Silent brain infarcts and early cognitive outcomes after transcatheter aortic valve implantation: a systematic review and meta-analysis

Abstract

Background Silent brain infarcts (SBIs) are frequently identified after transcatheter aortic valve implantation (TAVI), when patients are screened with diffusion-weighted magnetic resonance imaging (DW-MRI). Outside the cardiac literature, SBIs have been correlated with progressive cognitive dysfunction; however, their prognostic utility after TAVI remains uncertain. This study’s main goals were to explore (i) the incidence of and potential risk factors for SBI after TAVI; and (ii) the effect of SBI on early post-procedural cognitive dysfunction (PCD). Methods and results A systematic literature review was performed to identify all publications reporting SBI incidence, as detected by DW-MRI after TAVI. Silent brain infarct incidence, baseline characteristics, and the incidence of early PCD were evaluated via meta-analysis and meta-regression models. We identified 39 relevant studies encapsulating 2408 patients. Out of 2171 patients who underwent post-procedural DW-MRI, 1601 were found to have at least one new SBI (pooled effect size 0.76, 95% CI: 0.72–0.81). The incidence of reported stroke with focal neurological deficits was 3%. Meta-regression noted that diabetes, chronic renal disease, 3-Tesla MRI, and pre-dilation were associated with increased SBI risk. The prevalence of early PCD increased during follow-up, from 16% at 10.0 ± 6.3 days to 26% at 6.1 ± 1.7 months and meta-regression suggested an association between the mean number of new SBI and incidence of PCD. The use of cerebral embolic protection devices (CEPDs) appeared to decrease the volume of SBI, but not their overall incidence. Conclusions Silent brain infarcts are common after TAVI; and diabetes, kidney disease, and pre-dilation increase overall SBI risk. While higher numbers of new SBIs appear to adversely affect early neurocognitive outcomes, long-term follow-up studies remain necessary as TAVI expands to low-risk patient populations. The use of CEPD did not result in a significant decrease in the occurrence of SBI.

The 2020 American College of Cardiology/ American Heart Association (ACC/AHA) Guideline for the Management of Patients with Valvular Heart Disease. Should the World Jump In?

“…The prevalence of early post-procedural cognitive dysfunction (PCD) increased during follow-up, from 16% at 10.0±6.3 days to 26% at 6.1±1.7 months and meta-regression suggested an association between the mean number of new SBI and incidence of PCD. These data underline the importance of long-term follow-up, as several studies reveal a temporal association with cognitive dysfunction with mean follow-up times between 3.6 and 5.2 years, while those with short follow-up periods generally failed to detect any association [ 48 ] .…”

Asymptomatic Stroke in the Setting of Percutaneous Non-Coronary Intervention Procedures

“…SBIs exhibit a higher incidence than clinical strokes in patients undergoing aortic valve replacement, and they are observed more frequently after TAVR than after SAVR (at least 70% [36] and 44% [37] respectively). The presence of multiple lesions and a bilateral distribution suggests an embolic etiology and particulates likely originate from the aortic valve and aorta [38].…”

How to reduce uncommon but severe transcatheter aortic valve implantation complications: stroke, thrombosis, endocarditis, cognitive decline?

“…The number of SBI per patient depends on the strength of the MRI magnet used—a stronger magnet showing more small lesions. 11 The presence of SBIs is associated with prevalence of conventional stroke risk factors (diabetes and chronic kidney disease) but procedural factors such as balloon pre-dilations have been associated with more lesions per patient. 11 Although termed ‘clinically silent’, the consequences of SBI lesions depend on their location within brain areas—when they affect areas without primary motor, sensory or linguistic functions they remain silent.…”

“…As stated previously, EPDs do not reduce the absolute number of new SBIs but have been associated with smaller volume of lesions and smaller total SBI volume. 11 It is therefore difficult to give strong evidence-based recommendations on EPD during TAVI. The ongoing PROTECTED TAVR trial (clinicaltrials.gov NCT 04149535) will randomize 3000 patients undergoing TAVI to cerebral protection vs. no EPD with a clinical primary endpoint (stroke at 72 h) and should provide more definitive answers.…”

“…Despite the limitations, it has been shown that the mean number and not just the incidence of SBI might be associated with post-procedural cognitive dysfunction after TAVI and that a threshold effect exist—a certain volume of infarcted brain is required before cognition decline becomes clinically evident. 7 , 11 In a meta-analysis the use of EPD, by reducing microembolic load, was found to have a significant association with lower prevalence of cognitive decline up to 1-week post-TAVI. However, this effect was no longer significant at 1 month.…”