Measuring cNP is useful as a diagnostic and prognostic tool (10, 11, 12). In non-rejecting transplanted patients, despite the normalization of endothelin-1 plasma levels and diastolic and systolic functions, BNP remains high by comparison with control subjects (9). Plasma BNP levels during acute rejection episodes do not correlate with hemodynamic variables but correlate with the levels of regulated on activation, normal T expressed and secreted, insulin growth factor binding protein-1 and neutrophil activating protein-2 (4). During an acute cardiac allograft rejection episode, BNP – but not atrial natriuretic peptide (ANP) – plasma levels increase significantly above pre-rejection values independently of the surgical technique used (8). However, studies on cardiac transplant patients have shown that plasma cNP levels remain high even after intra-cardiac pressures normalize following transplantation (7). Increased left ventricular end-diastolic wall stress and left ventricular end-systolic wall stress correlate with an increase in plasma cNP in heart failure (5, 6). Neurohumoral stimuli include endothelin-1, angiotensin II, adrenergic agonists and various cytokines (4). This phenomenon is referred to as stretch-secretion coupling (3). The main mechanical stimulus for the secretion of cNP is the increased pressure in the cardiac chambers leading to stretching of the myocardial fibers. ![]() Increased secretion of cNP is a result of both mechanical and neurohumoral stimuli (1, 2). These findings posed the question as to why it is that in some patients the plasma levels of cardiac natriuretic peptides (cNP) are unexpectedly low, and what is their value in the prognosis for these patients? LVEF was 66% and plasma BNP and NT-proBNP were 10 and <20 pg/ml, respectively (reference values for age and sex: BNP median 31 pg/ml, percentile 25–75th, 14-49 pg/ml NT-proBNP median 25 pg/ml, percentile 5–95th, 5–88 pg/ml). The echocardiogram showed mild hypokinesia of the basal segment of the inferior wall and mild dilation of left ventricle with eccentric hypertrophy. He was in stable condition without chest pain, in NYHA class II. His BMI was 44.3 kg/m 2 and his waist circumference 137 cm. No coronary angiography was done due to his weight (144 kg). Patient B, 58 years of age, had suffered a non-ST-elevation myocardial infarction two years earlier, and had received standard treatment. Plasma BNP and NT-proBNP were 72 and 100 pg/ml, respectively (reference values for age and sex: BNP median 28 pg/ml (percentile 25–75th, 10–58 pg/ml) NT-proBNP median 45 pg/ml (percentile 5–95th, 14–140 pg/ml)). The echocardiogram showed apical and lateral hypokinesia with left ventricular ejection fraction (LVEF) of 58%. His BMI was 34.8 kg/m 2, waist circumference 116 cm and was stable without chest pain in NYHA class I. Their glomerular filtration rate was normal (>75 ml/min per 1.73 m 2 ), HbA1c was 70% stenosis on a diagonal artery, which was not treated and showed no significant stenosis in the remaining coronary arteries. Both were hypertensive with hyper cholesterolemia and hypertriglyceridemia. ![]() Two male patients with type 2 diabetes (T2D) and coronary heart disease had plasma levels of brain natriuretic peptide (BNP) and N-terminal probrain natriuretic peptide (NT-proBNP) measured as part of routine evaluation. Understanding this role should help define novel principles in the treatment of cardiometabolic disease. Together, these observations suggest that the cNP system plays a role in the pathophysiology of metabolic vascular disease. ![]() Highly elevated cNP levels are generally observed in patients with systolic heart failure or high blood pressure, while obese and type-2 diabetics display reduced cNP levels. In human association studies in patients without heart disease higher cNP concentrations were observed in lean, insulin-sensitive subjects. Clinically, these properties lead to browning of white adipose tissue and to increased muscular oxidative capacity. Recent lines of evidence suggest important metabolic effects of the cNP system, which has been shown to activate lipolysis, enhance lipid oxidation and mitochondrial respiration. The clinical significance of cNP plasma levels has been shown to differ in obese and non-obese subjects. cNP secretion from the heart is increased by humoral and mechanical stimuli. In addition, it has been shown that cNP plasma levels are strong predictors of cardiovascular events and mortality in populations with no apparent heart disease as well as in patients with established cardiac pathology. Since their discovery in 1981, the cardiac natriuretic peptides (cNP) atrial natriuretic peptide (also referred to as atrial natriuretic factor) and brain natriuretic peptide have been well characterised in terms of their renal and cardiovascular actions.
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