New studies searching for markers predictive of mortality and morbidity in hypertension are published in this issue of the Journal of Hypertension. Strandberg et al. (pp. 1797–1804) report the findings from the prospective Helsinki Businessmen Study, showing that lower blood pressure (BP) in midlife is associated with longer life (a substantial 7.5-year age-adjusted difference in the mean survival between men with normal BP and men with SBP at least 160 mmHg or DBP at least 100 mmHg) and better physical functioning and general health-related quality of life in old age. Cuspidi et al. (pp. 1879–1887) have analysed the data from the Pressioni Arteriose Monitorate e Loro Associazioni (PAMELA) prospective population study with a follow-up of 148 months and found that aortic root diameter (as assessed by echocardiography) indexed to height is predictive of the incident nonfatal and fatal cardiovascular events, and support that assessment of the aortic root diameter in addition to left ventricular mass may refine cardiovascular risk stratification and preventive strategies in the general population. In a cross-sectional study measuring 24-h aortic and brachial BP, Protogerou et al. (pp. 1805–1814) found a higher discriminatory ability of 24-h average aortic than brachial SBP to detect the presence of left ventricular hypertrophy. In an accompanying comment, Salvi et al. (pp. 1774–1777) discuss the reliability of central BP and explain why recent European Society of Hypertension/European Society of Cardiology hypertension guidelines  did not recommend the routine clinical measurement of central BP.
Furthermore, in this same issue of the journal a systematic review and meta-analysis of the recent studies comparing central and brachial SBP shows that noninvasive estimation of central BP is device and technique dependent, and the authors call for caution in applying these devices and techniques across the clinical studies (Narayan et al., pp. 1727–1740).
In a prospective study of pregnant women, Chen et al. (pp. 1833–1841) found that foetal and maternal plasma angiotensin (1–7) concentrations were independently associated with preterm birth, a known risk factor for hypertension later in life. Indeed, another article in this issue, using data from the Avon Longitudinal Study of Parents and Children (Howe et al., pp. 1789–1796), confirm that small size at birth followed by rapid adiposity gain in infancy and continued overweight or obesity are associated with high BP in young adulthood, thus emphasizing the importance of maintaining normal weight in childhood for the prevention of high BP. Finally, the association of hypertension prevalence with socioeconomic inequalities is illustrated in a comprehensive epidemiological study in Iran (Fateh et al., pp. 1782–1788).
A group of pathophysiological studies in animals have explored the ability of aldosterone to increase reactive oxygen species production and induce endothelial dysfunction in cerebral arteries independent of the BP changes (Chrissobolis et al., pp. 1815–1821); the BP increase induced by a high phosphate diet through an increase in renin mediated by the parathormone (Bozic et al. pp. 1822–1832); a new NKCC2 interacting partner (β1NK) involved in the modulation of NKCC2 intracellular trafficking and possibly in the regulation of BP (Carmosino et al., pp. 1842–1853). In an accompanying editorial, Grisk (pp. 1778–1779) reviews the role of NKCC2 and remarks that the difference in the amount of β1NK in NKCC2 containing multiprotein complexes between SHR and WKY and the functional data provided by Carmosino et al. are important criteria to suggest that β1NK content in such complexes is related to BP.
A group of studies focus on several aspects of cardiac involvement in hypertension. Kloch-Badelek et al. (pp. 1854–1861) demonstrate moderate heritability of various indexes reflecting left ventricular diastolic function in nuclear families. Yang et al. (pp. 1862–1869) report that normotensive individuals with an exaggerated BP response to exercise exhibit impairment in longitudinal myocardial function. Tadic et al. (pp. 1870–1878), by using two-dimensional speckle tracking analyses, found that left ventricular mechanics is impaired in individuals with the metabolic syndrome.
A group of studies deal with problems of immediate therapeutic interest. de Beus et al. (pp. 1751–1761) review the evidence that sympathetic activity is increased in chronic kidney disease and raise the point whether these patients may be particularly responsive to renal denervation, a question that appears relevant at a time when specific indications for this procedure should be sought for. Directly recorded muscle sympathetic nerve activity was the target of another study (Inomata et al., pp. 1898–1904), which reports the recently developed calcium channel blocker, azelnidipine, compared with amlodipine, is accompanied by a significantly lower sympathetic activity. In an accompanying comment, Grassi (pp. 1780–1781) discusses whether the effects of azelnidipine can really be defined as sympathoinhibitory or whether it simply represents the absence of a sympathoexcitatory action.
A further systematic review and meta-analysis of the randomized controlled trials using continuous positive airway pressure (cPAP) in patients with obstructive sleep apnoea confirms cPAP induces significant BP reductions, but these are rather small (Schein et al., pp. 1762–1773). A review of the available trial evidence on the effects of BP and LDL-cholesterol lowering in the primary and secondary prevention of stroke, and on cognitive decline is published (pp. 1741–1750) as an introduction to the presentation of the design of the Stroke in Hypertension Optimal Treatment (SHOT) randomized trial, recently initiated as a joint endeavour of the European Society of Hypertension and the Chinese Hypertension League (pp. 1888–1897).
Conflicts of interest
There are no conflicts of interest.
1. Mancia G, Fagard R, Narkiewicz K, Redon J, Zanchetti A, Böhm M, et al. The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). 2013 ESH/ESC guidelines for the management of arterial hypertension. J Hypertens