Atrial stunning: basics and clinical considerations

Abstract

Conversion of atrial fibrillation and flutter to sinus rhythm results in a transient mechanical dysfunction of atrium and atrial appendage, termed atrial stunning. Atrial stunning has been reported with all modes of conversion of atrial fibrillation and flutter to sinus rhythm including both transthoracic and low energy internal electrical, pharmacological, and spontaneous cardioversion, and conversion by overdrive pacing and by radiofrequency ablation. Atrial stunning is a function of the underlying arrhythmia becoming apparent at the restoration of sinus rhythm, not the function of the mode of conversion, and does not develop after the unsuccessful attempts of cardioversion or the delivery of electric current to the heart during rhythms other than atrial fibrillation or flutter. Tachycardia-induced atrial cardiomyopathy, cytosolic calcium accumulation, and atrial hibernation are the suggested mechanisms of atrial stunning. Atrial stunning is at maximum immediately after cardioversion and improves progressively with a complete resolution within a few minutes to 4–6 weeks depending on the duration of the preceding atrial fibrillation, atrial size, and structural heart disease. Atrial stunning causes postcardioversion thromboembolism despite restoration of sinus rhythm. Duration of anticoagulation therapy after successful cardioversion should depend on the duration of atrial stunning. Lack of improvement in cardiac output and functional recovery of patients immediately after cardioversion is attributed to the atrial stunning. Verapamil, acetylstrophenathidine, isoproterenol, and dofetilide have been reported to protect from atrial stunning in animal and small human studies. Right atrium stunning is less marked and improves earlier than that of left atrium, resulting in a differential atrial stunning explaining the rare occurrence of pulmonary edema after cardioversion.

Introduction

The cardioversion of atrial fibrillation and atrial flutter to sinus rhythm is associated with a cardioversion related transient mechanical dysfunction of the left atrium and left atrial appendage, termed atrial stunning [1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17], [18], [19], [20], [21], [22], [23], [24], [25], [26], [27], [28], [29], [30], [31]. The left atrial stunning results in a paradoxical reduction in the left atrial and left atrial appendage blood flow velocities despite reversion to sinus rhythm. There is a considerable evidence to suggest that the left atrial and left atrial appendage stunning is responsible for an increase in the risk of developing thromboembolic events for h to weeks after cardioversion of atrial fibrillation to sinus rhythm [6], [8], [17], [18], [32]. Furthermore, data suggest that left atrial stunning hampers the improvement in exercise tolerance, the time course of which parallels with the return of the atrial function [33], [34]. Historically, the postcardioversion left atrial mechanical dysfunction was initially documented by using direct left atrial pressure tracings [1], [2]. Later, it has been uniformly confirmed by numerous transthoracic and transesophageal echo and Doppler studies [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17], [18], [19], [20], [21], [22], [23], [24], [25], [26], [27], [28], [29], [30], [31].

Due to the loss of organized atrial contraction, atrial fibrillation predisposes to the development of thromboembolism and results in a 5-fold increase in the risk of stroke [35], [36], [37], [38]. The two important aspects considered in the treatment of patients with atrial fibrillation are the long-term use of anticoagulation therapy to prevent thomboembolism and the long-term use of atrioventricular node-blocking drugs for control of ventricular rates [37], [38], [39], [40], [41]. Cardioversion of atrial fibrillation and maintaining the sinus rhythm is the best measure to control the heart rate, eliminating the need of the use of atrioventricular node-blocking drugs, and is considered to abate the need of the long-term use of anticoagulation, abolishing the risk of major bleeding or intracranial hemorrhage potentially associated with the use of anticoagulation therapy [42], [43], [44], [45]. However, interestingly, cardioversion of atrial fibrillation by itself predisposes to and increases the short-term risk of thromboembolic episodes, including stroke [32], [42], [46]. Two mechanisms have been suggested underlying this short-term increase in the risk of thromboembolic events after cardioversion of atrial fibrillation. Initially, it was thought that the organized atrial contraction restored after cardioversion may dislodge fresh thrombi that had been formed during atrial fibrillation [47]. Later, a number of transthoracic and transesophageal echocardiographic studies, mostly conducted in the last decade, demonstrated that although sinus rhythm is restored and the atrial contractions are organized after successful cardioversion, the mechanical function of left atrial and left atrial appendage is paradoxically depressed resulting in a decrease in the left atrial and left atrial appendage blood flow velocities and development of an echogenic swirling pattern of blood flow with potential to development of new thrombi [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17], [18], [19], [20], [21], [22], [23], [24], [25], [26], [27], [28], [29], [30], [31], [47], [48], [49], [50], [51], [52], [53], [54], [55], [56], [57], [58], [59], [60], [61], [62], [63], [64], [65], [66], [67], [68], [69], [70], [71], [72], [73], [74], [75], [76], [77], [78], [79], [80]. Similar studies, but in a smaller number, have observed parallel findings in right atrium.