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Aims: The incidence and prognosis of symptomatic heart failure following acute myocardial infarction (AMI) in the primary percutaneous coronary intervention era have rarely been reported in the literature. This study aimed to (i) determine the incidence of heart failure admission among AMI survivors, (ii) compare 1 year outcomes between patients with heart failure admission and those without, and (iii) identify the independent risk factors associated with heart failure admission. Methods and results: The Japan Acute Myocardial Infarction Registry is a prospective multicentre registry from which data on consecutively enrolled patients with AMI from 50 institutions between 2015 and 2017 were obtained. Among the 3411 patients enrolled, 3226 who survived until discharge were included in this study. The primary endpoint was all‐cause mortality. The secondary endpoints were major adverse cardiovascular events (defined as cardiovascular mortality, non‐fatal myocardial infarction, or non‐fatal cerebral infarction) and major bleeding events corresponding to Bleeding Academic Research Consortium Type 3 or 5. Clinical outcomes were compared between the patients who were and were not admitted for heart failure. Over a median follow‐up of 12 months, 124 patients (3.8%) were admitted due to heart failure. Independent risk factors for heart failure admission included older age, female sex, Killip class ≥2 on admission, left ventricular ejection fraction <40%, estimated glomerular filtration rate ≤30 mL/min/1.73 m2, a history of malignancy, and non‐use of angiotensin‐converting enzyme inhibitors at discharge. The cumulative incidence of all‐cause mortality was significantly higher in the heart failure admission group than in the no heart failure admission group (11.3% vs. 2.5%, P < 0.001). The rates of major adverse cardiovascular events (16.9% vs. 2.7%, P < 0.001) and major bleeding (6.5% vs. 1.6%, P < 0.001) were significantly higher in the heart failure admission group. Heart failure admission was associated with a higher risk of all‐cause mortality, even after adjusting for potential confounders (adjusted hazard ratio: 2.41, 95% confidence interval: 1.33–4.39, P = 0.004). Conclusions: Utilizing real‐world data of the contemporary percutaneous coronary intervention era from the Japan Acute Myocardial Infarction Registry database, this study demonstrates that the heart failure admission of AMI survivors was significantly associated with higher all‐cause mortality rates. [ABSTRACT FROM AUTHOR]

Aims: This study aimed to examine the prognostic significance of a history of cancer and atrial fibrillation (AF) in antithrombotic therapy for patients with chronic heart failure (CHF). Methods and results: We enrolled consecutive 4876 CHF patients (69 ± 12 years; women, 31.9%) in our multicentre, hospital‐based cohort study, the Chronic Heart Failure Analysis and Registry in the Tohoku District‐2 (CHART‐2), with a median follow‐up of 8.7 years. Among them, 14% and 41% had a history of cancer and AF, respectively. AF patients with a history of cancer were older, more frequently men. History of cancer was not statistically associated with higher rate of composite of stroke, systemic thrombosis, and major bleeding defined by International Society on Thrombosis and Haemostasis [Fine–Gray sub‐distribution hazard ratio (sHR) accounting for the competing risk of all‐cause death, 0.91; 95% confidence interval (CI), 0.56–1.48; P = 0.715]. The patients with history of cancer and AF had a heightened risk for the composite of stroke, systemic thrombosis, and major bleeding (sHR, 1.64; 95% CI, 1.04–2.60; P = 0.033), especially in those aged >75 years (sHR, 2.14; 95% CI, 1.01–4.53; P = 0.046) and those with ischaemic heart disease (IHD; 2.48; 1.30–4.72; P = 0.006). Furthermore, 36% of AF patients with a history of cancer did not receive anticoagulant therapy. Conclusions: The CHF patients with history of cancer and AF had higher risk for stroke, systemic thrombosis, and major bleeding, especially in the elderly and those with IHD, but considerable number of the patients did not receive anticoagulant therapy, indicating the need for better optimal anticoagulation strategy. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Aims: We aimed to examine temporal changes in left ventricular (LV) structures and their prognostic impacts in patients with heart failure (HF) and preserved ejection fraction (HFpEF). Methods and results: In the Chronic Heart Failure Analysis and Registry in the Tohoku District‐2 (CHART‐2) study (n = 10 219), we divided 2698 consecutive HFpEF patients (68.9 ± 12.2 years, 32.1% female) into three groups by LV hypertrophy (LVH) and enlargement (LVE) at baseline: (−)LVH/(−)LVE (n = 989), (+)LVH/(−)LVE (n = 1448), and (+)LVH/(+)LVE (n = 261). We examined temporal changes in LV structures and their prognostic impacts during a median 8.7‐year follow‐up. From (−)LVH/(−)LVE, (+)LVH/(−)LVE to (+)LVH/(+)LVE at baseline, the incidence of the primary outcome, a composite of cardiovascular death or HF admission, significantly increased. Among 1808 patients who underwent echocardiography at both baseline and 1 year, we noted substantial group transitions from baseline to 1 year; the transition rates from (−)LVH/(−)LVE to (+)LVH/(−)LVE, from (+)LVH/(−)LVE to (−)LVH/(−)LVE, from (+)LVH/(−)LVE to (+)LVH/(+)LVE, and from (+)LVH/(+)LVE to (+)LVH/(−)LVE were 27% (182/671), 22% (213/967), 6% (59/967), and 26% (44/170), respectively. In the univariable Cox proportional hazard model, patients who transitioned from (+)LVH/(−)LVE to (+)LVH/(+)LVE or remained in (+)LVH/(+)LVE had the worst subsequent prognosis [hazard ratio (HR) 4.65, 95% confidence interval (CI) 3.09–6.99, P < 0.001; HR 4.01, 95% CI 2.85–5.65, P < 0.001, respectively], as compared with those who remained in (−)LVH/(−)LVE. These results were unchanged after adjustment for the covariates including baseline LV ejection fraction (LVEF) and 1‐year LVEF change. Conclusion: In HFpEF patients, LV structures dynamically change over time with significant prognostic impacts, where patients who develop LVE with LVH have the worst prognosis. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Although several factors, including heart failure (HF) and inflammation, are known to increase the incidence of cancer, it remains unknown whether HF may increase cancer mortality, especially with a reference to inflammation. We examined 8843 consecutive cardiovascular patients without a prior history of cancer in our CHART-2 Study (mean 68 yrs., female 30.9%). As compared with patients without HF (Stage A/B, N = 4622), those with HF (Stage C/D, N = 4221) were characterized by higher prevalence of diabetes, previous myocardial infarction, atrial fibrillation, and stroke. During the median 6.5-year follow-up (52,675 person-years), 282 cancer deaths occurred. HF patients had significantly higher cancer mortality than those without HF in both the overall (3.7 vs, 2.8%, hazard ratio (HR) 1.42, 95% confidence interval (CI) 1.12–1.79, P = 0.004) and the propensity score-matched cohorts (HR 1.46, 95%CI 1.10–1.93, P = 0.008), which was confirmed in the competing risk models. The multivariable Cox proportional hazard model in the matched cohort showed that HF was associated with increased cancer mortality in patients with C-reactive protein (CRP) ≥ 2.0 mg/L (HR 1.87, 95%CI 1.18–2.96, P = 0.008) at baseline, but not in those with CRP < 2.0 mg/L (HR 0.89, 95%CI 0.54–1.45, P = 0.64) (P for interaction = 0.03). Furthermore, temporal changes in CRP levels were associated with cancer death in the overall cohort; HF patients with CRP ≥ 2.0 mg/L at both baseline and 1-year had significantly increased cancer death, while those with CRP ≥ 2.0 mg/L at baseline and < 2.0 mg/L at 1-year not. These results provide the first evidence that HF is associated with increased cancer death, especially when associated with prolonged inflammation. • We examined whether heart failure (HF) increases cancer mortality. • HF patients had significantly higher cancer mortality than those without HF. • Temporal changes in C-reactive protein levels were associated with cancer death. [ABSTRACT FROM AUTHOR]

Background: The new category of heart failure (HF), HF with mid-range left ventricular ejection fraction (LVEF) (HFmrEF), has recently been proposed. However, the clinical features of HFmrEF, with reference to HF with preserved LVEF (HFpEF) and HF with reduced LVEF (HFrEF) in the same HF cohort, remain to be fully examined.Methods and Results: In the Chronic Heart Failure Analysis and Registry in the Tohoku District-2 Study, we examined 3480 consecutive HF patients with echocardiography data consisting of 2154 HFpEF (LVEF ≥50%), 596 HFmrEF (LVEF 40-49%) and 730 HFrEF (LVEF <40%). While clinical characteristics and prognostic factors of HFmrEF were intermediate between HFpEF and HFrEF, prognosis of HFmrEF resembled HFpEF and the prognostic impact of cardiovascular medications in HFmrEF resembled that of HFrEF. Analysis of LVEF transition among the three groups revealed that HFmrEF and HFrEF dynamically transitioned to other categories, especially within 1 year, whereas HFpEF did not; HFmrEF at registration transitioned to HFpEF and HFrEF by 44% and 16% at 1 year, and 45% and 21% at 3 years, respectively. Landmark analysis demonstrated that, regardless of HF stages at registration, HFmrEF patients at 1 year had mortality comparable to that of HFpEF patients, which was better than HFrEF patients, but HFmrEF patients at registration had increased mortality when transitioned to HFrEF at 1 year.Conclusions: These results indicate that clinical characteristics of HFmrEF are intermediate between HFpEF and HFrEF and that HFmrEF dynamically transitions to HFpEF or HFrEF, especially within 1 year, suggesting that HFmrEF represents a transitional status or an overlap zone between HFpEF and HFrEF, rather than an independent entity of HF. [ABSTRACT FROM AUTHOR]

Aims It is still controversial whether elevated baseline heart rate ( HR) is associated with higher mortality in patients with heart failure ( HF) with preserved ejection fraction ( HFpEF). We compared the impacts of baseline HR on mortality in patients with HFpEF and those with HF with reduced ejection fraction ( HFrEF). Methods and results We enrolled consecutive 2688 patients in Stage C or D HF with sinus rhythm from our Chronic Heart Failure Analysis and Registry in the Tohoku District 2 ( CHART-2) Study ( n = 10 219). The prognostic impact of HR increase was compared between the two groups, defined as left ventricular ejection fraction of < 50% ( HFrEF) and > 50% ( HFpEF). Cox regression analysis revealed that elevated baseline HR was associated with increased all-cause mortality in both groups [hazard ratio for the highest tertile ( HH) 1.77 in HFrEF, P = 0.008; HH1.82 in HFpEF, P = 0.001]. However, as for mode of death, elevated HR was associated with cardiovascular ( CV) death in HFpEF ( HH 2.17, P = 0.012), but the association was modest in HFrEF ( HH1.49, P = 0.14): in particular, impact on HF death was different between HFpEF ( HH 3.79, P = 0.020) and HFrEF ( HH 1.07, P = 0.864). In contrast, the prognostic impact of baseline HR on non- CV death was noted only in patients with HFrEF. β-Blocker therapy was associated with reduced HF mortality in HFrEF (hazard ratio 0.49, P = 0.038) but not in HFpEF (hazard ratio 0.64, P = 0.321). Conclusions Elevated HR was associated with increased CV death in HFpEF compared with HFrEF, although its impact on all-cause mortality was comparable between the two groups. [ABSTRACT FROM AUTHOR]

Introduction: Basigin is a multifunctional protein that induces MMPs and is strongly upregulated in patients with cardiovascular diseases. We have shown that basigin enhances cardiac hypertrophy and fibrosis in a mouse model of heart failure (HF). Hypothesis: Soluble form of basigin (sBsg) can be a biomarker in patients with chronic HF. Methods: This cohort study included 1,075 hypertensive patients with chronic HF treated with ACE inhibitors, beta-blockers, or both (mean age 66 years, 74% male, mean left ventricular ejection fraction 54%). In this prospective, open-label, blinded endpoint study, patients were randomized to the addition of olmesartan to baseline therapy or control. Serum levels of sBsg were measured in samples from 1,075 patients, and were compared with 11 conventional risk factors plus BNP with respect to all-cause death and hospitalization for worsening HF. Results: During a median follow-up of 4.7 years, we found that higher serum sBsg levels (>5365 pg/mL) predicted all-cause death and HF hospitalization in patients with chronic HF. Moreover, patients with increased serum sBsg during follow-up (Δ>1094 pg/mL) predicted poorer prognosis in those patients. Importantly, the combination of sBsg and BNP was more significantly associated with all-cause death, HF hospitalization, and additional use of medication for HF than sBsg or BNP alone. In multivariable analysis, sBsg remained independently associated with all-cause death and HF hospitalization (hazard ratio, 1.6; 95% confidence interval [CI], 1.2 to 2.2; P =0.004). Incorporation of sBsg into a full-adjusted model for all-cause death (including clinical variables and BNP) improved discrimination (C-statistic 0.74, P =0.001) and calibration, and significantly improved reclassification (integrated discrimination improvement 0.04; 95% CI, 0.03 to 0.06; P <0.001; net reclassification index, 0.35; 95% CI, 0.21 to 0.49; P <0.001). Finally, in HF patients with higher sBsg levels, the addition of olmesartan treatment significantly reduced sBsg levels after 3-year follow-up. Patients with reduced sBsg levels had better prognosis than those with increased sBsg levels. Conclusions: Serum levels of sBsg have a prognostic impact in chronic HF patients. [ABSTRACT FROM AUTHOR]