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Hypertension-related mortality and morbidity

Zanchetti, Alberto

doi: 10.1097/HJH.0000000000000725
EDITOR'S CORNER

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 02 50320484; e-mail: alberto.zanchetti@unimi.it

A large number of articles published in the current issue of the Journal of Hypertension are focused on the relationship of hypertension or hypertension-associated phenotypes with mortality and morbidity.

Patel et al. (pp. 2046–2053) present data from a longitudinal study of 9260 hypertensive adults followed for 40 years, and report that in these individuals, serum phosphate and calcium were significantly associated with reduced all-cause and cardiovascular survival. Chung et al. (pp. 2099–2106) in a retrospective observational study of 1161 patients hospitalized for an acute ischemic stroke within 4 h of onset find that blood pressure variability during the first 72 h is independently and linearly correlated with the development of early neurological deterioration. In an accompanying commentary, Kjeldsen and Berge (pp. 2020–2021) cite data from the Scandinavian Candesartan Acute Stroke Trial (SCAST) showing less neurological deterioration in patients with small to moderate fall in SBP from day 1 to 2, compared with patients with a rise or a large fall in SBP. Rakugi et al. (pp. 2165–2172) report the results of a subanalysis of the Combinations of Olmesartan (COLM) trial, in which the angiotensin receptor blocker olmesartan was compared in its combinations with a calcium antagonist or with a diuretic. Visit-to-visit variability of SBP was smaller in the olmesartan-calcium antagonist than in the olmesartan–diuretic combination, particularly in the very elderly group (75–84 years), in which cardiovascular event incidence was lower in the calcium-antagonist than in the diuretic-based combination. Gutierrez et al. (pp. 2115–2122) examine relations between pulsatile and steady components of blood pressure and MRI measures of cerebral small vessel disease in the Northern Manhattan Study cohort, which is a stroke-free random sample of middle-aged and older members of the local community, and report a differential association between the various blood pressure components and the different types of small vessel disease in the brain. In an accompanying commentary, Mitchell (pp. 2025–2028) underscores the important contribution of aortic stiffness and pulsatile haemodynamics in vascular brain damage and suggests that further investigation in this area may open new avenues for prevention of age-related cognitive decline. Hopes for a more effective prevention of cerebrovascular disease and cognitive dysfunction are not encouraged by a report from the Czech post-MONICA study: Cifkova et al. (pp. 2107–2114) find that cardiovascular risk factors are highly prevalent and poorly controlled among patients surviving their first-ever ischemic stroke, against the reasonable expectation that control would be better in these patients, given the frequency of severe disability. In a thoughtful accompanying editorial, Chalmers (pp. 2022–2024) raises the argument that recent guidelines in various parts of the world pointing out that trial evidence for lower blood pressure thresholds and targets is scanty may have weakened efforts towards better blood pressure control even in high risk patients, and recognizes the urgent need for more clinical trials aiming at clarifying the matter. Chalmers (pp. 2029–2031) also provides an editorial commentary of another article in this issue of the Journal (Peters et al., pp. 2156–2164) with data from the Newcastle 85+ Study. In this population-based cohort study recruiting individuals aged 85 years via practices in Newcastle (UK), Peters et al. have found an association between use of calcium antagonists and less cognitive decline over 3 years. As the authors recognize, the study is observational and the number of individuals involved is small, and in his editorial, Chalmers reiterates an invitation to explore this clinically important problem by the best approach, namely, large adequate randomized trials.

Early biomarkers of renal disease in the plasma of patients with hypertension or diabetes have been searched for by Pena et al. (pp. 2123–2132), who report that plasma proteomics may predict the transition in albuminuria stage in these patients. The influence of blood pressure control on microvascular complications and mortality in diabetic patients has been investigated by Walraven et al. (pp. 2091–2098) in 5711 patients followed up for 5.7 years, in whom at least two blood pressure follow-up measurements were available. They show that in 15% of these patients, a suboptimal blood pressure control pattern over time occurred, associated with an increased risk of microvascular complications. In an accompanying editorial, Nilsson (pp. 2018–2019) appreciates the value of studying trajectories over time in blood pressure control in patients at high risk, but calls attention to an enigmatic finding in the study by Walraven et al., namely, that the subgroup with the worst control (’nonresponsive’) was found at a lower risk of total mortality than the well controlled majority group, and suggests this may be a spurious finding.

Cuspidi et al. (pp. 2133–2140) have re-examined the relation of left ventricular geometry with all-cause mortality in the 1716 individuals representative of the general population of Monza enrolled in the Pressioni Arteriose Monitorate E Loro Associazioni (PAMELA) study. They conclude that the new classification system of left ventricular geometry patterns proposed by the Dallas Heart Institute may improve mortality risk stratification. Left ventricular mass is also the objective of another article in this issue of the Journal: Cioffi et al. (pp. 2141–2149) report that an inappropriate left ventricular mass is found in two-third of a large group of patients with rheumatoid arthritis without overt cardiac disease, which is associated with left ventricular systolic dysfunction and concentric geometry.

Other articles focus on morbidity association with hypertension-related arterial stiffness. Kheder-Elfekih et al. (pp. 2010–2015) review the mechanisms by which increased arterial stiffness in older individuals can damage the kidney and reduce the beneficial effects of blood pressure lowering. Bellinazzi et al. (pp. 2054–2060) report that in their cohort of 403 hypertensive patients followed up for about 4 years, a lower common carotid systolic flow velocity/systolic arterial diameter ratio was associated with major cardiovascular events independent of cardiovascular prediction models such as the Framingham risk score and carotid intima–media thickness. The authors suggest that this index may be a promising approach to identify hypertensive individuals at an increased risk for future cardiovascular events. In an accompanying editorial commentary, Cameron (pp. 2016–2017) points out that the eventual demonstration of clinical utility of a new index obviously requires multisite uptake and results from a wide variety of cohorts. In his opinion, the hypothesis and initial data presented by Bellinazzi et al., while lacking repeatability/reproducibility, are consistent with quantification of target system damage and seem to conform to biological plausibility, but whether the suggested parameter adds sufficient clinical reclassification remains to be demonstrated. In a cohort of 853 hypertensive patients followed up for about 8 years, Cremer et al. (pp. 2150–2155) find that an index of arterial stiffness is a strong predictor of incident atrial fibrillation, independently of age, 24-h pulse pressure and left atrial diameter. In communities of African ancestry, Sibiya et al. (pp. 2083–2090) find that reflected rather than forward wave pressures account for brachial pressure-independent relations of aortic pressure with end-organ changes.

Finally, two important review articles from the Reference Values for Arterial Measurements Collaboration (pp. 1981–2009) provide much needed age and sex-specific reference intervals of local carotid and local femoral stiffness: carotid data are derived from 3601 healthy individuals and femoral data from 1489 healthy individuals from 24 research centres.

Other articles in this issue are focused on other aspects of epidemiology, genetics and treatment. In a large cohort of 2078 patients attending a cardiac rehabilitation programme at the University of Michigan, Giorgini et al. (pp. 2032–2038) report that short-term exposures to fine particulate matter pollution (PM 2.5), even at low concentrations within current air quality standards, are associated with significant increases in blood pressure. Okello et al. (pp. 2039–2045) observed a high incidence of hypertension in HIV-infected persons on antiretroviral therapy in rural Uganda, and increased risk with lower CD4+ cell counts at treatment initiation. Thijs et al. (pp. 2075–2082) present the results of animal and human experiments investigating the mechanisms of hypertension induced by the antiangiogenesis agent, sunitinib. In animals, exposure to high concentrations of sunitinib reduced endothelium-dependent vasodilation by reducing endothelial release of nitric oxide, whereas in humans, reduced endothelium-dependent vasodilation did not precede the development of hypertension in patients treated with sunitinib. Marques-Vidal et al. (pp. 2173–2178) report results of a prospective observational study to investigate the association of angiotensin receptor blockers with inflammatory markers, showing that these agents were not associated with reduced levels of the three inflammatory markers tested [C-reactive protein (CRP), interleukin (IL)-1β, IL-6]. Alvan et al. (pp. 2061–2067) find significant heritability estimates for both ambulatory and office blood pressure in a Swiss population-based study, and Akehurst et al. (pp. 2068–2074) report the results of a pilot study identifying microRNA-206 as a novel factor upregulated in preeclampsia within the maternal circulation and in placental tissue.

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There are no conflicts of interest.

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