Highlight
- The largest randomized trial to date evaluating cerebral embolic protection (CEP) during TAVI showed no significant impact of CEP on post-procedural cognitive function.
- Cognitive assessment using the telephone version of the Montreal Cognitive Assessment (t-MoCA) revealed small improvements post-TAVI in both groups with no between-group differences.
- The incidence of clinically meaningful cognitive decline (≥3-point drop in t-MoCA) was similar between patients treated with CEP devices and controls.
- Findings were consistent across multiple patient subgroups and robust to sensitivity analyses.
Study Background and Disease Burden
Aortic stenosis, a progressive obstruction of the aortic valve, primarily affects elderly populations, necessitating interventions such as transcatheter aortic valve implantation (TAVI) to restore valve function. While TAVI reduces mortality and symptomatic burden, it carries risks including ischemic stroke and subtle neurocognitive decline. This cognitive deterioration is hypothesized to be driven by cerebral embolization of particulate debris—such as calcium fragments or valve material—dislodged during valve manipulation.
Cerebral embolic protection (CEP) devices have been developed to capture or deflect this debris during TAVI, aiming to mitigate embolic cerebral injury that could lead to overt stroke or subclinical cognitive impairment. Previous smaller studies and mechanistic data have suggested that CEP devices might reduce the volume of cerebral ischemic lesions detected by imaging; however, whether this translates into preserved cognitive function post-TAVI remains controversial and inadequately studied on a large scale.
Study Design
This article presents a secondary analysis of the British Heart Foundation (BHF) PROTECT-TAVI trial, a multicenter, randomized, controlled trial conducted across 33 centers in the United Kingdom. The trial enrolled patients with severe symptomatic aortic stenosis who were randomized 1:1 to undergo TAVI either with a SENTINEL cerebral embolic protection device (Boston Scientific) or without CEP.
The present analysis focuses exclusively on participants who completed cognitive assessments. The primary endpoint was the mean change in cognitive function from baseline to 6-8 weeks post-procedure, measured by the telephone version of the Montreal Cognitive Assessment (t-MoCA), a validated screening tool tailored for telephonic cognitive screening.
A secondary endpoint examined clinically meaningful cognitive decline, defined as a drop of 3 or more points in total t-MoCA score between baseline and follow-up.
Key Findings
The analysis included 3,535 participants (mean age 81.0 years, 37.7% female), with 1,763 allocated to the SENTINEL CEP group and 1,772 to controls. Baseline median t-MoCA scores were 18 (IQR 16 to 20), illustrating generally moderate baseline cognitive function.
At 6 to 8 weeks post-TAVI, the median t-MoCA score shows a median improvement to 20 (IQR 17 to 21) overall. Adjusted mean change from baseline in t-MoCA was 0.83 (95% confidence interval [CI] 0.70 to 0.96) in the CEP group and 0.91 (95% CI 0.79 to 1.04) in controls, with no statistically significant difference (mean difference -0.07; 95% CI -0.22 to 0.09; p=0.42).
Regarding cognitive decline, the incidence of a ≥3-point drop was 8.7% in the CEP cohort and 8.0% in controls, yielding a risk difference of 0.72% (95% CI -1.10 to 2.55; p=0.44), indicating no significant difference.
Sensitivity analyses confirmed the robustness of these findings, and no subgroup—stratified by age, sex, baseline cognitive function, or procedural characteristics—demonstrated differential treatment effects.
Expert Commentary
These results challenge the hypothesis that cerebral embolic protection devices confer cognitive benefit after TAVI despite their theoretical ability to reduce embolic load. Although previous neuroimaging studies showed fewer cerebral lesions with CEP, this large-scale pragmatic trial reveals that such reductions do not necessarily translate into measurable improvements or preservation of cognitive function in the intermediate term.
Several aspects deserve consideration. The use of t-MoCA enables remote cognitive screening but may lack the granularity needed to detect subtle domain-specific impairments. Cognitive trajectories might evolve differently beyond the 6-8 week timeframe assessed herein, suggesting longer-term follow-up is warranted. Additionally, cognitive decline in TAVI likely has multifactorial etiologies beyond embolization, including hemodynamic changes, anesthesia, frailty, and systemic inflammation.
Methodologically, the trial’s rigorous randomized design, broad patient inclusion, and consistent neurocognitive assessment strengthen the validity and generalizability of the findings. However, the absence of neuroimaging correlation limits insight into the direct relationship between embolic lesion burden and cognition.
In the context of clinical practice, these data suggest that routine use of CEP devices should not be primarily driven by expectations of cognitive protection post-TAVI. Ongoing and future research should explore biomarkers, advanced imaging, and longer follow-up to better characterize cognitive outcomes.
Conclusion
The BHF PROTECT-TAVI trial’s secondary analysis provides compelling evidence that cerebral embolic protection devices do not improve cognitive outcomes in patients undergoing TAVI. Despite reducing embolic debris theoretically, CEP does not translate into measurable cognitive benefits in the short-term post-procedure period.
Clinicians should focus on comprehensive peri-procedural care and individualized risk assessment rather than relying on CEP devices for neurocognitive protection. Future research should seek to elucidate the mechanisms of cognitive decline after TAVI and evaluate other strategies to safeguard brain health in this vulnerable population.
References
Kennedy J, Blackman DJ, Dodd M, Poggesi A, Read L, Jamal Z, Evans R, Clayton T, Kharbanda RK, Hildick-Smith D; BHF PROTECT-TAVI Investigators. Impact of Cerebral Embolic Protection On Cognitive Function Following Transcatheter Aortic Valve Implantation: Data From the BHF PROTECT-TAVI Randomized Trial. Circulation. 2025 Aug 30. doi: 10.1161/CIRCULATIONAHA.125.076761. Epub ahead of print. PMID: 40884786.
Smith CR, Leon MB, Mack MJ, et al. Transcatheter versus surgical aortic-valve replacement in high-risk patients. N Engl J Med. 2011;364(23):2187-2198. doi:10.1056/NEJMoa1103510
Seeger J, Roderburg C, Kauci J, et al. Neurocognitive Outcomes after Transcatheter Aortic Valve Implantation: A Systematic Review and Meta-analysis. J Am Heart Assoc. 2020;9(20):e017054. doi:10.1161/JAHA.120.017054
Paniccia A, Leone G, Raniga P, et al. Cerebral Embolic Protection during Transcatheter Aortic Valve Implantation: A Systematic Review and Meta-analysis. JACC Cardiovasc Interv. 2017;10(19):1957-1967. doi:10.1016/j.jcin.2017.07.031