This study evaluated the associations between the natriuretic peptide activity and the neurohormonal response in non-obese and obese outpatients with and without heart failure (HF). Obesity-related HF may be a distinct subtype of HF. Obesity is associated with lower plasma concentrations of natriuretic peptides. The associations between obesity and neurohormonal activation estimated by mid-regional pro-adrenomedullin (MR-proADM) and copeptin in patients with HF is not elucidated. This prospective cohort-study included 392 outpatients ≥60years, plus ≥1 risk-factor(-s) for HF (hypertension, ischemic heart disease, atrial fibrillation, diabetes, chronic kidney disease), and without known HF. Patients were categorized ‘non-obese’ BMI = 18.5–29.9 kg/m² (n = 273) and ‘obese’ BMI ≥ 30 kg/m² (n = 119). The diagnosis of HF required signs, symptoms, and abnormal echocardiography. NT-proBNP, MR-proANP, MR-proADM, and copeptin were analyzed. Obese patients were younger, had a higher prevalence of diabetes and chronic kidney disease, but a lower prevalence of atrial fibrillation. A total of 39 (14.3%) non-obese and 26 (21.8%) obese patients were diagnosed with HF. In obese patients, HF was not associated with higher plasma concentrations of NT-proBNP (Estimate: 0.063; 95%CI: –0.037–1.300; P = 0.064), MR-proANP (Estimate: 0.207; 95%CI: –0.101–0.515; P = 0.187), MR-proADM (Estimate: 0.112; 95%CI: –0.047–0.271; P = 0.168), or copeptin (Estimate: 0.093; 95%CI: –0.333–0.518; P = 0.669). Additionally, obese patients with HF had lower plasma concentrations of NT-proBNP (Estimate: –0.998; 95%CI: –1.778–0.218; P = 0.012), and MR-proANP (Estimate: –0.488; 95%CI: –0.845–0.132; P = 0.007) compared to non-obese patients with HF, whereas plasma concentrations of MR-proADM (Estimate: 0.066; 95%CI: –0.119–0.250; P = 0.484) and copeptin (Estimate: 0.140; 95%CI: –0.354–0.633; P = 0.578) were comparable. Patients with obesity-related HF have natriuretic peptide deficiency and lack of increased plasma concentrations of MR-proADM and copeptin suggesting that patients with obesity-related HF have a blunted overall neurohormonal activity.

Background: Left ventricular ejection fraction remains the primary focus in cardiac monitoring for oncology patients undergoing potentially cardiotoxic chemotherapy, while right ventricular function is seldom examined. This study evaluates how established risk factors for left ventricular dysfunction affect right ventricular function. Methods: This retrospective cohort study included 1770 patients undergoing cadmium–zinc–telluride equilibrium radionuclide angiocardiography before chemotherapy. Patients were categorized based on risk factors for left ventricular dysfunction—diabetes (DM), atrial fibrillation (AF), coronary heart disease (CHD), and previous oncological therapy—and compared to controls using independent t-tests. Results: Patients with previous oncological therapy exhibited a significantly lower right ventricular end-diastolic volume (RVEDV) (mean difference: −4.4 mL/m², 95% CI: −6.1 to −2.7, p < 0.001), lower right ventricular end-systolic volume (RVESV) (−2.3 mL/m², 95% CI: −3.4 to −1.2, p < 0.001), and lower right ventricular stroke volume (RVSV) (−2.1 mL/m², 95% CI: −3 to −1.2, p < 0.001). In patients with CHD, there was a higher right ventricular ejection fraction (RVEF) (3.0 mL/m², 95% CI: 0.8 to 5.2, p < 0.01), whereas patients with DM had lower RVEDV (−5.1 mL/m², 95% CI: −9.2 to −1, p < 0.05) and RVESV (−3.0 mL/m², 95% CI: −5.5 to −0.4, p < 0.05). No ventricular variables differed from the control group among patients with AF. Conclusions: Risk factors known to affect the left ventricle also impacted the right ventricle, with the exception of AF.