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Journal of Hypertension:
doi: 10.1097/HJH.0b013e32835d2a34
Editor's Corner

Editor's Corner: a look at current hypertension research from this issue content

Zanchetti, Alberto

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Istituto Auxologico Italiano and Centro Interuniversitario di Fisiologia Clinica e Ipertensione, Università di Milano, Milan, Italy

Correspondence to Professor Alberto Zanchetti, Centro di Fisiologia Clinica e Ipertensione, Università di Milano, Via F. Sforza 35, 20122 Milano, Italy. E-mail:

Received 28 November, 2012

Accepted 28 November, 2012

If a journal content is a microcosm reflecting what is happening in research in the ‘gran teatro del mundo’, the wide theatre of the world, it is relevant that the current issue of the Journal of Hypertension opens with the Latin American consensus document on hypertension in patients with type-2 diabetes mellitus (pp. 223–238). Management guidelines and consensus documents prepared by experts in different regions of the world are welcome, as they reflect the prevalent local epidemiology, the specific type of organization of medical care, and are a better instrument for improving health and fighting disease than guidelines intended to be applied in the whole world indiscriminately.

Development of new methodologies and devices and the precision and reproducibility of those currently employed are given due space in this issue of the Journal, as was the case in the January issue wherein attention was given to the accuracy/inaccuracy of various methods for calculating central blood pressure. A new device for measuring blood pressure noninvasively based on the pulse delay time technique is presented by Fujikawa et al. (pp. 278–286), who have favourably tested their triple-cuff device according to guidelines. An editorial by Avolio and Parati places this new study in the context of attempts during more than a century to improve blood pressure measurements by making them less operator-dependent and more reproducible (pp. 251–252).

An extensive review by Hodgkinson et al. (pp. 239–250) of the accuracy of ambulatory blood pressure monitors raises some concern by showing that 50% of the 24 studies that passed a validation protocol nonetheless found a difference of at least 5 mmHg between the test device and the reference standard for 30% or more of the readings, a blood pressure difference that in prospective studies implies a 20% difference in cardiovascular outcomes. A study by Atkinson et al. (pp. 287–291) and its commentary by Cipollone and Muiesan (pp. 253–255) debate the specificity and reproducibility of the most widely noninvasive methods for endothelial function evaluation, flow-mediated dilation. The logarithmic-derived general linear model proposed by Atkinson et al. (pp. 287–291) presents itself as a more reliable model to be used in every clinical setting, and it is expected to be widely tested to confirm its usefulness as a more reliable marker of cardiovascular risk. Finally, the sensitivity of electrocardiographic criteria to detect left ventricular hypertrophy in obese individuals is challenged by a study of Maunganidze et al. (pp. 377–383) in a group of African ancestry: none of the current voltage criteria have been found sufficiently performing to be recommended for use in obesity. In an accompanying editorial including a valuable review of current information about the association of left ventricular hypertrophy with obesity, Cuspidi et al. (pp. 256–258) remark that also echocardiography, although undoubtedly more sensitive than electrocardiography, has a limitation in obesity because the ultrasonographic view of left ventricular wall interfaces is hampered by increased chest wall impedence.

Two epidemiological studies investigate the relation between blood pressure and cardiovascular outcomes. Kondo et al. (pp. 263–270) report that in young and middle-age Japanese men with high-normal or slightly elevated blood pressure incidence of cardiovascular disease events is increased among smokers only. Daugherty et al. (pp. 271–277), using a large database of 177 521 patients with incident hypertension, find some interesting differences in incident outcomes between men and women, with the latter being less likely to die by any cause and to be hospitalized for myocardial infarction or stroke, but more likely to develop chronic kidney disease compared with men. A cross-sectional study of a cohort of Swedish individuals undergoing ambulatory home polysomnography [Zou et al. (pp. 345–351)] report that short sleep time is associated with hypertension. Finally, the possibility that hypertension is associated with chronic exposure to inorganic arsenic in drinking water is discussed in a study by Kunrath et al. (pp. 361–369), who find that arsenic exposure can increase stress-induced blood pressure hyperreactivity and poor blood pressure recovery.

As usual, a number of studies concern problems of experimental pathophysiology. Batenburg et al. (pp. 292–302) report that a (pro)renin receptor antagonist counteracts the beneficial effect of the renin inhibitor aliskiren on vascular dysfunction in diabetic hypertensive rats, but not its effects on blood pressure suggesting that (pro)renin receptor blockade is unlikely to be a new tool to further suppress the renin–angiotensin system on top of existing blockers. Chávez-Canales et al. (pp. 303–311) show that insulin induces activation and phosphorylation of the renal NaCl cotransporter, suggesting this effect could play a role in arterial hypertension associated with hyperinsulinemic states. Goonetilleke et al. (pp. 312–320) provide electrophysiological evidence for enhanced purinergic function in the SHR, and Honetschlägerová et al. (pp. 321–332) report that the antihypertensive actions of soluble epoxide hydrolase inhibition in an angiotensin-dependent malignant form of experimental hypertension are nitric oxide-dependent. Finally, Brand et al. (pp. 333–344) describe oxidative stress-mediated genotoxic effects of angiotensin II in mice, suggesting a mutagenic potential of angiotensin may be responsible, at least in part, for the increased cancer risk reported in hypertensive individuals.

A number of studies obviously address problems of therapeutic interest. Kasiakogias et al. (pp. 352–360) report that hypertensive patients with moderate-to-severe sleep apnoea had similar blood pressure values (including ambulatory blood pressure) irrespectively of good adherence or lack of adherence to continuous airway pressure (cPAP) application. This extends data summarized in the sleep apnoea consensus document recently published in the Journal of Hypertension (J Hypertens 2012; 30: 633–646), by showing that the antihypertensive effectiveness of cPAP remains scarce also during long-term application (longer than 3 years).

A 6-month randomized controlled trial in prediabetic postmenopausal women with prehypertension or hypertension shows that administration of soy protein and isoflavones reduces SBP as well as endothelial cytokines, thus supporting previous results of animal experiments and observational studies [study by Liu et al. (pp. 384–392)]. Another randomized controlled trial has investigated the effects of different antihypertensive agents on endothelial function measured by flow-mediated dilatation: Dorresteijn et al. (pp. 393–403) report flow-mediated dilatation was increased by renin-inhibition (aliskiren), but not by simpathoinhibition (moxonidine) or diuretic therapy (hydrochlorothiazide), although it remains to be established whether the endothelial effect specifically results from renin inhibition or from the more marked blood pressure reduction occurring with aliskiren. The effects of various drug therapies in the obese hypertension are commented in an editorial by Egan and Grassi (pp. 259–260).

More effective drug treatment for so-called resistant hypertension continues to attract the interest of investigators: Jansen et al. (pp. 404–413) confirm that add-on therapy with the aldosterone-receptor antagonist eplerenone effectively lowers blood pressure in these patients, but that the effect is unrelated to circulating renin–angiotensin–aldosterone system activity and renal mineralocorticoid receptor activity. The mechanisms of treatment resistance in these difficult to treat patients remains debated: in the 2602 resistant hypertensive patients of the REasons for Geographic And Racial Differences in Stroke (REGARDS) study, Shimbo et al. (pp. 370–376) have explored the role of unhealthy lifestyle factors, such as obesity, physical inactivity, smoking, alcohol consumption, low DASH diet score, finding that none of these unhealthy life factors were associated with resistance to treatment.

Finally, the recent publication on the New England Journal of Medicine (Epub 3 November 2012) of the data of the Aliskiren Trial in Type 2 Diabetes Using Cardio-Renal Endpoints (ALTITUDE) trial, a placebo-controlled trial in which the renin inhibitor aliskiren was administered to diabetic patients on top of either an ACE-inhibitor or an angiotensin receptor blocker, is interestingly complemented by the publication in this issue of the Journal of Hypertension of an analysis of diabetic patients included in the going Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ON-TARGET) trial who were also exposed to double blockade of the renin–angiotensin system (ramipril and telmisartan) and compared with those exposed to a single blocker only (either ramipril or telmisartan). As reported by Mann et al. (pp. 414–421), in ON-TARGET diabetics double blockade was not accompanied by any excess of stroke, but by an excess of adverse events, namely acute dialysis, hyperkalaemia and hypotension. These results very closely parallel those reported in ALTITUDE, and the two studies together are supportive of the recommendation not to use double blockade of the renin system, at least in the majority of hypertensive patients. A stimulating editorial commentary by John Chalmers (pp. 261–262) underlines two major questions arising from the very similar results of ALTITUDE and ON-TARGET: why does dual renin blockade fail to reduce the risk of stroke despite a few mmHg lower SBP with dual therapy rather than with monotherapy, when stroke is considered the most sensitive vascular outcome to blood pressure changes? Why does dual blockade cause an excess of renal dysfunction compared with monotherapy despite a reduction in incidence and progression of proteinuria usually considered as a safe index of progression of renal disease and of an increased risk of cardiovascular outcomes? Should some of our certainties be challenged?

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