Randomized trial suggests carotid endarterectomy does not affect dementia risk

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Alison Halliday

Carotid endarterectomy (CEA) does not appear to either reduce or increase the risk of dementia, despite it having been shown to reduce stroke risk. This is according to 20-year results from the ACST-1 trial, published online ahead of print in the European Journal of Vascular and Endovascular Surgery (EJVES).

ACST-1 (Asymptomatic carotid surgery trial) showed that surgery for asymptomatic carotid stenosis significantly reduces long-term stroke risk, Alison Halliday, MS FRCS, a professor of vascular surgery at the University of Oxford, Oxford, England, and colleagues write. They note, however, that the effect of CEA on later dementia is “uncertain.”

The investigators underline the fact that prolonged follow-up of trial participants is now possible with the linkage of national electronic records. In addition, they note that dementia records have a good positive predictive value for clinical diagnosis, though they are likely to underestimate the true risk. The combination of these factors, the authors write, “provides the opportunity to investigate the longer-term effects of CEA on incident dementia.”

In the present study, the researchers randomly allocated all U.K. and Swedish patients in ACST-1 (n=1,601/3,120) to either immediate CEA (n=796) or deferral of CEA (i.e. no intervention was performed unless or until triggered by ipsilateral transient ischemic attack or stroke; n=805) and followed them for 16–26 years, to study effects on dementia. The median follow-up was 19.4 years (interquartile range, 16.9–21.7).

Halliday et al report that dementia was recorded in 107 immediate CEA patients and 115 allocated delayed surgery. A total of 1,290 patients died, 1,091 before any dementia diagnosis, they add.

The investigators found that dementia incidence rose with age and with female sex (men, 8.3% aged <70 years at trial entry vs. 15.1% aged ≥70; women, 15.1% aged <70 years at trial entry vs. 22.4% aged ≥70 years) and was higher in those with pre-existing cerebral infarction (silent or with prior symptoms, 20.2% vs. 13.6%, respectively).

In addition, the authors relay that dementia risk was similar in both randomized groups: 6.7% vs. 6.6% at 10 years and 14.3% vs. 15.5% at 20 years, respectively.

The dementia hazard ratio (HR) was 0.98 (95% confidence interval [CI], 0.75–1.28; p=0.89), with no heterogeneity in the neutral effect of immediate CEA on dementia related to age, carotid stenosis, blood pressure, diabetes, country of residence, or medical treatments at trial entry (heterogeneity values: p>0.05), Halliday and colleagues detail.

Considering the main strengths of their research, Halliday et al highlight the fact that early CEA was randomly allocated, and so intervention and control groups were matched for known confounders at recruitment. In addition, they write that the use of electronic health records reduces potential bias, because the electronic health record includes participants who may not respond to active follow-up.

The authors also recognize some limitations. They acknowledge that face-to-face interviews of participants throughout follow-up would have been the “ideal method” to detect cognitive impairment and dementia, but this was not possible. They also state that dementia may be under ascertained using electrical records and that there was no consistent dementia ascertainment over time. In addition, they remark that the study confidence interval did not exclude a proportional benefit or hazard of about 25%.

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