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Background: Lifetime risk for cardiovascular (CV) disease is high but predicting incident events on an individual level remains difficult. Single measurements of galectin-3, a marker of tissue fibrosis, predict mortality and new-onset heart failure (HF). Persistently elevated levels may indicate a clinically silent disease process., Objectives: Our aim was to establish the value of serial galectin-3 measurements to predict CV outcomes in the general population., Methods: Plasma galectin-3 was measured in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study at baseline and after ∼4 years. Changes in serial galectin-3 were expressed as categorical changes or absolute change from baseline and were related to subsequent outcome., Results: Serial galectin-3 was measured in 5958 subjects (mean age 49±12 years; 49% female). The median duration of follow-up was 8.3 years. Persistently elevated galectin-3 (defined as highest quartile at baseline and highest quartile during visit 2, n=757 subjects) was associated with a higher risk for new-onset HF, CV mortality, all-cause mortality, new-onset atrial fibrillation and CV events, compared with subjects with non-persistently elevated galectin-3. After multivariable adjustments for baseline characteristics, serial galectin-3 remained an independent predictor of new-onset HF (HR 1.85 (1.10-3.13); p=0.02) but not for other outcomes. Serial measurements provided more accurate prognostic value to predict new-onset HF, compared with a single baseline measurement (Harrell's C: 0.72 (0.68-0.75) vs 0.68 (0.65-0.72); p=0.002, respectively) with significant net reclassification., Conclusions: Persistently elevated galectin-3 predicts new-onset HF after adjustment for covariates, and serial measurements provide more accurate prognostic information compared with single determination of galectin-3. This may help to identify individuals who are at risk for incident HF and might provide a measure to monitor interventions., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/)

Background: Sex differences in patients with established heart failure have been well described, but much less is known in the development of heart failure., Methods: We studied sex-specific incidence and risk of new-onset heart failure in 8592 subjects (mean age 49.2 ± 12.7 years; 50.1 % women) of the Prevention of REnal and Vascular ENdstage Disease (PREVEND) study and distinguished reduced and preserved ejection fraction (HFrEF <40 % and HFpEF >50 %)., Results: Of 374 cases with incident heart failure, 241 (64.4 %) occurred in men and 133 (35.6 %) in women (median follow-up 12.5 years; 96,550 person-years). Men developed heart failure earlier (7.0 vs. 8.6 years; P < 0.001). Incidence rates per 1,000 person-years in women compared to men were lower for HFrEF (1.2 vs. 3.0 %; P < 0.001), but higher for HFpEF (1.2 vs. 0.7 %; P < 0.001). Women developed HFpEF later in life than HFrEF (75.1 vs. 69.7 years; P = 0.033), while men showed no significant difference (72.2 vs. 69.5 years; P = 0.116). Multivariable competing risks analyses showed that women had lower risk for HFrEF (subhazard ratio = 0.47; 95 % CI 0.29-0.76, P = 0.002) but higher risk for HFpEF (subhazard ratio = 2.16; 95 % CI 1.21-3.83, P = 0.009) than men. Among all risk factors, only atrial fibrillation had a sex-specific predictive value and increased risk specifically for women (P-for interaction = 0.016)., Conclusions: In a middle-aged population, men developed heart failure more frequently and at a younger age than women. However, women had higher risk for HFpEF, with atrial fibrillation being a specific female risk factor.

Background: 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., Methods and Results: 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., Conclusions: 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., (© 2014 American Heart Association, Inc.)