A View on the Interrelationship between Obesity and Natriuretic Peptide Measurements: Can Dysregulation in pro–B-type Natriuretic Peptide Glycosylation Explain Decreased B-type Natriuretic Peptide Concentrations in Obese Heart Failure Patients?

B-type natriuretic peptide (BNP)3 and N-terminal proBNP (NT-proBNP) are peptides produced in the heart in response to increased wall stretch and volume overload. As their production and secretion increases in the heart with the progression of heart failure (HF), plasma BNP and its N-terminal counterpart (i.e., NT-proBNP) have emerged as useful and cost-effective HF biomarkers (1, 2). Since the discovery of BNPs in 1988, much effort has been made to precisely determine the BNP and NT-proBNP levels via immunoassays for reliable HF diagnostics. As a result, the measurement of these biomarkers is globally accepted and used as a tool by clinicians to diagnose acute and chronic HF, stratify risk, and monitor response to therapy (3). HF is a global pandemic that is constantly increasing in prevalence. Unfortunately, the proportion of HF patients with significant obesity has also increased dramatically owing to the increase in obesity in the general population. Recent data suggest an inverse relationship between BNP/NT-proBNP concentrations and body mass index (BMI). Obesity is a risk factor for systemic hypertension, hyperlipidemia, diabetes mellitus, and left ventricular hypertrophy, all of which are conditions associated with an increased prevalence of HF. However, the applications of BNP and NT-proBNP as biomarkers in obese patients are limited, as the relationship between their levels and myocardial stiffness is complex. Considering that the established clinical thresholds are not relevant to distinguish HF from non-HF conditions among obese patients, the interpretation of results and clinical decisions are further complicated.