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New evidence and critical reappraisal of available evidence: the task of a scientific journal

Zanchetti, Alberto

doi: 10.1097/HJH.0000000000000461
EDITOR'S CORNER
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Istituto Auxologico Italiano and Centro Interuniversitario di Fisiologia Clinica e Ipertensione, Università di Milano, Milan, Italy

Correspondence to Alberto Zanchetti, Centro di Fisiologia Clinica e Ipertensione, Università di Milano, Via F. Sforza, 35, 20122 Milan, Italy. Tel: +39 02 50320484; e-mail: alberto.zanchetti@unimi.it

The task of a scientific journal spans from providing space for carefully reviewed new experimental and clinical evidence as well as a forum for critical reappraisal of available evidence. Although scientific knowledge and medical practice progress through innovating research, this on its turn is usually generated from a critical examination of existing knowledge showing the gaps of current understanding to be filled, the inconsistencies of available data to be solved, the opinions taken for evidence, thus opening the way to meaningful new studies and to beneficial changes in medical practice. Our readers know that the Journal of Hypertension has always given space to both approaches, but will have noted that recently we have published a larger number of critical reviews, though still giving a majority space to new original research. In this issue, there are as many as five reviews or meta-analyses instead of the usual two or three. We hope our readers will appreciate this and find them useful for planning their future research.

Among reviews, Deng (pp. 3–13) takes advantage of rat models of systolic and diastolic heart failure to unravel the genetic components known as quantitative trait loci (QTLs) initiating systolic and diastolic function. From their analyses, novel pathways emerge, which deserve to be investigated in human heart failure and may provide new diagnostic tools and innovative therapeutic targets. Dornas et al. (pp. 14–23) have carried out a meta-analysis of recent studies in animal models of hypertension investigating the blood pressure effects of the superoxide dismutase mimetic, tempol and conclude antioxidant treatment with tempol can reduce blood pressure, suggesting that reactive oxygen species play a role in the pathogenesis of animal models of hypertension.

The results of another interesting meta-analysis are published by Cuspidi et al. (pp. 24–32), who show that individuals diagnosed with white-coat hypertension have alterations in cardiac structure and function intermediate between those in sustained hypertensive individuals and those in normotensive controls. In the authors’ view, these data further support the concept that white-coat hypertension should no longer be considered a fully benign condition. Mancia and Giannattasio (pp. 33–43) review diagnosis and treatment of isolated systolic hypertension and underline that there is evidence that, in this type of hypertension, cardiovascular outcomes are independently associated with arterial stiffness and blood pressure lowering significantly reduces outcomes. Nevertheless, current hypertensive treatments have limited effects on arterial stiffness and development of new agents capable of affecting vascular ageing is highly desirable. Isidori et al. (pp. 44–60) summarize and discuss the controversies on the pathogenesis of hypertension in Cushing's syndrome and offer a pathophysiology-oriented therapeutic algorithm to rationalize the treatment of hypertension in this syndrome.

The same areas dealt with by reviews are also touched by original papers in the same issue of the Journal. In addition to Deng's review on genetics of heart failure, another study by Park et al. (pp. 69–76) investigates synergistic effects on blood pressure of genetic variations in CYP1A1 and CYP1B1 and serum levels of 25-hydroxyvitamin D, especially in individuals currently on treatment for hypertension. The role of oxidative stress in vascular responses in an animal hypertension model has been explored by García-Redondo et al. (pp. 77–87), who report that in Wistar Kyoto normotensive rats, contractile vascular responses to H2O2 are mediated by c-Src via modulation of thromboxane A2 (TXA2) release, but in spontaneously hypertensive rats, the vascular responses are c-Src independent and TXA2 release is mediated through Rho kinase. In placentas from pregnancies complicated by preeclampsia, Gao et al. (pp. 106–117) find that oxidative stress induces increased autophagy in trophoblasts on endothelial cells that affects trophoblast invasion and the placental vasculature.

Ambulatory blood pressure effects on target organs are discussed not only in the review by Cuspidi et al., but Stabouli et al. (pp. 88–95) also describe the possible effects of increased SBP variability on arterial stiffness in children and adolescents. Macdonald-Wallis et al. (pp. 96–105) report normal ranges for blood pressure values at different gestation ages and maternal subgroups, and suggest whole population and stratified normograms as reference to identify abnormal trajectories. This application is discussed by Gaillard and Jaddoe in an accompanying comment (pp. 61–62), with the conclusion that further research is needed to examine whether these reference charts can really improve prediction of adverse pregnancy outcomes.

The review by Isidori et al. on Cushing's syndrome is accompanied by an original article by Berge et al. (pp. 118–125) on primary aldosteronism, showing that this is associated with lower levels of prorenin than essential hypertension and suggesting that the aldosterone/prorenin ratio might be included in the diagnostic work-up of primary aldosteronism.

A number of other articles deal with hypertension-related organ damage. Vethe et al. (pp. 126–135) publish a proteomic study of the renal cortex in the two-kidney, one-clip rat model, suggesting periostin, especially in combination with transgelin and creatine kinase type-B, as possible proteomic signals to distinguish hypertensive nephrosclerotic from normal tissue. In a large prospective cohort study of rural Chinese, Wang et al. (pp. 136–143) show a dose–response relationship between baseline SBP and DBPs and decline in estimated glomerular filtration rate. González et al. (pp. 144–152) publish evidence that in an animal model, the inflammatory cytokine interleukin (IL)-6 plays an important role in hypertensive heart damage, while Pucci et al. (pp. 153–160) in a considerable cohort of never-treated hypertensive individuals, report aortic characteristic impedance is significantly associated with left ventricular mass. The latter observation is commented by Butlin and Avolio (63–65), who underline the potential clinical use of noninvasive measurements of aortic haemodynamic parameters, but remark further studies are required to confirm the potential advantages of the methodology.

Finally, a number of original articles are focused on aspects of potential therapeutic importance. In an animal model of hypertension, Vaněčková et al. (pp. 161–169) show that the ETA blocker, atrasentan, lowers blood pressure by reducing Ca2+ influx through L-type voltage-dependent calcium channels, and in a rat model of ischemic stroke Alhusban et al. (pp. 170–180) find that the first nonpeptide angiotensin receptor 2 (AT2R) agonist, compound 21, is neurovascular protective and improves stroke outcome possibly through increasing neurotrophin activity. This observation is commented upon by Thorin et al. in an accompanying editorial (pp. 66–68), who remark that, because the mechanism of action of compound 21 relies on a functional endothelium, the concept of stimulating AT2R for neuroprotection is probably limited to a small population of younger individuals with a limited burden of cardiovascular risk with successful thrombolysis following ischemic stroke. On the clinical side, Wallbach et al. (pp. 181–186) report new data on baroreflex activation therapy in resistant hypertension, showing that the procedure, in addition to lowering peripheral blood pressure, also reduces central blood pressure.

This issue also includes an obituary of Professor Peter van Zwieten. He was a protagonist in the hypertension research scene for several decades, and an Associate Editor of the Journal of Hypertension from 1995 to 2013, acting as Guest Editor for all manuscripts submitted by members of the Editorial team in Milan. I would like to add the expression of my deepest regret for the loss of a great scientist and a dear friend.

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ACKNOWLEDGEMENTS

Conflicts of interest

There are no conflicts of interest.

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