N-terminal-pro-brain natriuretic peptide, but not brain natriuretic peptide, is increased in patients with severe obesity

Abstract

Elevated body mass index (BMI) has been reported as a risk factor for heart failure. Prevention of heart failure through identification and management of risk factors and preclinical phases of the disease is a priority. Levels of natriuretic peptides as well as activity of their receptors have been found altered in obese persons with some conflicting results. We investigated cardiac involvement in severely obese patients by determining N-terminal-pro-brain natriuretic peptide (NT-proBNP) and brain natriuretic peptide (BNP) and attempting to correlate the levels of these peptides in serum and plasma, respectively, with BMI, duration of obesity, waist circumference, and echocardiographic parameters. Thirty-three patients with severe obesity (mean BMI: 46.39 kg/m 2 , mean age: 39 years) were studied. The control group contained 30 healthy age-matched individuals (BMI: <25 kg/m 2 , mean age: 43 years). The t-test and Spearman correlation were used for statistical analysis. Log-NT-proBNP was significantly higher (P = 0.003) in obese patients (mean 1.67, 95% CI: 1.50-1.83 log pg/mL) compared to controls (mean: 1.32, 95% CI: 1.17-1.47 log pg/ mL). The Log-NT-proBNP concentration correlated with duration of obesity (r = 0.339, P < 0.004). No difference was detected in the Log-BNP concentration (P = 0.63) of obese patients (mean: 0.73, 95% CI: 0.46-1.00 log pg/mL) compared to controls (mean: 0.66, 95% CI: 0.51-0.81 log pg/mL). NT-proBNP, but not BNP, is increased in severely obese patients and its concentration in serum is correlated with duration of obesity. NT-proBNP may be useful as an early diagnostic tool for the detection of cardiac burden due to severe obesity.

Natriuretic peptides: linking heart and adipose tissue in obesity and related conditions – a systematic review

“…Authors who specifically studied very obese patients did not find lower natriuretic peptide levels in patients with morbid obesity. Class 3 obese patients (body mass index ≥ 40 kg m −2 ) showed significantly higher levels of N‐terminal pro‐B‐type natriuretic peptide (57–59) and BNP (60) than lean and class 2 (body mass index between 30 and 40 kg m −2 ) patients respectively. This difference may also be related to underdiagnosis of heart failure in the severely obese population, as most of these studies based heart failure diagnosis on clinical history, thorax radiographs and electrocardiogram.…”

Cardiac function in growth hormone deficient patients before and after 1 year with replacement therapy: a magnetic resonance imaging study

“…Therefore it can be questioned if our discordant results concerning the natriuretic peptides can be related to cardiac function in patients with GHD. As an alternative explanation fat free mass may have influenced levels of NT-proBNP at baseline as well as after treatment [58,59]. In addition the discordant results between NT-proBNP and BNP may raise the question if there could be a direct effect of IGF-I on processing and clearance of the different components of the B-type natriuretic peptide molecule.…”

The conundrum of patients with obesity, exercise intolerance, elevated ventricular filling pressures and a measured ejection fraction in the normal range

“…In the absence of oedema, the increase in cardiac filling pressures may remain clinically undetected for long periods of time, especially if the reduced exercise capacity is attributed to obesity rather than hypervolaemia . Circulating levels of natriuretic peptides are low or normal in obese people and no longer reliably reflect increases in cardiac filling pressures or wall stress . Echocardiography reveals left atrial and left ventricular enlargement, increased E/e' ratios (indicative of cardiac overfilling) and abnormalities in regional strain, but these subtle changes are often ignored by clinicians or attributed to associated hypertension.…”

“…States of HOHF typically result from anatomical or physiological abnormalities that lead to marked decline in systemic vascular resistance. The most obvious physiological cause for the systemic vasodilatation in obesity‐related HOHF is the striking increase in natriuretic peptides in these patients, particularly when compared with the suppressed levels seen in most obese people . Endogenous vasodilatory peptides (e.g.…”