P3‐136: LOW CARDIAC INDEX IS ASSOCIATED WITH INCIDENT DEMENTIA AND ALZHEIMER'S DISEASE: THE FRAMINGHAM HEART STUDY

Cross-sectional epidemiological and clinical research suggest lower cardiac index is related to markers of abnormal brain aging, such as smaller brain volume, increased white matter hyperintensities, and worse cognitive performance. It is unknown whether lower resting cardiac index is a risk factor for incident dementia or Alzheimer's disease (AD). 1034 Framingham Offspring Cohort participants free from clinical stroke, transient ischemic attack, or dementia constituted our sample (69±6 years; 53% women). Multivariable-adjusted proportional hazard models adjusting for age, sex, education, systolic blood pressure, diabetes mellitus, prevalent cardiovascular disease (CVD), and apolipoprotein E4 status were used to relate cardiac MRI-assessed cardiac index (cardiac output/body surface area, L/min/m 2) to incident all-cause dementia and AD. Over a median 7.3 year follow-up period, 26 participants developed dementia, including 21 AD cases. In multivariable-adjusted models, each one standard deviation unit decrease in cardiac index increased the relative risk of dementia (HR=1.77, p=0.01) and AD (HR=1.73, p=0.03). If participants with clinically prevalent CVD and atrial fibrillation were excluded (n=209), each one standard deviation unit decrease in cardiac index continued to increase the relative risk of dementia (HR=3.54, p=0.01) and AD (HR=3.45, p=0.02). Among community dwelling adults age 60 years and older, lower cardiac index is associated with increased risk of incident dementia and AD over a median follow-up period of 7 years. When participants with prevalent CVD and atrial fibrillation were excluded from analyses, lower cardiac index was still associated with increased risk of incident dementia and AD. Systemic hemodynamics may affect cerebral hemodynamics in older adults with a lifetime burden of vascular risk factors and subsequent modest compromises in cerebral circulation control. Such age-related changes may contribute to the pathogenesis or exacerbation of amyloid deposition, subsequent neuronal injury, and vascular pathology. Further investigation into the mechanisms underlying this increased risk is merited for identifying targets for primary prevention or therapeutic interventions.