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 0250320484, e-mail: firstname.lastname@example.org, email@example.com
This issue is opened by a review and meta-analysis of population-based observational studies investigating the relation between psoriasis and hypertension (Armstrong et al., pp. 433–443). Despite the difficulties in ascertaining the associations between common diseases, the meta-analysis concludes that psoriasis and psoriatic arthritis are associated with greater prevalence of hypertension. Another epidemiological study explores the role of parity as predictor of early hypertension during menopausal transition (Giubertoni et al., pp. 501–507).
Current interest in improving the predictive role of traditional cardiovascular risk factors for subsequent outcomes is illustrated by a series of papers exploring the additional predictive role of signs of organ damage. In the general Japanese population of the Hisayama study, adding an index of arterial stiffness, pulse wave velocity, to traditional risk factors was shown to increase significantly the area under the receiver operating characteristic curve (Ninomiya et al., pp. 477–483). Likewise, Vernooij et al. (pp. 492–500) report that presence of organ damage increases the risk for a vascular outcome, as well as for mortality, in proportion to the number of organs involved. Courand et al. (pp. 484–491) have studied hypertensive patients after a very long follow-up (35 years) and found that the presence of aortic atherosclerosis or cardiac disease increases the prognostic significance of heart rate for cardiovascular outcomes.
A number of other papers investigate aspects of hypertension-associated organ damage. In a South African community sample, Maunganidze et al. (pp. 568–575) have found strong relationships between estimated glomerular filtration rate and left ventricular mass irrespective of the presence of hypertension and independent of 24-h and aortic blood pressure. They suggest that nonhemodynamic factors may explain a considerable proportion of the relationship between early glomerular dysfunction and left ventricular hypertrophy. Left ventricular hypertrophy is the topic of other three articles. Zhao et al. (pp. 576–586) outline the possible role of profilin-1 in the cardiac hypertrophy of the spontaneously hypertensive rats, by finding attenuated and, respectively, enhanced myocardial hypertrophy and fibrosis in animals in which the profilin-1 gene was knocked down or, respectively, overexpressed. Ravasa et al. (pp. 587–594) add further important information to the evidence built up by their group about the correlation of cardiotrophin-1 with left ventricular mass. These important data are commented by Schillaci and Perlini (pp. 474–476), who discuss the point whether the available evidence is enough to support the use of cardiotrophin-1 as a screening tool for hypertensive heart disease in the clinical practice. Kwon et al. (pp. 601–609) find that left ventricular systolic dyssynchrony is quite frequent among hypertensive patients, and independently associated with subclinical left ventricular systolic dysfunction. Finally, Diederichsen et al. (pp. 595–600) report that electrocardiographic signs of left ventricular hypertrophy and/or strain have no apparent relationship with coronary artery calcification, suggesting the two sets of marker identify different subjects. Zhang et al. (pp. 554–559) bring forth new evidence showing differences in the characteristics of elastic and muscular arteries, by finding that pulse wave velocity in a typical elastic arterial system (carotid-femoral) markedly increases with age, brachial blood pressure, and plasma glucose, whereas pulse wave velocity in a predominantly muscular system (carotid-pedis) is much less dependent on age and blood pressure. In an Italian nationwide survey on high blood pressure in HIV infection, Schillaci et al. (pp. 560–567) report a higher symmetric ambulatory arterial stiffness index, which may play a role in increasing the cardiovascular risk of these patients.
Salt intake is also the subject of several papers. Quelhas–Santos et al. (pp. 543–553) describe the effects of normal and high sodium intake on plasma and urinary renalase in partially nephrectomized rats as compared with sham-operated animals. Low and high sodium diets have also been found to influence the acute phase protein, hemopexin, in such a way that plasma hemopexin is significantly lower in healthy men on high rather than low sodium balance when the pressure response to angiotensin II is larger. This suggests activated hemopexin might be considered as a factor mediating angiotensin II effects upon blood pressure by modulating AT1-receptor availability (Krikken et al. pp. 537–542). Finally, DuPont et al. (pp. 530–536) show that a high sodium diet may have detrimental effects on the cardiovascular system also in so-called salt-resistant individuals: in these individuals, a 7-day high sodium intake, though unaffecting blood pressure, significantly reduced flow-mediated vasodilatation, indicating salt intake may impair endothelial function independently of changes in blood pressure. The several possible mechanisms involved in the pressure independent vascular injury induced by high salt are discussed by Stier in a thoughtful editorial commentary (pp. 472–473).
Other articles in this issue concern endothelial function. An extensive review by Lankhorst et al. (pp. 444–454) of the endothelial effects of antiangiogenesis agents (frequently used nowadays in the treatment of various forms of cancers) shows a blood pressure increase associated with elevated circulating and urinary levels of endothelin-1, an effect that can be prevented or reverted by endothelin receptor blockers. Interference of inflammatory signals in endothelial cells by tomato extracts and carotenoids has also been observed in cultured endothelial cell models through inhibition of nuclear factor-kB signaling (Armoza et al., pp. 521–529).
At least a paper on hypertension genetics usually appears in each issue of the Journal of Hypertension: in the current issue, Määttä et al. (pp. 516–520) report a significant association between STK39 (serine/threonine kinase) genetic variant rs6749447 and hypertension in a Finnish cohort.
Technical aspects of blood pressure measurement are debated by Hirata et al. (pp. 508–515), who compare the utility of the generalized transfer function and the late systolic shoulder of the radial pressure waveform for estimating seated central SBP and seated c-augmentation index, concluding that both methods are well suited. Salvi et al. (pp. 469–471) comment on this topic discussing values and limitations of both methods, and underlying that validation of arterial tonometry in different subjects’ positions may contribute to a larger diffusion of this technique.
Telemonitoring of home blood pressure is reviewed by Omboni et al. (pp. 455–468) as a novel approach to improve therapeutic adherence. In their meta-analysis, the authors find a better control of both SBP and DBP by telemonitoring than by usual care, due to a larger prescription of antihypertensive medications, without any significant difference in therapeutic adherence, however. Telemonitoring remained more costly compared with usual care. The question whether the additional cost of new procedures makes antihypertensive management more successful can be considered in the light of another article published in this issue (Parati et al., pp. 616–623), showing that in a large-scale, practice-based observational cohort, morning and smooth 24-h ambulatory blood pressure control is achieved in less than 50% of treated hypertensive patients.
Finally, resistant hypertension continues to be the focus of a lot of clinical and research interest. Schmieder et al. (pp. 610–615) have compared two large international cohorts, one of hypertensive patients defined as resistant according to guidelines, the other of uncontrolled hypertensive patients: in addition to the known risks to physical health, resistant hypertension has been found to present a substantial emotional burden to the patients.
For treatment of resistant hypertension, recourse to aldosterone antagonists is now recommended. Amar et al. (pp. 624–629) report a sequential comparison of aldosterone synthase inhibition and mineralocorticoid receptor antagonism: in patients with primary aldosteronism, the effects on blood pressure, potassium, and plasma renin concentrations of the mineralocorticoid receptor antagonist eplerenone were found to be more marked than those of a new aldosterone synthase inhibitor, LCI699. Introduction of this new class of drugs in the treatment of resistant hypertension should therefore apparently wait for a more effective agent.
Conflicts of interest
There are no conflicts of interest.
© 2013 Lippincott Williams & Wilkins, Inc.