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Large and small vessel disease and other aspects of hypertension

Zanchetti, Alberto

doi: 10.1097/HJH.0000000000000785

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. Tel: +39 02 50320484; e-mail:

Involvement of large and small vessels by hypertension and mechanisms of vascular wall damage are major topics of a consistent group of articles in the current issue of the Journal of Hypertension.

Butler et al. (pp. 2463–2470) report that in the Atherosclerosis Risk in Communities cohort, there were significant differences in both the average baseline pulse pressure and the annual rate of change in pulse pressure between men and women, and between African–Americans and Caucasians, with diabetes and obesity exerting the strongest effects. An accompanying commentary by Schillaci and Pucci (pp. 2389–2391) underlines that the paper by Butler et al. clearly shows that pulse pressure widening is not only an unavoidable effect of aging, but it is strongly influenced by cardiovascular risk factors. In the Campania-Salute registry of treated hypertensive patients risk of incident carotid atherosclerotic plaques did not depend on blood pressure control and type of antihypertensive therapy, but was related to the magnitude of initial intima–media thickness, suggesting that an antihypertensive treatment strategy to stop progress of vascular disease might be difficult to achieve once vascular damage is established (Izzo et al., pp. 2471–2476).

Jablonski et al. (pp. 2477–2482) report observations supporting the hypothesis that suppression of the proinflammatory nuclear factor κB (NFκB) signaling may partially mediate the lower aortic stiffness in adults who regularly perform aerobic exercise. In another mechanistic study, Lenders et al. (pp. 2455–2462) find that differential responses of endothelial sodium channel (ENaC) inhibition by amiloride in human ex-vivo vessels correlate with arterial stiffness. Ji et al. (pp. 2431–2442) have observed that neuropeptide W (NPW-23) regulates ICa,L via the G protein-coupled receptor 7, which is mediated by PLC/PKC signaling, and such a mechanism also plays a role in modulating vascular myogenic tone. Behuliak et al. (pp. 2443–2454) have investigated the importance of the RhoA/Rho-kinase pathway for blood pressure and vascular tone control in the spontaneous hypertensive rat. Lammertyn et al. (pp. 2483–2490) report that hemostatic alterations are linked to early retinal microvascular changes. In a double-blind, randomized, placebo-controlled study, Jumar et al. (pp. 2491–2499) find that treatment with aliskiren, given on top of valsartan, improves altered vascular remodeling in hypertensive patients. In an accompanying commentary, Savoia and Grassi (pp. 2392–2394) remark that aliskiren given on top of valsartan reduced blood pressure more than placebo, and therefore, it is uncertain whether the more pronounced effect on vascular remodeling and arterial stiffness was due to blood pressure reduction or to an independent effect of dual renin–angiotensin system blockade. Finally, an extensive review is devoted to the possible role of hypertension in the pathogenesis of age-related macular degeneration. Katsi et al. (pp. 2382–2388) conclude that most epidemiological studies have found hypertension to be a risk for macular degeneration, but there are no data to support the view that antihypertensive medication and the successful management of hypertension have a positive effect.

Two studies have investigated the effects of treatment on blood pressure variability. In a post-hoc analysis of the Losartan Intervention For Endpoints reduction trial, Vishram et al. (pp. 2422–2430) have found that visit-to-visit blood pressure variability during the trial was associated with the incidence of the composite endpoint and stroke, but not with incidence of myocardial infarction and organ damage. In resistant hypertensive patients receiving renal denervation, Ewen et al. (pp. 2512–2518) find the procedure was followed by reduced blood pressure variability even when office blood pressure was not reduced. In another study, the same group of authors (Ewen et al., pp. 2519–2525) also report that blood pressure changes following renal denervation are related to changes in total peripheral resistance.

Another group of studies focus on epidemiological aspects of hypertension. Kunutsor et al. (pp. 2373–2381), as a result of a careful review and meta-analysis of available data, conclude gamma-glutamyltransferase is linearly associated with the risk of hypertension. Khanam et al. (pp. 2399–2406) report high prevalence of undiagnosed hypertension in rural areas of Bangladesh and more than 50% of the treated hypertensive patients to be uncontrolled. Tabara et al. (pp. 2407–2413) summarize results from the population sample of the Nagahama study, indicating that several factors affect spot urine Na/K ratio, but these factors are not substantial enough to confound the association between Na/K ratio and blood pressure. Wu et al. (pp. 2414–2421) report that low temperature and high air pollution may act synergistically to increase blood pressure in healthy adults, and call attention to the potential health implications of these findings.

Two studies focus on primary aldosteronism. Manolopoulou et al. (pp. 2500–2511) have verified that the new automated chemiluminescence immunoassay allowing the simultaneous measurement of plasma aldosterone (PAC) and plasma renin concentrations (PRC) presents a convenient alternative for the measurement of PAC and PRC on a single automated analyzer, thus, facilitating screening and diagnosis of primary aldosteronism. Rossi et al. (pp. 2546–2549) illustrate a case report of a normoaldosteronemic aldosterone-producing adenoma. In this case, development of a novel monoclonal antibody for the human CYP11B2 (aldosterone syntase) allowed identification of a CYP11B2-positive adenoma in the resected adrenal.

Two other studies have direct implications on drug treatment of hypertension. In resistant hypertensive patients, Beaussier et al. (pp. 2526–2533) find that blood pressure can be more easily controlled and organ damage can more easily regress following sequential nephron blockade than sequential renin–angiotensin system blockade, but only in patients with acceptable medication adherence. The important, although difficult, issue of drug adherence in hypertension, even in controlled clinical trials, is critically discussed by Burnier and Wuerzner (pp. 2395–2398) in an accompanying editorial commentary. Finally, Fadl Elmula et al. (pp. 2534–2545) report the results of a randomized study comparing treatment guided by noninvasive hemodynamic monitoring associated with a drug selected algorithm and conventional treatment, and show similar reductions in ambulatory daytime and office SBP with the two approaches.

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Conflicts of interest

There are no conflicts of interest.

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