P2‐106: Echocardiography vortex formation time reveal cardiac diastolic transmitral flow dysfunction in Alzheimer's disease patients

Alzheimer's disease (AD) shares several risk factors with cardiovascular disease. As a continuation of our studies concerning the potential pathological role of the cardiovascular axis on AD brain perfusion, we studied general cardiac performance by echocardiography. Previous studies have demonstrated that reduced cerebral perfusion in AD could be due to left ventricular (LV) dysfunction. Optimal diastolic hemodynamic conditions are determined by an efficient transmitral blood flow and vortex formation time (VFT). In general, a vortex ring forming alongside a jet entering a body of fluid results in a more efficient fluid transport compared to a straight jet. Echocardiography was performed on 45 individuals, 22 in the AD group (15 males and 7 females, mean age 80.1 ± 6.7 years) and 23 in the ND group (15 females and 8 males, mean age 76.5 ± 6.7 years). Standard apical and parasternal echocardiographic projections and transmitral Doppler flow velocity measurements were recorded for subsequent analyses. Early (E) and atrial (A) components of LV filling velocities were not statistically different between the AD and ND groups; however, abnormal E/A < 1.0 was found in both groups. The LV septal and posterior walls were at a threshold of normal or mildly increased diastolic thickness, with significantly thicker LV walls in the AD group, while LV volumes and ejection fraction were normal. The VFT in AD and ND subjects was outside of the optimal range and significantly lower in the former (AD 3.33 ± 1.17 and ND 4.00 ± 0.85, p = 0.0183). These observations are consistent with age-dependent diastolic relaxation dysfunction and preserved LV systolic function. The VFT values indicate that in the AD group, the relaxation impairment negatively impacted diastolic vortex formation, possibly due to myocardial structural remodeling, suggesting suboptimal blood transport rheology. We speculate that this suboptimal hemodynamic efficiency represents a patho-physiological link between the pronounced LV relaxation dysfunction and ultimate cognitive dysfunction in the AD patients.