ArticleScientific reports2024
Neurohormonal activation pattern in patients with atrial septal defect.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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).
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