Left atrial appendage isolation: The asymmetrically sharp double edge sword

Abstract

The relationship between atrial fibrillation and stroke remains an enigma. Our earlier explanation where stasis during atrial fibrillation was visualized leading to thrombus formation and subsequent embolization perhaps during conversions to sinus rhythm now appear to have been simplistic. Recent data from continuous monitoring with indwelling pacemakers have shown that stroke in patients with atrial fibrillation may be more likely to occur when the patient is in sinus rhythm! 1 Further, relatively brief paroxysms of atrial fibrillation in a diabetic elderly female with a prior history of stroke are far more likely to result in a cardioembolic event within a year than continuous permanent atrial fibrillation in a younger patient without such history and a structurally normal heart. Thus, it appears that atrial fibrillation and stroke are epiphenomena not having a predictable causal role. As a corollary, therefore, ablation for atrial fibrillation even if successful has yet to be shown conclusively to eliminate stroke risk. Despite these confusing pathophysiological conundrum, a common player for both atrial fibrillation and stroke is the left atrial appendage (LAA). Undoubtedly, the most common location for an echocardiographically identifiable thrombus in the atrium is the left atrial appendage. Extrapulmonary triggers 2 for atrial fibrillation have recently been identified to originate in the LAA. Furthermore, reduction in the electrically active atrial mass by isolating or amputating the LAA may have a role in substrate modification for persistent atrial fibrillation as well. 3,4 Isolating the appendage, however, removes a principle component of LAA blood flow from active contraction and may paradoxically increase the risk of stroke, something all appendage and fibrillatory therapies have aimed to minimize. In this issue of the journal, Chen et al 5 describe such a case of a rapidly progressing thrombus in the LAA despite ablation that included isolation and continued anticoagulation. They provide us with a concise description of a rescue approach to manage this difficult situation. | ELECTRICAL ISOLATION AND STROKELAA contraction is not the sole determinant of blood transit into and out of this important capacitance subchamber of the atrium. A multicomponent often quadriphasic flow transiting the appendage is determined by LAA contraction, relaxation, left ventricular contraction and relaxation, and the compliance and conduit role of the body of the left atrium. Thus, with electrical isolation, appendage velocities are abnormal but flow still occurs as long as the remaining components are intact and robust. However, if appendage isolation is done in a patient with a noncompliant atrium, depressed ventricular function, and abnormal diastolic function of the left ventricle, then profound changes in appendage flow not dissimilar to what is seen in atrial fibrillation occur and understandably may give rise to dangerous stasis and thrombus formation even with ongoing anticoagulation. 6 2 | MANAGING THROMBUS POST-L...