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Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm

Authors
Gregory YH Lip, MD, FRCPE, FESC, FACC
Jordan M Prutkin, MD, MHS, FHRS
Section Editor
Bradley P Knight, MD, FACC
Deputy Editor
Gordon M Saperia, MD, FACC

INTRODUCTION

Atrial fibrillation (AF) can lead to a fall in cardiac output that is often clinically significant. Potential consequences include a fall in blood pressure, decreased exercise capacity, and pulmonary congestion, all of which are manifestations of heart failure (HF) (table 1). In addition, AF and HF often occur together, and each may predispose to the other [1].

The hemodynamic effects of AF and of cardioversion will be reviewed here. The clinical aspects and treatment of AF in patients with HF and cardiomyopathy are discussed separately. (See "The management of atrial fibrillation in patients with heart failure".)

ADVERSE HEMODYNAMICS IN AF

Many patients with atrial fibrillation (AF) develop a modest decline in left ventricular performance that typically returns to the previous baseline following reversion to sinus rhythm [2-5]. The magnitude of this effect and its reversibility were illustrated in a report of 15 patients with AF who were successfully cardioverted and maintained sinus rhythm for one month; 11 of these patients maintained sinus rhythm for three months [4]. The mean duration of AF was three months (range 5 to 254 days). The following findings were noted after cardioversion:

The mean left ventricular ejection fraction (LVEF) increased from 47 percent at baseline to 55 percent immediately after cardioversion to 61 percent at one month; there was no further increase at three months. The improvement in LVEF occurred in all but one patient. The maximum improvement in LVEF by one month coincides with the time to full recovery of left atrial contractile function [6]. (See 'Atrial stunning' below.)

The increase in LVEF was primarily due to enhanced diastolic filling resulting from two factors: (1) an increase in cycle length, which may involve both regularization of the heart rate and avoidance of short cycle lengths that impair ventricular contractility; and (2) the return of left atrial contractile function, as determined by peak A wave velocity, which increases the atrial contribution to ventricular filling [3,4].

             

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Literature review current through: Nov 2016. | This topic last updated: Tue Nov 03 00:00:00 GMT+00:00 2015.
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