PULSE-COR REGISTRY

Abstract

Objective: The pathogenesis of LV diastolic failure development remains unknown. The aim to maintain this registry was to evaluate ventricle-arterial interactions with the help of pulse wave contour analysis (PWA), pulse wave velocity (PWV) analysis and echocardiographic parameters along with evaluation additional factors. Design and method: We included 553 patients with AH who were hospitalized in the Symptomatic hypertension department NSC Institute of cardiology n.a. acad. M.D. Strazhesko. Final analysis included 320 patients, that underwent all necessary diagnostic procedures. PWA and PWV analysis were performed using SphygmoCor device (AtCor, Australia) with determination of central SBP (cSBP), augmentation index (Aix) and normalized Aix ([email protected]), carotid-femoral PWV (cfPWV). Also we measured CAVI and ankle-brachial index (ABI) with the mean of VaSera 1500 (Fukuda Denshi, Japan). Ultrasound diagnostics included vascular ultrasound with intima-media thickness (IMT) measurement. Echocardiography was performed according ASE standartized protocol, LV diastolic function was evaluated according to ASE 2016 guidelines. Ventricle-arterial coupling (VAC) was evaluated using formula, described in literature. Results: Mean SBP/DBP was 154,5 ± 1,5/92,8 ± 0,9 mmHg. VAC was significantly associated with woman sex (r = 0,276; p < 0,05), office SBP (r = 0,351; p < 0,05), E/A (r = 0,215; p < 0,001), IVRT (r = −0,127; p < 0,05), Dt (−0,131; p < 0,05), LV ejection fraction (EF) (r = 0,9; p < 0,05), LVMMI (r = −0,195; p < 0,01), mitral annulus motion (s′) (r = 0,272; p < 0,001), left ventricle wall stress (LVWS) (r = −0,169; p < 0,01), CAVI (r = 0,561; p < 0,01). E/A was significantly associated with age (r = −0,373; p < 0,001), cSBP (r = −0,308; p < 0,01), IMT (r = −0,297; p < 0,05), EF (r = 0,170; p < 0,001), s′ (r = 0,253; p < 0,001), ABI (r = 0,253; p < 0,05), cfPWV (r = −,0374; p < 0,05), [email protected] (r = −0,360; p < 0,05). E/e′ was correlated with BMI (r = 0,291; p < 0,05), office SBP (r = 0,208; p < 0,05), E/A (r = 0,340; p < 0,001), IVRT (r = 0,291; p < 0,001), Dt (r = 0,248; p < 0,001), EF (r = −0,109; p < 0,05), LVMMI (r = 0,303; p < 0,001), s′ (r = −0,263, p < 0,05), ABI (r = 0,258; p < 0,05). Conclusions: Our findings demonstrates that low arterial elasticity is really involved in LV diastolic dysfunction formation. Moreover, CAVI was the only parameter significantly associated with VAC. That is why CAVI may not only diagnose arterial stiffening but also may demonstrate how it increases LV load.