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Physical activity (PA) in the daily life is strongly related to prognosis in patients with or at high risk of heart failure (HF). However, factors limiting habitual exercise and their prognostic impacts remain unknown in HF patients. We sent questionnaires asking factors limiting habitual exercise in the daily life to 8370 patients with Stage A/B/C/D HF in our nationwide registry and received valid responses from 4935 patients (mean age 71.8 years, 71.0% male). Among the 5 components consisting of “busyness”, “weak will”, “dislike, “socioeconomic reasons” and “diseases” in the questionnaires, “busyness” (34.5%) and “diseases” (34.7%) were the most frequently reported factors limiting habitual exercise, while “socioeconomic reasons” were the least (15.3%). Multiple Cox proportional hazard models indicated that “busyness”and “diseases” were associated with better (hazard ratio (HR) 0.53, 95% confidence interval (CI) 0.39–0.72, P  < 0.001) and worse prognosis (HR 1.57, 95% CI 1.21–1.98, P  < 0.001), respectively, while other components were not. Furthermore, it was noted that, while prognostic relevance of “busyness” limiting exercise did not differ by age or sex, negative impact of “diseases” was particularly evident in patients with age < 75 years ( P for interaction < 0.01). Factors limiting habitual exercise were associated with “busyness” and “diseases”, but not with “weak will”, “dislike, or “socioeconomic reasons”. While “busyness” was associated with better prognosis regardless of age and sex, “diseases” was associated with worse prognosis in younger populations. Thus, physicians may pay more attentions to the reasons that limit exercise in the daily lives of HF patients rather than the low amount of exercise itself.

We aimed to compare the usefulness of plasma levels of B-type natriuretic peptide (BNP) for long-term risk stratification among patients with heart failure (HF) with preserved left ventricular ejection fraction (LVEF) (HFpEF), borderline HFpEF, and HF with reduced LVEF (HFrEF) in the same HF cohort. In the CHART-2 Study ( N  = 10,219), we categorized 4301 consecutive Stage C/D HF patients (mean age 68.7 years, female 32.4%) into 3 groups: HFpEF (LVEF ≥ 50%, N  = 2893), borderline HFpEF (LVEF 40–50%, N  = 666), and HFrEF (LVEF ≤ 40%, N  = 742). During the median 6.3-year follow-up, all-cause deaths occurred in 887 HFpEF, 330 borderline HFpEF, and 330 HFrEF patients. Although median BNP levels increased from HFpEF, borderline HFpEF to HFrEF (85.3, 126 and 208 pg/ml, respectively, P  < 0.001), the relationship between log 2 BNP levels and the mortality risk was comparable among the 3 groups. As compared with patients with BNP < 30 pg/ml, those with 30–99, 100–299 and ≥ 300 pg/ml had comparably increasing mortality risk among the 3 groups (hazard ratio 2.5, 4.7 and 7.8 in HFpEF, 2.1, 4.2 and 7.0 in borderline HFpEF, and 3.0, 4.7 and 9.5 in HFrEF, respectively, all P  < 0.001). BNP levels have comparable prognostic impact among HFpEF, borderline HFpEF, and HFrEF patients.

This study examined the effects of pemafibrate, a selective peroxisome proliferator-activated receptor α agonist, on the serum biochemical parameters of male patients with coronary artery disease and metabolic syndrome (MetS). This was a post hoc analysis of a randomized, crossover study that treated hypertriglyceridemia with pemafibrate or bezafibrate for 24 weeks, followed by a crossover of another 24 weeks. Of the 60 patients enrolled in the study, 55 were male. Forty-one of 55 male patients were found to have MetS. In this sub-analysis, male patients with MetS (MetS group, n  = 41) and those without MetS (non-MetS group, n  = 14) were compared. The primary endpoint was a change in fasting serum triglyceride (TG) levels during pemafibrate therapy, and the secondary endpoints were changes in insulin resistance-related markers and liver function parameters. S erum TG levels significantly decreased (MetS group, from 266.6 to 148.0 mg/dL, p  < 0.001; non-MetS group, from 203.9 to 97.6 mg/dL, p  < 0.001); however, a percent change (%Change) was not significantly different between the groups (− 44.1% vs. − 51.6%, p  = 0.084). Serum insulin levels and homeostasis model assessment of insulin resistance significantly decreased in the MetS group but not in the non-MetS group. %Change in liver enzyme levels was markedly decreased in the MetS group compared with that in the non-MetS group (alanine aminotransferase, − 25.1% vs. − 11.3%, p  = 0.027; gamma-glutamyl transferase, − 45.8% vs. − 36.2%, p  = 0.020). In conclusion, pemafibrate can effectively decrease TG levels in patients with MetS, and it may be a more efficient drug for improving insulin resistance and liver function in such patients.

Patients with adult congenital heart disease (ACHD) are at increased risk of developing late cardiovascular complication. However, little is known about the predictive factors for long-term outcome. The Model for End-Stage Liver Disease eXcluding INR (MELD-XI) score was originally developed to assess cirrhotic patients and has the prognostic value for heart failure (HF) patients. In the present study, we examined whether the score also has the prognostic value in this population. We retrospectively examined 637 ACHD patients (mean age 31.0 years) who visited our Tohoku University hospital from 1995 to 2015. MELD-XI score was calculated as follows; 11.76 x ln(serum creatinine) + 5.11 x ln(serum total bilirubin) + 9.44. We compared the long-term outcomes between the high (≥10.4) and the low (<10.4) score groups. The cutoff value of MELD-XI score was determined based on the survival classification and regression tree (CART) analysis. The major adverse cardiac event (MACE) was defined as a composite of cardiac death, HF hospitalization, and lethal ventricular arrhythmias. During a mean follow-up period of 8.6 years (interquartile range 4.4-11.4 years), MACE was noted in 51 patients, including HF hospitalization in 37, cardiac death in 8, and lethal ventricular arrhythmias in 6. In Kaplan-Meier analysis, the high score group had significantly worse MACE-free survival compared with the low score group (log-rank, P<0.001). Multivariable Cox regression analysis showed that the MELD-XI score remained a significant predictor of MACE (hazard ratio 1.36, confidence interval 1.17-1.58, P<0.001) even after adjusting for patient characteristics, such as sex, functional status, estimated glomerular filtration rate, and cardiac function. Furthermore, CART analysis revealed that the MELD-XI score was the most important variable for predicting MACE. These results demonstrate that the MELD-XI score can effectively predict MACE in ACHD patients, indicating that ACHD patients with high MELD-XI score need to be closely followed.

Background We examined the effect of switching from angiotensin receptor-neprilysin inhibitor (ARNI) to angiotensin-receptor blocker (ARB) on plasma levels of natriuretic peptides and myocardial remodeling. Methods This is a prospective study that included 11 patients with heart failure (HF) treated with ARNI. The patients were divided into two groups: 5 patients who continued treatment with sacubitril/valsartan 194/206 mg/day (ARNI-continue group) and 6 patients who were switched to valsartan 160 mg/day (ARB-switch group). The primary endpoint was percent change (%Change) in plasma A-, B-, and N-terminal pro-B-type natriuretic peptide (ANP, BNP, and NT-proBNP) levels from the baseline to week 24. The secondary endpoint was the change in echocardiographic parameters related to myocardial remodeling from the baseline to week 24. Results ANP levels in the ARB-switch group significantly decreased (from 1155.7 ± 592.6 pg/mL to 231.6 ± 233.8 pg/mL, p  = 0.035), whereas those in the ARNI-continue group were not significant ( p  = 0.180). The %Change of decrease in ANP levels was significantly greater in the ARB-switch group than the ARNI-continue group (− 76.9% vs. −9.1%, p  = 0.009). BNP levels were not significantly different between the baseline and week 24 in both groups. NT-proBNP levels in the ARB-switch group increased from 1185.3 ± 835.6 pg/mL to 1515.2 ± 1213.5 pg/mL, although the changes were not statistically significant ( p  = 0.345). The %Change of increase in NT-proBNP levels was significantly greater in the ARB-switch group than the ARNI-continue group (57.9% vs. 17.3%, p  = 0.016). In the ARB-switch group, there was a significant increase in left ventricular (LV) end-systolic volume (from 41.3 ± 24.1 mL/m 2 to 71.4 ± 8.8 mL/m 2 , p  = 0.043) and LV peak-systolic wall stress (from 187.0 ± 42.7 × 10 3 dynes/cm 2 to 279.7 ± 34.1 × 10 3 dynes/cm 2 , p  = 0.012) from the baseline to week 24 and a trend toward a decrease in LV ejection fraction ( p  = 0.080). In the ARNI-continue group, no differences in echocardiographic parameters were observed from the baseline to week 24. Conclusion Switching from ARNI to ARB may worsen HF due to returning to myocardial remodeling induced by a sustained decline in ANP levels.

We herein report a case of sudden death in a 20s male who presented with fever 1 week before and with abdominal pain and vomiting 2 days before death. Laboratory findings at the time of death were suspected the onset of fulminant type 1 diabetes accompanied by diabetic ketoacidosis and acute renal failure. A postmortem blood examination at several sites showed elevated levels of glucose and β-hydroxybutyrate, lower levels of C-peptide, insulin, 1,5-anhydroglucitol, and HbA1c of less than 8.7% based on the diagnostic criteria of FT1DM. Furthermore, glucose levels in vitreous humor and cerebrospinal fluid were very high. These results showed reflecting antemortem hyperglycemia. Postmortem serum pancreatic enzyme levels of lipase and elastase 1 were high. Antibodies to insulin, insulinoma-associated antigen-2 (IA-2), and zinc transporter 8 (ZnT8) were negative, while antibodies to glutamic acid decarboxylase (GAD) slightly exceeded the reference range (< 1.5 U/mL). Immunostaining of insulin in pancreatic tissue showed no positive cells in contrast to glucagon. We presented that FT1DM was diagnosed even 3 days postmortem, as compared with the antemortem clinical examination.

Aims Prognostic impacts of serum uric acid (UA) levels in patients with chronic heart failure (CHF) remain inconclusive, especially for the whole range of serum UA levels. Methods and results In the Chronic Heart Failure Registry and Analysis in the Tohoku District‐2 (CHART‐2) study, we enrolled 4652 consecutive patients with CHF and classified them into four groups based on baseline serum UA levels by the Classification and Regression Tree: G1 (<3.8 mg/dL, N = 313), G2 (3.8–7.1 mg/dL, N = 3070), G3 (7.2–9.2 mg/dL, N = 1018), and G4 (>9.2 mg/dL, N = 251). Mean age was 71 ± 12, 69 ± 12, 68 ± 13, and 69 ± 15 years in G1, G2, G3, and G4, respectively (P < 0.001). During the median follow‐up of 6.3 years, in G1, G2, G3, and G4, 111 (35%), 905 (29%), 370 (36%), and 139 (55%) patients died and 79 (25%), 729 (24%), 300 (29%), and 115 (46%) experienced heart failure hospitalization, respectively (both P < 0.001). G1 was characterized by a significantly high prevalence of women as compared with G2, G3, and G4 (59%, 32%, 24%, and 23%, respectively). Serum creatinine levels (0.8 ± 0.4, 0.9 ± 0.4, 1.2 ± 0.6, and 1.4 ± 0.8 mg/dL, respectively), prevalence of atrial fibrillation (34%, 39%, 45%, and 50%, respectively), and diuretics use (36%, 45%, 67%, and 89%, respectively) increased from G1, G2, G3 to G4 (all P < 0.001), while left ventricular ejection fraction decreased from G1, G2, G3 to G4 (59 ± 15, 58 ± 15, 54 ± 15, and 52 ± 17%, respectively, P < 0.001). Multivariable Cox proportional hazards models showed that, as compared with G2, both G1 and G4 had increased incidence of all‐cause death [adjusted hazard ratio (aHR) 1.34, 95% confidence interval (CI) 1.08–1.67, P = 0.009; aHR 1.28, 95% CI 1.02–1.61, P = 0.037, respectively] and heart failure admission (aHR 1.39, 95% CI 1.09–1.78, P = 0.008 and aHR 1.35, 95% CI, 1.06–1.71, P = 0.014, respectively). This U‐shaped relationship was evident in the elderly patients. Furthermore, abnormal transitions to either higher or lower levels of serum UA from G2 were associated with increased mortality (aHR 1.29, 95% CI 1.06–1.57, P = 0.012; aHR 1.57, 95% CI 1.12–2.20, P = 0.009). Conclusions These results demonstrate that serum UA levels have the U‐shaped prognostic effects and abnormal transitions to either higher or lower levels are associated with poor prognosis in the elderly patients with CHF.

To ensure that experiences and lessons learned from the unprecedented 2011 Great East Japan Earthquake are used to improve future disaster planning, the Japan Diabetes Society (JDS) launched the “Research and Survey Committee for Establishing Disaster Diabetes Care Systems Based on Relevant Findings from the Great East Japan Earthquake” under the supervision of the Chairman of the JDS. The Committee conducted a questionnaire survey among patients with diabetes, physicians, disaster medical assistance teams (DMATs), nurses, pharmacists, and nutritionists in disaster areas about the events they saw happening, the situations they found difficult to handle, and the needs that they felt required to be met during the 2011 Great East Japan Earthquake. A total of 3,481 completed questionnaires were received. Based on these and other experiences and lessons reported following the 2011 Great East Japan Earthquake and the 2004 Niigata-Chuetsu Earthquakes, the current “Manual for Disaster Diabetes Care” has been developed by the members of the Committee and other invited authors from relevant specialties. To our knowledge, the current Manual is the world’s first to focus on emergency diabetes care, with this digest English version translated from the Japanese original. It is sincerely hoped that patients with diabetes and healthcare providers around the world will find this manual helpful in promoting disaster preparedness and implementing disaster relief.

In forensic practice, it may be necessary to identify the source of the tissue at crime scenes and elsewhere. We examined the physiological presence of myosin light chain 1 (MLC1), a structural protein in striated muscle, and designed a method that can identify human skeletal muscle from tissue fragments with very small sample consumption by quantitative analysis of MLC1. The MLC1 content in human muscles was compared with that in 13 different animal muscles and human organs, excluding horse muscles. The mean MLC1 content in the investigated iliopsoas muscles was 0.89 mg/g wet weight. For species identification, it is possible to differentiate human muscles from the muscles of other animal species except for horse. The MLC1 content in various human organs is very low, and differentiation between muscles and other organs is easy. The results showed that this method is highly sensitive, has good organ and species specificity, and is thought to be useful for the preliminary analysis of tissue fragments. •Identified human skeletal muscle using MLC1 detection via enzyme immunoassay.•MLC1 content in human iliopsoas muscles averages 0.89 mg/g wet weight.•Method differentiates human muscles from 14 animal species, except horse.•MLC1 content is significantly low in human organs, except the heart.