Key result
Obesity in HF links to ~39% lower BNP levels despite similar severity.
Why the study?
Obesity is a major risk factor for heart failure with uncertain mechanisms, and natriuretic peptides and lipolysis are physiologically linked.
Observational (n=318)
Absolute Event Rate: 205% vs 335%
p-value: p=0.0007
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“We and others have previously demonstrated that obesity also affects plasma levels of cardiac biomarkers, and that higher BMI is associated with lower plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels.”
“The present paper supports the hypothesis that relative NP deficiency may exist in some individuals, particularly in obese persons, and speculates about various mechanisms, such as increased clearance secondary to up-regulation of neprilysin (NEP) and/or the NP clearance receptor (NPR-C), as well as impaired NP production.”
“An inverse relationship between body mass index (BMI) and natriuretic peptides levels complicates the biomarker's use in obese patients, who typically exhibit lower levels, potentially delaying heart failure diagnosis and treatment, and leading to worsened outcomes.”
Obesity-linked BNP suppression may require adjusted HF diagnostic thresholds; leaves open prognostic and therapeutic implications.
OBJECTIVES This investigation evaluated the relationship between obesity and B-type natriuretic peptide (BNP) in heart failure. BACKGROUND Obesity is a major risk factor for the development of heart failure, but the precise mechanisms remain uncertain. Physiologically, natriuretic peptides and lipolysis are closely linked. METHODS A total of 318 patients with heart failure were evaluated between June 2001 and June 2002. Levels of BNP were compared in obese (body mass index [BMI] > or =30 kg/m(2)) and nonobese (BMI <30 kg/m(2)) patients with respect to New York Heart Association functional class and lean body weight-adjusted peak aerobic oxygen consumption. In a subset of 36 patients, plasma levels of tumor necrosis factor-alpha, interleukin-6, and soluble intercellular adhesion molecule-1 were measured. RESULTS The population's BMI was 29.4 +/- 6.6 kg/m(2); 24% were lean (BMI <25 kg/m(2)), 31% overweight (BMI > or =25 to 29.9 kg/m(2)), and 45% obese (BMI > or =30 kg/m(2)). Obese patients were younger, more often African American, and more likely to have a history of antecedent hypertension, but less likely to have coronary artery disease and with only a trend toward diabetes mellitus. Levels of BNP were significantly lower in obese than in nonobese subjects (205 +/- 22 and 335 +/- 39 pg/ml, respectively; p = 0.0007), despite a similar severity of heart failure and cytokine levels. Multivariate regression analysis identified BMI as an independent negative correlate of BNP level. There were no differences in emergency department visits, heart failure hospitalization, or death between the obese and nonobese patients at 12-month follow-up. CONCLUSIONS Our investigation indicates that a state of reduced natriuretic peptide level exists in the obese individual with heart failure.
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Mehra et al. (2004) conducted an observational in heart failure (n=318). Obesity (BMI ≥30 kg/m²) vs. Nonobese (BMI <30 kg/m²) was evaluated on B-type natriuretic peptide (BNP) levels (p=0.0007). Obese patients with heart failure had significantly lower B-type natriuretic peptide levels than nonobese patients (205 vs 335 pg/ml; p=0.0007), despite similar heart failure severity.
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