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Aims: As part of the Toon Health Study, which is an ongoing population-based cohort study, we aimed to develop a prediction model for N-terminal pro-brain natriuretic peptide (NT-proBNP) in a general Japanese population. We sought to explore the influence of various demographic and clinical factors on NT-proBNP levels and assess the model's performance. In addition, our objectives included internal validation and investigation of the diagnostic potential of the observed-to-predicted NT-proBNP ratio (OPR) at baseline for predicting the risk of heart failure with preserved ejection fraction (HFpEF)., Methods and Results: In this prospective cohort study, participants were recruited from Toon City, Japan, as part of the larger Toon Health Study, focusing on cardiovascular risk factors. We measured the NT-proBNP levels and used linear regression with penalization (ridge regression) to develop the model. The model incorporated 10 prespecified predictors (age, gender, body mass index, diastolic blood pressure, heart rate, haemoglobin, albumin, total cholesterol, haemoglobin A1c, and estimated glomerular filtration rate) and underwent assessment using R 2 and root mean squared error (RMSE). Internal validation was conducted through bootstrapping. In a post hoc analysis, we explored the OPR's diagnostic potential using 5 year follow-up data (n = 636) to predict the elevation of NT-proBNP > 125 pg/mL at the 5 year follow-up as the risk of HFpEF. A total of 2505 participants (age: 60.4 ± 12.9 years, men: 35%) were enrolled in this study. There was a linear relationship between the observed and predicted values of NT-proBNP in which the logarithm of observed NT-proBNP was <6, which corresponds to 403 pg/mL in NT-proBNP. The prediction model demonstrated satisfactory performance (R 2 : 0.291, RMSE: 0.688), with age identified as a dominant predictor. The stability of the model was underscored by the internal validation. The OPR at baseline predicted NT-proBNP > 125 pg/mL at the 5 year follow-up with an area under the curve of 0.793., Conclusions: This study introduces the first prediction model for NT-proBNP in a general Japanese population. Although the model has acceptable performance, ongoing refinement is essential. Our transparent approach to model development, alongside a web-based interactive tool, lays the groundwork for further improvements and external validation. The OPR holds potential for predicting the future risk of HFpEF. This research contributes to understanding the nuanced influence of patient backgrounds on levels of NT-proBNP in asymptomatic individuals within the context of a broader population-based cohort study., (© 2024 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

We investigated the independent and incremental role of worsening arterial stiffness in new-onset heart failure (HF) in patients with preclinical HF. We retrospectively studied 456 consecutive asymptomatic patients with HF risk factors (hypertension, obesity, type 2 diabetes mellitus, atrial fibrillation and ischemic heart disease) who underwent paired applanation tonometry examinations (median interval of 2.4 years) during 2006-2011. Brachial ankle pulse wave velocity (baPWV) was measured as a surrogate marker of arterial stiffness. Patients were followed up for admission for new-onset HF over a median duration of 4.9 years after the second examination. HF was observed in 30 patients (7%). The change in baPWV (∆baPWV) was significantly associated with hospitalization for new-onset HF, independent of and incremental to comorbidities, renal dysfunction, left ventricular (LV) dysfunction and baPWV at baseline. Even in patients with an LV ejection fraction of ⩾40%, ∆baPWV was significantly associated with hospitalization for new-onset HF after similar adjustments. When the patients were divided into groups based on this cutoff value of ⩾15% ∆baPWV and the generally accepted external cutoff value of ⩾1750 cm s -1 for baseline baPWV, the Kaplan-Meier estimates of the time of hospitalization for new-onset HF showed that a higher rate of HF was associated with higher baPWV at baseline and higher ∆baPWV (P=0.00005). In asymptomatic patients with cardiovascular risk factors, the deterioration in arterial stiffness was associated with hospitalization for new-onset HF, independent of and incremental with the clinical LV function and increased stiffness parameters at baseline.

Aims: Traditional criteria for heart transplantation by cardiopulmonary exercise testing (CPX) include peak oxygen uptake (VO2) < 14 mL/kg/min. Reaching a sufficient exercise load is challenging for patients with refractory heart failure (HF) because of their exercise intolerance. Recently, a substantial impact of right ventricular (RV) dysfunction was highlighted on urgent heart transplantation and mortality. This study aims to investigate the impact of RV contractile reserve, assessed by low‐load exercise stress echocardiography (ESE), on exercise intolerance defined as peak VO2 < 14 mL/kg/min, in patients with HF. Methods and results: We prospectively examined 67 consecutive patients hospitalized for HF who underwent ESE and CPX under a stabilized HF condition. Although low‐load ESE was defined as 25 W load exercise, an increment in RV systolic (s′) velocity was regarded as the preservation of RV contractile reserve. All patients completed low‐load ESE. During low‐load ESE, the variation in RV s′ velocity significantly correlated with peak VO2 (r = 0.787, P < 0.001). The change in RV s′ velocity during low‐load ESE accurately identified patients with peak VO2 < 14 mL/kg/min (area under the curve, 0.95; sensitivity, 92%; specificity, 85%). The intraclass correlation coefficient for intra‐observer and inter‐observer agreement for the change in RV s′ velocity was 0.96 (95% confidence interval, 0.88–0.99, P < 0.001) and 0.86 (95% confidence interval, 0.64–0.95, P < 0.001), respectively. The RV‐to‐pulmonary circulation (PC) coupling, which was assessed by the slope of the relationship between RV s′ velocity and pulmonary artery systolic pressure at rest and low‐load exercise, was worse in the low‐peak VO2 group (<14 mL/kg/min) than the preserved‐peak VO2 group (≥14 mL/kg/min). Conclusions: The change in RV s′ velocity during low‐load ESE could estimate the exercise capacity in HF patients. The assessments of RV contractile reserve and RV‐to‐PC coupling could be clinically beneficial to distinguish high‐risk HF patients. [ABSTRACT FROM AUTHOR]