ABC | Volume 110, Nº2, February 2018

Original Article Amaral et al Autonomic and vascular control in prehypertensive patients Arq Bras Cardiol. 2018; 110(2):166-174 Table 3 – Arterial baroreflex function Variable Normotensive (n = 13) Prehypertensive (n = 9) p SBP-iRR LF Central frequency (Hz) 0,10 ± 0,02 0,10 ± 0,01 0,58 a LF Phase shift (rad) -0,96 ± 0,33 - 0,94 ± 0,31 0,90 a LF Coherence 0,85 ± 0,08 0,79 ±0,14 0,15 a Resp-iRR LF Central frequency (Hz) 0,14 [0,10-0,15] 0,10 [0,07-0,12] 0,08 b LF Coherence 0,47 ± 0,19 0,42 ± 0,16 0,56 a Central frequency HF (Hz) 0,29 [0,28-0,30] 0,32 [0,27-0,33] 0,42 b HF Coherence 0,96 [0,91-0,98] 0,93 [0,92-0,95] 0,22 b Data presented as mean ± standard deviation of mean or median [interquartile range]; a unpaired Student t test; b : Mann-Whitney U-test; iRR-RR interval; SBP: systolic blood pressure; LF: low frequency; HF: high frequency. characteristics of the population studied, such as the presence of FHSAH in both groups, since individuals with this risk factor have demonstrated vascular dysfunction in several studies. 6,7 In addition to FHSAH, pre-hypertensive volunteers in this study had higher cardiac and contractility rates, which may have triggered a local vasodilatory homeostatic response in an attempt to alleviate pressure elevation, 12 although this mechanism failed systematically in view of the fact that no difference was observed between groups in peripheral vascular resistance. No studies were found that investigated the association between cardiac and contractility indices and vascular conductance in prehypertensive patients. In hypertensive patients with hyperkinetic circulation, characterized by elevation of cardiac index and mean arterial pressure, Stevo et al. 29 observed greater forearm muscle blood flow compared to normotensive individuals. However, in this study the calculation of vascular conductance was not performed. Thus, future studies should investigate the association between these variables in pre‑hypertensive individuals with a family history of arterial hypertension. According to Davis et al., 12 BP elevation in prehypertension results from hereditary disorders that present a set of genetic determinants and pathogenic traits that act on hemodynamic and autonomic events in series and trigger the SAH. In this scenario, autonomic alterations appear to be the first changes observed in prehypertensive patients. 12 However, although changes in the spectral indices of cardiac autonomic modulation in prehypertensive patients have been demonstrated in other studies, 8,30 in this one, they were not observed. Lin et al., 13 who also observed LF and HF components in normalized units, as well as the LF/HF ratio of heart rate variability, similar among normotensive and prehypertensive youngsters, reported results similar to ours. A possible explanation for these contradictory results is the population studied. In this study, we evaluated normotensive and pre-hypertensive individuals with FHSAH, while the other studies did not control the distribution of this risk factor in the analyzed groups. Thus, since alterations in cardiac autonomic modulation have been demonstrated in normotensive individuals with hypertensive father and / or mother, 4,5 further studies are needed to elucidate these alterations in individuals who have both risk factors, prehypertension and FHSAH. Regarding the autonomic peripheral modulation, in this study we verified dysfunctions in this system in the prehypertensive individuals. We observed a higher LF component of SBP variability in prehypertensive patients compared to normotensive patients, which shows a greater performance of vascular tone sympathetic modulation as well as myogenic vascular function in this population. 23 Similar results were reported by Hering et al. 31 and Seravalle et al. 9 who evaluated individuals with normal-high pressure and also observed greater peripheral sympathetic modulation, assessed by the microneurography technique, in these individuals when compared to normotensive individuals. The variability of SBP, as well as elevation of pressure levels, has been recognized as an important risk factor for target organ damage. 32 In this study, pre-hypertensive individuals presented greater variance of SBP in relation to normotensive individuals, corroborating the results of Duprez et al. 33 However, these authors did not report the FHSAH of study participants. BP fluctuations are triggered by multiple systems including the renin-angiotensin system, baroreflex, myogenic vascular response, and release of nitric oxide. 23 Thus, the elevations of the LF and VLF components observed in this study may be related to the increase in SBP variability through changes in myogenic vascular function. 23 The HF component, which appears to be related to endothelial nitric oxide 23 , was similar between the groups and did not appear to be involved in increased pressure variability. In addition, this study demonstrated a reduction in the baroreflex control of heart rate in prehypertensive individuals when compared to normotensive individuals, a factor that may also be related to the increased pressure variability and peripheral sympatheticmodulation observed. 34 The results of this study corroborate the findings of previous studies 9,11,13 that also observed reduction of baroreflex sensitivity in prehypertensive patients. However, this is the first to demonstrate autonomic changes in prehypertensive patients with FHSAH in relation to normotensive individuals with the same risk factor. 171