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Contrary to earlier research, a Framingham Heart Study analysis found no significant dementia risk tied to transient ischemic attack over 2 decades.
A recent study found no significant difference in dementia incidence over a 20-year follow-up among individuals who had or did not have a transient ischemic attack.1
“Our findings challenge our initial hypothesis and diverge from certain existing literature studies that have proposed persistent cognitive decline following [transient ischemic attack],” wrote investigators, led by Vasileios‐Arsenios Lioutas, MD, from the department of neurology at Beth Israel Deaconess Medical Center, Harvard Medical School. “It is noteworthy, however, that other studies suggest cognitive impairment after [transient ischemic attack] is a transient phenomenon, potentially part of an acute confusional state or delirium.”
According to the Cleveland Clinic, multi-infarct dementia results from a series of small strokes—transient ischemic attacks.2 Transient ischemic attacks and strokes share symptoms, but the former may be milder. Risk factors for multi-infarct dementia include hypertension, diabetes, conditions that can cause blood clots (atherosclerosis, coronary heart disease, heart valve disease, and carotid artery disease), hyperlipidemia, and smoking.
Despite existing data, the link between transient ischemic attack and dementia is still under-characterized. Investigators aimed to determine the long-term incidence of dementia following a transient ischemic attack and whether the attack prompts changes in vascular risk factors. The primary outcome was the 20-year incidence of all-cause dementia.
The team recruited participants from a nested, matched, longitudinal cohort study within the community-based Framingham Heart Study. Participants without dementia or transient ischemic attack (n = 1485) were matched 5:1 by age and sex to 297 participants with first incident transient ischemic attack at > 60 years. The arm with incident transient ischemic attack had a sample of 47% men and a mean age of 72.7 ±7.7 years. Participants with transient ischemic attack were more likely to have hypertension (78% vs 67%; P = .0006), coronary heart disease (37% vs 7%; P = .018), and atrial fibrillation (11% vs 7%; P = .018).
Over a follow-up of 8.9 years, 19% and 24% of patients with and without transient ischemic attack, respectively, developed dementia (hazard ratio [HR], 0.93; 95% confidence interval [CI], 0.71 – 1.24; P = .063). The association remained after adjusting for strokes and the competing risk of death. Once the team removed case-control sets with interim stroke, 25% and 24% of participants with and without transient ischemic attack, respectively, developed dementia (HR, 1.17; 95% CI, 0.78 – 1.73; P = .448).
“It is still unclear whether this represents a true lack of association between [transient ischemic attack] and cognitive decline or a true but relatively small risk exists but can be mitigated by early initiation and consistent adherence with secondary prevention,” the team wrote.
The analysis showed that participants with transient ischemic attack were more likely to have a reduction in the frequency of smoking (18% to 11%; P = .025), an increase in anticoagulant use (3% to 18%; P = .0005), and a slight increase in aspirin use (46% to 61%; P = .052).
Furthermore, participants who started anticoagulation after transient ischemic attack had a greater likelihood of developing dementia (HR, 4.71; 95% CI, 1.89 – 11.71; P < .001). This was observed after adjusting for atrial fibrillation (HR, 4.01; 95% CI, 1.57–10.20; P = .0005).
No participants in either arm experienced changes in their mean SBP or had high systolic SBP (SBP > 149 mm Hg).
“Prospective studies with well‐matched controls, active cognitive surveillance, and sufficiently long follow‐up are necessary to better characterize the cognitive repercussions of [transient ischemic attack] and the impact of secondary stroke prevention in cognitive health,” investigators wrote.
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