Stroke, TIA, and Silent Microemboli

Stroke and TIA
Embolism of air or thrombus is one of the most significant complications of AF ablation, and both are potential causes of cerebral, coronary, and peripheral vascular compromise.
The incidence of thromboembolism associated with AF ablation is reported to be between 0% and 7%.242,489,503,532,533,655,673,796,798,799,806,920,921,1202,1203,1204 More than two-thirds of the clinical trials reviewed for preparation of this document reported one or more cerebro-vascular events. Thromboembolic events typically occur within 24 hours of the ablation procedure, with the high-risk period extending for the first 2 weeks following ablation.798,1204 In one series that surveyed 26 embolic stroke events that occurred in a series of 3060 patients, long-term neurological outcomes were as follows: severe impairment (3 patients, with 2 possibly related deaths); moderate impairment (10 patients); mild impairment (9 patients); and unknown (4 patients).1202
A number of potential explanations for the development of thromboembolic complications have been proposed. These include the development of thrombi on or within stationary sheaths or ablation catheters positioned within the LA, char formation at the tip of the ablation catheter and at the site of ablation, disruption of a thrombus located in the atrium prior to the ablation procedure, and electrical cardioversion during procedures.875 Incidence of these events can be reduced by a combination of detailed preprocedural imaging, a strict anticoagulation protocol, meticulous attention to sheath management, and careful control of RF energy to minimize the risk of char formation. Of the writing group members, 68% report maintaining a constant heparinized flush through all long sheaths with access to the LA, and most heparinize to an ACT >300 seconds before transseptal catheterization.
Diagnosis of a symptomatic thromboembolic event is usually straightforward when ischemia or infarction results from arterial occlusion interrupting perfusion of dependent tissue. The potential manifestations depend on where the occlusion occurs, whether it be intracranial, coronary arterial, abdominal, or in other peripheral arterial beds. We have previously discussed the prevention of thromboembolism by intraprocedural and postprocedural anticoagulation in Section 7: Technical Aspects of Ablation to Maximize Safety and Anticoagulation. Treatment of a thromboembolic event will vary according to the location of the embolus. Peripheral arterial embolization might be amenable to surgical thrombectomy, whereas cerebral embolization has traditionally been managed conservatively and the consequences accepted. There is growing interest, however, in aggressive early management of such events, using either thrombolytic drugs or percutaneous interventional techniques. Some delay in diagnosis of a thromboembolic event that occurs during an ablation procedure while a patient is under general anesthesia cannot be avoided.

Asymptomatic Cerebral Emboli
ACE is defined as an occlusion of a blood vessel in the brain due to an embolus that does not result in any acute clinical symptoms and is therefore “silent.”800,1205 Emboli can result from a thrombus, air, gas, tissue, or fat. During an AF ablation procedure, potential sources of these microemboli include thrombi, which can develop on intracardiac catheters; sheath materials; air introduction through a sheath during catheter insertion or exchanges; dislodgement of thrombi in the heart; or as a result of thrombi or gas that forms during the ablation process. Diffusion-weighted MRI (DW-MRI), with or without fluid-attenuated inversion recovery (FLAIR) imaging, is very sensitive for identifying acute ischemic injury and can detect a cerebral lesion created by an embolus as early as 30 minutes postablation.
The first report of ACE lesions following AF ablation was published in 2006.1206 In this report, 2 of 20 patients developed new asymptomatic cerebral lesions on MRI, following AF ablation. Subsequent to this report, multiple studies have reported that DW-MRI can detect new acute lesions created by emboli, following up to 50% of AF ablation procedures.723,724,800,1205,1207,1208,1209
The incidence of this complication initially appeared to vary according to the system used for ablation, and was reported to be highest with the use of nonirrigated circumferential multielectrode ablation catheters with duty cycled phased RF energy.1209,1210 Based on these findings, modifications were made in anticoagulation, sheath management, and energy delivery protocols. Following introduction of these modifications, two subsequent studies reported a 2% or lower incidence of ACE lesions with use of this same circular phased RF ablation catheter.728,731,1211 One study examined the important question concerning whether these lesions persist on repeat DW-MRI and T2 FLAIR scanning. In this study, 14 patients who had 50 new silent cerebral emboli detected post-AF ablation had a repeat MRI a median of 3 months later. It was notable that 47 of the 50 lesions (94%) resolved in the interim. The three lesions in three patients that produced a residual defect at repeat scanning were initially >10 mm in size, and one of these patients had neurological symptoms. When considering the significance of the ACE lesions that have been observed following AF ablation, it is important to note that cerebral embolism has also been observed after most types of cardiac invasive procedures, including coronary angiography, carotid artery stenting, and cardiac valve replacement.1212,1213 Importantly, as of now, a direct link between silent cerebral embolism and a decline in neurocognitive function has not been proven.800,1205,1211,1212 However, one study has reported mild postoperative neurocognitive dysfunction in 13% of patients undergoing ablation for PAF and in 20% undergoing ablation for persistent AF. The precise mechanism of this neurocognitive dysfunction and its possible link to ACE lesions needs to be explored further.1214
A decade after the first description of ACE lesions following AF ablation, a tremendous amount of new knowledge has been generated concerning this important complication of AF ablation.800,1205,1211,1215,1216 These efforts have resulted in a striking decrease in the incidence of this complication. During this period of time, studies have identified a number of techniques to lower the risk of ACE lesions, including (1) aggressive anticoagulation prior to, during, and following ablation; (2) careful sheath management; (3) modifications in the delivery of phased RF energy; and (4) choice of ablation energy source and lesion sets. The long-term prognostic implications of ACE following AF ablation remain unclear. Because multiple studies have reported that the majority of acute lesions regress without evidence of chronic glial scar when reassessed several weeks to months later, the occurrence of long-term sequelae appears unlikely.1205 Nevertheless, there is a possibility of long-term sequelae, given the association between silent cerebral infarcts and an increased long-term risk of dementia.1217 While further work remains, the amount of progress is striking and will benefit our patients in the long term.