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Despite a wide choice of effective antihypertensive treatments, blood pressure (BP) in roughly half of hypertensive subjects is not controlled. Resistant hypertension is defined as an uncontrolled BP despite optimal doses of three antihypertensive treatments, including a diuretic. After confirmation of resistant BP using home BP measurement or 24-hour ambulatory BP monitoring (ABPM), patients usually go through a work-up to rule out secondary hypertension. If secondary hypertension is ruled out, the recent European guidelines on hypertension consider baroreceptor stimulation or renal denervation to be possible options. The prevalence of resistant primary hypertension may reach up to 10% in specialized centres. The two proposed non-pharmacological therapeutic strategies have been developed recently to inhibit sympathetic overactivity in resistant hypertension. Among them, baroreceptor activation therapy (BAT) is an innovative approach that interferes with baroreflex function. The first-generation BAT device (Rheos(®); CVRx, Inc., Minneapolis, MN, USA) demonstrated good efficacy in lowering office BP and ABPM, but had an insufficient safety profile due to complex surgery. The second-generation BAT device (Barostim neo™ system; CVRx, Inc.) seems to share the same BP-lowering efficacy but has a better safety profile. We report the first French case of baroreceptor stimulation for hypertension using the Barostim neo™ system. We also discuss the pathophysiological features of and current levels of evidence for this technique., (Copyright © 2014 Elsevier Masson SAS. All rights reserved.)

There are many variations in blood pressure, ranging from that observed between systole and diastole (pulse pressure) to slower daily or seasonal variations. This variability has many facets, for example the simple concept of variation around the mean blood pressure and the more complex spectral, chaos or fractal analysis... Some of these concepts are still the subject of fundamental research and have no current clinical applications. Others, however, are already part of our evaluation of hypertensive patients or used as prognostic factors in cardiac failure or myocardial infarction. Blood pressure variability, either the pulse pressure or 24 hour variability, is associated with a higher incidence of cardiovascular complications. Although the causality of the relationship is uncertain, patients with the greatest variability seem to be at higher risk. In addition to this prognostic impact, the study of changes in blood pressure by spectral analysis may also provide indices of adrenergic tone or sympathovagal equilibrium which may be useful clinically. Finally, the combined study of blood pressure variability and heart rate lead to the baroreflex, the sensitivity of which integrates major risk factors such as blood pressure, age, heart rate and serum cholesterol. This baroreflex could be a useful parameter for stratification of cardiovascular risk. This has already been demonstrated in patients at high risk, such as those with cardiac failure or myocardial infarction.

Objective: Estimating the risk entailed by classical risk factors like blood pressure (BP) or serum cholesterol may be difficult because of their variability and the often unknown duration of exposure. Having variables integrating the impact of those classical risk factors on the cardiovascular system would probably aid the prediction of cardiovascular events. The present study aimed at determining whether cardiac baroreflex sensitivity (BRS), correlates with several risk factors and thus is a good candidate for being such an integrative variable. As a comparison, left ventricular mass (LVM), pulse wave velocity (PWV), and creatinine were also tested for association with risk factors., Design: A total of 302 subjects referred for hypertension, were considered. They had a 24-h BP recording and a determination of BRS by two different methods (sequence and alpha coefficient), in two different positions (lying and standing). They were also tested for the presence of left ventricular hypertrophy (LVH) (by echocardiography and electrocardiogram) and had a PWV measurement. Biological testing included serum lipids, blood glucose, creatinine, proteinuria and urinary excretion of microalbumin., Results: There was a strong correlation between the two methods of BRS measurement in each position (P < 0.001). BRS determined by the sequence method in the lying position was correlated significantly and independently with age, 24-h systolic BP, heart rate, and serum cholesterol with P values < 0.001, < 0.001, < 0.01, and < 0.05, respectively. In an univariate analysis, BRS was also correlated with echocardiographic LVM index (r = -0.21, P < 0.05) and PWV (r = -0.27, P < 0.001), which possibly reflects its dependence on both vascular and cardiac damages., Conclusion: The present study supports the hypothesis that BRS could encompass the impact over time of several risk factors on the cardiovascular system. Thus, it may constitute a valuable parameter in assessing more precisely the risk of cardiovascular events.

This experiment aimed at 1) comparing the spontaneous baroreflex sensitivity (SBRS) in Lyon genetically hypertensive (LH), normotensive (LN), and low blood pressure (LL) rats and 2) assessing some aspects of the mechanisms of its impairment in LH rats. Baroreflex was studied in control animals after an early chronic converting enzyme inhibition with perindopril and after a 4-wk infusion of ANG II in perindopril-treated rats. The SBRS was determined with a previously validated method, using statistical dependence between blood pressure (BP) and heart rate values recorded in freely moving animals. LH rats exhibited high BP, cardiac hypertrophy, and decreased SBRS (LH, 1.3 +/- 0.2; LN, 2.5 +/- 0.4; LL, 2.2 +/- 0.4 beats . min-1 . mmHg-1). Perindopril prevented the development of hypertension and cardiac hypertrophy and normalized SBRS. BP rose in LH and LL rats after ANG II infusion, but only LH rats, which developed a cardiac hypertrophy, had an impaired SBRS (LH, 1.1 +/- 0.2; LN, 2.5 +/- 0.2; LL, 2.8 +/- 0.3 beats . min-1 . mmHg-1). This impairment was partially reversed by an acute ANG II blockade with losartan. These results demonstrate that high BP does not account for the decreased SBRS in LH rats. SBRS impairment could result either from cardiac hypertrophy or from the direct effect of ANG II on the baroreflex loop.

A new method was developed to evaluate the cardiac baroreflex sensitivity (BRS) from spontaneous mean arterial pressure (MAP) and heart rate (HR) changes in conscious rats. It relies on the determination of the statistical dependence between MAP and HR values. In 13 control rats, 12 rats with a pharmacologically induced hypertension, and 7 rats with a chronic sinoaortic denervation (SAD), dependent (MAP, HR) couples related to the baroreflex activity were selected to determine the spontaneous BRS (Sp-BRS). In control and hypertensive rats, pharmacological BRS (Ph-BRS) was estimated using graded bolus intravenous doses of vasoactive drugs. Ph-BRS was significantly lower in hypertensive than in control rats. Sp-BRS was determined in 10 control and 10 hypertensive rats and was strongly correlated with Ph-BRS (r = 0.83, n = 20, P < 0.0001). Sp-BRS could be evaluated in six SAD rats and was profoundly decreased (-86%, P < 0.001) compared with control rats. In conclusion, this work validates the estimation of the cardiac BRS from spontaneous MAP and HR variations with use of (MAP, HR) couples of values that are statistically dependent.

Objective: To investigate the link between cardiac hypertrophy, elevated blood pressure level and baroreflex impairment, we assessed cardiac baroreflex function in a hypertensive model almost devoid of cardiac hypertrophy, obtained by nitric oxide synthesis inhibition., Methods: Thirteen adult male Wistar rats were treated orally with NG-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg per 24 h) for 4 weeks. Fifteen control rats received tap water. At the end of the treatment aortic blood pressure was recorded continuously and the baroreceptor-heart rate curve was assessed by bolus injections of phenylephrine and sodium nitroprusside (10 different doses of each)., Results: Mean blood pressure was higher in L-NAME rats than in control rats, whereas body weight was similar. Total heart weight and left ventricular weight did not differ between the groups. Cardiac baroreflex was reset in hypertensive rats, as indicated by a rightwards shift of the mean blood pressure-heart rate curve. Its gain was decreased significantly in L-NAME rats, whereas the heart rate range was not different between the two groups., Conclusion: L-NAME hypertensive rats exhibit an original impairment of cardiac baroreflex, characterized by a range-independent decreased gain which is not due to cardiac hypertrophy.