in isolated coronary arteries and endothelial nitric-oxide synthase phosphorylation were impaired in old mice compared with that in young mice and were improved by MitoTEMPO treatment. Mitochondria from the old mice myocardium showed lower rates of complex I-dependent and II-dependent respiration compared with that from young mice. Supplementation of MitoTEMPO in old mice improved the respiration rates and efficiency of ATP generation in mitochondria to a level similar to that of young mice. CONCLUSION: Resolution of oxidative stress in mitochondria by MitoTEMPO in old mice restored cardiac function and the capacity of coronary vasodilation to the same magnitude observed in young mice. An antioxidant strategy targeting mitochondria could have a therapeutic benefit in heart disease with senescence.

Associations of dipeptidyl peptidase-4 inhibitors with mortality in hospitalized heart failure patients with diabetes mellitus.

BACKGROUND: Heart failure (HF) and diabetes mellitus (DM) often co-exist. Treatment of DM in HF patients is challenging because some therapies for DM are contraindicated in HF. Although previous experimental studies have reported that dipeptidyl peptidase-4 (DPP-4) inhibitors improve cardiovascular function, whether DPP-4 inhibition improves mortality of HF patients with DM remains unclear. Therefore, we examined the impact of DPP-4 inhibition on mortality in hospitalized HF patients using propensity score analyses. METHODS AND RESULTS: We performed observational study analysed by propensity score method with 962 hospitalized HF patients. Of these patients, 293 (30.5%) had DM, and 122 of these DM patients were treated with DPP-4 inhibitors. Propensity scores for treatment with DPP-4 inhibitors were estimated for each patient by logistic regression with clinically relevant baseline variables. The propensity-matched 1:1 cohorts were assessed based on propensity scores (DPP-4 inhibitors, n = 83, and non-DPP-4 inhibitors, n = 83). Kaplan-Meier analysis in the propensity score-matched cohort demonstrated that cardiac and all-cause mortality was significantly lower in the DPP-4 inhibitor group than in the non-DPP-4 inhibitor group (cardiac mortality: 4.8% vs. 18.1%, P = 0.015; all-cause mortality: 14.5% vs. 41.0%, P = 0.003, by a log-rank test). In the multivariable Cox proportional hazard analyses, after adjusting for other potential confounding factors, the use of DPP-4 inhibitors was an independent predictor of all-cause mortality (pre-matched cohort: hazard ratio 0.467, P = 0.010; post-matched cohort: hazard ratio 0.370, P = 0.003) in HF patients with DM. CONCLUSIONS: Our data suggest that DPP-4 inhibitors may improve cardiac and all-cause mortality in hospitalized HF patients with DM.

Senescence marker protein-30 deficiency impairs angiogenesis under ischemia.

Aging decreases collateral-dependent flow recovery following acute arterial obstruction. However, the mechanisms are partially understood, therefore critical management has been lacked in clinical setting. Senescence marker protein-30 (SMP30) is a novel aging marker, which is assumed to act as an anti-aging factor in various organs. Therefore, we studied the effect of SMP30 on ischemia-induced collateral growth in SMP30 knockout (KO) mice, young and old C57BL/6 mice. The SMP30 expression in gastrocnemius tissue was decreased in old mice compared to that of young mice. The recovery of cutaneous blood flow in hind limb after femoral artery ligation and tissue capillary density recoveries were suppressed in SMP30 KO and old mice compared to those in young mice. Nitric oxide generation induced by l-arginine and GSH/GSSG in aorta of SMP30 KO and old mice were lower than those in young mice. The levels of NADPH oxidase activity and superoxide production in the ischemic tissue were higher in SMP30 KO and old mice than in young mice. The phosphorylated eNOS and Akt levels and VEGF levels in ischemic muscle were lower in SMP30 KO and old mice than in young mice. Deficiency of SMP30 exacerbates oxidative stress related to NADPH oxidase activity enhancement and impairs eNOS activity, which leads to rarefaction of angiogenesis induced by ischemia. These results suggest that SMP30 plays a key role in disrupting collateral growth under ischemia in aging.

Predominance of Abdominal Visceral Adipose Tissue Reflects the Presence of Aortic Valve Calcification.

Background. Aortic valve calcification (AVC) is a common feature of aging and is related to coronary artery disease. Although abdominal visceral adipose tissue (VAT) plays fundamental roles in coronary artery disease, the relationship between abdominal VAT and AVC is not fully understood. Methods. We investigated 259 patients who underwent cardiac and abdominal computed tomography (CT). AVC was defined as calcified lesion on the aortic valve by CT. %abdominal VAT was calculated as abdominal VAT area/total adipose tissue area. Results. AVC was detected in 75 patients, and these patients showed higher %abdominal VAT (44% versus 38%, p < 0.05) compared to those without AVC. When the cutoff value of %abdominal VAT was set at 40.9%, the area under the curve to diagnose AVC was 0.626. Multivariable logistic regression analysis showed that age (OR 1.120, 95% CI 1.078-1.168, p < 0.01), diabetes (OR 2.587, 95% CI 1.323-5.130, p < 0.01), and %abdominal VAT (OR 1.032, 95% CI 1.003-1.065, p < 0.05) were independent risk factors for AVC. The net reclassification improvement value for detecting AVC was increased when %abdominal VAT was added to the model: 0.5093 (95% CI 0.2489-0.7697, p < 0.01). Conclusion. We determined that predominance of VAT is associated with AVC.

Relationship of hyperuricemia with mortality in heart failure patients with preserved ejection fraction.

Serum uric acid is a predictor of cardiovascular mortality in heart failure with reduced ejection fraction. However, the impact of uric acid on heart failure with preserved ejection fraction (HFpEF) remains unclear. Here, we investigated the association between hyperuricemia and mortality in HFpEF patients. Consecutive 424 patients, who were admitted to our hospital for decompensated heart failure and diagnosed as having HFpEF, were divided into two groups based on presence of hyperuricemia (serum uric acid ≥7 mg/dl or taking antihyperuricemic agents). We compared patient characteristics, echocardiographic data, cardio-ankle vascular index, and cardiopulmonary exercise test findings between the two groups and prospectively followed cardiac and all-cause mortality. Compared with the non-hyperuricemia group (n = 170), the hyperuricemia group (n = 254) had a higher prevalence of hypertension (P = 0.013), diabetes mellitus (P = 0.01), dyslipidemia (P = 0.038), atrial fibrillation (P = 0.001), and use of diuretics (P < 0.001). Cardio-ankle vascular index (8.7 vs. 7.5, P < 0.001) and V̇e/V̇co2 slope (34.9 vs. 31.9, P = 0.02) were also higher. In addition, peak V̇o2 (14.9 vs. 17.9 ml·kg(-1)·min(-1), P < 0.001) was lower. In the follow-up period (mean 897 days), cardiac and all-cause mortalities were significantly higher in those with hyperuricemia (P = 0.006 and P = 0.004, respectively). In the multivariable Cox proportional hazard analyses after adjustment for several confounding factors including chronic kidney disease and use of diuretics, hyperuricemia was an independent predictor of all-cause mortality (hazard ratio 1.98, 95% confidence interval 1.036-3.793, P = 0.039). Hyperuricemia is associated with arterial stiffness, impaired exercise capacity, and high mortality in HFpEF.

Beneficial Effects of Positive Airway Pressure Therapy for Sleep-Disordered Breathing in Heart Failure Patients With Preserved Left Ventricular Ejection Fraction.

BACKGROUND: Right-heart dysfunction is associated with poor prognosis in heart failure with preserved left ventricular ejection fraction (HFpEF). It remains unclear whether sleep-disordered breathing (SDB) treatment using positive airway pressure (PAP) improves right-heart and pulmonary function and exercise capacity and reduces mortality rates of HFpEF patients. HYPOTHESIS: PAP may improve right-heart and pulmonary function, exercise capacity and prognosis in HFpEF patients with SDB. METHODS: One hundred nine consecutive patients with HFpEF (left ventricular ejection fraction >50%) and moderate to severe SDB (apnea-hypopnea index ≥15/h) treated with medications were divided into 2 groups: 31 patients with PAP (PAP group) and 78 patients without PAP (non-PAP group). Right ventricular fractional area change (RV-FAC), tricuspid valve regurgitation pressure gradient (TR-PG), tricuspid valve E/E', forced expiratory volume in 1 second/forced vital capacity (FEV1 /FVC), percentage of vital capacity, and peak VO2 were determined before and 6 months later, and all-cause mortality was followed up for 916 days. RESULTS: All parameters improved in the PAP group (RV-FAC, 36.0% -46.5%; TR-PG, 31.1 mm Hg-22.4 mm Hg; tricuspid valve E/E', 7.8-5.1; FEV1 /FVC, 83.9%-89.8%; percentage of vital capacity, 83.5%-89.9%; and peak VO2 , 16.6 mL/kg/min-19.6 mL/kg/min; P <0.05, respectively) but not in the non-PAP group. Importantly, all-cause mortality was significantly lower in the PAP group than in the non-PAP group (0% vs 12.8%; log-rank P = 0.014). CONCLUSIONS: Positive airway pressure improves right-heart and pulmonary function and exercise capacity and may reduce all-cause mortality in patients with HFpEF and SDB.

Association of Hypocalcemia With Mortality in Hospitalized Patients With Heart Failure and Chronic Kidney Disease.

BACKGROUND: Chronic kidney disease--mineral and bone disorders (CKD-MBD) are associated with vascular calcification and abnormal electrolytes that lead to cardiovascular disease and mortality. CKD-MBD is identified by imbalances in serum calcium (Ca), phosphate, and parathyroid hormone (PTH). Although the relation of phosphate and PTH with the prognosis of HF patients has been reported, the association of Ca with prognosis in patients with heart failure (HF) and CKD remains unclear. METHODS AND RESULTS: We examined 191 patients admitted for HF and CKD (estimated glomerular filtration rate <60 mL min(-1) 1.73 m(-2)), and they were divided into 2 groups based on levels of corrected Ca: low Ca (Ca <8.4 mg/dL; n = 32) and normal-high Ca (8.4 ≤Ca; n = 159). We compared laboratory and echocardiographic findings, as well as followed cardiac and all-cause mortality. The low-Ca group had 1) higher levels of alkaline phosphatase (308.9 vs. 261.0 U/L; P = .026), 2) lower levels of 1,25-dihydroxy vitamin D (26.1 vs. 45.0 pg/mL; P = .011) and hydrogen carbonate (22.4 vs. 24.5 mmol/L; P = .031), and 3) a tendency to have a higher PTH level (87.5 vs. 58.6 pg/mL; P = .084). In contrast, left and right ventricular systolic function, estimated glomerular filtration rate, urine protein, phosphate, sodium, potassium, magnesium, and zinc did not differ between the 2 groups. In the Kaplan-Meier analysis, cardiac and all-cause mortality were significantly higher in the low-Ca group than in the normal-high-Ca group (P < .05). In the multivariable Cox proportional hazard analyses, hypocalcemia was an independent predictor of all-cause mortality in HF and CKD patients (P < .05). CONCLUSIONS: Hypocalcemia was an independent predictor of all-cause mortality in HF and CKD patients.

Impact of peripheral artery disease on prognosis in hospitalized heart failure patients.

BACKGROUND: The impact of peripheral artery disease (PAD) on heart failure (HF) prognosis remains unclear. METHODS AND RESULTS: A total of 388 consecutive decompensated HF patients were divided into 2 groups based on the presence of PAD: HF with PAD (PAD group, n=101, 26.0%) and HF without PAD (non-PAD group, n=287, 74.0%). We compared clinical features, echocardiographic parameters, cardiopulmonary exercise testing results, laboratory findings, as well as cardiac, non-cardiac, and all-cause mortality between the 2 groups. The PAD group, as compared with the non-PAD group, had (1) higher prevalence of coronary artery disease (40.6 vs. 27.5%, P=0.011) and cerebrovascular disease (34.7 vs. 18.2%, P=0.001); (2) higher tumor necrosis factor-α (1.82 vs. 1.49 pg/ml, P=0.023), C-reactive protein (0.32 vs. 0.19 mg/dl, P=0.045), and troponin T (0.039 vs. 0.021 ng/ml, P=0.019); (3) lower LVEF (42.4 vs. 48.5%, P<0.001); (4) lower peak V̇O2(13.4 vs. 15.9 ml·kg(-1)·min(-1), P=0.001); and (5) higher V̇E/V̇CO2slope (38.8 vs. 33.7, P<0.001). On Kaplan-Meier analysis, cardiac, non-cardiac, and all-cause mortality were significantly higher in the PAD group than in the non-PAD group (P<0.05, respectively). On Cox proportional hazard analysis after adjusting for confounding factors, PAD was an independent predictor of cardiac and all-cause mortality (P<0.05, respectively) in HF patients. CONCLUSIONS: PAD was common and an independent predictor of cardiac and all-cause mortality in HF patients.

Epicardial adipose tissue reflects the presence of coronary artery disease: comparison with abdominal visceral adipose tissue.

Accumulation of visceral adipose tissue is associated with a risk of coronary artery disease (CAD). The aim of this study was to examine whether different types of adipose tissue depot may play differential roles in the progression of CAD. Consecutive 174 patients who underwent both computed tomography (CT) and echocardiography were analyzed. Cardiac and abdominal CT scans were performed to measure epicardial and abdominal visceral adipose tissue (EAT and abdominal VAT, resp.). Out of 174 patients, 109 and 113 patients, respectively, presented coronary calcification (CC) and coronary atheromatous plaque (CP). The EAT and abdominal VAT areas were larger in patients with CP compared to those without it. Interestingly, the EAT area was larger in patients with CC compared to those without CC, whereas no difference was observed in the abdominal VAT area between patients with CC and those without. Multivariable logistic regression analysis revealed that the presence of echocardiographic EAT was an independent predictor of CP and CC, but the abdominal VAT area was not. These results suggest that EAT and abdominal VAT may play differential pathological roles in CAD. Given the importance of CC and CP, we should consider the precise assessment of CAD when echocardiographic EAT is detected.

Impact of sleep-disordered breathing on myocardial damage and metabolism in patients with chronic heart failure.

Sleep-disordered breathing (SDB) has a critical association with mortality and morbidity of patients with chronic heart failure (CHF). Troponin T is a marker of ongoing myocardial damage and predicts adverse clinical outcomes in patients with CHF. Carnitine plays an important role in the utilization of fatty acids in the myocardium. It has been reported that myocardial carnitine levels decrease in the failing heart. We hypothesized that plasma troponin T and carnitine are increased due to the leakage from damaged cardiomyocytes or the alteration of myocardial metabolism in CHF patients with SDB. We examined the relation of plasma troponin T and carnitine levels with severity of SDB in CHF. We used portable sleep monitor and measured the apnea-hypopnea index (AHI), plasma levels of high-sensitive troponin T and carnitine in 131 CHF patients. These patients were divided into three groups based on AHI: group A (None-mild SDB AHI < 15/h, n = 45), group B (Moderate SDB 15 ≤ AHI < 30/h, n = 32) and group C (Severe SDB AHI ≥ 30/h, n = 54). Levels of high-sensitive troponin T and plasm total carnitine were significantly higher in group C than in groups A and B [high-sensitive troponin T; group A 0.009 (0.005-0.016), group B 0.012 (0.006-0.021), group C 0.021 (0.011-0.039) ng/ml, total carnitine; group A 61.0 ± 15.1, group B 65.0 ± 13.5, group C 73.3 ± 17.5 µmol/l, P < 0.01 vs. group A and P < 0.05 vs. group B, respectively]. Furthermore, in the multiple regression analysis, the independent factors to determine plasma levels of log (high-sensitive troponin T) were high-sensitive C-reactive protein and AHI, and the independent factors to determine plasma levels of carnitine were glomerular filtration rate and AHI. The present study suggests that SDB is associated with latent myocardial damage and alteration of myocardial carnitine metabolism in patients with CHF, presented by higher circulating troponin T and carnitine levels.

Serum cholinesterase is an important prognostic factor in chronic heart failure.

We determine the importance of indicators of nutrition including lymphocyte, total protein, albumin, cholinesterase and body mass index, and compare the prognostic significance in chronic heart failure (CHF). We examined consecutive 465 CHF patients (376 males, age 62 ± 14 years) who underwent cardiopulmonary exercise testing, echocardiography and blood examination including indicators of nutrition at the same time in our hospital. The patients were followed up [median period 766 days (interquartile range 500-1060)] to register cardiac deaths and rehospitalization due to worsening heart failure. There were 180 cardiac events during the follow-up periods. Patients with cardiac events had lower cholinesterase level than those without events (P < 0.001). On the receiver operating characteristic analysis, the best cut-off value for cholinesterase was 240 U/l (area under the curve 0.720). In the Kaplan-Meier analysis, patients with cholinesterase <240 U/l had significantly higher cardiac event rates than those with cholinesterase >240 U/l. Multivariable Cox proportional hazards model demonstrated that NYHA class III [hazard ratio (HR): 1.688, 95 % confidence interval (CI) 1.062-2.684, P = 0.027], eGFR (HR: 0.983, 95 % CI 0.971-0.995, P = 0.006), sodium concentration (HR: 0.947, 95 % CI 0.897-0.999, P < 0.046), log BNP (HR: 1.880, 95 % CI 1.509-2.341, P < 0.001), cholinesterase (HR: 0.996, 95 % CI 0.993-0.998, P = 0.002) and exertional periodic breathing (HR: 1.619, 95 % CI 1.098-2.388, P = 0.015) were independent factors to predict adverse clinical outcomes. Serum cholinesterase level was an important prognostic factor in CHF.

Comparisons of prognostic factors between young and elderly patients with chronic heart failure.

AIM: The purpose in the present study was to compare prognostic risk factors between older and younger chronic heart failure (CHF) patients. METHODS: We examined 598 consecutive CHF patients (476 men and 122 women, mean age 61.4 ± 14.3 years) who underwent cardiopulmonary exercise testing, echocardiography and blood examination. We divided the 598 patients into two groups: the elderly group (age ≥75 years, n = 123) and the young group (age <75, n = 475). We compared blood testing data, exercise capacity, cardiac function and prognosis between the two groups. Patients were followed up (median 782 days) to register cardiac deaths or rehospitalization as a result of worsening heart failure. RESULTS: Patients in the elderly group were associated with higher frequencies of atrial fibrillation and diuretic use than those in the young group. Patients in the elderly group had lower hemoglobin concentration, more impaired renal function, higher plasma B-type natriuretic peptide (BNP) levels, smaller left ventricular volume, longer deceleration time of early mitral wave and lower exercise capacity than those in the young group. There were 199 cardiac events during follow-up periods. As expected, Kaplan-Meier analysis showed that patients in the elderly group had higher cardiac event rates than those in the young group. In the young group, multivariable Cox hazard analysis showed that hemoglobin concentration, log BNP and peak VO(2) were independent predictors related to cardiac events. In contrast, in the elderly group, estimated glomerular filtration rate, atrial fibrillation and peak VO(2) were independent factors to predict adverse clinical outcomes. CONCLUSIONS: Prognostic factors were different between the elderly and young patients in CHF.

Impact of body mass index on mortality in heart failure patients.

BACKGROUND: Higher body mass index (BMI) is associated with incident heart failure (HF), but paradoxically associated with better prognosis, recognized as the obesity paradox in HF. However, the impact of BMI on detailed prognosis on HF and the mechanism of obesity paradox remain still unclear. MATERIALS AND METHODS: We researched consecutive 648 patients admitted for HF as follows: underweight (BMI < 18·5 kg/m(2) , n = 86), normal (18·5 ≤ BMI < 25, n = 380), overweight (25 ≤ BMI < 30, n = 147) and obese (30 ≤ BMI, n = 35) and compared the results from their laboratory tests and echocardiography. We also followed cardiac and all-cause mortality. RESULTS: Obese group had a higher prevalence of obesity-related comorbidity (hypertension, diabetes, dyslipidemia); however, tumour necrosis factor-α, adiponectin, troponin T and systolic pulmonary arterial pressure were higher in the underweight group than in the other groups (P < 0·05, respectively). Left and right ventricular systolic function did not differ among the groups. In the Kaplan-Meier analysis, cardiac and all-cause mortality progressively increased from obese to overweight, normal and underweight group. Importantly, in the Cox proportional hazard analyses after adjusting for known risk factors, BMI was an independent predictor of cardiac and all-cause mortality (P < 0·01, respectively) in HF patients. CONCLUSIONS: Body mass index was an independent predictor of cardiac death and all-cause mortality in HF patients. Furthermore, lower BMI was associated with higher circulating levels of tumour necrosis factor-α, adiponectin and troponin T and higher systolic pulmonary arterial pressure.

Liver dysfunction assessed by model for end-stage liver disease excluding INR (MELD-XI) scoring system predicts adverse prognosis in heart failure.

AIMS: Liver dysfunction due to heart failure (HF) is often referred to as cardiac or congestive hepatopathy. The composite Model for End-Stage Liver Disease excluding INR (MELD-XI) is a robust scoring system of liver function, and a high score is associated with poor prognosis in advanced HF patients with a heart transplantation and/or ventricular assist device. However, the impact of MELD-XI on the prognosis of HF patients in general remains unclear. METHODS AND RESULTS: We retrospectively analyzed 562 patients who were admitted to our hospital for the treatment of decompensated HF. A MELD-XI score was graded, and patients were divided into two groups based on the median value of MELD-XI score: Group L (MELD-XI <10, n = 289) and Group H (MELD-XI ≥10, n = 273). We compared all-cause mortality and echocardiographic findings between the two groups. In the follow-up period (mean 471 days), 104 deaths (62 cardiac deaths and 42 non-cardiac deaths) were observed. The event (cardiac death, non-cardiac death, all-cause death)-free rate was significantly higher in group L than in group H (logrank P<0.05, respectively). In the Cox proportional hazard analysis, a high MELD-XI score was found to be an independent predictor of cardiac deaths and all-cause mortality in HF patients. Regarding echocardiographic parameters, right atrial and ventricular areas, inferior vena cava diameter, and systolic pulmonary artery pressure were higher in group H than in group L (P<0.05, respectively). CONCLUSIONS: The MELD-XI scoring system, a marker of liver function, can identify high-risk patients with right heart volume overload, higher pulmonary arterial pressure and multiple organ failure associated with HF.