From the pathophysiological to the epidemiological approach to hypertension research

Two major sets of papers in the current issue of the Journal of Hypertension are focused – one on exploring pathophysiological mechanisms accompanying experimental and human hypertension, and the other on large epidemiological studies mostly searching for predictors of hypertension development and subsequent cardiovascular outcomes. As usual, the wide span of hypertension research methods and targets is illustrated in the Journal content. The current issue opens with a detailed review by Deng (pp. 669–680) on the contribution that experimental models of hypertension have provided to an insight of the polygenic mechanisms of hypertension. A.Y. Deng, who has greatly contributed to this research area, illustrates how epistasis genetics can mechanistically unravel the order and regulatory relationships between certain blood pressure quantitative trait loci and facilitate mechanism-based diagnosis and treatment of hypertension. Two studies focus on immunological and inflammatory aspects of experimental hypertension. Machado Cardoso et al. (pp. 763–772) report that exercise (swimming training) prevents some of the alterations present in lymphocytes of rats with L-NAME-induced hypertension, whereas Katsuki et al. (pp. 773–783) find that a decrease in Foxp3+ regulatory T-cell proportion is crucial for the development of hypertension and cardiac hypertrophy in the stroke-prone spontaneously hypertensive rat. Also, in the spontaneously hypertensive rat, Liu et al. (pp. 784–790) provide evidence that the reduced glucagon-like peptide-1 receptor (GLP-1R) expression in the renal arteries is mediated through protein kinase Cß (PKCß) up-regulation. Markers of renal alterations have been searched in human hypertension also. Rhee et al. (pp. 836–842) have performed a metabolomic study of renal venous plasma from individuals with unilateral atherosclerotic renal artery stenosis to examine how impaired renal blood flow may impact small molecule handling, but report that metabolomic profiling does not differentiate venous efferent from the stenotic and the contralateral kidney. A metabolomic study has been completed by Menni et al. on a large cohort of female twins (pp. 791–796): of the 280 known metabolites measured, uridine, phenylacetylglutamine and serine were strongly correlated with pulse wave velocity; interestingly, uridine was not correlated with blood pressure and traditional risk factors, but was correlated with gene expression levels of the purinergic receptor P2Y. In their accompanying comment, Redón and Monleón (pp. 698–699) remark that the combination of metabolomics and gene-based information in clinical samples may help to increase our understanding of the mechanisms of disease. Other biochemical correlates of arterial stiffening have been searched for by Semba et al. (pp. 797–803), who report that in older, community-dwelling adults, serum carboxymethyl-lysine – an advanced glycation end product – is significantly associated with indices of arterial stiffness. Early changes in cardiovascular regulation have been investigated by Maloberti et al. (pp. 804–809) in a number of children with the Williams–Buren syndrome, a genetic disorder that involves the elastin gene: they report no change in pulse wave velocity, but a higher augmentation index and reflection magnitude, limited to the night period. Two other papers focus on pathophysiological mechanisms of cardiac alterations related to hypertension. Rivera-Torres et al. (pp. 843–850) have found that the Notch pathway is activated in the vasculature of mice with hypertension and left ventricular hypertrophy, and its inhibition via inducible genetic γ-secretase deletion protects against both conditions. They also report preliminary observations of an elevated expression of the Notch target HES5 in vascular tissue from hypertensive patients with (but not without) left ventricular hypertrophy, thus supporting the translational potential of their observations in mice. Fernández-Solà et al. (pp. 851–859) report their results in a remarkable number of heart samples from human donors: the presence of hypertension in the donor significantly decreases insulin-like growth factor-1 (IGF-1) expression, whereas myostatin myocardial expression increases in the presence of structural cardiomyopathy, independently of its origin (hypertensive or nonhypertensive). The group of epidemiological papers in the current issue of the Journal largely consists of prospective or cross-sectional studies investigating predictors or correlates of hypertension, organ damage or outcomes. Li et al. (pp. 704–710) report that incidence of hypertension in Indigenous Australians is nearly double that of the general Australian population, high prevalence of obesity and diabetes contributing to this excess. In another Australian study, prenatal life stress associated positively with offspring BMI, but inversely with SBP and systolic prehypertension in young adult offspring (Bhat et al., pp. 711–719). In the prospective Western New York Health Study, Stranges and Donahue (pp. 720–726) have found that measures of health-related quality of life may represent independent predictors of hypertension risk, at least among women. Roderjan et al. (pp. 827–835) have investigated correlates of aortic stiffness changes in patients with resistant hypertension, whereas El-Bikai et al. (pp. 727–735) report that in a large Canadian cohort – CARTaGENE – hypertension, low bone mineral density and arterial stiffness are strongly associated with height, and shorter stature, low body mineral density and fractures correlate with increased arterial stiffness. In a general population, García-Ortiz et al. (pp. 818–826) have found that measurement of the retinal arteriovenous ratio may be used as an assessment of asymptomatic vascular damage in large arteries, lower retinal arteriovenous ratios being associated with increases in carotid intima–media thickness, augmentation index and pulse wave velocity. From an 11-year long prospective study, Thompson et al. (pp. 810–817) conclude that calcified carotid plaques may predict mortality and cardiovascular outcomes independent of traditional cardiovascular disease risk factors and may serve as an additional risk assessment in the elderly. The role of hypertension on prognosis of patients with acute coronary syndromes has been retrospectively investigated by Erne et al. (pp. 860–867) in a large registry of 41 771 patients: the outcome of those with pre-existing hypertension was found to be associated with an improved in-hospital prognosis, but the effect was not long-lasting. In an editorial comment, Volpe and Tocci (pp. 700–701) conclude that available evidence suggests caution in drastically lowering blood pressure in hypertensive patients, particularly when asymptomatic coronary disease is suspected, but further, more specific clinical studies are needed. An analysis of the prospective Gubbio population study by Lanti et al. (pp. 736–744) has been done to confute the frequently held concept that antihypertensive treatment should be considered a risk factor for major cardiovascular events in epidemiological studies: in the Gubbio cohort, the relative risk of treated but controlled hypertensive patients, though initially higher, became equal to that of nonhypertensive patients after adjustment for age, achieved blood pressure and other risk factors; likewise, risk of treated but uncontrolled hypertensive patients was similar to that of untreated hypertensive patients. In the large hypertensive cohort from the Campania Salute Network, de Simone et al. (pp. 745–754), by applying the new left ventricular geometric classification including the category of dilated left ventricular hypertrophy, conclude in favor of the importance of the volume load coexisting with the pressure overload in determining the risk of left ventricular hypertrophy. This topic is further discussed in an editorial commentary by Kahan (pp. 690–692). As usual, therapeutic topics have also been investigated by other papers in this issue of the Journal. The role of specific medical or surgical treatment of primary aldosteronism on the associated carotid intima-media thickening has been investigated by Holaj et al. (pp. 874–882), who report the long-term effects of the two types of intervention are comparable. In an extensive review and meta-analysis, Fan et al. (pp. 681–689) find that in Chinese patients with hypertension and hyperuricemia, losartan and other antihypertensive agents have similar effects on blood pressure, but losartan is significantly more effective in lowering serum uric acid levels. Marques-Vidal et al. (pp. 868–873) have calculated that shifting from the Joint National Committee (JNC)-7 report to the JNC-8 report or from the 2007 to the 2013 European Society of Hypertension-European Society of Cardiology (ESH-ESC) guidelines would remarkably decrease the prevalence of patients eligible for treatment and increase the percentage of treated patients within blood pressure goals, with considerable potential savings in antihypertensive drug treatment. These calculations and their implications are commented by Mancia, the coordinator of the ESH-ESC guidelines (pp. 702–703). A final paper by Nunan et al. (pp. 755–762) is focused on the diagnostic accuracy of self-monitored blood pressure, and they conclude that hypertension can be ruled out in the majority of individuals with elevated clinic blood pressure using the average of the first five consecutive days of self-monitored blood pressure. In an accompanying comment, Stergiou and Ntineri (pp. 693–697) remark that, while there is international consensus on the optimal home blood pressure measurement schedule to be applied in clinical practice, there are other aspects that remain uncertain. ACKNOWLEDGEMENTS Conflicts of interest There are no conflicts of interest

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