Are plasma levels of atrial natriuretic peptide, N-terminal ProANP, and brain natriuretic peptide affected by the presence of coronary artery disease?

N-Terminal ProANP, and Brain Natriuretic Peptide Affected by the Presence of Coronary Artery Disease? To the Editor: We read with great interest the recent article by BibbinsDomingo et al1 on plasma brain natriuretic peptide (BNP) in outpatients with stable coronary disease. They concluded that elevated levels of BNP are independently associated with inducible ischemia in outpatients with stable coronary disease, particularly among those who have a history of myocardial infarction. Previous studies have demonstrated that transient myocardial ischemia stimulates the secretion of atrial natriuretic peptide (ANP) and N-terminal ProANP (N-ANP); because of its longer half-life, N-ANP may be a better marker than ANP for the detection of high-grade coronary artery stenosis.2–4 However, whether plasma BNP levels are increased in patients with coronary artery stenosis who have normal left ventricular function remains unknown. To examine whether coronary artery stenosis affects plasma ANP, N-ANP, and BNP levels, we recently measured these peptide levels in 104 patients with normal left ventricular systolic function who had a suspected diagnosis of angina pectoris.5 Plasma levels of all 3 of these natriuretic peptides were higher in patients with coronary artery stenosis (major coronary artery stenosis 75%) (n 65) than in those without stenosis (n 39), whereas hemodynamic variables were similar. Multiple logistic regression analysis revealed that N-ANP (per 100 fmol/mL increase; odds ratio 1.9 [95% CI 1.2 to 2.6], P 0.01), but not ANP (per 10 pg/mL increase; odds ratio 0.9 [95% CI 0.5 to 1.2], P 0.41) or BNP (per 10 pg/mL increase; odds ratio 1.1 [95% CI 0.8 to 1.4], P 0.73), was independently associated with coronary artery stenosis after adjusting for clinical and demographic variables. Furthermore, we measured these natriuretic peptides before and 3 to 6 months after percutaneous coronary intervention in patients with myocardial infarction of recent onset (n 58). Plasma levels of ANP, N-ANP, and BNP significantly decreased in patients without restenosis (n 46) (ANP, 91 15 to 39 7 pg/mL; BNP, 134 28.9 to 41 9 pg/mL; N-ANP, 688 81 to 407 52 fmol/mL; all P 0.05). In contrast, these natriuretic peptide levels did not change after coronary intervention in patients with restenosis (n 12) (ANP, 57 19 to 50 20; BNP, 102 35 to 57 13; N-ANP, 567 178 to 508 126; all NS). Our results support the findings of Bibbins-Domingo et al1; however, we propose that N-ANP may be more useful for the discrimination of clinically significant coronary artery stenosis than BNP because of its different sites of production, mechanisms of release, and metabolic characteristics.