Results:

Using linear regression analysis and adjusting the associations between AD status and cardiac function for age, the investigators found that age predicts a reduction in diastolic function by mitral valve E/A ratio (MVE/A). They divided the study cohort into three age groups (<65, 65-80, and >80 years of age). They found that a correlation between AD and anticipated decline of myocardial function was present in the first age tertile (1.20 ± 0.18 vs. 1.34 ± 0.12). This appeared to be better explained by defects in myocardial compliance because such a pattern was not shown for the atrial component (A) of the MVE/A. Using a linear regression F-test (p < 0.05), the investigators observed a pattern that was consistent with poorer diastolic function at earlier ages among the AD participants, conforming with the pathogenesis of AD as a disease of anticipated aging. They also found increased left ventricular septal and inferior wall thickness, respectively, in the older AD participants (p < 0.05 for each). Using immunoblotting and enzyme-linked immunosorbent assay (ELISA), the investigators found that like in the brain, Aß₄₀ and Aß₄₂ were present in the heart, and their expression was increased in AD. They also found that AD cardiomyocytes displayed slower velocities of relaxation (R50 [time to 50% relaxation]: 0.272 vs. 0.238) and prolonged Ca²⁺ transients (time-to-peak: 0.544 vs. 0.151; R90: 0.328 vs. 0.084) compared with controls, indicating a defect in Ca²⁺ homeostasis.