Effect of the Maze Procedure for Atrial Fibrillation on Atrial and Brain Natriuretic Peptide

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Abstract

We studied plasma levels of atrial and brain natriuretic peptides at rest and after exercise before and after intracardiac surgery with and without the maze procedure in patients with chronic heart failure secondary to valvular heart disease. The present study found that an increased response of both cardiac natriuretic peptides is attenuated with resulting water retention after the maze procedure.

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Cited by (38)

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    ANP is an important neurohormonal regulator that plays a vital role in cardiovascular homeostasis by regulating natriuresis and diuresis in response to volume expansion to maintain adequate salt and water balance (10). Earlier studies in patients who underwent a maze procedure with bilateral atrial appendectomies demonstrated reduced ANP in the early post-operative phase (11,12) that remained low at 2 years (12). Despite the decrease in ANP levels, there were no reported data on its impact on systemic blood pressure until the recent observations from our group performing epicardial LAAE in patients with AF (6,7).

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    Several investigators have demonstrated that the level of plasma ANP decreased after bilateral atrial appendectomy in animal models. In clinical settings, attenuation of ANP has been found in patients after the maze procedure and bilateral atrial appendectomy.20,21 This implies that amputation of both atrial appendages could affect renal function.

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    The challenge is to understand the association between AF and the elevations of NT-proBNP seen in those patients without acute HF. Recent data suggest that BNP and NT-proBNP levels may be correlated with the presence of AF6,7,11-18 and that natriuretic peptide values may decline significantly after conversion from AF to normal sinus rhythm,19-25 suggesting a mechanism in this arrhythmia that leads to an increase in BNP or NT-proBNP. Possible mechanisms include a primary increase in natriuretic peptide production induced by AF, and/or a secondary increase due to impaired cardiac function, ventricular wall stress, or increased ventricular filling pressures without clinically overt HF.14,26

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