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Highlights of the December issue

Mancia, Giuseppe

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doi: 10.1097/HJH.0000000000001969
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The December issue of the Journal of Hypertension devotes the initial part (pp. 2284–2309) to a short version of the hypertension guidelines of the European Society of Cardiology (ESC) and the European Society of Hypertension (ESH), which were published in extenso in the October issue of the Journal. The same was done for the 2007 and 2013 ESH/ESC guidelines, for which a short ‘practice’ version consisting of Tables, Figures and Recommendations connected by short explicatory sentences complemented the full one 2–3 months later. The ‘practice’ version is appreciated by physicians who find the rather detailed explanations of the evidence that leads to diagnostic and treatment recommendations too complex. Complex explanations are not without merit either because guidelines have an educational purpose and because many recommendations are based on expert opinions rather than evidence, which makes mention of their rationale even more necessary. Yet, there is no question that an additional simpler text, easy and quick to be consulted when needed, also has a value.

The following articles focus on vascular aspects, epidemiology and treatment of hypertension. Vascular aspects include an article by Pucci et al. (pp. 2316–2323) who explored the genetic vs. the environmental determinants of arterial stiffness, measured by pulse wave velocity, in 368 adult twins, 214 and 154 of whom were monozygotic and dizygotic, respectively. On the basis of the role played by additive genetic, shared environment and unique environment, the authors come to the important conclusion that arterial stiffness has a prevailing genetic determinant, which suggests that there may be a strong genetic participation in vascular ageing, for which arterial stiffening is regarded to be one of the best available measures. Obviously, this does not mean that environmental factors are not involved, and indeed, their role is emphasized by the article of Vallée et al. (pp. 2324–2332) on 514 hypertensive diabetic patients in whom arterial stiffness was also measured by pulse wave velocity. The conclusion drawn from this rather large group is that in this clinical condition, arterial stiffness has an extensively multifactorial modulation, the factors involved ranging from a history of cardiovascular events, to organ damage, lipid profile and even drug treatment, including insulin. The factors involved in the determination of arterial stiffness are also addressed by Strauss et al. (pp. 2333–2339) who make the interesting observation that in young black and white women, arterial stiffness bears a relationship with 24-h urinary excretion of marinobufagenin, a steroid with cardiotonic effects. There is currently a large and growing number of studies on the mechanistic aspects of the alterations of large artery mechanical properties, whose elucidation is preliminary to any substantial progress on the therapeutic ability to counteract their stiffening and thus prevent the development as well as favour the control of systolic hypertension. In this setting, the subsequent papers have a specific interest. Nilsson et al. (pp. 2340–2349) examined the clinical characteristics of middle age individuals at the 10% lower end of the pulse wave velocity distribution (and thus with lowest values of arterial stiffness and the highest score for what is referred to as healthy vascular aging) using the cohorts adhering to the “MARE” consortium. compared with the 10% individuals at the opposite side of the arterial stiffness spectrum, those with the lowest pulse wave velocity exhibited a much better cardiovascular risk profile, i.e. less diabetes, hypertension, metabolic syndrome, etc. Interestingly, the calculated age gain of the lowest arterial stiffness group amounted to 14 years, which suggests (in line with the observations of Vallée et al.) that the role played by concomitant adverse conditions is substantial. Korkmaz-Icöz et al. (pp. 2350–2361) show that, in rats made hypertensive by mechanical pressure loading (aortic banding), unloading is capable of improving the pressure-dependent structural and functional alterations of the arterial wall, with a reduction in their fibrotic and collagen components and a recovery of the impaired endothelial-dependent and independent vasorelaxation. Finally, Kozakova et al. (pp. 2362–2368) tested, in a large number of individuals, the possibility to measure central pulse pressure via a radiofrequency-based tracking of the distension of the carotid wall by the intravascular pressure. As emphasized by the authors and supported by an Editorial commentary of Avolio (pp. 2310–2311) this paves the way to the collection of central blood pressure (BP) data by routine examination of the extracranial carotid tree, which guidelines list as important for the assessment of organ damage. In the article by Kozakova et al. the central BP value obtained by the wall tracking approach correlated more closely with organ damage (carotid intima-media thickness and left ventricular mass) than peripheral BP, suggesting that this information may refine the quantification of cardiovascular risk.

The following two articles deal with salt, one reporting on the ability of high salt diet to blunt nitric oxide-dependent vasodilatation in mice (Liu et al., pp. 2369–2379) and the other (Rezaei et al., pp. 2380–2389) on the high salt intake in the adult Iranian population, whose daily mean salt consumption was found to be greater than 9.5 g, with a daily intake twice that recommended by the WHO in more than 41% of the study sample. The remaining epidemiological contributions relate to BP and associated risk factors. Marques et al. (pp. 2390–2397) show that popliteal artery plaques were more than twice as frequent in smokers than in nonsmokers (39 vs. 19%, P < 0.001). Interestingly, nonsmokers with popliteal plaques showed a more adverse cardiovascular risk profile (older age, hypertension, dyslipidaemia and diabetes) than smokers, which may emphasize the paramount importance of smoking alone for the genesis of peripheral atherosclerosis. Borrelli et al. (pp. 2398–2405) expand the evidence on the prognostic relevance of ‘short-term’ BP variability by showing that, in 465 patients with chronic kidney disease, 24-h, daytime or night-time BP variations independently predict renal outcomes as measured by end-stage renal disease or a major decline (≥50%) of glomerular filtration rate. BP variability was quantified not only by the standard deviation but also by the coefficient of variation of the mean ambulatory values, which minimized the confounding problem of the relationship of variability to the mean BP value, which has so far weakened the conclusion of many other papers. Fu et al. (pp. 2406–2413) provide a comprehensive description of the adiposity patterns of a large sample (n = 135 825) of middle-aged and older Chinese from the China National Stroke Prevention Project, confirming that in all instances, there is a relationship with the BP values, although somewhat surprisingly, general adiposity was more closely related to BP than central adiposity. Ngueta and Ndjaboue (pp. 2414–2419) show, from the US NHANES data-base, that having a sexual intercourse before age 19 may considerably increase (>30%) the risk of developing hypertension (defined by the new US guidelines criteria as ≥ 130/85 mmHg) later in life. The data are not easy to be interpreted because the effect was markedly different according to the women's ethnicity, i.e. non-hispanic whites, hispanic whites and non-hispanic blacks. There is also in this type of study the possible confounding effect of the association of early sexual activity with poor environmental conditions, more stressful personal interrelationships and more frequent exposure to risk factors. The study by Ngueta and Ndjaboue, however, was obtained from almost 40,000 women in whom the relationship between early sex and new onset hypertension was manifest even after adjustment for important potential confounders, including socio-economic factors such as the poverty-to-income ratio of the family, suggesting that factors other than those mentioned above may be involved. Finally, Krishnamoorthy et al. (pp. 2420–2424) describe the results of an analysis of people with polycythemia vera, using a large US registry. Polycythemic patients were 0.1% of hospital discharge patients. Except for diabetes and chronic kidney disease, these patients exhibited a significant increase in the prevalence of all cardiovascular risk factors and events compared with controls, including hypertension (61 vs. 46%, P < 0.0001). Using a specific terminology for the association of polycythemia vera and hypertension, that is the Gaisböck syndrome, is thus clinically justified.

The remaining articles of the December issue of the Journal deal with antihypertensive treatment, the device-based one in particular. Haggart et al. (pp. 2425–2433) report the results of a US retrospective study on the BP control rate of young (18–39 years old) hypertensive men and women from academic practice in the midwest of the Country. Overall, BP control was achieved in 48% of the study sample, which is more than what has been reported in most other countries, although probably not too far from the BP control rate reported for the general US populations. Interestingly, control was definitively lower in young men than in young women (−39%), a finding that reflects sex-related data in several previous studies but that more recently has not been confirmed by some reports. Lee et al. (pp. 2434–2443) show that in diabetic hypertensive patients of the Korea National Health Insurance cohort, the risk of cardiovascular events, renal events and mortality was less if systolic BP was reduced to less than 140 mmHg (and diastolic BP to <80 mmHg), whereas the benefit was not clear for those achieving a systolic BP value of less than 130 mmHg, at variance from the recommended targets of the European and American guidelines. As for all observational studies, the data suffer from the absence of randomized group comparisons, which does not allow to exclude an origin of the results from baseline clinical differences. They offer, however, a view of real-life medicine, which should not be overlooked in the evolving knowledge and opinions on this important issue. Moreira et al. (pp. 2444–2452) show that in the spontaneously hypertensive rats, central long-term stimulation of cardiac preganglionic neurons in the dorsal motor vagal nucleus can reduce BP, thus having a therapeutic effect when, as it is known to occur in the spontaneously hypertensive rat model, neural factors participate in the genesis of the BP elevation. Device-based treatment of hypertension has not been recommended for routine use by the recent European guidelines, because evidence of BP reduction and cardiovascular protection is still limited. Experimental and clinical research is active, however, and additional relevant data are continuously made available. In this context, this issue of the journal offers three contributions. Wolf et al. (pp. 2453–2459) validated in the porcine model another radiofrequency method for renal denervation (the Iberis-Bloom method) by showing that the resulting reduction of the norepinephrine concentration in the kidney was similar to that obtained by the widely used Symplicity-Spyral method. The results are discussed in an editorial commentary by an expert in this area of research, professor M. Esler, who also comments on the necrotic areas that the renal tissue showed with both denervation methods. Without challenging the absence of clinical complications consistently reported by the renal denervation studies, this suggests that the safety of this procedure should be matter of persistent attention. Xu et al. (pp. 2460–2470) show that in 67 hypertensive patients the pressor response to delivery of radiofrequency energy to the renal artery (documented in previous studies and believe to result from sympathetic activation) was related to the subsequent BP response to renal denervation, namely the patients showing little BP increase to the acute energy delivery manoeuver were those in whom the BP reduction after renal denervation was small or absent. This represents a potentially important finding because the wide range of the BP effects of renal denervation makes the inability to predict which patients with resistant hypertension might benefit of the procedure a weak aspect of the renal denervation approach. Finally, the case report that closes the December issue addresses another therapeutic device under study, that is the creation of an arteriovenous fistula. In a patient with severe hypertension resistant to drug treatment, the authors (Jung et al., pp. 2471–2477) implanted a central arteriovenous coupler device. Implantation was followed by an immediate BP decrease, which persisted for the 3.5 years of follow-up, with signs and symptoms of right heart overload (as expected from this intervention), which were, however, controlled by optimizing diuretic therapy. The available evidence, potential and drawbacks of the procedure are discussed in an accompanying editorial of de Leeuw and Kroon (pp. 2314–2315).


Conflicts of interest

The author has no conflict of interest.

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