Neurohormonal activation pattern in patients with atrial septal defect

• Published in: Scientific reports Vol. 14; no. 1; pp. 29980 - 9
• Main Authors: Çetin Güvenç, Rengin, Koç Ada, Saniye, Güvenç, Tolga Sinan, Çelik, Fatma Betül, Polat Ocaklı, Ezgi, Al Arfaj, Abdullah Ayar, Güllü, Hakan, Özer, Nihat, Çekmen, Mustafa Baki, Çalışkan, Mustafa
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 02.12.2024; Nature Publishing Group; Nature Portfolio
• Subjects: 631/45/776; 692/4019/592/75/1539; Adult; Aldosterone; Aldosterone - blood; Argipressin; Atrial septal defect; Blood; Cardiac arrhythmia; Cardiovascular disease; Case-Control Studies; Congenital diseases; Endothelin; Endothelin 1; Endothelin-1 - blood; Female; Glycopeptides - blood; Heart failure; Heart Septal Defects, Atrial - blood; Heart Septal Defects, Atrial - physiopathology; Humanities and Social Sciences; Humans; Laboratories; Male; Middle Aged; multidisciplinary; Natriuretic Peptide, Brain - blood; Neurohormonal activation; Neurotransmitter Agents - blood; Neurotransmitter Agents - metabolism; Neurotransmitters; Noradrenaline; Norepinephrine; Norepinephrine - blood; Peptides; Plasma; Pulmonary arteries; Pulmonary hypertension; Renin; Renin - blood; Science; Science (multidisciplinary); Vasoconstriction; Vasopressin; Atrial septal defect; Endothelin; Neurohormonal activation; Aldosterone; Noradrenaline
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-024-78950-x

Atrial septal defects (ASD) divert flow from systemic to pulmonary circulation, and some degree of plasma volume expansion and neurohormonal activation are necessary to maintain the effective circulatory volume. The aim of the present study was to understand the patterns of neurohormonal activation in ASD patients. 16 ASD patients and 10 controls were enrolled. Fasting blood samples were collected prior to procedure and 48 h after defect closure. At baseline, renin (185.0(79.0—437.0 vs. 79.4(60.8—110.0),  p  = 0.04), aldosterone (20.2 ± 7.6 vs. 11.7 ± 2.8,  p  < 0.001), copeptin (43.6 ± 27.5 vs. 16.4 ± 8.7,  p  = 0.002) and both natriuretic peptides were higher in ASD patients, while noradrenaline (113.0 ± 61.3 vs. 178.0 ± 49.4,  p  = 0.009) and endothelin-1 (2.93 ± 2.00 vs. 5.06 ± 1.25,  p  = 0.006) were higher in controls. After ASD closure, only NT-proBNP reduced significantly ( p  = 0.02). There were negative correlations between defect area with noradrenaline ( r =-0.73,  p  = 0.002) and with endothelin-1 ( r =-0.59,  p  = 0.02). Present findings suggest that in patients with an ASD, there is an increase in neurohormones that are related to regulation of plasma volume (aldosterone and arginine vasopressin) with simultaneous reductions in neurohormones related to vasoconstriction in systemic and pulmonary beds (noradrenaline and endothelin-1).