Page 23 - Journal of Structural Heart Disease Volume 4, Issue 1

Original Scienti c Article
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TAVR is the gold standard therapy for inoperable patients with symptomatic severe AS [1, 3]. Recent- ly, TAVR has been indicated for intermediate risk pa- tients [2]. The use of TAVR in a wider range of patient populations has paralleled improvements in valve technology aimed at reducing the risk of complica- tions such as vascular injury and stroke [25]. The 30- day stroke rate in the PARTNER 1A trial was signi - cantly higher among patients in the TAVR group than among patients in the medical therapy group (6.7% vs. 1.7%, P = 0.04) or the SAVR group (5.5% vs. 2.4%, P = 0.04) [1, 3]. In the PARTNER 1A trial, 38% of strokes occurred within 2 days and 58% within 30 days in pa- tients undergoing TAVR. Risk factors for stroke in the PARTNER 1A trial were use of TAVR and small native aortic valve area [9]. The risk of post-TAVR stroke in other studies ranged between 1.7% and 8.4% [7, 26, 27]. This wide di erence in reported stroke rate in the literature is likely secondary to inconsistencies in the de nitions of acute neurological events. However, a systematic review of the literature shows that stroke rates have declined over the last decade as delivery systems have become smaller, the systematic use of heparin has increased, and technical experience has improved [7, 25, 28].
The mechanism of stroke in TAVR is multifactorial but largely thought to be secondary to embolization. This may be in part due to liberation of calci c materi- al during valve implantation. Other factors contribut- ing to the development of stroke are manipulation of wires and catheters at the level of the aortic arch and root during the transfemoral approach and manip- ulation of the apex during the transapical approach [29]. Although studies have implicated embolization during the procedure as a potential cause of stroke [30], and bilateral carotid disease is a predictive fac- tor for post-procedure stroke [12], the main source of emboli remains unclear. Clinically silent emboli to the brain have been detected in the majority of pa- tients after TAVR [14, 16, 24, 31]. Several studies have used transcranial Doppler to identify high-intensity transient signal (HITS) as a surrogate for microembo- lization. Procedural HITS was identi ed in all patients, with the highest HITS detected for the transfemoral approach with the self-expanding Medtronic Core Valve, mainly during implantation [14, 29, 30]. In our study, neuroimaging testing was not used to deter-
mine the impact of carotid compression on the bur- den of asymptomatic microembolization. The valve design did not seem to alter the risk of stroke after TAVR. The FRANCE 2 Registry showed no statistically signi cant di erence between the balloon-expand- ing Edwards SAPIEN valve and the self-expanding Core Valve in terms of stroke outcome [32].
The use of carotid compression to in uence cere- bral embolization during cardiac procedures is con- troversial, with little published data in support of this practice. Asahi et al. [33] used magnetic resonance an- giography to examine the e ects of unilateral carotid compression on cerebral ow patterns in two human volunteers. They demonstrated clear changes in per- fusion patterns and ow directions within the cere- bral vasculature that recovered with decompression. Hillebrand et al. [18] studied 20 patients undergoing a variety of open cardiac surgeries and performed transcranial Doppler of the middle cerebral artery. They found that digital carotid compression reduced the incidence of cerebral emboli during aortic cannu- lation and declamping. The lack of e cacy of carotid compression during TAVR in the present study may be explained by the fact that microemboli occur during every step of TAVR, not just during valve deployment, as shown by TCD monitoring [14], although there is clearly a peak during valve positioning and deploy- ment. In addition, there is no consensus on the timing and level of pressure that should be applied to poten- tially prevent stroke.
Another approach to preventing stroke after TAVR is the use of embolic protection devices. There is evi- dence to suggest that the use of embolic protection devices is associated with a smaller volume of silent ischemic lesions and a smaller total volume of lesions, but there is no related decrease in clinically relevant strokes [34] and no signi cant change in neurocogni- tive function [15, 16, 24].
Although the speci c causes of ischemic stroke in TAVR patients have yet to be fully identi ed, several factors may increase a patient’s risk of post-procedure stroke, including chronic kidney disease, new onset atrial brillation [11, 21], post-deployment balloon di- lation, and pure aortic stenosis without regurgitation [26]. Because stroke increases a patient’s risk for mor- tality [35] and can negatively impact quality of life for patients and their families [36], and there is evidence
Journal of Structural Heart Disease, February 2018
Volume 4, Issue 1:9-16