Abstract

For a long time, the problem of the formation of diastolic dysfunction (DD) of the left ventricle (LV) in patients with arterial hypertension (AH) remained insufficiently studied. It was demonstrated that the formation of LV DD is largely related to the increase in stiffness of this heart chamber. We decided to evaluate the extent to which increased LV stiffness, determined noninvasively by echocardiography, is associated with LV diastolic dysfunction and determine the relationship of this method with arterial stiffness indicators for which validated methods have been developed.Materials and methods. A one-center registry called PULSE-COR was established in 2011 and is still in operation. There were 779 AH participants in our sample. A distinct cohort of patients (n=283) with essential AH and no substantial comorbidities were found from the final analysis, which comprised 320 patients who had undergone all requisite diagnostic procedures. Our tool of choice for measuring carotid-femoral pulse wave velocity (cfPWV) was the SphygmoCor device (AtCor, Australia). We also used the VaSera 1500 device (Fukuda Denshi, Japan) to measure cardio-ankle vascular index (CAVI) and ankle-brachial index (ABI). Vascular ultrasound and intima-media thickness measurement (IMT) were included in the ultrasound diagnosis. The ASE 2016 recommendations were followed for the evaluation of diastolic LV function, and the standardized ASE protocol was followed for echocardiography. A standardized formula was used to assess the ventriculo-arterial coupling (VAC) which also included LV end-systolic elastance (Ees) and arterial elastance (Ea) evaluation. We conducted Spearman correlation analysis to identify relationships.Results and discussion. Our cohort were patients with AH, 51 % males; the mean age was 53.6±2.0 years. Mean office blood pressure (BP) was 159.8±4.5 mm Hg for systolic (SBP), 97.9±2.6 mm Hg for diastolic (DBP), 62.0±3.5 mm Hg for pulse blood (PBP) BP, and 76.6±2.2 bits per minute was the mean heart rate (HR). Both the left and right CAVI (R=0.698; p=0.012 and R=0.683; p=0.014) showed a strong correlation with VAC. Both E/A and E/e showed a substantial correlation with ABI (R=0.716; p=0.006 and R=0.764; p=0.002, respectively). cfPWV was linked with nearly the same parameters (R=0.248; p=0.001 for correlation with IMT, R=0.382; p=0.01 for correlation with low-density lipoproteins). Ea was substantially associated with IMT (R=0.491; p=0.24), total cholesterol (R=0.499; p=0.07), and low-density lipoproteins (R=0.687; p=0.001). Ees was substantially correlated with end diastolic volume (R=0.644; p=0.001), blood lymphocytes (R=–0.678; p=0.001), E/A (R=0.159; p=0.007), and E/e’ (R=–0.130; p=0.029).Conclusions. We have found a substantial correlation between validated arterial stiffness measurements and non-invasive LV stiffness evaluation parameters (VAC). VAC also was associated with LV diastolic function parameters

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