Both the International and European Societies of Hypertension are obviously interested in hypertension problems worldwide, which present similarities and differences based on ethnicities and economic resources. The Journal of Hypertension reflects these interests of the sponsoring scientific societies and of its readers worldwide. The current issue publishes a number of papers that directly address some of these problems. In 2011, the European Society of Hypertension established a Working Group on ‘Cardiovascular Risk in Low Resource Settings’, which brought together cardiologists, diabetologists, nephrologists, clinical trialists, epidemiologists, economists and stake holders, and the Working Group now reports a consensus document on how to assess cardiovascular risk in low-resource countries (Modesti et al., pp. 951–960). Baena et al. (pp. 961–973) publish a meta-analysis of studies on the effects of lifestyle-related intervention on blood pressure in low-to-medium-income countries. Lifestyle interventions may be of value in preventing and reducing blood pressure in these lower-resource countries. Nevertheless, the overall quality and sample size of the studies were found to be low, with larger effects being reported by smaller samples and shorter studies. Grootveld et al. (pp. 990–997) report a comparative study of an ethnic Dutch, South Asian Surinamese and African Surinamese population living in the Netherlands: a higher incidence of hypertension was found among the South Asian Surinamese and, in particular, African Surinamese than among the Dutch. The ethnic differences in the incidence of hypertension were only partly explained by body composition. In an editorial commentary, Masuo (pp. 974–976) remarks that Grootveld et al.'s study, being a perspective one, will have further opportunities to clarify which factor, in addition to body composition (genetic, environmental including diet, socioeconomic, etc.), is more important in the development of hypertension. In a prospective cohorts of Inner Mongolians, Tang et al. (pp. 1091–1096) evaluated the cumulative effect of hypertension and alcohol on stroke incidence and found hypertension to be an independent risk factor of stroke and that drinkers with hypertension are at the highest risk.
Other papers in the current issue deal with measurement of risk factors in populations and assessment of cardiovascular risk. Mente et al. (pp. 1005–1015) present the results of an important validation study of three formulae to estimate sodium and potassium excretion from a single morning fasting urine compared to 24-h measures, and conclude the Kawasaki formula, compared with the Tanaka and INTERSALT formulae, is the most valid and least biased method of estimating 24-h sodium excretion from a single morning fasting urine, and is suitable for population studies of sodium intake. Ruilope in an accompanying editorial (p. 977) remarks that one of the strengths of the study consists in the fact that the data were obtained from general population samples in 11 different countries. Pan et al. (pp. 998–1004) have examined the association between uric acid and high blood pressure in a multiethnic study of Chinese children and adolescents, and found a significant positive association.
Regarding assessment of cardiovascular risk, Vinyoles et al. (pp. 1016–1024) have taken advantage of the large database of the Spanish Ambulatory Blood Pressure Monitoring registry (32 569 hypertensive patients included) to estimate the night-time heart rate cut-off point best predicting the value of office tachycardia considered a cardiovascular risk factor, and found a mean night-time heart rate more than 66 beats per minute is a good predictor of cardiovascular risk office tachycardia. Vishram et al. (pp. 1025–1033) summarize the results of the large MOnica Risk Genetics Archiving and Monograph project including 85 772 apparently healthy Europeans and Australians followed up for an average of 13.3 years, and report SBP was superior to DBP at all ages to predict coronary heart disease (CHD) mortality, but for stroke and all-cause mortality, there was a gradual age-related shift from DBP (superior up to 26 years) to SBP (superior above age 63), with both SBP and DBP being important at intermediate ages. In a thoughtful editorial commentary, van Bortel (pp. 978–980) underlines the importance age-related changes in arterial stiffness play in the changing predictivity of SBP and DBP, and the usefulness of taking into account target organ damage in the assessment of cardiovascular risk and in treatment guidance. The latter concept is further supported by the prospective study published by Greve et al. (pp. 1034–1041), in which sub-clinical organ damage, and especially atherosclerotic plaques or albuminuria, added prognostic information with moderate or intermediate risk.
Other papers in this issue deal with hypertension-related organ damage or outcomes. Tabara et al. (pp. 1084–1090) show postprandial blood pressure decline is an overlooked risk marker for asymptomatic lacunar infarction. This finding is commented by Parati and Bilo (pp. 983–985), who underline the importance of the finding, but also remark the interpretative difficulties due to its cross-sectional nature. Wohlfahrt et al. (pp. 1097–1103), by studying a cohort of patients after their first ischaemic stroke, report data, suggesting that aortic stiffness, by reducing the buffering function of the aorta, may increase flow pulsatility into the cerebral arterioles and thus contribute to the pathogenesis of lacunar stroke. Experimental studies in Wistar rats fed a high-fat diet, published by Martínez-Martínez (pp. 1104–1114), suggest that leptin locally produced in the heart may affect collagen turnover, thus participating in development of fibrosis. Collagen synthesis induced by leptin seems to be mediated by the production of galectin-3, transforming growth factor ß (TGF-ß) and connective tissue growth factor (CTGF) through oxidative stress.
Uhm et al. (pp. 1115–1120) report that first-degree atrioventricular block is an independent risk factor for future development of advanced atrioventricular blockade, atrial fibrillation and left-ventricular dysfunction in patients with hypertension. In their editorial commentary, Bang and Okin (pp. 986–987) remark that the electrocardiogram is an inexpensive and widely available procedure which provides convincing predictive value in patients with cardiovascular disease, but whether first-degree atrioventricular block will become a widely utilized marker of cardiovascular risk will require further assessment in additional populations and under differing treatment conditions. Finally, Perlini et al. (pp. 1121–1131), in a prospective study of a large cohort of patients with cardiac amyloidosis with preserved ejection fraction, report that depressed circumferential mid-wall fractional shortening is a powerful predictor of survival.
Another group of papers deals with therapeutic aspects or has therapeutic potentials. In spontaneously hypertensive rats, van den Elsen et al. (pp. 1050–1058) show that dietary fish oil lowers blood pressure and improves endothelial function in association with suppression of sphingolipid-dependent contraction. Zhang et al. (pp. 1059–1067) have investigated the cardiovascular and sympathetic responses to administration of the peptide, salusin-ß, into the rostral ventrolateral medulla of renovascular hypertensive rats, and concluded that salusin-ß activates the sympathetic nervous system to increase blood pressure via the NAD(P)H oxidase enzyme complex and generation of superoxide anion. In a comprehensive commentary, Matsumura (pp. 981–982) suggests this mechanism may account for their previous findings that the exaggerated pressor response to glutamate in the medulla of the spontaneously hypertensive rat was attenuated by chronic treatment with an angiotensin receptor antagonist, but remarks that, although superoxide anions are likely to mediate the cardiovascular action of salusin-ß in the medulla, the overall physiological role of salusin-ß on the central regulation of blood pressure has not been fully investigated. Further studies will be needed to better understand the mechanisms of interactions between salusin-ß, oxidative stress and angiotensin II in hypertension.
Xu et al. (pp. 1075–1083) report that some antihypertensive drugs used in pregnancy may improve the cellular interaction between trophoblast and endothelial cells exposed to tissue necrosis factor-α. Wolak et al. (pp. 1132–1137) show that doxazosin treatment for hypertension is associated with adverse cardiac outcome only among patients with moderate to severe ischaemia on myocardial perfusion imaging. Escobar et al. (pp. 1138–1145), by reviewing evolution of therapy inertia in primary care setting in Spain during 2002-2010, find that therapeutic inertia has decreased, but no therapeutic action is actually taken yet. In their commentary, Volpe and Tocci (pp. 988–989) call for improving educational and behavioural interventions for reducing physicians’ inertia and increasing patients’ adherence to prescribed medications. Corrao et al. (pp. 1146–1153), after analysing data about more than one hundred thousand individuals on antihypertensive treatment in Lombardy during 2008 conclude that generic products are not responsible for the high rate of discontinuation from antihypertensive drug therapy.
Finally, the span of topics covered by papers published in this issue of the Journal is completed by a genetic study by Zhu et al. (pp. 1042–1049), showing that genetic variants in nicotinic acetylcholine receptor genes jointly contribute to kidney function in American Indians, and by a study on the diagnosis of hypertension in children (Outdili et al., pp. 1068–1074), showing that the blood pressure-to-height ratio at a single visit had a high performance to identify hypertension in children.
Conflicts of interest
There are no conflicts of interest