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Understanding link between vascular disease, dementia critical for elderly
Adults aged at least 80 years are more likely to experience the effects of dementia than CVD, according to research published in the Journal of the American College of Cardiology.
Coronary artery calcium (CAC) was identified as a determinant of mortality, CHD and MI in this population.
Lewis H. K uller, MD, DrPH , emeritus professor, department of epidemiology, Graduate School of Public Health, University of Pittsburgh, and colleagues investigated the link between CAC, carotid intima-media thickness, stenosis and ankle-brachial index — all measures of subclinical CVD — with the risk for dementia, CHD and all-cause mortality. The study included 532 older adults who participated in the Cardiovascular Health Study–Cognition Study between 1998 and 2013. The mean age was 93 years.
All participants underwent a yearly cognitive evaluation at the clinic or during home visits. Electron bean tomography scanning was used to measure CAC.
The final analysis included 311 of 433 patients who did not have clinical CAD in 1998 or 1999. Of those, the majority were white women (n = 157).
According to the findings, 36% of patients had a CAC score > 400 Hounsfield units. An elevated CAC score was associated with increased total mortality (HR = 1.73; 95% CI, 1.18-2.54). Although only 16% of the 422 deaths reported were determined to be caused by dementia, 64% of all patients who died had been diagnosed with dementia before their death. Twenty-five percent of the deaths were determined to be due to CHD.
Women and blacks, the researchers reported, had lower CAC scores and fewer white women had dementia (P = .19).
In addition, lower ankle-brachial index was associated with increased risk for dementia for white women, whereas maximal percent stenosis was a strong predictor of dementia for white men. By the end of the study, only 9% of the remaining patients did not have dementia.
“As age at first [MI] continues to rise, dementia will be an important comorbidity and will affect treatment decisions and outcomes,” Kuller said in a press release. “If delay or prevention of atherosclerosis resulted in the reduction or slowing of progression of brain disease and subsequent incidence of dementia, then there is the potential for a very substantial impact on reducing the majority of dementia in very old ages.”
Kuller also said there is a need “to test such hypotheses by substantially modifying risk factors, slowing the progression of atherosclerosis and determining whether such an effect will substantially reduce the incidence of dementia and specific neuropathology among older patients.”
In a related editorial, Walter Swardfager, PhD, and Sandra E. Black, MD, both of the LC Campbell Cognitive Neurology Unit, Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, Toronto, noted that these findings emphasize “the importance of determining whether preventing atherosclerosis will also prevent Alzheimer’s disease. The question is germane because [Alzheimer’s disease] is the most common dementia diagnosis, and the clinical risk factors for [it] are also risk factors for atherosclerosis.”
What is still unknown, according to Swardfager and Black, is “how exactly [Alzheimer’s disease] and vascular disease may be co-contributors or causally related.
“As more individuals live to older ages, we can expect a dramatic increase in the incidence and prevalence of dementia. Atherosclerosis, even if clinically undeclared, will likely contribute to these cases, suggesting the importance of pharmacological and nonpharmacological management of vascular risk factors beginning in midlife.” – by Tracey Romero
D isclosure: The study was supported by NHLBI, the National Institute of Neurological Disorders and Stroke, and the National Institute on Aging. The researchers report no relevant financial disclosures. Swardfager reports receiving funding from the department of psychiatry at the Sunnybrook Research Institute and from the Canadian Partnership for Stroke Recovery. Black reports receiving funding from the Brill Chair in Neurology in the department of medicine at the University of Toronto and the Toronto Dementia Research Alliance as well as institutional grants from Biogen Idec, Cognoptix, Eli Lilly, GE Healthcare, Novartis, Pfizer, Roche, Transition Therapeutics and personal honoraria from Boehringer Ingelheim, Merck and Novartis.