Arterial Stiffness and Ventricular Arterial Coupling and Pulsatative Load on the Left Ventricle in Patients with Hypertension with Initial and Fulminant Heart Failure and Preserved Ejection Fraction According to E/e’ Estimates

Abstract

The objective: was to evaluate the cardiac structure and the contribution of arterial and ventricular stiffness to the mechanism of impaired cardiac hemodynamics and the development of clinical symptoms of HFpEF.

Materials and methods. We attracted to the study prospectively 103 haemodynamically stable patients 43 to 85 years (mean age 65,4±10,8 years) with clinical signs and symptoms of HF with NYHA II–III with hypertension 1 degree that treated with antihypertensive therapy and EF LV ≥50%, signs of DD according to Doppler echoCG. Patients were tested for the levels of the NTproBNP, in addition to standard laboratory parameters. The pulse wave velocity (carotid-femoral) and hemodynamic indices were determined using aplanation tonometry. Echocardiography was determined standard values and diastolic stress test was obtained. HFpEF was diagnosis according to the recommendations of ESC2016. In case of presence or absence of elevation of E/E’ at rest >13 in addition to the structural criteria, patients were divided into three groups. Group 1 consisted of patients with levels of NTproBNP <125 pg/ml and having the structural criteria and group 2 allocated to the patient’s in the presence of structural criteria level NTproBNP > 125 pg/ml, patients that with levels of NTproBNP >125 mg including elevated levels of E/E’ > 13 made group 3.

Results. The groups 1 (without HF) consisted of 11 (10.6%) group 2 – 28 (27,18%), the groups have 3 – 64 (62,1%) patients. Signs of NYHA II were present in all patients of the 1st group and in 78,5% – 2 groups (p>0,05), whereas in group 3 NYHA ІІІ (64,0%) prevailed (p<0,01). The NTproBNP level progressively increased from 1 to 3 groups (all p<0,01). According to EchoCG, there was an increase in end diastolic index and end systolic index in patients of group 3, compared with those in group 1, was accompanied to decrease in LV EF (by 11,5%; p<0,05), with a progressive increase in LVMI and LAVI (p<0,01). In evaluating the indicators of diastolic LV function, an increase in the indicators of active relaxation of the LV myocardium was observed, e’lateral, e’septal and their average value from 1 to 3 groups (p<0,01). When evaluating the performance brachial and central arterial pressure level brachial central pulsative arterial pressure in the three groups were not different (p>0,05). The analysis of SAP indices augmentation in the aorta showed a significant increase in AP and Alx 75 only patients in group 3 as compared with the other two groups, that noted as increase of PWV (as compared with those in groups 1 and 2; p<0,01). At the same time, the endothelial dependent vasodilation was already reduced in patients of group 2 from initial HF (compared with group 1 by 38,5%; p<0,01) in the absence of significant differences compared to patients with HF and E/e’ > 13 at rest (p>0,05). Patients of all groups were comparable in Ea (p>0,05). Patients in Group 2 have decrease Ees index compared with patients in Group 1 12,8% (p<0,01), which was accompanied by an increase Ea/Ees (21%; p<0,01). At the same time, in group 3, the values of both indicators did not differ from those in group 2 from the initial HF (p>0,05).

Conclusions.1. In patients with AH and HFpEF, compared with those without HF, a violation of the ventricular-arterial coupling is noted by reducing the final systolic stiffness of theLV. With an initial HF with an increase of left venricular pressure according to E/e’ > 13 only with exercice, these changes are accompanied by an increase in LVMI and LAVI by 7,7% and 5,1% and a moderate decrease in myocardial relaxation (e’ average by 23%).

2. The progression of heart failure with E/e’ > 13 at rest is not accompanied by subsequent modifications of ventricular–arterial coupling, but is associated with increased augmentation pulse wave, AP, Alx 75 and PWV and development of eccentric LV hypertrophy and a decrease in LV EF by 11,5%.