Most of the articles in the current issue of the Journal of Hypertension focus on diagnostic and therapeutic aspects.
Tadic et al. (pp. 744–753) review the main principles of left ventricular dynamics and summarize the clinical significance of left ventricular strain in hypertensive patients, underlying the finding that particularly longitudinal strain was proved as a stronger independent predictor of cardiovascular and total morbidity than left ventricular ejection fraction and suggesting its evaluation may become part of everyday clinical practice. Iacobaeus et al. (pp. 857–866) provide interesting data on cardiac function, myocardial mechanoenergetic efficiency and ventricular–arterial coupling in normal pregnancy, which may represent a useful comparison for studies on hypertensive pregnancies.
A group of articles investigate diagnostic aspects of pulse wave analysis and pulse wave velocity (PWV) measurement. A type of pulse wave analysis, the pulsed wave separation analysis (WSA), has been introduced to quantitatively estimate the forward and backward pressure components. In this issue, Cauwenberghs et al. (pp. 867–875) have evaluated feasibility and usefulness of WSA in a sample of the Flemish Study on Environment, Genes and Health Outcomes population. They report the WSA algorithm was found to have low feasibility in older individuals with unfavourable hemodynamics, and favour the use of the composite central pulse pressure for prediction of left ventricular dysfunction. Light and shade of pulse wave analysis are extensively discussed by de Simone and Mancusi in an accompanying editorial (pp. 765–767), who remember that an easy method to analyze ventricular vascular interactions across the entire cardiac cycle, as pointed out by Cauwenberghs et al., is the pulse pressure/stroke index (PP/SVi) ratio, which has been demonstrated to be particularly useful for the prediction of incident heart failure. Influence of different confounders on arterial stiffness, as measured by PWV, has been investigated in two studies. Buus et al. (pp. 815–823) have compared several cardiovascular indices, including PWV and augmentation index (AIx), in young to middle-aged individuals genetically predisposed for hypertension (Danish Hypertension Prevention Project) and their spouses, and found that AIx but not vascular stiffness were higher in genetically predisposed individuals, and that AIx were also higher in women than men. Topouchian et al. (pp. 824–833) present data from a large European multicenter study [Advanced Approach to Arterial Stiffness (AAAS) Study], showing a differential impact of age and metabolic syndrome on two different methods of evaluating arterial stiffness, carotid–femoral PWV (cf-PWV) and the cardio-ankle vascular index (CAVI), age having a more pronounced effect on CAVI and metabolic syndrome on cf-PWV. This article is accompanied by a careful review of limits and strengths of the two methods of assessing arterial stiffness by Grillo and Salvi (pp. 759–764), who point out that the presentation of CAVI and cf-PWV as two pictures of the same subject from different angles may be misleading, and although the diagnostic usefulness of cf-PWV is consolidated, the role of CAVI is still debated. They conclude that only longitudinal studies, such as the prospective component of AAAS will be able to clarify the respective roles of CAVI and cf-PWV. Finally, a Mendelian randomization study by Gottsäter et al. (pp. 809–814) in individuals from the population-based Malmö Diet Cancer study has investigated a potential set of genetic cardiometabolic traits and arterial stiffness, and reports that genetically elevated fasting plasma glucose but not genetically elevated risk of type 2 diabetes was associated with arterial stiffness.
A large number of articles in the current issue of the Journal of Hypertension have impact on different therapeutic aspects of hypertension. Among lifestyle interventions, sodium restriction and physical activity have been investigated. D’Elia et al. (pp. 734–743) present the results of a systematic search and meta-analysis of randomized controlled studies on the effect of dietary sodium restriction on arterial stiffness and report that restriction of dietary sodium reduces arterial stiffness, the effect being at least in part independent of the changes in blood pressure (BP). In an accompanying editorial commentary, Salvi et al. (pp. 754–758) raise the possibility that in addition to the level of sodium intake, also the individual degree of sodium sensitivity, likely to have a genetic background, may play a role. The readers interested in the evaluation of dietary sodium may read another article (Vidal-Petiot et al., pp. 785–792) on the debated issue of the accuracy of different formulae to estimate 24-h sodium intake from a fasting morning urine sample. The authors conclude that all formulae have poor precision and accuracy: although they are not suitable for estimating individual sodium intake, their potential value in population studies cannot be discussed.
Concerning physical activity, Fan et al. (pp. 793–800) publish the results of a 7-year prospective cohort study of more than 150 000 participants from 10 different areas across China, showing a higher level of physical activity was associated with a reduction in all-cause and cardiovascular mortality, independent of the activity intensity. Some relation with aspects of lifestyle can be found in a pathophysiological study by Li et al. (pp. 801–808) in an experimental model of obesity-induced hypertension, showing that enhanced cannabinoid (CB1) receptor-mediated neurotransmission in the rostral ventrolateral medulla may play a role in the development of this type of hypertension and the associated increase in renal sympathetic activity.
A larger set of studies refer to aspects of pharmacological treatment of hypertension. Because of some evidence that BP variability may provide independent prognostic information, the effects of different antihypertensive treatment strategies on BP variability are of some interest. Omboni et al. (pp. 720–733) present the results of a pooled individual data analysis of 24-h BP variability in 10 studies based on olmesartan monotherapy or combination therapy, and report that olmesartan in combination with a dihydropyridine calcium channel blocker or thiazide diuretic reduces 24-h BP variability more than placebo or monotherapies. Readers may be interested to read another article in this issue, in which Veloudi and Sharman (pp. 711–719) carefully review the different methodologies used for measuring BP variability on different time scales: short-time (24-h ambulatory BP), mid-term (home BP on several days) and long-term (visit-to-visit clinic BP).
Fuchs et al. (pp. 933–938) publish the results of a randomized clinical trial carried out across Brazil, testing the effects of low-dose diuretic therapy (chlorthalidone 12.5 mg and amiloride 2.5 mg daily) versus placebo in adults with hypertension over 18 months of treatment: the diuretic therapy significantly reduced SBP by 2.8 mmHg compared with placebo, but most participants in both the active and placebo groups continued to have BP in the prehypertension range or progressed to hypertension. Nagai et al. (pp. 924–932) report interesting data on prevalence, treatment and control of hypertension in the population of Fukushima Prefecture before and after the 2011 Great East Japan Earthquake, and Jessen et al. (pp. 779–784) publish data on trends in hypertension and hypertension treatment between 2005 and 2015 in Mozambique.
Sex differences in antihypertensive treatment have been studied insufficiently. In this issue of the journal, Deborde et al. (pp. 939–946) investigated sex differences in antihypertensive treatment in France among 17 856 patients in a tertiary hypertension unit, finding women were more frequently treated with diuretics and beta-blockers, but less frequently with angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers than men. Foy et al. (pp. 904–915) have analyzed the results of the Systolic Blood Pressure Intervention Study (SPRINT) by gender, concluding that more aggressive lowering of SBP resulted in no heterogeneity of effect between men and women on cardiovascular or renal outcomes, or on rates of serious adverse events. In an accompanying commentary, Delles and Currie (pp. 768–770), however, call attention on several differences in baseline risk factors between women and men, and underuse of ACE inhibitors and statins in women, thus further underlining the need of more studies into sex differences in hypertension and hypertension management. The SPRINT study, by showing the benefits of aggressive SBP-lowering treatment, has given occasion to Okin et al. (pp. 916–923) to analyze the relationship of all-cause mortality to on-treatment SBP in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study they had previously conducted: their analysis shows that in LIFE, achievement of an average SBP lower than 142 mmHg was associated with reduced mortality whenever baseline SBP was 164 mmHg or less but with increased mortality whenever baseline SBP was higher. The authors suggest that the lower mortality associated with a lower SBP target in SPRINT may not be applicable to patients with considerably higher baseline SBP values. In an accompanying commentary, Jennings (pp. 771–772) raises the point whether analyzing one trial can help explaining the results of another one, and suggests that the hypothesis made by Okin et al. can only be tested by repeating SPRINT in different populations. The readers interested in the different relationships between BP and different patients’ characteristics may read another article in the current issue (Wijsman et al. pp. 773–778) describing different associations of DBP with cardiovascular events in the older patients of the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER) with or without a history of preexisting cardiovascular diseases.
In few other articles, a more basic approach provides useful therapeutic prospectives. Witte et al. (pp. 892–903) show that sunitinib-induced hypertension, a frequent complication nowadays of cancer treatment, is highly sensitive to blockers of the renal epithelial sodium channel and thiazides may be particularly suitable for its treatment. Yang et al. (pp. 834–846) present data in mice revealing an important role of the AKT2-IL6 pathway in mediating hypertension induced by angiotensin II in combination with a high-salt diet; Podesser et al. (pp. 847–856) identify Tenascin-C as a novel-signaling mechanism contributing to left ventricular remodeling via matrix medulloproteinases (MMPs) upregulation, cardiomyocyte hypertrophy and myocardial fibrosis under chronic pressure overload in mice; and, finally, Zhai et al. (pp. 876–891) indicate that calcitonin gene-related peptide (CGRP) is protective against ischemia-induced neuronal cell injury and progression of cognitive decline in mice. Whether these interesting pathophysiological findings will help identifying novel candidates for treatment of hypertension and its complications is an open question for further investigations.
A final therapeutic article reports the results of a randomized titrate-to-target study comparing azilsartan medoxomil combined with chlorthalidone with olmesartan and hydrochlorothiazide in systolic hypertension (Cushman et al., pp. 947–956), finding the former combination reduced SBP to a significantly greater extent than the latter.
Conflicts of interest
There are no conflicts of interest.