Different contribution of sympathetic nerve activity to arterial velocity pulse index in hypertensive patients with and without diastolic dysfunction

Abstract

Abstract Introduction Left ventricular diastolic dysfunction (LVDD) is the main cause of heart failure with preserved ejection fraction (HFpEF). LVDD is related not only to arterial stiffness but also sympathetic nerve activity (SNA). Recent study demonstrated that increased muscle sympathetic nerve activity (MSNA) may be one of contributing factor for arterial stiffness. In clinical practice, Cardio-ankle vascular index (CAVI) provides a reproducible index of arterial stiffness, independent of blood pressure (BP). Recently, Arterial Velocity pulse Index (AVI), which is an index of arterial reflected waves, have been proposed as new index of arterial stiffness. We reported that AVI was associated with MSNA in hypertensive (HT) patients. However, it is still uncertain the effect of LVDD on the association between AVI and SNA in HT patients. Thus, we tested the hypothesis that AVI would be increased and related to MSNA in HT patients with LVDD. Methods Patients with essential HT subjects were included in this study. HT was diagnosed as systolic blood pressure (SBP) ≥140mmHg or diastolic blood pressure (DBP) ≥90mmHg. Patients with secondary HT was excluded. AVI was measured from left upper arm by NAS-1000 (Nihon Koden, Japan). CAVI was measured by VaSera VS-1500A (Fukuda Denshi, Japan). Transthoracic echocardiography was performed by trained sonographers. SNA was evaluated by direct recording of MSNA from peroneal nerves. Results 25 HT patients were included (age 63±14 years, Male/Female 9/16). They were divided into two groups according to E/e' (no LVDD group, E/e' ≤9, N=12; LVDD group, E/e' >9, N=13). There were no significant differences between no LVDD and LVDD groups in age (63±9 vs 69±9 years p=0.205), body mass index (23±3 vs 24±4 p=0.355), BP (SBP 139±16 vs 144±20mmHg p=0.524, DBP 87±15 vs 78±14mmHg p=0.167). LV Ejection Fraction (EF) and Stroke Volume (SV) did not differ between two groups (EF 66±7 vs 69±6% p=0.471, SV 58±7 vs 62±14ml p=0.599). MSNA had tendency to increase in LVDD group compared to no LVDD group (MSNA 53±10 vs 44±12 bursts/100 heartbeats, p=0.052). Contrary to our hypothesis, AVI and CAVI did not differ between two groups (AVI 27±7 vs 29±7 p=0.398, CAVI 8.7±1.4 vs 8.6±1.4 p=0.894). However, a significant correlation was seen between AVI and MSNA in no LVDD group (r=0.57, p<0.05), but no correlation in LVDD group. There is no correlation between CAVI and MSNA in no LVDD and LVDD group. Significant relationship was observed between AVI and CAVI in LVDD group (r=0.61, p<0.05), but no relationship in no LVDD group. Conclusion AVI was significantly associated with MSNA in HT patients without LVDD, but not with LVDD. CAVI was related to AVI in HT patients with LVDD, but not without LVDD. MSNA was slightly increased in HT patients with LVDD compared to without LVDD. These results indicate that augmented SNA could contribute to the increase in arterial stiffness in HT patients without LVDD, however, this contribution might be attenuated in HT patients with LVDD. Funding Acknowledgement Type of funding sources: None.