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Background--Heart failure (HF) is a prevalent and deadly disease, and preventive strategies focused on at-risk individuals are needed. Current HF prediction models have not examined HF subtypes. We sought to develop and validate risk prediction models for HF with preserved and reduced ejection fraction (HFpEF, HFrEF). Methods and Results--Of 28,820 participants from 4 community-based cohorts, 982 developed incident HFpEF and 909 HFrEF during a median follow-up of 12 years. Three cohorts were combined, and a 2:1 random split was used for derivation and internal validation, with the fourth cohort as external validation. Models accounted for multiple competing risks (death, other HF subtype, and unclassified HF). The HFpEF-specific model included age, sex, systolic blood pressure, body mass index, antihypertensive treatment, and previous myocardial infarction; it had good discrimination in derivation (c-statistic 0.80; 95% confidence interval [CI], 0.78-0.82) and validation samples (internal: 0.79; 95% CI, 0.77-0.82 and external: 0.76; 95% CI: 0.71-0.80). The HFrEF-specific model additionally included smoking, left ventricular hypertrophy, left bundle branch block, and diabetes mellitus; it had good discrimination in derivation (c-statistic 0.82; 95% CI, 0.80-0.84) and validation samples (internal: 0.80; 95% CI, 0.78-0.83 and external: 0.76; 95% CI, 0.71-0.80). Age was more strongly associated with HFpEF, and male sex, left ventricular hypertrophy, bundle branch block, previous myocardial infarction, and smoking with HFrEF (P value for each comparison =0.02). Conclusions--We describe and validate risk prediction models for HF subtypes and show good discrimination in a large sample. Some risk factors differed between HFpEF and HFrEF, supporting the notion of pathogenetic differences among HF subtypes. [ABSTRACT FROM AUTHOR]

We aim to identify and quantify the value of biomarkers for incident new-onset heart failure (HF) in a community-based cohort and subgroups based on cardiovascular risk and evaluate the prognostic value of 13 biomarkers for HF with reduced and preserved ejection fraction.Thirteen biomarkers reflecting diverse pathophysiologic domains were examined in 8569 HF-free participants in Prevention of Vascular and Renal Endstage Disease (mean age, 49 years; 50% men). Subjects were categorized in 2 risk groups based on cardiovascular history. Incremental value per biomarker was assessed using Harrell C-indices. One hundred sixty-eight subjects (2.4%) were diagnosed with new-onset HF in the low-risk group (n=6915; Framingham Risk Score, 5.9%) and 206 (12.2%) subjects in the high-risk group (n=1654; Framingham Risk Score, 18.6%). The association of natriuretic peptides, adrenomedullin, endothelin, and galectin-3 with new-onset HF was stronger in the high-risk group (all P<0.05). Troponin-T, high-sensitive C-reactive protein, urinary albumin excretion, and cystatin-C had similar risk for new-onset HF between both risk groups. The best model for new-onset HF included the combination of N-terminal pro-B-type natriuretic peptide, troponin-T, and urinary albumin excretion, increasing model accuracy to 0.81 (9.5%, P<0.001) in the high-risk group. Except for a modest effect of cystatin-C, no biomarker was associated with increased risk for HF with preserved ejection fraction.Risk stratification increases the incremental value per biomarker to predict new-onset HF, especially HF with reduced ejection fraction. We suggest that routine biomarker testing should be limited to the use of natriuretic peptides and troponin-T in patients with increased cardiovascular risk. [ABSTRACT FROM AUTHOR]

The article focuses on a genome-wide association study (GWAS) on the plasma levels of midregional-proadrenomedullin (MR-pro-ADM) and C-terminal-pro-endothelin-1 (CT-prot-ET-1). It notes that the release of nitric oxide (NO) and vasoactive peptides such as endothelin-1 (ET-1) and adrenomedullin (ADM) mediates the control of vascular tone. It states that the GWAS led to the identification of a novel role for the plasma kallikrein related to MR-pro-ADM and CT-pro-ET-1 regulation.