Cardiac Hormones as Diagnostic Tools in Heart Failure

Abstract

In patients with heart failure, plasma levels of atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), and the N-terminal fragments of their prohormones (N-ANP and N-BNP) are elevated, because the cardiac hormonal system is activated by increased wall stretch due to increased volume and pressure overload. Patients suspected of having heart failure can be selected for further investigations on the basis of having an elevated plasma concentration of N-ANP, BNP, and N-BNP. High levels of cardiac hormones identify those at greatest risk for future serious cardiovascular events. Moreover, adjusting heart failure treatment to reduce plasma levels of N-BNP may improve outcome. Cardiac hormones are most useful clinically as a rule-out test. In acutely symptomatic patients, a very high negative predictive value is coupled with a relatively high positive predictive value. Measurement of cardiac hormones in patients with heart failure may reduce the need for hospitalizations and for more expensive investigations such as echocardiography. However, there have also been conflicting reports on the diagnostic value of cardiac hormones, they are not specific for any disease, and the magnitude of the effects of age and gender on BNP in the normal subgroup suggests that these parameters need to be considered when interpreting cardiac hormone levels.

Circulating levels of pro‐atrial natriuretic peptide in lower respiratory tract infections

“…We did not measure D-dimers, which have also been propagated as prognostic parameter in CAP [31]. Natriuretic peptides have emerged as reliable markers for congestive heart failure [3,[9][10][11]. In a selected cohort of patients with dyspnoea predominantly caused by underlying congestive heart failure, B-type natriuretic peptide (BNP) was shown to have better accuracy to predict death in concomitant CAP when compared with the PSI [32,33].…”

“…In addition to the clinical evaluation, a novel approach to estimate the presence of an infection and to grade its severity and its treatment response is the use of biomarkers. Thereby, the MR-proANP level may mirror both, the inflammatory cytokine response correlated with the severity of pneumonia, as well as the presence of disease-relevant comorbidities, namely heart failure and renal dysfunction [7][8][9][10][11]. Therefore, we investigated MR-proANP levels in a well-defined cohort of 545 consecutive patients with lower respiratory tract infections, to evaluate its prognostic use for the severity of disease and outcome.…”

Distinct regulation of B-type natriuretic peptide transcription by p38 MAPK isoforms

“…Natriuretic peptides atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are cardiac hormones released into circulation by myocytes to protect the cardiovascular system against increased hemodynamic load and decrease blood pressure by increasing salt and water excretion and by promoting vasodilatation (reviewed in de Bold et al, 1996;Ruskoaho, 2003;Kuwahara and Nakao, 2010). Increased expression of natriuretic peptides is a sign of hemodynamic overload of the heart and, at least in experimental setting, can be used to measure the hypertrophic response in the heart.…”

Natriuretic Peptides in the Regulation of Cardiovascular Physiology and Metabolic Events

“…In 1983–1984, ANP was then isolated and purified, and the amino acid sequence was determined in rats and humans. Whereas atrial ANP levels are higher than those in ventricles, the ventricular myocardium becomes a major source for circulating ANP in failing hearts owing to larger mass 2. In 1988, a homologous peptide with similar biological activities was isolated from porcine brain and named BNP 3.…”

“…The key stimulant for release of ANP and BNP from the heart is myocardial stretch, whereas the third family member, CNP, is mainly released from endothelial cells in response to various cytokines2 as depicted in Figure 1. Classically, ANP and BNP exert diuretic, natriuretic, and hypotensive actions, and genetic variations of the NPPA‐NPPB locus that increase the circulating levels of ANP and BNP in patients have been shown to offer protection from hypertension 4.…”