Page 19 - Journal of Structural Heart Disease Volume 4, Issue 1

Original Scienti c Article
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al was signi cantly higher among TAVR patients than among SAVR patients (5.5% vs. 2.4%, P = 0.04) in the high-risk cohort [1]. Published 5-year outcomes of the PARTNER 1 trial showed a similar incidence of stroke or transient ischemic attack (TIA) between TAVR and SAVR patients (15.9% vs. 14.7%, P = 0.3) [5]. More re- cent data show stroke rates of 3.4% at 30 days in the FRANCE 2 Registry study [6] and procedural/in-hos- pital stroke rates of 1.8% in the Transcatheter Valve Treatment Sentinel Pilot Registry [7]. Although the incidence of stroke is declining [8], stroke is strongly associated increased morbidity and mortality [9, 10].
The mechanism of stroke after TAVR is presumably embolic in most cases and may di er depending on the timing of stroke and route of access. Howev- er, a history of carotid disease may be one predictor of post-procedure strokes [11-13]. Multiple studies utilizing magnetic resonance imaging, trans-crani- al Doppler, and ltered and retrieved material have documented nearly universal embolic phenomena during TAVR [14-17]. Hypothetically, stroke preven- tion can be achieved by minimizing the amount of microemboli showering from the aorta to the brain during TAVR implantation. Anecdotally, several TAVR programs in the United States and Europe perform carotid compression during TAVR to minimize the risk of stroke or TIA [18]. The rationale for this concerns both direct occlusion of the arteries during a period of embolic showering and a change in ow diverting emboli from entering cerebral circulation. Here, we examined the association between carotid compres- sion during TAVR and post-procedural incidence of TIA and stroke.
Materials and Methods
Patient Population
The study included patients with symptomatic severe AS who underwent TAVR at the University of Utah Hospital, Washington University Medical Center, or Banner Health Center in Phoenix, Arizona between February 1, 2012 and April 1, 2016. Collected data were part of the Transcatheter Valve Therapy registry. For the purposes of this study, the intervention of in- terest was whether the patient received carotid com- pression during the TAVR procedure as documented in the clinical operative report. Patient eligibility for
TAVR was decided at each site by the heart team, which included interventional cardiologists, cardio- thoracic surgeons, imaging cardiologists, and cardi- ac anesthesiologists. Members of the heart teams at all three centers were similarly trained and quali ed to treat TAVR patients. Enrolled patients were divid- ed into two groups: Group I included patients who underwent TAVR without carotid compression, and Group II included patients who underwent TAVR with carotid compression. The valve technologies included in the study were SAPIEN XT and S3 (Ed- ward Lifesciences, Irvine, California, USA). To control for any potential di erences in pathophysiology re- lated to access approach, only patients who under- went a TAVR procedure via the transfemoral access route were included in this study. Patients whose pre-procedure carotid stenosis status had not been measured were not included in the study, nor were patients with bilateral carotid disease. All patients for whom anticoagulation medication was not contrain- dicated received dual anti-platelet therapy with aspi- rin and clopidogrel for 6 months after TAVR. Intrave- nous heparin was administered during the procedure to obtain an activated clotting time goal of >300 s. Taking into account contraindications, there was no signi cant di erence between groups with regard to the administration of anticoagulation medication at discharge (98.4% for Group I vs. 97.5% for Group II, P = 0.95).
At the University of Utah Hospital, it is standard practice to perform carotid compression on patients receiving SAPIEN valves; however, carotid compres- sion is not used at the other two centers, therefore data from these centers served as a control. Carotid compression is de ned as bilateral external compres- sion of the carotid arteries and is performed coinci- dent with rapid pacing. In this study, carotid compres- sion was initiated 2 s before rapid pacing and released 3 s after rapid pacing was discontinued, with the av- erage duration of carotid compression lasting 30–45 s. Carotid compression was completed manually with enough pressure to feel the carotid compressed and was completed by the assisting physician. Stroke and TIA were de ned according to Valve Academic Re- search Consortium (VARC) criteria [19]. TIA was de- ned as a new focal or global neurological de cit with symptom resolution within 24 hours of onset in the
Journal of Structural Heart Disease, February 2018
Volume 4, Issue 1:9-16