A new study, published in Circulation: Cardiovascular Interventions, shows that one fifth of patients undergoing transcatheter aortic valve implantation (TAVI) have evidence of carotid artery disease. It also indicates that while the presence of carotid disease may be a marker of higher cardiovascular burden, it is not itself a risk factor for stroke or mortality after TAVI.
Authors Ajar Kochar (Duke Clinical Research Institute, Duke University of School of Medicine, Durham, USA) and others report that the biological mechanism underpinning periprocedural stroke in TAVI are “incompletely understood”. They note that periprocedural debris embolisation is one potential mechanism of stroke in this context but add that strokes (at 30 days) still occur in patients who undergo TAVI with cerebral protection devices (such as Sentinel, Claret Medical). “These findings suggest either current technologies do not sufficiently reduce the risk of periprocedural debris embolisation or there are other mechanisms for TAVI-associated stroke,” Kochar et al write.
According to the authors, another potential mechanism is the presence of the disease—given that it is associated with an increased risk of stroke in patients undergoing surgical aortic valve replacement. Therefore, the aim of the present study was to evaluate incidence among TAVI patients, the relationship between severity of disease and cardiovascular outcomes, and its influence on 30-day and one-year stroke mortality.
Using data from three US registries, Kochar et al identified 29,143 patients who underwent TAVI between October 2013 and September 2015 (in the USA). Of these, 6,410 had carotid disease (22%). In most cases (50–79%), the car was of moderate severity.
Looking at unadjusted outcomes, the presence of the disease was associated with a significantly increased risk of stroke at 30 days and at one year. Similarly, carotid disease was associated with a significantly increased risk of mortality both at 30 days and at one year. These risks increased with increasing severity.
However, in an adjusted analysis, the condition was no longer associated with a significantly increased risk with stroke or mortality at 30 days. Nor were there, after adjustment for patient characteristics, any significantly differences in the risk of stroke or mortality at one year between patients with and those without carotid disease. The authors state: “Even after incorporating the degree of stenosis, there was no significant adjusted association between severity and 30-day or one-year risks of stroke or mortality.”
Kochar et al observe that, on the basis of their findings, “carotid disease is possibly a marker for patients with a higher mortality burden” but does not itself “result in a higher risk of stroke or mortality”. “Further supporting this notion that the disease is a marker for a large comorbidity burden are the higher unadjusted one-year cumulative incidence rates for both myocardial infarction and bleeding rates compared with no carotid patients,” they add.
They conclude: “Despite technological improvements, post-TAVI stroke is still a major complication; our results suggest carotid disease does not influence this risk of stroke.”