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Aims: Heart failure remained consistent as one of the biggest cardiovascular problems in Indonesia. Hyponatraemia is a common electrolyte disorder among patients presented with heart failure; however, the prognostic value for worsening heart failure has not been well defined. Methods and results: We studied 134 patients admitted with acute heart failure and investigated the relationship between admission serum sodium and the composite clinical outcomes of all‐cause mortality and hospitalization ambispectively with a follow‐up duration of 6 months. We also try to look for low sodium‐level impacts in several conditions. Among 134 patients, 84 patients presented with low sodium during admission, defined as a serum sodium level of <135 mEq/L, and it was associated with higher composite clinical outcome risk [odds ratio (OR), 5.9; 95% confidence interval (CI), 2.8–12.0; P < 0.001]. Moreover, hyponatraemia impacts on composite endpoints were driven by both parameters; it was independently associated with mortality (OR, 3.1; 95% CI, 1.4–6.8; P = 0.003) and rehospitalization (OR, 5.3; 95% CI, 2.4–11.7; P < 0.001). This result remained consistent in most subgroups. Conclusions: On‐admission hyponatraemia is a predictor for 6 month mortality and rehospitalization. Further work is needed to determine if correction of hyponatraemia translates into clinical benefit. [ABSTRACT FROM AUTHOR]

Aims: In recent years, survival in patients with breast cancer has increased. Despite the improvement in outcomes of those patients, the risk of treatment‐related cardiotoxicity remains high, and its presence has been associated with a higher risk of treatment termination and thus lower therapeutic efficacy. Prior trials demonstrated that a preventive initiation of heart failure drugs, including the renin–angiotensin–aldosterone inhibitors, might reduce the risk of treatment‐related cardiotoxicity. However, to date, no study investigated the efficacy of sacubitril/valsartan, a novel antineurohormonal drug shown to be superior to the previous therapies, in the prevention of cardiotoxicity in patients with early‐stage breast cancer, which is the aim of the trial. Methods and results: MAINSTREAM is a randomized, placebo‐controlled, double‐blind, multicentre, clinical trial. After the run‐in period, a total of 480 patients with early breast cancer undergoing treatment with anthracyclines and/or anti‐human epidermal growth factor receptor 2 drugs will be randomized to the highest tolerated dose of sacubitril/valsartan, being preferably 97/103 mg twice daily or placebo in 1:1 ratio. The patients will be monitored, including routine transthoracic echocardiography (TTE) and laboratory biomarker monitoring, for 24 months. The primary endpoint of the trial will be the occurrence of a decrease in left ventricular ejection fraction by ≥5% in TTE within 24 months. The key secondary endpoints will be the composite endpoint of death from any cause or hospitalization for heart failure, as well as other imaging, laboratory, and clinical outcomes, including the occurrence of the cancer therapy‐related cardiac dysfunction resulting in the necessity to initiate treatment. The first patients are expected to be recruited in the coming months, and the estimated completion of the study and publication of the results are expected in December 2027, pending recruitment. Conclusions: The MAINSTREAM trial will determine the efficacy and safety of treatment with sacubitril/valsartan as a prevention of cardiotoxicity in patients with early breast cancer (ClinicalTrials.gov number: NCT05465031). [ABSTRACT FROM AUTHOR]

Aims: Early start and patient profile‐oriented heart failure (HF) management has been recommended. In this post hoc analysis from the SHIFT trial, we analysed the treatment effects of ivabradine in HF patients with systolic blood pressure (SBP) < 110 mmHg, resting heart rate (RHR) ≥ 75 b.p.m., left ventricular ejection fraction (LVEF) ≤ 25%, New York Heart Association (NYHA) Class III/IV, and their combination. Methods and results: The SHIFT trial enrolled 6505 patients (LVEF ≤ 35% and RHR ≥ 70 b.p.m.), randomized to ivabradine or placebo on the background of guideline‐defined standard care. Compared with placebo, ivabradine was associated with a similar relative risk reduction of the primary endpoint (cardiovascular death or HF hospitalization) in patients with SBP < 110 and ≥110 mmHg [hazard ratio (HR) 0.89, 95% confidence interval (CI) 0.74–1.08 vs. HR 0.80, 95% CI 0.72–0.89, P interaction = 0.34], LVEF ≤ 25% and >25% (HR 0.85, 95% CI 0.72–1.01 vs. HR 0.80, 95% CI 0.71–0.90, P interaction = 0.53), and NYHA III–IV and II (HR 0.83, 95% CI 0.74–0.94 vs. HR 0.81, 95% CI 0.69–0.94, P interaction = 0.79). The effect was more pronounced in patients with RHR ≥ 75 compared with <75 (HR 0.76, 95% CI 0.68–0.85 vs. HR 0.97, 95% CI 0.81–0.1.16, P interaction = 0.02). When combining these profiling parameters, treatment with ivabradine was also associated with risk reductions comparable with patients with low‐risk profiles for the primary endpoint (relative risk reduction 29%), cardiovascular death (11%), HF death (49%), and HF hospitalization (38%; all P values for interaction: 0.40). No safety concerns were observed between study groups. Conclusions: Our analysis shows that RHR reduction with ivabradine is effective and improves clinical outcomes in HF patients across various risk indicators such as low SBP, high RHR, low LVEF, and high NYHA class to a similar extent and without safety concern. [ABSTRACT FROM AUTHOR]

Aims: Chronic heart failure (CHF) remains a major health issue worldwide. In the present study, we aimed to identify novel circulating biomarkers for CHF using serum proteomics technology and to validate the biomarker in three independent cohorts. Methods and results: The isobaric tags for relative and absolute quantitation technology was utilized to identify the potential biomarkers of CHF. The validation was conducted in three independent cohort. Cohort A included 223 patients with ischaemic heart disease (IHD) and 321 patients with ischaemic heart failure (IHF) from the CORFCHD‐PCI study. Cohort B recruited 817 patients with IHD and 1139 patients with IHF from the PRACTICE study. Cohort C enrolled 559 non‐ischaemic heart disease patients with CHF (n = 316) or without CHF (n = 243). We found the expression of a‐1 antitrypsin (AAT) was elevated significantly in patients with CHF compared with that in the patients with stable IHD using statistical and bioinformatics analyses. In a validation study, there was a significant difference between patients with stable IHD and patients with IHF in AAT concentration either in cohort A (1.35 ± 0.40 vs. 1.64 ± 0.56, P < 0.001) or in cohort B (1.37 ± 0.42 vs. 1.70 ± 0.48, P < 0.001). The area under the receiver operating characteristic curve was 0.70 [95% confidence interval (CI): 0.66 to 0.74, P < 0.001] in cohort A and 0.74 (95% CI: 0.72 to 0.76, P < 0.001) in cohort B. Furthermore, AAT was negative correlated with left ventricular ejection fraction (r = −0.261, P < 0.001). After adjusting for confounders using a multivariate logistic regression analysis, AAT remained an independent association with CHF in both cohort A (OR = 3.14, 95% CI: 1.667 to 5.90, P < 0.001) and cohort B (OR = 4.10, 95% CI: 2.97 to 5.65, P < 0.001). This association was also validated in cohort C (OR = 1.86, 95% CI: 1.02 to 3.38, P = 0.043). Conclusions: The present study suggests that serum AAT is a reliable biomarker for CHF in a Chinese population. [ABSTRACT FROM AUTHOR]

Aims: Currently, no incident heart failure (HF) risk score that is in regular use in a general population is available. We aimed to develop this and compare with existing HF risk scores. Methods and results: Participants in the third wave (2006–08) of the population‐based Trøndelag Health Study 3 (HUNT3) were included if they reported no previous HF. Any hospital diagnoses captured during follow‐up (until the end of 2018) of HF, cardiomyopathy, or hypertensive heart disease were assessed by an experienced cardiologist. Valid HF events were defined as symptoms/signs of HF and objective evidence of structural/functional abnormality of the heart at rest. The model was compared with slightly modified HF risk scores (the Health Aging and Body Composition HF risk score, the Framingham HF risk score, the Pooled Cohort equations to Prevent HF risk score, and NORRISK 2). Among 36 511 participants (mean ± SD age of 57.9 ± 13.3 years, 55.4% female), with a mean follow‐up of 10.2 ± 1.3 years, 1366 developed HF (incidence rate of 3.66 per 1000 participant years). Out of the 38 relevant clinical variables assessed, we identified 12 (atrial fibrillation being the strongest) that independently predicted an HF event. The final model demonstrated good discrimination (C statistics = 0.904) and calibration, was stable in internal validation, and performed well compared with existing risk scores. The model identified that, at enrolment, 31 391 (86%), 2386 (7%), 1246 (3%), and 1488 (4%) had low, low‐intermediate, high‐intermediate, and high 10‐year HF risk, respectively. Conclusions: Twelve clinical variables independently predicted 10‐year HF risk. The model may serve well as the foundation of a practical, online risk score for HF in general practice. Trial Registration: ClinicalTrials.gov Identifier: NCT04648852. [ABSTRACT FROM AUTHOR]

Aims: Previous studies demonstrated the relationship between hypochloraemia and poor prognosis in patients hospitalized for acute heart failure (AHF). However, the usefulness of chloride in clinical practice remains uncertain, notably in very old patients with predominantly heart failure (HF) with preserved ejection fraction (HFpEF). We aimed to evaluate the prognostic impact of chloride in a cohort of very aged patients with AHF and the possible existence of different phenotypes of hypochloraemia with distinct clinical significance. Methods and results: It was an observational study of 429 patients hospitalized for AHF in which chloraemia was measured. Two different phenotypes of hypochloraemia were identified by their relationship with estimated plasma volume status (ePVS) as a proxy of intravascular congestion. The endpoint of interest was time to all‐cause mortality and the composite of death and/or HF readmission. A multivariable Cox proportional hazard regression model was constructed to analyse the endpoints. The median age was 85 (78–92) years, 266 (62%) were women, and 80% had HFpEF. After multivariable analysis, chloraemia, but not natraemia, was associated with the risk of death and HF readmission in a U‐shaped pattern. The phenotype characterized by hypochloraemia and low ePVS (depletional) was associated with an increased risk of mortality when compared with patients with normochloraemia [hazard ratio (HR) 1.86, P = 0.008]. In contrast, hypochloraemia with high ePVS (dilutional) had no prognostic significance (HR 0.94, P = 0.855). Conclusions: In very old patients hospitalized with AHF, plasma chloride was associated with the risk of death and HF readmission in a U‐shaped pattern and could potentially be used for congestion phenotyping. [ABSTRACT FROM AUTHOR]

Aims: Although various non‐invasive cardiac examinations are known to be predictive of long‐term outcomes in patients with heart failure (HF), combining them properly would provide synergism. We aimed to show that non‐invasive cardiac assessments targeting left ventricular filling pressure (LVFP), left atrial remodelling, and exercise capacity would provide better prognostication in combination. Methods and results: This prospective observational study included consecutive hospitalized stage A–C HF patients evaluated with N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP), echocardiography including two‐dimensional speckle tracking, and cardiopulmonary exercise testing. According to NT‐proBNP and echocardiographic semi‐quantitative LVFP grading (Echo‐LVFP), patients were classified into three LVFP groups: normal range of both Echo‐LVFP and NT‐proBNP (Group 1), normal range of Echo‐LVFP but elevated NT‐proBNP (Group 2), and elevated Echo‐LVFP and NT‐proBNP (Group 3). The adverse outcome was defined as a composite of cardiovascular death, non‐fatal acute coronary syndrome, acute stroke, or HF‐related hospitalization. Among 224 HF patients (mean age of 63.8 ± 11.6 years, 158 men) analysed, 160 (71.4%) had ischaemic aetiology. During the follow‐up of 18.6 ± 9.8 months, event‐free survival in Group 2 (n = 56, age of 65.4 ± 12.4) was better than that in Group 3 (n = 45, age of 68.5 ± 11.5) but worse than that in Group 1 (n = 123, mean age of 61.4 ± 10.5) (log‐rank P < 0.001). Mechanical left atrial dysfunction (peak longitudinal strain <28%) (adjusted hazard ratio 5.69, 95% confidence interval 1.06–4.48) and limited exercise capacity (peak VO2 per +5 mL/kg/min) (adjusted hazard ratio 0.63, 95% confidence interval 0.46–0.87) were also predictable adverse outcomes. Serial addition of peak VO2 and left atrial strain to the model incrementally enhanced the predictive power of LVFP‐based risk stratification for adverse outcomes. Conclusions: The combination of NT‐proBNP and Echo‐LVFP could be used to predict adverse outcomes in patients with HF of various stages. Left atrial mechanics and exercise capacity are incremental to prognostication. Non‐invasive test findings could be strategically combined to provide an integrative profile of cardiac performance. [ABSTRACT FROM AUTHOR]

Aims: We assessed the diagnostic yield of genetic testing and the relationship of left ventricular (LV) reverse remodelling (LVRR) with the presence of DNA pathogenic (P) or likely pathogenic (LP) variants in patients with dilated cardiomyopathy (DCM). Methods and results: From 680 outpatients followed at the Heart Failure Outpatient Clinic of our institution, we selected subjects with a diagnosis of DCM as defined by LV ejection fraction (LVEF) ≤40% and LV dilatation not explained by coronary artery disease or other causes. All patients were offered genetic investigation of 42 disease‐associated DCM genes with next‐generation sequencing. Seventy patients fulfilled the definition of DCM and 66 underwent genetic investigation. We identified 18 P/LP variants in 16 patients, with a diagnostic yield of 24%. The most common variants were truncating TTN variants (n = 7), followed by LMNA (n = 3), cytoskeleton Z‐disc (n = 3), ion channel (n = 2), motor sarcomeric (n = 2), and desmosomal (n = 1) genes. After a median follow‐up of 53 months (inter‐quartile range 20–111), patients without P/LP variants exhibited higher systolic and diastolic blood pressure, lower plasma brain natriuretic peptide levels, and a larger extent of LVRR, as reflected by the increase in LVEF (+14% vs. +1%, P = 0.0008) and decrease in indexed LV end‐diastolic diameter (−6.5 vs. −2 mm/m2, P = 0.03) compared with patients with P/LP variants. Conclusions: Our results confirm the high diagnostic yield of genetic testing in selected DCM patients and suggest that identification of P/LP variants in DCM portends poorer LVRR in response to guideline‐directed medical therapy. [ABSTRACT FROM AUTHOR]

We witnessed major advances in the management of heart failure (HF) in 2022. Results of recent clinical and preclinical investigations aid preventive strategies, diagnostic efforts, and therapeutic interventions, and collectively, they hold promises for a more effective HF care for the near future. Accordingly, currently available information extends the 2021 European Society of Cardiology guidelines and provides a solid background for the introduction of improved clinical approaches in the number of HF‐related cases. Elaboration on the relationships between epidemiological data and risk factors lead to better understanding of the pathophysiology of HF with reduced ejection fraction and HF with preserved ejection fraction. The clinical consequences of valvular dysfunctions are increasingly interpreted not only in their haemodynamic consequences but also in association with their pathogenetic factors and modern corrective treatment possibilities. The influence of coronavirus disease 2019 pandemic on the clinical care of HF appeared to be less intense in 2022 than before; hence, this period allowed to refine coronavirus disease 2019 management options for HF patients. Moreover, cardio‐oncology emerges as a new subdiscipline providing significant improvements in clinical outcomes for oncology patients. Furthermore, the introduction of state‐of‐the‐art molecular biologic methods, multi‐omic approaches forecast improved phenotyping and precision medicine for HF. All above aspects are addressed in this article that highlights a selection of papers published in ESC Heart Failure in 2022. [ABSTRACT FROM AUTHOR]

Aims: Knowledge of long‐term outcomes in patients with atrial fibrillation (AF) remains limited. We sought to evaluate the risk of new‐onset heart failure (HF) in patients with AF and a low cardiovascular risk profile. Methods and results: Data from the Swedish National Patient Register were used to identify all patients with a first‐time diagnosis of AF without underlying cardiovascular disease at baseline between 1987 and 2018. Each patient was compared with two controls without AF from the National Total Population Register. In total, 227 811 patients and 452 712 controls were included. During a mean follow‐up of 9.1 (standard deviation 7.0) years, the hazard ratio (HR) for new‐onset HF was 3.55 [95% confidence interval (CI) 3.51–3.60] in patients compared with controls. Women with AF (18–34 years) had HR for HF onset 24.6 (95% CI 7.59–80.0) and men HR 9.86 (95% CI 6.81–14.27). The highest risk was within 1 year in patients 18–34 years, HR 103.9 (95% CI 46.3–233.1). The incidence rate within 1 year increased from 6.2 (95% CI 4.5–8.6) per 1000 person‐years in young patients (18–34 years) to 142.8 (95% CI 139.4–146.3) per 1000 person‐years among older patients (>80 years). Conclusions: Patients studied had a three‐fold higher risk of developing HF compared with controls. Young patients, particularly women, carry up to 100‐fold increased risk to develop HF within 1 year after AF. Further studies in patients with AF and low cardiovascular risk profile are needed to prevent serious complications such as HF. [ABSTRACT FROM AUTHOR]

Aims: The early identification and appropriate management may provide clinically meaningful and substained benefits in patients with acute heart failure (AHF). This study aimed to develop an integrative nomogram with myocardial perfusion imaging (MPI) for predicting the risk of all‐cause mortality in AHF patients. Methods and results: Prospective study of 147 patients with AHF who received gated MPI (59.0 [47.5, 68.0] years; 78.2% males) were enrolled and followed for the primary endpoint of all‐cause mortality. We analysed the demographic information, laboratory tests, electrocardiogram, and transthoracic echocardiogram by the least absolute shrinkage and selection operator (LASSO) regression for selection of key features. A multivariate stepwise Cox analysis was performed to identify independent risk factors and construct a nomogram. The predictive values of the constructed model were compared by Kaplan–Meier curve, area under the curves (AUCs), calibration plots, continuous net reclassification improvement, integrated discrimination improvement, and decision curve analysis. The 1, 3, and 5 year cumulative rates of death were 10%, 22%, and 29%, respectively. Diastolic blood pressure [hazard ratio (HR) 0.96, 95% confidence interval (CI) 0.93–0.99; P = 0.017], valvular heart disease (HR 3.05, 95% CI 1.36–6.83; P = 0.007), cardiac resynchronization therapy (HR 0.37, 95% CI 0.17–0.82; P = 0.014), N‐terminal pro‐B‐type natriuretic peptide (per 100 pg/mL; HR 1.02, 95% CI 1.01–1.03; P < 0.001), and rest scar burden (HR 1.03, 95% CI 1.01–1.06; P = 0.008) were independent risk factors for patients with AHF. The cross‐validated AUCs (95% CI) of nomogram constructed by diastolic blood pressure, valvular heart disease, cardiac resynchronization therapy, N‐terminal pro‐B‐type natriuretic peptide, and rest scar burden were 0.88 (0.73–1.00), 0.83 (0.70–0.97), and 0.79 (0.62–0.95) at 1, 3, and 5 years, respectively. Continuous net reclassification improvement and integrated discrimination improvement were also observed, and the decision curve analysis identified the greater net benefit of the nomogram across a wide range of threshold probabilities (0–100% at 1 and 3 years; 0–61% and 62–100% at 5 years) compared with dismissing the included factors or using either factor alone. Conclusions: A predictive nomogram for the risk of all‐cause mortality in patients with AHF was developed and validated in this study. The nomogram incorporated the rest scar burden by MPI is highly predictive, and may help to better stratify clinical risk and guide treatment decisions in patients with AHF. [ABSTRACT FROM AUTHOR]

Although the development of therapies and tools for the improved management of heart failure (HF) continues apace, day‐to‐day management in clinical practice is often far from ideal. A Cardiovascular Round Table workshop was convened by the European Society of Cardiology (ESC) to identify barriers to the optimal implementation of therapies and guidelines and to consider mitigation strategies to improve patient outcomes in the future. Key challenges identified included the complexity of HF itself and its treatment, financial constraints and the perception of HF treatments as costly, failure to meet the needs of patients, suboptimal outpatient management, and the fragmented nature of healthcare systems. It was discussed that ongoing initiatives may help to address some of these barriers, such as changes incorporated into the 2021 ESC HF guideline, ESC Heart Failure Association quality indicators, quality improvement registries (e.g. EuroHeart), new ESC guidelines for patients, and the universal definition of HF. Additional priority action points discussed to promote further improvements included revised definitions of HF 'phenotypes' based on trial data, the development of implementation strategies, improved affordability, greater regulator/payer involvement, increased patient education, further development of patient‐reported outcomes, better incorporation of guidelines into primary care systems, and targeted education for primary care practitioners. Finally, it was concluded that overarching changes are needed to improve current HF care models, such as the development of a standardized pathway, with a common adaptable digital backbone, decision‐making support, and data integration, to ensure that the model 'learns' as the management of HF continues to evolve. [ABSTRACT FROM AUTHOR]

Aims: Multiple prediction score models have been validated to predict major adverse events in patients with heart failure. However, these scores do not include variables related to the type of follow‐up. This study aimed to evaluate the impact of a protocol‐based follow‐up programme of patients with heart failure regarding scores accuracy for predicting hospitalizations and mortality occurring during the first year after hospital discharge. Methods and results: Data from two heart failure populations were collected: one composed of patients included in a protocol‐based follow‐up programme after an index hospitalization for acute heart failure and a second one—the control group—composed of patients not included in a multidisciplinary HF management programme after discharge. For each patient, the risk of hospitalization and/or mortality within a period of 12 months after discharge was calculated using four different scores: BCN Bio‐HF Calculator, COACH Risk Engine, MAGGIC Risk Calculator, and Seattle Heart Failure Model. The accuracy of each score was established using the area under the receiver operating characteristic curve (AUC), calibration graphs, and discordance calculation. AUC comparison was established by the DeLong method. The protocol‐based follow‐up programme group included 56 patients, and the control group, 106 patients, with no significant differences between groups (median age: 67 years vs. 68.4 years; male sex: 58% vs. 55%; median ejection fraction: 28.2% vs. 30.5%; functional class II: 60.7% vs. 56.2%, I: 30.4% vs. 31.9%; P = not significant). Hospitalization and mortality rates were significantly lower in the protocol‐based follow‐up programme group (21.4% vs. 54.7%; P < 0.001 and 5.4% vs. 17.9%; P < 0.001, respectively). When applied to the control group, COACH Risk Engine and BCN Bio‐HF Calculator had, respectively, good (AUC: 0.835) and reasonable (AUC: 0.712) accuracy to predict hospitalization. There was a significant reduction of COACH Risk Engine accuracy (AUC: 0.572; P = 0.011) and a non‐significant accuracy reduction of BCN Bio‐HF Calculator (AUC: 0.536; P = 0.1) when applied to the protocol‐based follow‐up programme group. All scores showed good accuracy to predict 1 year mortality (AUC: 0.863, 0.87, 0.818, and 0.82, respectively) when applied to the control group. However, when applied to the protocol‐based follow‐up programme group, a significant predictive accuracy reduction of COACH Risk Engine, BCN Bio‐HF Calculator, and MAGGIC Risk Calculator (AUC: 0.366, 0.642, and 0.277, P < 0.001, 0.002, and <0.001, respectively) was observed. Seattle Heart Failure Model had non‐significant reduction in its acuity (AUC: 0.597; P = 0.24). Conclusions: The accuracy of the aforementioned scores to predict major events in patients with heart failure is significantly reduced when they are applied to patients included in a multidisciplinary heart failure management programme. [ABSTRACT FROM AUTHOR]

In the last years, major progress has occurred in heart failure (HF) management. The 2023 ESC focused update of the 2021 HF guidelines introduced new key recommendations based on the results of the last years of science. First, two drugs, sodium-glucose co-transporter-2 (SGLT2) inhibitors and finerenone, a novel nonsteroidal, selective mineralocorticoid receptor antagonist (MRA), are recommended for the prevention of HF in patients with diabetic chronic kidney disease (CKD). Second, SGLT2 inhibitors are now recommended for the treatment of HF across the entire left ventricular ejection fraction spectrum. The benefits of quadruple therapy in patients with HF with reduced ejection fraction (HFrEF) are well established. Its rapid and early up-titration along with a close follow-up with frequent clinical and laboratory re-assessment after an episode of acute HF (the so-called 'high-intensity care' strategy) was associated with better outcomes in the STRONG-HF trial. Patients experiencing an episode of worsening HF might require a fifth drug, vericiguat. In the STEP-HFpEF-DM and STEP-HFpEF trials, semaglutide 2.4 mg once weekly administered for 1 year decreased body weight and significantly improved quality of life and the 6 min walk distance in obese patients with HF with preserved ejection fraction (HFpEF) with or without a history of diabetes. Further data on safety and efficacy, including also hard endpoints, are needed to support the addition of acetazolamide or hydrochlorothiazide to a standard diuretic regimen in patients hospitalized due to acute HF. In the meantime, PUSH-AHF supported the use of natriuresis-guided diuretic therapy. Further options and most recent evidence for the treatment of HF, including specific drugs for cardiomyopathies (i.e., mavacamten in hypertrophic cardiomyopathy and tafamidis in transthyretin cardiac amyloidosis), device therapies, cardiac contractility modulation and percutaneous treatment of valvulopathies, with the recent finding from the TRILUMINATE Pivotal trial, are also reviewed in this article., (© 2024 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

In addition in Riccardi et al,[1] in paragraph "Treatment of heart failure with reduced ejection fraction", section "Pharmacological therapies", sub-section "Sodium-glucose co-transporter-2 inhibitors" (page 4 out of 27) as regard the sentence "Tomasoni et al. reviewed growing evidence that support the early, upfront initiation of SGLT2is in both acute and chronic HF patients due to early benefits, with clinically meaningful reductions in clinical events that reach statistical significance within days to weeks, safety, and tolerability." only reference 100 is correct. References 1 Riccardi M, Sammartino AM, Piepoli M, Adamo M, Pagnesi M, Rosano G, Metra M, von Haehling S, Tomasoni D. Heart failure: an update from the last years and a look at the near future. [Extracted from the article]

Aims: Heart failure with preserved ejection fraction (HFpEF), which is caused by wide various conditions, has become a major public health problem. Transthyretin amyloid cardiomyopathy (ATTR‐CM), which is thought to be an underdiagnosed disease, can cause HFpEF. Non‐invasive diagnosis using 99mTechnetium (Tc)‐pyrophosphate (PYP) scintigraphy enables accurate diagnosis of ATTR‐CM. The aim of this study was to clarify the prevalence and characteristics of ATTR‐CM among Japanese patients with HFpEF. Methods and results: This study was a multicentre, prospective, observational study conducted in Japan. We enrolled 373 patients with HFpEF [left ventricular (LV) ejection fraction ≥50%] aged ≥65 years who were admitted to the department of cardiology from September 2018 to January 2022. A 99mTc‐PYP scintigraphy scan was performed during admission in all eligible patients. Cardiac 99mTc‐PYP retention was graded according to a previously reported visual scale ranging from 0 to 3 points. The scan was considered positive when it revealed moderate‐to‐severe 99mTc‐PYP uptake (Grade 2–3) in both ventricles. Patients were divided into ATTR‐CM and non‐ATTR‐CM patients according to positive (Grade 2–3) or negative (Grade 0–1) 99mTc‐PYP scintigraphy, respectively. Medical history, blood tests, electrocardiogram, echocardiography, and magnetic resonance imaging in the two groups of patients were compared. Among the 373 patients with HFpEF, 53 patients (14.2%; 95% confidence interval: 10.7–17.7) showed positive uptake on 99mTc‐PYP scintigraphy. An endomyocardial biopsy was performed in 32 patients and confirmed amyloidosis in all cases. There were no significant differences between the two groups in age, severity of heart failure as assessed by the New York Heart Association (NYHA) functional classification, renal function values, left ventricular ejection fraction, and tricuspid regurgitant pressure gradient (ATTR‐CM, n = 53 vs. non‐ATTR‐CM, n = 320). Patients in the ATTR‐CM group had a higher N‐terminal pro‐brain natriuretic peptide level [2314 (1081–3398) vs. 900 (415–1828), P < 0.001], higher sensitive troponin T level (0.074 ± 0.049 vs. 0.035 ± 0.038, P < 0.001), and higher mean LV maximal wall thickness [12.5 (11–14) vs. 10.5 (9.5–11.5), P < 0.001]. Conclusions: ATTR‐CM is an underdiagnosed disease with a significant prevalence in Japanese patients with HFpEF. This study showed that results of examinations for ATTR‐CM patients appear to be worse than those for non‐ATTR‐CM patients, but clinical severities of heart failure as assessed by the NYHA functional classification are similar in ATTR‐CM and non‐ATTR‐CM patients, and the clinical overlap between ATTR‐CM and non‐ATTR‐CM is high. [ABSTRACT FROM AUTHOR]

Aims: Heart failure (HF) is a progressive disease in which periods of clinical stability are interrupted by episodes of clinical deterioration known as worsening heart failure (WHF). Patients who develop WHF are at high risk of subsequent death, rehospitalization, and excessive healthcare costs. As such, WHF could be seen as a separate disease stage and precursor of advanced HF. Whether WHF has a substantial health, societal, and economic impact evidence regarding its multifactorial nature and the specific barriers in treatment, including advanced HF therapies, remains scarce. The CHAIN‐HF registry aims to describe the incidence, characteristics, current treatment, and outcomes of WHF. Additionally, it will promote structured regional collaboration and educate on increasing awareness for WHF and describe the implementation of guideline directed medical therapy and utilization of advanced HF therapies in a collaborative network. Methods and results: The CHAIN‐HF registry is a prospective, observational, and multicentre study from the collaborating hospitals (Rijnmond HF Network) in the Rotterdam area. Unselected and consecutive patients (irrespective of ejection fraction) with a WHF event will be included. Comprehensive data including demographics, co‐morbidities, treatment, and in‐hospital and post‐discharge outcomes will be collected. Notably, data on socio‐economic status, treatment decisions, and referral for advanced HF therapies will be included. Conclusions: CHAIN‐HF will be the first prospective, dedicated WHF registry in a collaborative network of hospitals that will provide robust real‐world evidence on the incidence, characteristics, and outcomes of WHF. Moreover, it will provide information on of the value of regional collaboration to improve awareness and outcomes of WHF. [ABSTRACT FROM AUTHOR]

Aims: There are currently limited therapeutic approaches for patients with heart failure with preserved ejection fraction (HFpEF) who have developed permanent atrial fibrillation (AF). We aimed to analyse the impact of ventricular irregularity on heart failure rehospitalization in patients with permanent AF and HFpEF. Methods and results: All 24 h ambulatory Holter monitoring performed in our centre within a month after a first heart failure hospitalization were screened. Patients with HFpEF and permanent AF were included in the retrospective analysis. The following parameters of ventricular irregularity were calculated over the 24 h recording period: standard deviation of all RR intervals (SDNN), coefficient of variation of SDNN (CV‐SDNN = SDNN/mean RR), root of the mean squared differences of successive RR intervals (RMSSD), and percentage of consecutive RR intervals with difference over 50 ms (pNN50). The primary endpoint was rehospitalization for acute heart failure (HFrH). From 2010 to 2021, 51/216 screened patients were included. During a median follow‐up of 3.13 years, 29/51 patients reached the primary endpoint. HFrH patients had higher SDNN (205 ± 65 vs. 154 ± 46 ms; P < 0.01), CV‐SDNN (26 ± 8% vs. 19 ± 5%, P < 0.01), RMSSD (182 ± 47 vs. 138 ± 65 ms, P = 0.013), and pNN50 (76 ± 9 vs. 58 ± 26, P < 0.001) when compared with patients with no HFrH. In multivariate analysis, all those parameters remained significantly associated with HFrH. Conclusions: In this pilot study, we found some evidences for a deleterious impact of excessive ventricular irregularity on HFrH in AF patients with HFpEF. Those new findings could pave the way for new prognosis and therapeutic approaches in this patients' population. [ABSTRACT FROM AUTHOR]

Aims: Ring‐like late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) imaging is a special LGE pattern in patients with chronic inflammatory cardiomyopathy (infl‐CMP), which is associated with cardiac dysfunction and ventricular remodelling and attributed to viral infection followed by bacterial and parasitic infections. Data on the combination of CMR imaging and clinical parameters that can add long‐term prognostic value in patients with infl‐CMP are still rare. We aimed to evaluate the prognostic value of CMR in risk stratification in this kind of patients. Methods and results: A total of 319 consecutive patients with clinically suspected myocarditis were retrospectively identified. Forty‐seven patients with ring‐like LGE on CMR who diagnosed as infl‐CMP, and 72 patients with other LGE pattern were eligible for standardized follow‐up. The left ventricle (LV) and right ventricle function and mass were analyses by CMR. Myocardial strain of the ventricles was evaluated by feature tracking. Major (cardiac death, resuscitated cardiac arrest, ventricular assist device, transplantation, and appropriate implantable cardioverter‐defibrillator shock) and minor (rehospitalization due to heart failure and sustained atrial fibrillation) adverse cardiovascular events were assessed during follow‐up since the date of nCMR examination. Cox proportional hazards model was used to investigate which of the prognostic factors identified by univariable analysis were significantly associated with cardiac events. In the ring‐like LGE group, adverse cardiac events occurred in 14 (31.11%) patients, including 7 deaths (15.56%), 6 (13.33%) heart‐failure hospitalizations, and 1 (2.22%) case of sustained atrial fibrillation during the mean follow‐up period of 70.15 ± 45.68 months (interquartile range: 32.83–103.71 months). No major or minor adverse cardiac event occurred in the other LGE pattern group, except rehospitalization in one patient due to arrhythmia. Further analyses of ring‐like LGE group by univariable and Multivariable Cox proportional hazard regression analysis showed that body mass index (BMI) (hazard ratio [HR]: 0.54, 95% confidence interval [CI]: 0.40–0.73, P = 0.000), right ventricle cardiac index (RVCI) (HR: 0.31, 95% CI: 0.14–0.71, P = 0.002), LV basal peak circumferential strain (LV‐PCSbasal) (HR: 1.26, 95% CI: 1.11–1.43, P = 0.000) were independently associated with the long‐term outcome. Receiver operator characteristic curve indicated that the cut‐off of LV‐PCSBasal was −7.95%, and it has added prognostic value to BMI and RVCI. Conclusions: For infl‐CMP patients with ring‐like LGE on CMR, low BMI and RVCI were associated with a poor prognosis. LV‐PCSBasal with a cut‐off of −7.95% can add prognostic value for patients with infl‐CMP who have ring‐like LGE. [ABSTRACT FROM AUTHOR]

Aims: Liver fibrosis scores (LFSs) are non‐invasive and effective tools for estimating cardiovascular risks. To better understand the advantages and limitations of currently available LFSs, we determined to compare the predictive values of LFSs in heart failure with preserved ejection fraction (HFpEF) for primary composite outcome, atrial fibrillation (AF), and other clinical outcomes. Methods and results: This was a secondary analysis of the TOPCAT trial, and 3212 HFpEF patients were enrolled. Five LFSs, namely, non‐alcoholic fatty liver disease fibrosis score (NFS), fibrosis‐4 score (FIB‐4), BARD, aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio, and Health Utilities Index (HUI) scores were adopted. Cox proportional hazard model and competing risk regression model were performed to assess the associations between LFSs and outcomes. The discriminatory power of each LFS was evaluated by calculating the area under the curves (AUCs). During a median follow‐up of 3.3 years, a 1‐point increase in the NFS [hazard ratio (HR) 1.10; 95% confidence interval (CI) 1.04–1.17], BARD (HR 1.19; 95% CI 1.10–1.30), and HUI (HR 1.44; 95% CI 1.09–1.89) scores was associated with an increased risk of primary outcome. Patients with high levels of NFS (HR 1.63; 95% CI 1.26–2.13), BARD (HR 1.64; 95% CI 1.25–2.15), AST/ALT ratio (HR 1.30; 95% CI 1.05–1.60), and HUI (HR 1.25; 95% CI 1.02–1.53) were at an increased risk of primary outcome. Subjects who developed AF were more likely to have high NFS (HR 2.21; 95% CI 1.13–4.32). High levels of NFS and HUI scores were a significant predictor of any hospitalization and hospitalization for heart failure. The AUCs for the NFS in predicting primary outcome (0.672; 95% CI 0.642–0.702) and incident of AF (0.678; 95% CI 0.622–0.734) were higher than other LFSs. Conclusions: In light of these findings, NFS appears to have superior predictive and prognostic utility compared with AST/ALT ratio, FIB‐4, BARD, and HUI scores. Clinical trial registration: (https://clinicaltrials.gov). Unique identifier: NCT00094302. [ABSTRACT FROM AUTHOR]

Aims: Heart failure (HF) is an increasing concern worldwide. A rising HF burden is expected due to the prospected future demographic changes with aging populations. Consequently, the long‐term follow‐up and treatment will be performed increasingly by primary care physicians in the future. Contemporary data on HF patients in primary care are needed to plan and ensure an effective and safe follow‐up of future patients. Methods and results: The electronic patient journals of 148 primary care clinics in Denmark were searched in a standardized manner to identify patients with HF [code K77 of the International Classification of Primary Care, Second Edition]. Prespecified variables including demographic information, clinical variables, co‐morbidities, prescribed medications, and setting of follow‐up were recorded. In total, 1111 patients were included in the study. The mean timepoint for the HF diagnosis was August 2018. In 95% of cases, the diagnosis of HF was made in a specialized setting. The echocardiogram data used for phenotyping were available in 1042 (94%) of the 1111 patients. HF with reduced ejection fraction (HFrEF) was present in 43%, recovered HFrEF in 31%, and HF with mildly reduced (HFmrEF) or preserved ejection fraction (HFpEF) in 26%. In patients with HFrEF or recovered HFrEF, fundamental treatments were prescribed in 86% for angiotensin converting enzyme inhibitor (ACEI), angiotensin receptor blocker (ARB), or angiotensin receptor neprilysin inhibitor (ARNI), in 82% for beta‐blocker, in 38% for mineralocorticoid receptor antagonist (MRA), and in 12% for sodium‐glucose co‐transporter‐2 inhibitor (SGLT2i). Older patients were treated to a significantly lesser extent than young patients for all drug classes [odds ratio (OR) point estimates 0.50 to 0.69, all P‐values < 0.05]. In patients with HFmrEF or HFpEF, an ACEI, ARB, or ARNI was prescribed in 67%, beta‐blocker in 67%, MRA in 22%, and SGLT2i in 7.4% with significantly lower probability of treatment compared to patients with HFrEF or recovered HFrEF [OR point estimates 0.33 to 0.57, all P‐values < 0.05]. The setting of follow‐up was available in 96% of patients. Irrespective of HF phenotype, follow‐up was performed solely in primary care in 64%. These patients were generally treated to a lesser extent with HF therapies compared with patients where follow‐up included specialized care, yet differences were generally small. Conclusions: HFrEF is the most common phenotype of HF in primary care followed by recovered HFrEF and fundamental therapies are markedly underutilized. Initiatives to increase the use of recommended therapies are needed to improve the future care of patients with HF. [ABSTRACT FROM AUTHOR]

Aims: Heart failure (HF) is a global health burden and new strategies to achieve timely diagnosis and early intervention are urgently needed. Natriuretic peptide (NP) testing can be used to screen for left ventricular systolic dysfunction (LVSD), but evidence on test performance is mixed, and international HF guidelines differ in their recommendations. Our aim was to summarize the evidence on diagnostic accuracy of NP screening for LVSD in general and high‐risk community populations and estimate optimal screening thresholds. Methods: We searched relevant databases up to August 2020 for studies with a screened community population of over 100 adults reporting NP performance to diagnose LVSD. Study inclusion, quality assessment, and data extraction were conducted independently and in duplicate. Diagnostic test meta‐analysis used hierarchical summary receiver operating characteristic curves to obtain estimates of pooled accuracy to detect LVSD, with optimal thresholds obtained to maximize the sum of sensitivity and specificity. Results: Twenty‐four studies were identified, involving 26 565 participants: eight studies in high‐risk populations (at least one cardiovascular risk factor), 12 studies in general populations, and four in both high‐risk and general populations combined. For detecting LVSD in screened high‐risk populations with N‐terminal prohormone brain natriuretic peptide (NT‐proBNP), the pooled sensitivity was 0.87 [95% confidence interval (CI) 0.73–0.94] and specificity 0.84 (95% CI 0.55–0.96); for BNP, sensitivity was 0.75 (95% CI 0.65–0.83) and specificity 0.78 (95% CI 0.72–0.84). Heterogeneity between studies was high with variations in positivity threshold. Due to a paucity of high‐risk studies that assessed NP performance at multiple thresholds, it was not possible to calculate optimal thresholds for LVSD screening in high‐risk populations alone. To provide an indication of where the positivity threshold might lie, the pooled accuracy for LVSD screening in high‐risk and general community populations were combined and gave an optimal cut‐off of 311 pg/mL [sensitivity 0.74 (95% CI 0.53–0.88), specificity 0.85 (95% CI 0.68–0.93)] for NT‐proBNP and 49 pg/mL [sensitivity 0.68 (95% CI 0.45–0.85), specificity 0.81 (0.67–0.90)] for BNP. Conclusions: Our findings suggest that in high‐risk community populations NP screening may accurately detect LVSD, potentially providing an important opportunity for diagnosis and early intervention. Our study highlights an urgent need for further prospective studies, as well as an individual participant data meta‐analysis, to more precisely evaluate diagnostic accuracy and identify optimal screening thresholds in specifically defined community‐based populations to inform future guideline recommendations. [ABSTRACT FROM AUTHOR]

Aims: No studies have comprehensively compared the efficacy of sodium‐glucose cotransporter‐2 (SGLT2) inhibitors, renin–angiotensin system (RAS) inhibitors, and angiotensin receptor neprilysin (ARN) inhibitors based on different type of heart failure, including heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). The aim of this network meta‐analysis was to evaluate the relative efficacy of SGLT2 inhibitor (SGLT2i), RAS inhibitor (RASi) and ARN inhibitor (ARNI) in different types of heart failure. Methods: A systemic literature search was performed from inception to 19 November 2022 for randomized control trials assessing the risk of cardiovascular (CV) death or hospitalization for heart failure (HHF) of these drugs in HF. A network meta‐analysis was performed. Risk ratio (RR) with 95% confidence intervals (CI) were synthesized. Results: Seventeen studies were selected with a total of 61 489 patients. In patients with HFrEF, ARNI led to a reduced risk of a composite outcome of CV death or HHF when compared with placebo (RR = 0.83, 95% CI 0.77–0.89). Similar trends were observed when focusing on the outcome of CV death or HHF alone. In patients with HFpEF, SGLT2i showed the beneficial effects on the CV death or HHF events when compared with placebo and RASi (RR = 0.82, 95% CI 0.74–0.92; RR = 1.16, 95% CI 1.02–1.31). For CV death, all these three drugs could not show beneficial effects in HFpEF. For the incidence of HHF in HFpEF, both SGLT2i and ARNI demonstrated the beneficial effects but SGLT2i was superior to ARNI. There were no differences in the events of discontinuation under these drugs when compared with placebo or each other in either HFrEF or HFpEF patients. SGLT2i showed the least renal injury among these interventions in HFrEF and there were no differences in the incidence of renal injury of these interventions in HFpEF. Conclusions: Among these drugs, ARNI showed the greatest ability to lower the incidence of CV death or HHF and SGLT2i exerted the least renal injury in patients with HFrEF. In patients with HFpEF, SGLT2i was associated with a reduction in the risk of CV death or HHF. There were no differences in the incidence of renal injury of these interventions in HFpEF. The intolerance of these drugs were comparable in both HFrEF and HFpEF. [ABSTRACT FROM AUTHOR]

Aims: This study aimed to clarify the relationship between cardiovascular prognosis and left ventricular hypertrophy (LVH) in patients with severe aortic stenosis who underwent transcatheter aortic valve replacement (TAVR) and to investigate the relationship between cardiac sympathetic nerve (CSN) function and these factors using 123I‐metaiodobenzylguanidine scintigraphy. Methods and results: In this single‐centre, retrospective observational study, 349 patients who underwent TAVR at our institution between July 2017 and May 2020 were divided into two groups: those with severe LVH pre‐operatively [severe LVH (+) group] and those without LVH pre‐operatively [severe LVH (−) group]. The rates of freedom from cardiovascular events (cardiovascular death and heart failure hospitalization) were compared. The relationship between changes in left ventricular mass index (LVMi) and changes in delay heart–mediastinum ratio (H/M) from before TAVR to 6 months after TAVR was also investigated. The event‐free rate was significantly lower in the severe LVH (+) group (87.1% vs. 96.0%, log‐rank P = 0.021). The severe LVH (+) group exhibited a significantly lower delay H/M value, scored by 123I‐metaiodobenzylguanidine scintigraphy, than the severe LVH (−) group (2.33 [1.92–2.67] vs. 2.67 [2.17–3.68], respectively, P < 0.001). Moreover, the event‐free rate of post‐operative cardiovascular events was lower among patients with a delay H/M value < 2.50 than that among other patients (87.7% vs. 97.2%, log‐rank P = 0.012). LVMi was significantly higher (115 [99–130] vs. 90 [78–111] g/m2, P < 0.001) and delay H/M value was significantly lower (2.53 [1.98–2.83] vs. 2.71 [2.25–3.19], P = 0.025) in the severe LVH (+) group than in the severe LVH (−) group at 6 months after TAVR. Patients with improved LVH at 6 months after TAVR also had increased delay H/M (from 2.51 [2.01–2.81] to 2.67 [2.26–3.02], P < 0.001), whereas those without improved LVH had no significant change in delay H/M (from 2.64 [2.23–3.06] to 2.53 [1.97–3.00], P = 0.829). Conclusions: Severe LVH before TAVR is a prognostic factor for poor post‐operative cardiovascular outcomes. LVH associated with aortic stenosis and CSN function are correlated, suggesting their involvement in LVH prognosis. [ABSTRACT FROM AUTHOR]

Aims: This study aimed to investigate the prognostic value of dynamic changes in left ventricular ejection fraction (EF) for cardiovascular (CV) outcomes in an all‐comer heart failure (HF) population with reduced EF (HFrEF, EF < 40%). We sought to identify independent factors related to improvement in EF and to identify risk factors for increased risk of CV events in the subgroups of improved EF (iEF) and non‐improved EF (niEF), respecively. Methods and results: This is a retrospective sub‐analysis from the REDEAL HF trial, which included consecutive patients with chronic HF who were hospitalized from July 2009 to December 2017. Baseline and follow‐up echocardiography data (interval ≥12 months) of 573 consecutive patients with HFrEF were analysed. iEF was defined as absolute improvement in EF ≥ 10% and follow‐up EF over 40%. The primary endpoint was defined as a composite endpoint of cardiovascular (CV) death, CV hospitalization, or appropriate implantable cardioverter‐defibrillator (ICD) therapy for ventricular arrhythmia. EF improved in 37.2% of patients with HFrEF during follow‐up (median period of 17 months). iEF was independently associated with shorter HF duration (>4 vs. ≤4 years, odd ratio [OR] = 0.477, 95% CI 0.305–0.745), no coronary artery disease (CAD vs. no CAD, OR = 0.583, 95% CI 0.396–0.858), and no ICD implantation (ICD vs. no ICD, OR = 0.341, 95% CI 0.228–0.511). Compared with niEF, iEF was significantly and independently associated with lower all‐cause mortality (22.1% vs. 31.1%, P = 0.019; hazard ratio [HR] = 0.674, 95% CI 0.469–0.968), lower CV mortality (8.9% vs. 16.1%, P = 0.015; HR = 0.539, 95% CI 0.317–0.916), and lower CV events risk (27.2% vs. 49.2%, P < 0.001; HR 0.519, 95% CI 0.381–0.708), after adjustment for age, sex, duration of HF, and other clinical risk factors. Hypertension (HR = 2.452, P = 0.032) and elevated N‐terminal prohormone of brain natriuretic peptide (NT‐proBNP >1153 pg/mL, HR = 4.372, P < 0.001) were identified as independent risk factors for CV events in the iEF subgroup. ICD implantation (HR = 1.533, P = 0.011), elevated NT‐proBNP (HR = 1.626, P = 0.018), increased left atrial volume index (HR = 1.461, P = 0.021), reduced lateral mitral annular plane systolic excursion (HR = 1.478, P = 0.025), and reduced tricuspid plane systolic excursion (HR = 1.491, P = 0.039) were identified as risk factors for CV events in the niEF subgroup. Conclusions: Improvement in EF is independently related to the longer survival and lower CV related mortality and hospitalization rate of HFrEF. Elevated baseline NT‐proBNP is identified as the strongest prognostic factor associated with increased CV events risk in HFrEF patients both with and without improved EF, regardless of age, sex, duration of HF, and other clinical risk factors. [ABSTRACT FROM AUTHOR]

Aims: Hyperkalaemia is observed frequently in heart failure (HF) patients and is associated with an impaired prognosis and underuse of mineralocorticoid receptor antagonists (MRAs). However, the effects of serum potassium on prescription of the full guideline recommended daily dose of 50 mg in real‐world daily practice are unknown. Therefore, we investigated serum potassium and its association with the prescribed MRA dose in a large cohort of chronic HF patients. Methods and results: A total of 5346 patients with chronic HF with a left ventricular ejection fraction ≤40% from 34 Dutch outpatient HF clinics between 2013 and 2016 were analysed on serum potassium and MRA (spironolactone and eplenerone) dose. Data were stratified by potassium as a serum potassium level <4.0, 4.0 to 5.0 or >5.0 mmol/L. Multivariable logistic regression models were used to assess the association between serum potassium and MRA dose and to adjust for potential confounders. Mean serum potassium was 4.4 ± 0.5 mmol/L and hyperkalaemia (serum potassium >5.0 mmol/L) was present in 399 patients (7.5%). MRA was used in 3091 patients (58.1%). Patients with hyperkalaemia significantly less often received ≥100% of the target dose (50 mg) compared with patients with a serum potassium between 4.0–5.0 mmol/L and <4.0 mmol/L (7.7% vs. 9.5% vs. 13.6% respectively, P = 0.0078). In the multivariable regression analyses, patients with hyperkalaemia were significantly less likely to receive ≥100% of the target dose compared with patients with serum potassium 4.0–5.0 mmol/L (OR 0.38, 95% CI 0.15–0.97, P = 0.044). Additionally, a one unit increase in serum potassium was significantly associated with a lower odds of receiving ≥100% of the target dose (OR 0.69, 95% CI 0.49–0.98, P = 0.036). Conclusions: In this large registry of real‐world chronic HF patients, both an increase in serum potassium and hyperkalaemia were associated with a lower odds of receiving the guideline‐recommended MRA dose. [ABSTRACT FROM AUTHOR]

Aims: Heart failure (HF) is reported to be one of the major risks of bleeding events. On the other hand, HF patients frequently receive anticoagulants or antiplatelet therapy to manage various co‐morbidities. However, predictors of bleeding events in patients with HF have rarely been reported. This study aimed to evaluate the predictors of bleeding events and relationship between bleeding events and HF re‐hospitalizations. Methods and results: We included 1660 acute decompensated heart failure (ADHF) patients from the AURORA registry between January 2015 and December 2020. A total of 1429 patients were excluded because of history of HF admission, missing echocardiographic data at discharge, lost to follow‐up, haemodialysis and no antithrombotic drugs. Finally, we evaluated 231 patients from AURORA registry. The bleeding events were defined as Type 2 to 5 bleeding according to the Bleeding Academic Research Consortium definition. We divided our patients into the bleeding group and non‐bleeding group. We compared the baseline characteristics, medications, laboratory data, and echocardiographic data between the two groups. Median age was 78 (IQR 71–82) years old and male accounted for 59%. Approximately half of the patients had an antiplatelet therapy and 70% had an anticoagulant therapy. During a median follow‐up of 651 (IQR 357–1139) days, 32 patients (13.8%) suffered from bleeding events. The major driver of the registered events was gastrointestinal bleeding (n = 21, 65.6%), and the other events were cerebral bleeding (n = 4, 12.5%), intraarticular bleeding (n = 2, 6.3%), urogenital bleeding (n = 2, 6.3%), haemorrhagic pericardial effusions (n = 1, 3.1%), subcutaneous hematomas (n = 1, 3.1%), and haemothorax (n = 1, 3.1%). There was a significantly lower haemoglobin level (P < 0.01), higher proportion of inferior vena cava (IVC) diameter ≥21 mm (P < 0.01), and higher furosemide equivalent doses per kilogram (P < 0.01) in the bleeding group than non‐bleeding group. A multivariate analysis revealed an equivalent dose of furosemide per kilogram ≥0.66 mg/kg (hazard ratios (HR) of 2.64, 95% confidence interval (CI) 1.26–5.68, P = 0.01), haemoglobin ≤10.3 g/dL (HR of 2.43, 95% CI 1.14–5.03, P = 0.02), and IVC diameter ≥21 mm (HR of 2.79, 95% CI 1.16–6.29, P = 0.02) were independently associated with bleeding events. The Kaplan–Meier analysis showed that HF re‐hospitalization rates were higher in the bleeding group than non‐bleeding group (P = 0.04). Conclusions: High doses of oral loop diuretics, IVC dilatation, and anaemia were predictors of bleeding events in patients hospitalized with ADHF patients. In addition, bleeding events were associated with HF re‐hospitalizations. [ABSTRACT FROM AUTHOR]

Aims: Frailty in older patients with stage B heart failure with preserved ejection fraction (HFpEF) has not been fully explored. We evaluated the prevalence and prognostic significance of frailty in older patients diagnosed with stage B HFpEF. Methods: Our prospective cohort study included inpatients aged ≥65 years who were followed up for 3 years. Stage B HFpEF was defined as cardiac structural or functional abnormalities with a left ventricular ejection fraction (LVEF) ≥ 50% without signs or symptoms. Frailty was assessed using the Fried phenotype. The primary outcome was 3‐year all‐cause mortality or readmission. Results: Overall, 520 older inpatients diagnosed with stage B HFpEF [mean ± standard deviation age: 75.5 ± 6.25 years, male: 222 (42.7%)] were included in the study. Of these, 145 (27.9%) were frail. Frail patients were older (78.5 ± 6.23 vs. 74.3 ± 6.22 years, P < 0.001), with a lower body mass index (24.6 ± 3.60 vs. 25.7 ± 3.27 kg/m2, P = 0.001), higher level of N‐terminal pro‐B‐type natriuretic peptide [279 (interquartile range: 112.4, 596) vs. 140 (67.1, 266) pg/mL, P < 0.001], longer timed up‐and‐go test result (19.9 ± 9.71 vs. 13.3 ± 5.08 s, P < 0.001), and poorer performance in the short physical performance battery (4.1 ± 3.26 vs. 8.2 ± 2.62, P < 0.001), basic activities of daily living (BADL, 4.7 ± 1.71 vs. 5.7 ± 0.57, P < 0.001), and instrumental activities of daily living (IADL, 4.4 ± 2.73 vs. 7.4 ± 1.33, P < 0.001). Frail patients were more likely to have a Mini‐Mental State Examination (MMSE) score <24 (55.9% vs. 28.8%, P < 0.001) and take more than five medications (64.1% vs. 47.2%, P = 0.001). Frail patients had a higher incidence of all‐cause mortality or readmission (62.8% vs. 47.7%, P = 0.002), all‐cause readmission (56.6% vs. 45.9%, P = 0.029), and readmission for non‐heart failure (55.2% vs. 41.3%, P = 0.004) during the 3‐year follow‐up, with a 1.53‐fold (95%CI 1.11–2.11, P = 0.009) higher risk of all‐cause mortality or readmission, a 1.52‐fold (95%CI 1.09–2.11, P = 0.014) higher risk of all‐cause readmission, and a 1.70‐fold (95%CI 1.21–2.38, P = 0.002) higher risk of readmission for non‐clinical heart failure, adjusted for sex, age, polypharmacy, Athens Insomnia Scale, MMSE, LVEF, BADL, and IADL. Conclusions: Frailty is common in elderly patients with stage B HFpEF. Physical frailty, particularly low physical activity, can independently predict the long‐term prognosis in these patients. [ABSTRACT FROM AUTHOR]

Aims: Several patients with heart failure and reduced ejection fraction (HFrEF) do not receive renin–angiotensin–aldosterone system (RAAS) inhibitors at the recommended dose or at all, frequently due to actual or feared hyperkalaemia. Sodium zirconium cyclosilicate (SZC) is an orally administered non‐absorbed intestinal potassium binder proven to lower serum potassium concentrations. Methods and results: PRIORITIZE‐HF was an international, multicentre, parallel‐group, randomized, double‐blind, placebo‐controlled study to evaluate the benefits and risks of using SZC to intensify RAAS inhibitor therapy. Patients with symptomatic HFrEF were eligible and randomly assigned to receive SZC 5 g or placebo once daily for 12 weeks. Doses of study medication and RAAS inhibitors were titrated during the treatment period. The primary endpoint was the proportion of patients at 12 weeks in the following categories: (i) any RAAS inhibitor at less than target dose, and no MRA; (ii) any RAAS inhibitor at target dose and no MRA; (ii) MRA at less than target dose; and (iv) MRA at target dose. Due to challenges in participant management related to the COVID‐19 pandemic, the study was prematurely terminated with 182 randomized patients. There was no statistically significant difference in the distribution of patients by RAAS inhibitor treatment categories at 3 months (P = 0.43). The proportion of patients at target MRA dose was numerically higher in the SZC group (56.4%) compared with the placebo group (47.0%). Overall, SZC was well tolerated. Conclusions: PRIORITIZE‐HF was terminated prematurely due to COVID‐19 and did not demonstrate a statistically significant increase in the intensity of RAAS inhibitor therapies with the potassium‐reducing agent SZC compared with placebo. [ABSTRACT FROM AUTHOR]

Right ventricular (RV) function and its adaptation to increased afterload [RV–pulmonary arterial (PA) coupling] are crucial in various types of pulmonary hypertension, determining symptomatology and outcome. In the course of disease progression and increasing afterload, the right ventricle undergoes adaptive remodelling to maintain right‐sided cardiac output by increasing contractility. Exhaustion of compensatory RV remodelling (RV–PA uncoupling) finally leads to maladaptation and increase of cardiac volumes, resulting in heart failure. The gold‐standard measurement of RV–PA coupling is the ratio of contractility [end‐systolic elastance (Ees)] to afterload [arterial elastance (Ea)] derived from RV pressure–volume loops obtained by conductance catheterization. The optimal Ees/Ea ratio is between 1.5 and 2.0. RV–PA coupling in pulmonary hypertension has considerable reserve; the Ees/Ea threshold at which uncoupling occurs is estimated to be ~0.7. As RV conductance catheterization is invasive, complex, and not widely available, multiple non‐invasive echocardiographic surrogates for Ees/Ea have been investigated. One of the first described and best validated surrogates is the ratio of tricuspid annular plane systolic excursion to estimated pulmonary arterial systolic pressure (TAPSE/PASP), which has shown prognostic relevance in left‐sided heart failure and precapillary pulmonary hypertension. Other RV–PA coupling surrogates have been formed by replacing TAPSE with different echocardiographic measures of RV contractility, such as peak systolic tissue velocity of the lateral tricuspid annulus (S′), RV fractional area change, speckle tracking‐based RV free wall longitudinal strain and global longitudinal strain, and three‐dimensional RV ejection fraction. PASP‐independent surrogates have also been studied, including the ratios S′/RV end‐systolic area index, RV area change/RV end‐systolic area, and stroke volume/end‐systolic volume. Limitations of these non‐invasive surrogates include the influence of severe tricuspid regurgitation (which can cause distortion of longitudinal measurements and underestimation of PASP) and the angle dependence of TAPSE and PASP. Detection of early RV remodelling may require isolated analysis of single components of RV shortening along the radial and anteroposterior axes as well as the longitudinal axis. Multiple non‐invasive methods may need to be applied depending on the level of RV dysfunction. This review explains the mechanisms of RV (mal)adaptation to its load, describes the invasive assessment of RV–PA coupling, and provides an overview of studies of non‐invasive surrogate parameters, highlighting recently published works in this field. Further large‐scale prospective studies including gold‐standard validation are needed, as most studies to date had a retrospective, single‐centre design with a small number of participants, and validation against gold‐standard Ees/Ea was rarely performed. [ABSTRACT FROM AUTHOR]

Background: P‐wave indices have been used to predict incident atrial fibrillation (AF), stroke, and mortality. However, such indices derived from automated ECG measurements have not been explored for their predictive values in heart failure (HF). We investigated whether automated P‐wave indices can predict adverse outcomes in HF. Methods: This study included consecutive Chinese patients admitted to a single tertiary centre, presenting with HF but without prior AF, and with at least one baseline ECG, between 1 January 2010 and 31 December 2016, with last follow‐up of 31 December 2019. Results: A total of 2718 patients were included [median age: 77.4, interquartile range (IQR): (66.9–84.3) years; 47.9 males]. After a median follow‐up of 4.8 years (IQR: 1.9–9.0 years), 1150 patients developed AF (8.8/year), 339 developed stroke (2.6/year), 563 developed cardiovascular mortality (4.3/year), and 1972 had all‐cause mortality (15.1/year). Compared with 101–120 ms as a reference, maximum P‐wave durations predicted new‐onset AF at ≤90 ms [HR: 1.17(1.11, 1.50), P < 0.01], 131–140 ms [HR: 1.29(1.09, 1.54), P < 0.001], and ≥141 ms [HR: 1.52(1.32, 1.75), P < 0.001]. Similarly, they predicted cardiovascular mortality at ≤90 ms [HR: 1.50(1.08, 2.06), P < 0.001] or ≥141 ms [HR: 1.18(1.15, 1.45), P < 0.001], and all‐cause mortality at ≤90 ms [HR: 1.26(1.04, 1.51), P < 0.001], 131–140 ms [HR: 1.15(1.01, 1.32), P < 0.01], and ≥141 ms [HR: 1.31(1.18, 1.46), P < 0.001]. These remained significant after adjusting for significant demographics, past co‐morbidities, P‐wave dispersion, and maximum P‐wave amplitude. Conclusions: Extreme values of maximum P‐wave durations (≤90 ms and ≥141 ms) were significant predictors of new‐onset AF, cardiovascular mortality, and all‐cause mortality. [ABSTRACT FROM AUTHOR]

Aims: Increased red cell distribution width (RDW) is a poor prognostic factor in patients with heart failure (HF). However, only a few large‐scale studies have identified the clinical utility of RDW after adjusting for covariates affecting RDW. Methods and results: From January 2010 to April 2021, we retrospectively enrolled patients diagnosed with HF from three referral hospitals with available RDW data (taken within 3 months of HF diagnosis) using an integrated clinical data system. Patients with an ejection fraction (EF) < 50% or HFA‐PEFF (Heart Failure Association Pre‐test assessment, Echocardiography and natriuretic peptide, Functional testing, Final aetiology) score ≥ 2 without severe valvular heart disease or coronary revascularization were enrolled. The primary endpoint was all‐cause mortality, and cardiovascular mortality was also collected. Multivariable Cox regression analysis and stabilized inverse probability of treatment weighting (IPTW) were used to identify any association between RDW and all‐cause death by balancing covariates or compounding factors. The global χ2 score was calculated and discrimination analysis was performed to evaluate the incremental value of RDW in predicting prognosis. Among the 6599 participants enrolled in this study, 1256 (19.0%) cases of all‐cause death occurred, and the median duration of follow‐up was 887 (interquartile range 351–1589) days. Elevated RDW at the initial diagnosis was associated with poor prognosis [cumulative incidence: 819 (30.2%) vs. 437 (11.2%), relative risk 1.58, 95% confidence interval (CI) 1.51–1.67, log‐rank P < 0.001]. Multivariable Cox analysis showed that elevated RDW was a poor prognostic factor for the primary endpoint [hazard ratio (HR) 1.11, 95% CI 1.06–1.16, P < 0.001], independent of clinical risk factors, N‐terminal pro‐brain natriuretic peptide (NT‐proBNP), and EF, which was concordant with the stabilized IPTW (HR 1.29, 95% CI 1.10–1.49, P < 0.001). Adding RDW to model composed of traditional risk factors, NT‐proBNP, and echocardiographic parameters showed incremental prognostic value for predicting poor prognosis (area under the receiver operating characteristic curve, 0.799–0.826; P < 0.001). Conclusions: Increased RDW at the time of diagnosis is associated with poor prognosis in patients with HF, independent of clinical risk factors, such as NT‐proBNP, and echocardiographic parameters. Therefore, RDW may aid in the management of these patients beyond traditional risk factors. [ABSTRACT FROM AUTHOR]

To investigate the effectiveness of multicomponent integrated care on clinical outcomes among patients with chronic heart failure. We conducted a meta‐analysis of randomized clinical trials, published in English language from inception to 20 April 2022, with at least 3‐month implementation of multicomponent integrated care (defined as two or more quality improvement strategies from different domains, viz. the healthcare system, healthcare providers, and patients). The study outcomes were mortality (all‐cause or cardiovascular) and healthcare utilization (hospital readmission or emergency department visits). We pooled the risk ratio (RR) using Mantel–Haenszel test. A total of 105 trials (n = 37 607 patients with chronic heart failure; mean age 67.9 ± 7.3 years; median duration of intervention 12 months [interquartile range 6–12 months]) were analysed. Compared with usual care, multicomponent integrated care was associated with reduced risk for all‐cause mortality [RR 0.90, 95% confidence interval (CI) 0.86–0.95], cardiovascular mortality (RR 0.73, 95% CI 0.60–0.88), all‐cause hospital readmission (RR 0.95, 95% CI 0.91–1.00), heart failure‐related hospital readmission (RR 0.84, 95% CI 0.79–0.89), and all‐cause emergency department visits (RR 0.91, 95% CI 0.84–0.98). Heart failure‐related mortality (RR 0.94, 95% CI 0.74–1.18) and cardiovascular‐related hospital readmission (RR 0.90, 95% CI 0.79–1.03) were not significant. The top three quality improvement strategies for all‐cause mortality were promotion of self‐management (RR 0.86, 95% CI 0.79–0.93), facilitated patient–provider communication (RR 0.87, 95% CI 0.81–0.93), and e‐health (RR 0.88, 95% CI 0.81–0.96). Multicomponent integrated care reduced risks for mortality (all‐cause and cardiovascular related), hospital readmission (all‐cause and heart failure related), and all‐cause emergency department visits among patients with chronic heart failure. [ABSTRACT FROM AUTHOR]

Heart failure is a leading cause of morbidity and mortality, with relevant social and economic burden on global healthcare system. Although the development of novel diagnostic tools and the advance in therapies have deeply influenced the diagnosis and treatment of this disease, improving both prognosis and life expectancy of patients, hospitalization is still high, and mortality remains considerable. MicroRNAs are small endogenous RNA molecules that post‐transcriptionally regulate gene expression in both physiological and pathological processes. In recent years, microRNA have arisen as attractive therapeutic targets in the treatment of a wide spectrum of pathologies, including heart failure. In cardiac pathology, deregulation of microRNAs expression and function is associated to adverse outcome and heart failure progression. Circulating levels of specific microRNAs have emerged as useful biomarkers for the diagnosis of heart failure or as prognostic indicators. In the present review, we summarize the state of current research on the role of miRNAs as biomarkers for diagnosis and prognosis in patients with heart failure and their use as potential therapeutic targets for this condition. [ABSTRACT FROM AUTHOR]

Aims: The long‐term outcome in patients with heart failure (HF) after hospitalization may vary substantially depending on their age and left ventricular ejection fraction (LVEF). We aimed to assess the relative rates of cardiovascular death (CVD) and non‐CVD based on the age and how the rates differ under the updated LVEF classification system. Methods and results: Consecutively registered hospitalized patients with HF (N = 3558; 39.7% women with a mean age of 73.9 ± 13.3 years) were followed for a median of 2 (interquartile range, 0.8–3.1) years. The CVDs and non‐CVDs were evaluated based on age [young (<65 years), older (65–84 years), and very old (≥85 years)] and LVEF classification [HF with preserved EF (HFpEF; LVEF ≥50%) and non‐HFpEF (LVEF <50%)]. The adverse clinical events were adjudicated independently by a central committee. Overall, 1505 (42.3%) had HFpEF [young: n = 182 (12.1%), older: n = 894 (59.4%), very old: n = 429 (28.5%)], and 2053 (57.7%) had non‐HFpEF [young: n = 575 (28.0%), older: n = 1159 (56.5%), very old: n = 319 (15.5%)]. During the follow‐up, the crude incidence of all‐cause death was higher in non‐HFpEF than in HFpEF across all age groups (non‐HFpEF vs. HFpEF, young: 10.4% vs. 5.5%, log‐rank P = 0.10; older: 26.6% vs. 20.9%, log‐rank P = 0.002; very old: 36.7% vs. 31.7%, log‐rank P = 0.043). CVDs accounted for more than half of all deaths in non‐HFpEF (young 65.0%, older 64.2%, and very old 55.6%), whereas the proportion of CVDs remained less than half in HFpEF (young 50.0%, older 41.2%, very old 38.2%). HF readmission was associated with subsequent all‐cause death in non‐HFpEF [hazard ratio (HR): 1.72, 95% confidence interval (CI): 1.41–2.09, P < 0.001], but not in HFpEF (HR: 1.12, 95% CI: 0.87–1.43, P = 0.39). Conclusions: The probability of a non‐CVD increases in both LVEF categories with advancing age, but that it is greater in the HFpEF category. The findings indicate that mitigating CV‐related outcomes alone may be insufficient for treating HF in older population, particularly in the HFpEF category. [ABSTRACT FROM AUTHOR]

Aims: Acute viral myocarditis (AVMC) is the aetiology of heart failure (HF) with few specific treatments. The improvement of left ventricular ejection fraction (LVEF) is a critical predictor for the prognosis of AVMC. LCZ696 is a drug used in HF to improve LVEF, with a few research on AVMC. In this research, we evaluated the effects and mechanism of LCZ696 in improving LVEF in AVMC. Methods: Eighty 4‐week‐old male BALB/c mice were randomly divided into four groups of 20: Sham; Sham + LCZ696 (60 mg/kg/d); AVMC; AVMC + LCZ696. The above experiments were repeated by CVB3‐infected HL‐1 and Mdivi‐1 to down‐regulated dynamin‐related protein 1(Drp1). Adeno‐associated virus 9 (AAV9) with enhanced green fluorescent proteins (GFP) was injected to produce Drp1‐overexpression mice and set up four groups: AVMC group, AVMC + AAV group, AVMC + LCZ696 group, and AVMC + LCZ696 + AAV group (n = 20 in each group). LVEF was evaluated by echocardiography at a similar heart rate (HR) at d7, Drp1 (p‐Drp1), inflammation and apoptosis by histology and Western blot (WB), and mitochondrial by electron microscopy. Results: Cardiac function were injured in AVMC that LCZ696 reversed (LVEF, %: Sham: 68.99 ± 9.67; Sham + LCZ696: 71.96 ± 6.20; AVMC: 30.95 ± 6.40*; AVMC + LCZ696: 68.99 ± 9.67*#, *P < 0.05 vs. Sham, #P < 0.05 vs. AVMC). LCZ696 attenuated p‐Drp1 expression, inflammation, apoptosis, and mitochondrial fission (p‐Drp1/Drp1: Sham: 1; Sham + LCZ696: 1.37 ± 0.22; AVMC: 2.29 ± 0.36*; AVMC+LCZ696: 1.43 ± 0.08*#, *P < 0.05 vs. Sham, #P < 0.05 vs. AVMC). Some of the above results were repeated in CVB3‐infected HL‐1 cells and Mdivi‐1. AAV increased Drp1 expression and mitochondrial fission, inflammatory, and apoptosis. Compared with the AVMC + AAV group, the LVEF increased from 24.44 ± 0.03% to 32.33 ± 0.05% in the AVMC + LCZ696 + AAV group(P < 0.05), p‐Drp1/Drp1 decreased from 0.54 ± 0.12 to 0.42 ± 0.09*, and IL‐6, c‐IL‐1β, and c‐caspase‐3/caspase‐3 decreased from 1.07 ± 0.22 to 0.72 ± 0.08*, from 1.03 ± 0.14 to 0.79 ± 0.09*, and from 4.69 ± 0.29 to 0.92 ± 0.13*, respectively (*P < 0.05). Conclusions: LCZ696 has a protective effect on AVMC by improving LVEF and reducing inflammation and apoptosis, which may be due to the inhibition of Drp1‐mediated mitochondrial fission. [ABSTRACT FROM AUTHOR]

Over the last 15–20 years, remarkable developments of heart failure (HF) pharmacotherapies have been achieved. However, HF remains a global healthcare challenge with more than 64 million patients worldwide. Optimization of guideline‐directed chronic HF medical therapy is highly recommended with every patient visit to improve outcomes in patients with HF with reduced ejection fraction. However, the majority of patients in real‐world settings are treated with doses that are lower than those with proven efficacy in clinical trials, which might be due to concerns of adverse effects and inertia of physicians. Likewise, a significant proportion of patients still do not receive all drug classes that could improve their prognosis. The recent European Society of Cardiology guidelines do not provide detailed recommendations on how these drug classes should be implemented in the treatment of inpatients to allow for both safety and a high likelihood of efficacy. We therefore propose a practical approach algorithm to support physicians to treat HF patients in their daily practice. [ABSTRACT FROM AUTHOR]

Aims: We aim to investigate the correlation between high levels of the systemic immune‐inflammation index (SII) and long‐term mortality and major cardiovascular adverse events in advanced chronic heart failure patients with renal dysfunction. Methods and results: Seven hundred seventeen advanced chronic heart failure patients with renal dysfunction, who visited the First affiliated hospital of Zhengzhou University from September 2019 to December 2020, were included. All‐cause mortalities (ACM) were selected as primary endpoints and major cardiovascular adverse events (MACEs) as the secondary endpoints. Based on the receiver operating characteristic (ROC) curve and the Youden index, the optimal cut‐off values of SII for ACM and MACEs were 1228 and 1406. In the group where ACM were the primary endpoint, patients were categorized into the low‐SII group (n = 479) and the high‐SII group (n = 238). Patients in the group using MACEs as the secondary endpoint were also categorized into the low‐SII groups (n = 514) and the high‐SII groups (n = 203). Univariate and multivariate COX regression were used to screen the independent predictors for ACM and MACEs, revealing the relationship between SII levels and endpoints. According to the univariate COX analysis, SII was the risk factor (hazard ratio [HR] = 2.144, 95% confidence interval [CI]: 1.565–2.938, P < 0.001) for the ACM subgroup. It was also the risk factor (HR = 1.625, CI: 1.261–2.905, P < 0.001) for the MACEs subgroup. Multivariate COX regression analysis indicated that the occurrence of ACM and MACEs in high‐level SII and low‐level SII patients had statistical differences. The incidence of ACM increased by 70.3% (HR = 1.703; 95% CI: 1.200–2.337; P = 0.002) in patients of the high SII level group, the incidence of MACEs increased by 58.3% (HR = 1.583, 95% CI: 1.213–2.065, P = 0.001). Kaplan–Meier (K‐M) survival analysis further suggested that patients with a high SII level had an increased risk of having ACM (log‐rank P < 0.001) and MACEs (log‐rank P < 0.001) within 30 months. SII could be considered as a novel predictor of the occurrence of ACM and MACEs for patients with advanced chronic heart failure and renal dysfunction. Conclusions: This study suggested that SII is a novel independent predictor of mortality in advanced chronic heart failure patients with renal dysfunction, and it should be considered in current clinical management. [ABSTRACT FROM AUTHOR]

Aims: In heart failure (HF) with reduced left ventricular ejection fraction (HFrEF), the prognosis appears better in non‐ischaemic than in ischaemic aetiology. Infrequent diagnostic work‐up for ischaemic heart disease (IHD) in HF is reported. In this study, we compared short‐term response to initiated guideline‐directed medical treatment (GDMT) in recent‐onset HFrEF of non‐ischaemic (non‐IHF) vs. ischaemic (IHF) aetiology and evaluated the frequency of coronary investigation. Methods and results: Patients hospitalized with recent‐onset HFrEF [left ventricular ejection fraction (LVEF) < 40%] between 1 January 2016 and 31 December 2019 were included. Treatment response was determined by use of a hierarchical clinical composite outcome classifying each patient as worsened, improved, or unchanged based on hard outcomes (mortality, heart transplantation, and HF hospitalization) and soft outcomes (± ≥10 unit change in LVEF, ± ≥30% change in N‐terminal pro‐B‐type natriuretic peptide, and ± ≥1 point change in New York Heart Association functional class) during 28 weeks of follow‐up. The associations between baseline characteristics and composite changes were analysed with multiple logistic regression. Among the 364 patients analysed, 47 were not investigated for IHD. Comparing non‐IHF (n = 203) vs. IHF (n = 114), patients were younger (mean age 61.0 vs. 69.4 years, P < 0.001) with lower mean LVEF (26% vs. 31%, P < 0.001), but with similar male predominance (70.4% vs. 75.4%, P = 0.363). For non‐IHF vs. IHF, the composite outcomes were worsened (19.1% vs. 43.9%, P < 0.001) and improved (74.2% vs. 43.9%, P < 0.001). After multivariable adjustments, IHF was associated with increased odds for worsening [odds ratio (OR) 2.94; 95% confidence interval (CI) 1.51–5.74; P = 0.002] and decreased odds for improvement (OR 0.35; 95% CI 0.18–0.65; P < 0.001). In cases without previous IHD or new‐onset myocardial infarction (n = 261), a decision for coronary investigation was made in 69.0%. Conclusions: In recent‐onset HFrEF, patients with non‐IHF responded better to GDMT than patients with IHF. Almost one‐third of patients selected for follow‐up at HF clinics were never investigated for IHD. [ABSTRACT FROM AUTHOR]

Aims: The aim of this study was to assess the performance of these main scores in predicting prognosis in patients with heart failure (HF). Methods and results: A total of 2008 patients who were admitted to the Fourth People's Hospital of Zigong, Sichuan, from December 2016 to June 2019 and diagnosed with HF were included in the study. We compared the prognostic predictive performance of Seattle Heart Failure Model (SHFM), Meta‐Analysis Global Group in Chronic Heart Failure (MAGGIC‐HF) risk score, Get With the Guidelines‐Heart Failure programme (GWTG‐HF), Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure (ASCEND) risk scores, the Acute Decompensated Heart Failure National Registry (ADHERE) model, Barcelona Bio‐Heart Failure (BCN‐Bio‐HF) risk calculator, and Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico‐Heart Failure (GISSI‐HF) for the endpoints. The primary endpoint was 1 year all‐cause mortality and the secondary endpoint was the incidence of 28 day readmission post‐discharge. At 1 year follow‐up, 44 (2.21%) patients with HF died. Discrimination analyses showed that all risk scores performed reasonably well in predicting 1 year mortality, with areas under the receiver operating characteristic curve (AUCs) fluctuating between 0.757 and 0.822. GISSI‐HF showed the best discrimination with the AUC of 0.822 (0.768–0.876), followed by MAGGIC‐HF, BCN‐Bio‐HF, ASCEND, SHFM, GWTG‐HF, and ADHERE with AUCs of 0.819 (0.756–0.883), 0.812 (0.758–0.865), 0.802 (0.742–0.862), 0.787 (0.725–0.849), 0.762 (0.684–0.840), and 0.757 (0.681–0.833), respectively. All risk scores were similarly predictive of 28 day emergency readmissions, with AUCs fluctuating between 0.609 and 0.680. Overestimation of mortality occurred in all scores except the ASCEND. The risk scores remained with good prognostic discrimination in patients with biventricular HF and in the subgroup of patients taking angiotensin‐converting enzyme inhibitor/angiotensin II receptor blocker. Conclusions: Currently assessed risk scores have limited clinical utility, with fair accuracy and calibration in assessing patients' 1 year risk of death and poor accuracy in assessing patients' risk of readmission. There is a need to incorporate more patient‐level information, use more advanced technologies, and develop models for different subgroups of patients to achieve more practical, innovative, and accurate risk assessment tools. [ABSTRACT FROM AUTHOR]

Aims: Cellular communication network factor 1 (CCN1) is an independent predictor of MACE after ACS and elevated levels correlated with infarct size after STEMI. We compared the prognostic accuracy of baseline levels of CCN1, NT‐proBNP, hsTnT, and ST2 and changes in levels over time to predict the development of structural and functional alterations typical of LV remodelling. Methods: Serial 3‐T cMRI scans were performed to determine LVEF, LVEDV, LVESV, infarct size, and relative infarct size, which were correlated with serial measurements of the four biomarkers. The prognostic significance of these biomarkers was assessed by multiple logistic regression analysis by examining their performance in predicting dichotomized cardiac MRI values 12 months after STEMI based on their median. For each biomarker three models were created using baseline (BL), the Δ value (BL to 6 months), and the two values together as predictors. All models were adjusted for age and renal function. Receiver operator curves were plotted with area under the curve (AUC) to discriminate the prognostic accuracy of individual biomarkers for MRI‐based structural or functional changes. Results: A total of 44 predominantly male patients (88.6%) from the ETiCS (Etiology, Titre‐Course, and Survival) study were identified at a mean age of 55.5 ± 11.5 (SD) years treated by successful percutaneous coronary intervention (97.7%) at a rate of 95.5% stent implantation within a median pain‐to‐balloon time of 260 min (IQR 124–591). Biomarkers hsTnT and ST2 were identified as strong predictors (AUC > 0.7) of LVEDV and LVEF. BL measurement to predict LVEF [hsTnT: AUC 0.870 (95% CI: 0.756–0.983), ST2: AUC 0.763 (95% CI: 0.615–0.911)] and the Δ value BL‐6M [hsTnT: AUC 0.870 (95% CI: 0.756–0.983), ST2: AUC 0.809 (95% CI: 0.679–0.939)] showed a high prognostic value without a significant difference for the comparison of the BL model vs. the Δ‐value model (BL‐6M) for hsTnT (P = 1) and ST2 (P = 0.304). The combined model that included baseline and Δ value as predictors was not able to improve the ability to predict LVEF [hsTnT: AUC 0.891 (0.791–0.992), P = 0.444; ST2: AUC 0.778 (0.638–0.918), P = 0.799]. Baseline levels of CCN1 were closely associated with LVEDV at 12 months [AUC 0.708 (95% CI: 0.551–0.865)] and infarct size [AUC 0.703 (95% CI: 0.534–0.872)]. Conclusions: Baseline biomarker levels of hsTnT and ST2 were the strongest predictors of LVEF and LVEDV at 12 months after STEMI. The association of CCN1 with LVEDV and infarct size warrants further study into the underlying pathophysiology of this novel biomarker. [ABSTRACT FROM AUTHOR]

Aims: There are limited data about the relationship between body mass index (BMI) and left ventricular ejection fraction (EF) in patients with heart failure (HF). The study aims to assess the correlation between BMI and left ventricular EF under HF conditions. Methods and results: We derived the data from the Dryad Digital Repository for analysis, and the information of the original patients was obtained from the MIMIC‐III database by the data uploader. We performed smooth curve and two piecewise linear regression analyses to evaluate the association between BMI and EF in HF patients. A total of 962 participants were included in this study, with age of 73.7 ± 13.5 years, and 475 participants were male (49.4%). The results of the smooth curve supported a U‐shaped relationship between BMI and EF, and the inflection point was found to be a BMI of 23.3 kg/m2 in these HF patients. After adjusting for potential confounders, we found that EF decreased with increasing BMI up to the inflection point (β = −0.7, 95% CI −1.3 to −0.1, P = 0.028), whereas beyond the turning point, the relationship between EF and BMI showed a positive correlation (β = 0.2, 95% CI 0.1–0.3 P < 0.001). Importantly, ischaemic heart disease (interaction P = 0.0499) and hyperlipidaemia (interaction P = 0.0162) affected the association between BMI and EF in the lower BMI group (BMI < 23.3 kg/m2), although only diabetes mellitus (interaction P = 0.0255) altered the association between BMI and EF in the higher BMI group (BMI ≥ 23.3 kg/m2). Conclusions: In addition to higher BMI, we also found that lower BMI is related to higher EF in intensive care unit patients with HF, supporting a U‐shaped association between BMI and EF. [ABSTRACT FROM AUTHOR]

Aims: Inhibitors of SGLT2 (SGLT2i) have shown a positive impact in patients with chronic heart failure and reduced ejection fraction (HFrEF). Nonetheless, the direct effects of SGLT2i on cardiac cells and how their association with main drugs used for HFrEF affect the behaviour and signalling pathways of myocardial fibroblasts are still unknown. We aimed to determine the effects of dapagliflozin alone and in combination with sacubitril/valsartan (LCZ696) or spironolactone on the function of myocardial fibroblasts of patients with heart failure and reduced ejection fraction (HFrEF). Methods and results: Myocardial fibroblasts isolated from HFrEF patients (n = 5) were treated with dapagliflozin alone (1 nM–1 μM) or combined with LCZ696 (100 nM) or spironolactone (100 nM). The migratory rate was determined by wound‐healing scratch assay. Expression of heart failure (HF) markers and signalling pathways activation were analysed with multiplexed protein array. Commercially available cardiac fibroblasts from healthy donors were used as Control (n = 4). Fibroblasts from HFrEF show higher migratory rate compared with control (P = 0.0036), and increased expression of HF markers [fold‐change (Log2): COL1A1–1.3; IL‐1b–1.9; IL‐6–1.7; FN1–2.9 (P < 0.05)]. Dapagliflozin slowed the migration rate of HFrEF fibroblasts in a dose‐dependent manner and markedly decreased the expression of IL‐1β, IL‐6, MMP3, MMP9, GAL3, and FN1. SGLT2i had no effect on control fibroblasts. These effects were associated with decreased phosphorylation of AKT/GSK3 and PYK2 kinases and the signal transducer and activator of transcription (STAT). A combination of dapagliflozin + LCZ696 further decreased fibroblast migration, although it did not have a significant effect on the regulation of signalling pathways and the expression of biomarkers induced by SGLT2 inhibition alone. In contrast, the combination of dapagliflozin + spironolactone did not change the migration rate of fibroblast but significantly altered SGLT2i responses on MMP9, GAL3, and IL‐1b expression, in association with increased phosphorylation of the kinases AKT/GSK3 and ERK1/2. Conclusions: SGLT2i, LCZ696, and spironolactone modulate the function of isolated myocardial fibroblasts from HFrEF patients through the activation of different signalling pathways. The combination of SGLT2i + LCZ696 shows an additive effect on migration, while spironolactone modifies the signalling pathways activated by SGLT2i and its beneficial effects of biomarkers of heart failure. [ABSTRACT FROM AUTHOR]

Aims: Heart failure (HF) impairs all aspects of health‐related quality of life (HRQoL), but little is known about the effect of developing HF on HRQoL over time. We aimed to report changes in HRQoL over a 13‐year period. Methods and results: HRQoL was measured in the Echocardiographic Heart of England Screening (ECHOES) study and the ECHOES‐X follow‐up study (N = 1618) using the SF‐36 questionnaire (Version 1). Mixed modelling compared changes in HRQoL across diagnostic groups, adjusting for potential predictors and design variables. Patients who had developed HF with reduced ejection fraction (HFrEF) or HF with preserved ejection fraction (HFpEF) at rescreening had significantly greater reduction in physical functioning (PF) and role physical (RP) scores compared with those without HF; adjusted mean difference in PF: HFrEF −16.1, [95% confidence interval (CI) −22.2 to −10.1]; HFpEF −14.6, (95% CI −21.2 to −8.1); in RP: HFrEF −20.7, (95% CI −31.8 to −9.7); HFpEF −19.3, (95% CI −31.0 to −7.6). Changes in HRQoL of those with a HF diagnosis at baseline and rescreen, with exception of role emotion, were similar to those without HF but started from a much lower baseline score. Conclusions: People with a new diagnosis of HF at rescreening had a significant reduction in HRQoL. Conversely, for those with HF detected on initial screening, little change was observed in HRQoL scores on rescreening. Further research is required to understand the development of HF over time and to test interventions designed to prevent decline in HRQoL, potentially through earlier diagnosis and treatment optimization. [ABSTRACT FROM AUTHOR]

Aims: Heart failure (HF) remains a major public health problem with increasing prevalence in China. This study evaluated the clinical performance and quality measures for HF management to identify gaps in the standardization of care for patients hospitalized for HF in China. Methods and results: Following the results of China‐HF stage I (2012–2015), the second stage of the China‐HF was launched in 2017. Among 113 hospitals with ≥100 cases, the China‐HF Stage II assessed the quality of care measures for HF and compared results with previous data in China and the US‐based Get with The Guidelines‐Heart Failure (GWTG‐HF) registries. In total, 34 938 patients hospitalized with HF were enrolled from January 2017 to October 2020. Echocardiographic left ventricular function and natriuretic peptide test were performed in 93.7% and 93.0% of the cases, respectively. Adherence to standardized guidelines in China‐HF stage II was higher than that in the China‐HF stage I, but generally lower than GWTG‐HF registry with 78.2% of eligible patients was prescribed oral diuretics, 78.7% renin‐angiotensin‐system inhibitors, and 82.2% beta‐blockers. Implantable cardioverter‐defibrillators and cardiac resynchronization devices were implanted in 3.9% and 14.6%, respectively. In contrast, the proportion of eligible patients discharged with spironolactone (87.8%) was higher than GWTG‐HF. The median length of hospitalization was 9 (6, 12) days, and 938 (2.8%) patients died or withdrew from treatment during hospitalization. Conclusions: Despite significant improvements in the use of guideline‐recommended testing and therapy, there remain major gaps in quality of care for patients hospitalized for HF in China that are generally larger than gaps observed in the United States. [ABSTRACT FROM AUTHOR]

Aims: This study aims to determine the familial incidence of dilated (DCM) and hypertrophic cardiomyopathy (HCM) in first‐degree, second‐degree, and third‐degree relatives of affected individuals. Methods and results: In this population‐based multigenerational cohort study, full‐siblings, half‐siblings, and cousin pairs born to Swedish parents between 1932 and 2015 were included, and register‐based DCM and HCM diagnoses among relatives were ascertained. Adjusted odds ratios (ORs) for DCM and HCM were calculated for relatives of individuals with DCM and HCM compared with relatives of individuals without DCM and HCM for reference. Total study population included 6 334 979 subjects and consisted of 5 577 449 full‐siblings, 1 321 414 half‐siblings, and 3 952 137 cousins. Overall, 10 272 (0.16%) unique individuals were diagnosed with DCM and 3769 (0.06%) with HCM. Of these, 7716 (75.12%) and 2375 (63.01%) were males, respectively. Familial risk ORs for DCM were 5.35 [95% confidence intervals (CI): 4.85–5.90] for full‐siblings, 2.68 (95% CI:1.86–3.87) for half‐siblings, and 1.72 (95% CI:1.12–2.64) for cousins of affected individuals. The ORs for HCM were 42.44 (95% CI:37.66–47.82) for full‐siblings, 32.70 (95% CI:21.32–50.15) for half‐siblings, and 36.96 (95% CI:29.50–46.31) for cousins of affected individuals. In sex‐stratified analysis, relatives of affected females were found more likely to be affected than were relatives of affected males, with stronger aggregation observed for HCM. Conclusions: Familial risk of HCM and DCM is high and associated with genetic resemblance, with strongest aggregations observed in relatives of affected females with HCM, whereas this association was distinctly attenuated for DCM. The finding of a Carter effect, more pronounced in HCM, suggests a multifactorial threshold model of inheritance. [ABSTRACT FROM AUTHOR]

Aims: Abnormalities in potassium homeostasis are frequently seen in hospitalized patients. A poor outcome in heart failure (HF) has been linked to both hypokalaemia and hyperkalaemia. The studies on the connection between variations in potassium levels and all‐cause mortality remain scarce. We delineated trajectories of potassium levels and investigated the association of these trajectories with all‐cause mortality of critically ill patients with HF. Methods and results: A retrospective analysis of blood potassium levels (9 times) in patients with HF after being admitted to the intensive care unit (ICU). Potassium levels were divided into three groups according to the first serum potassium level in ICU and thereafter categorized as follows: hypokalaemia group (n = 336) (<3.5 mmol/L), normal blood potassium‐level group (n = 3322) (3.5–5.0 mmol/L), and hyperkalaemia group (n = 395) (>5.0 mmol/L). According to the group‐based trajectory modelling (GBTM), the hyperkalaemia group and the normal blood potassium‐level group can be divided into three trajectory groups: the low‐level stable group, the medium‐level stable group, and the high‐level decline group. The hypokalaemia group can be divided into two trajectory groups: the low‐level rise group and the high‐level rise group. A total of 4053 HF patients were included (mean age 71.81 ± 13.12 years, 54.90% males, 45.10% females). After adjusting for possible confounding variables, in the hyperkalaemia group, the low‐level stable group had lower 28 day [high‐level decline group vs. low‐level stable group hazard ratio (HR), 95% confidence interval (CI): 2.917, 1.555–5.473; P < 0.05] and 365 day (high‐level decline group vs. low‐level stable group HR, 95% CI: 2.854, 1.820–4.475; P < 0.05) all‐cause mortality. In the normal blood potassium‐level group, the medium‐level stable group had lower 28 day (medium‐level stable group vs. low‐level stable group HR, 95% CI: 0.776, 0.657–0.918; P < 0.05) and 365 day (medium‐level stable group vs. low‐level stable group HR, 95% CI: 0.827, 0.733–0.934; P < 0.05) all‐cause mortality. In the hypokalaemia group, the cumulative survival of the high‐level rise group and the low‐level rise group did not differ significantly. Conclusions: Critically ill patients with HF have blood potassium trajectories. And the trajectories are associated with all‐cause mortality for hyperkalaemia and normal blood potassium‐level patients. GBTM is a granular method to describe the evolution of blood potassium, which may increase the current knowledge of blood potassium‐level adjustment. [ABSTRACT FROM AUTHOR]

Aims: Secondary, or functional, mitral regurgitation (FMR) was recently recognized as a separate clinical entity, complicating heart failure with reduced ejection fraction (HFrEF) and entailing particularly poor outcome. Currently, there is a lack of targeted therapies for FMR due to the fact that pathomechanisms leading to FMR progression are incompletely understood. In this study, we sought to perform metabolomic profiling of HFrEF patients with severe FMR, comparing results to patients with no or mild FMR. Methods and results: Targeted plasma metabolomics and untargeted eicosanoid analyses were performed in samples drawn from HFrEF patients (n = 80) on optimal guideline‐directed medical therapy. Specifically, 17 eicosanoids and 188 metabolites were analysed. Forty‐seven patients (58.8%) had severe FMR, and 33 patients (41.2%) had no or non‐severe FMR. Comparison of eicosanoid levels between groups, accounting for age, body mass index, and sex, revealed significant up‐regulation of six eicosanoids (11,12‐EET, 13(R)‐HODE, 12(S)‐HETE, 8,9‐DiHETrE, metPGJ2, and 20‐HDoHE) in severe FMR patients. Metabolites did not differ significantly. In patients with severe FMR, but not in those without severe FMR, levels of 8,9‐DiHETrE above a cut‐off specified by receiver‐operating characteristic analysis independently predicted all‐cause mortality after a median follow‐up of 43 [interquartile range 38, 48] months [hazard ratio 12.488 (95% confidence interval 3.835–40.666), P < 0.0001]. Conclusions: We report the up‐regulation of various eicosanoids in patients with severe FMR, with 8,9‐DiHETrE appearing to predict mortality. Our observations may serve as a nucleus for further investigations into the causes and consequences of metabolic derangements in this important valvular abnormality. [ABSTRACT FROM AUTHOR]

Aims: Chronic heart failure (HF) is a common disease and one of the leading causes of death worldwide. Heart failure with preserved ejection fraction (HFpEF) and with reduced ejection fraction (HFrEF) are different diseases with distinct as well as comparable pathophysiologies and diverse responses to therapeutic agents. We aimed to identify possible pathobiochemical signalling pathways and biomarkers in HFpEF and HFrEF by using a broad proteomic approach. Methods and results: A total of 180 biomarkers in the plasma of a representative subgroup (71 years old) of HFpEF (70% female) with a left ventricular ejection fraction (LVEF) ≥ 50% and HFrEF (18% female) with an LVEF ≤ 40% patients (n = 127) from the Prevalence and Clinical Course of Diastolic Dysfunction and Diastolic Heart Failure (DIAST‐CHF) trial were examined and compared with a healthy control group (n = 40; 48% female). We were able to identify 35 proteins that were expressed significantly different in both HF groups compared with the control group. We determine 29 unique proteins expressed in HFpEF and 33 unique proteins in HFrEF. Significantly up‐regulated trefoil factor 3 (TFF3) and down‐regulated contactin‐1 could be identified as previously unknown biomarkers for HF. However, TFF3 is also a predictive factor for the occurrence of a cardiovascular event in HFpEF patients. In HFpEF, serine protease 27 was found at reduced levels for the first time, which could offer a new therapeutic target. Additionally, network analyses showed a special role of platelet‐derived growth factor subunit A, Dickkopf‐related protein 1, and tumour necrosis factor receptor superfamily member 6 in HFpEF patients, whereas perlecan and junctional adhesion molecule A stood out in the HFrEF group. Overall, signalling pathways of metabolic processes, cellular stress, and iron metabolism seemed to be important for HFrEF, whereas for HFpEF, oxygen stress, haemostasis, cell renewal, cell migration, and cell proliferation are in the foreground. Conclusions: The identified proteins and signalling pathways offer new therapeutic and diagnostic approaches for patients with chronic HF. [ABSTRACT FROM AUTHOR]

Aims: Identification and intervention of left ventricular hypertrophy (LVH) in essential hypertension (EH) are important for the prevention of adverse cardiovascular events. However, effective methods for diagnosing LVH are still lacking. This study aimed to explore the relationship between soluble ST2 (sST2) and LVH in EH patients to identify a potential specific biomarker for hypertensive LVH. Methods and results: This study included 97 EH patients. Based on the criteria for LVH, participants were divided into the LVH group (n = 52) and the non‐LVH group (n = 45). The level of serum sST2 was detected by enzyme‐linked immunosorbent assay. Pearson correlation analysis, logistic regression analysis, and receiver operating characteristic (ROC) curve analysis were used to investigate the potential of sST2 as a biomarker of LVH in EH patients. Compared with the non‐LVH group, the sST2 level was elevated in EH patients with LVH (P < 0.001). Pearson correlation analysis indicated that the sST2 level was positively correlated with the left ventricular mass index in EH patients (r = 0.454, P < 0.001). Logistic regression analysis showed that the odds ratio (OR) value of LVH was 2.990, suggesting that sST2 is an independent risk factor for LVH in EH patients [OR = 2.990, 95% confidence interval (CI), 1.650–5.419; P < 0.001]. The area under the ROC curve was 0.767 (95% CI, 0.669–0.866; P < 0.001), with a sensitivity of 0.808 and specificity of 0.689, indicating the possibility of considering sST2 as a biomarker for diagnosing LVH. Conclusions: Up‐regulation of sST2 is strongly related to LVH in EH patients, is an independent risk factor for hypertensive LVH, and can be used as a biomarker for the diagnosis of LVH. [ABSTRACT FROM AUTHOR]