Failure of Plasma Atrial Natriuretic Peptide Levels to Increase During Exercise in Patients with Chronic Atrial Fibrillation

It is generally accepted that plasma atrial natriuretic peptide release occurs secondary to atrial stretch. The influence of coordinated atrial contraction (AC) upon this process is not fully appreciated. The aim of the study was to determine the importance of coordinated AC upon peripheral atrial natriuretic peptide levels (α‐hANP) during exercise. Peripheral α‐hANP levels were measured at rest and during exercise in 12 patients with complete heart block (CHB) and permanent rate responsive pacemakers. Seven patients had coordinated AC and five had chronic atrial fibrillation (AE). Each patient performed three treadmill exercise tests. Maximal inspired oxygen volume (VO2 max) was determined during test 1. Tests 2 and 3 were performed to 70% VO2 max, the pacemaker being programmed to either VVI or VVIR mode. Plasma α‐hANP was measured using a two‐site immunoradiometric assay. At rest there was a small but significant difference between the two patient groups: AF 60.2 pg/mL versus AC 97.6 pg/mL; P = 0.03. During exercise in the AC patients, there was a significant increase in α‐hANP levels, in VVIR mode, to 238.4 pg/mL, and in VVI mode, to 207.9 pg/mL, P = 0.002 and 0.003, respectively. In those patients with chronic AF, there was no significant rise or fall in α‐hANP levels in either pacing mode, VVIR 65.2 pg/mL, VVI 46.6 pg/mL. Previous workers have suggested that α‐hANP release by nonfunctioning atria is normal. We have shown that the presence of coordinated AC is required for the release of α‐hANP during exercise in patients with CHB, and that this appears to be independent of ventricular rate.