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Studying arterial wall in hypertension

Zanchetti, Alberto

doi: 10.1097/HJH.0000000000000707
EDITOR'S CORNER
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Istituto Auxologico Italiano and Centro Interuniversitario di Fisiologia Clinica e Ipertensione, Università di Milano, Milan, Italy

Correspondence to Prof. Alberto Zanchetti, Centro di Fisiologia Clinica e Ipertensione, Università di Milano, Via F. Sforza, 35, 20122 Milano, Italy. Tel: +39 02 50320484; e-mail: alberto.zanchetti@unimi.it;alberto.zanchetti@auxologico.it

The area of hypertension research to which the most consistent number of articles are devoted in the current issue of the Journal of Hypertension is that of the functional properties of the arterial wall and their changes in hypertension. This obviously reflects the increasing interest that this area of research has raised in recent years. As all fast developing areas, the study of arterial wall properties has largely depended on advances in measurement technologies that are debated between experts. It is no surprise, therefore, that a number of articles on the arterial wall in this issue are focused on critical technical problems. An extensive review by Hayashi et al. (pp. 1742–1757) discusses theory and applications of arterial stiffness assessment with the Cardio Ankle Vascular Index (CAVI), which aims at obtaining an arterial stiffness index independent of blood pressure. In an original article, Pichler et al. (pp. 1868–1875) have compared two common techniques for measuring carotid-femoral pulse wave velocity, the Complior and SphygmoCor devices, and found their concordance is poor when the anatomical artery length is controlled for and in presence of cardiovascular risk factors. These differences result in a different classification of cardiovascular risk. Picone et al. (pp. 1876–1883) and Wassertheurer and Baumann (pp. 1884–1889) discuss the influence of radial waveform on estimation of central blood pressure. Picone et al. report that major brachial-to-radial amplification occurs in healthy people and increases with increasing age, thus contributing to underestimation of radial tonometry-derived central blood pressure. Wassertheurer and Baumann find that the association of SBP with all-cause mortality in prospective studies heavily depends on wave form calibration. In an accompanying editorial commentary, Avolio and Butlin (pp. 1761–1763) discuss several technical challenges raised by Wassertheurer and Baumann's data, and remark the article also shows the potential prognostic superiority of central over brachial pressure. Mirault et al. (pp. 1890–1896) have investigated a new emerging technique enabling direct measurement of carotid pulse wave velocity, ultrafast ultrasound imaging, and observe carotid stiffness changes over the cardiac cycle increase with age in healthy people. The authors also report a lower carotid stiffening in a cohort of patients with vascular Ehlers–Danlos syndrome, characterized by a defect in collagen type III.

Other articles are focused on nonmethodological aspects of arterial wall properties. Stancu et al. (pp. 1907–1921) have found that the soluble guanylate cyclase stimulator BAY 41-8543 improves aortic remodeling in a rat model of mild uremia, and van Dijk et al. (pp. 1897–1906), analyzing data from the large randomized controlled trial B-PROOF, report that, compared with placebo, B-vitamin supplementation, though lowering the elevated serum homocysteinemia of these patients, had no effect on pulse wave velocity and carotid intima–media thickness. Feistritzer et al. (pp. 1970–1976) found that aortic stiffness is associated with elevated high-sensitivity cardiac troponin T concentrations at a chronic stage (12 months) after ST-segment elevation myocardial infarction. Salvi and Parati (pp. 1767–1771), commenting these observations, elaborate on the hemodynamic mechanisms by which arterial stiffness influences coronary blood flow, and conclude that in clinical practice assessment of aortic distensibility should be included among the tests to screen for the risk of myocardial ischemia.

Other areas of hypertension research, such as epidemiology and obesity/diabetes, are also widely represented in the current issue of the Journal. Borghi et al. (pp. 1729–1741) review the most recent data pointing to an independent role of serum uric acid as a cardiovascular risk factor, and discuss the scope of intervention with urate-lowering drugs, particularly the xantine-oxidase inhibitors. In an interesting article, Rotar et al. (pp. 1772–1779) report cardiovascular health data of survivors of the Leningrad seige during the last World War, compared with age-matched and sex-matched individuals, and conclude that exposure to famine in childhood and intrauterine period of life was associated with higher prevalence of hypertension and shorter telomere length, but had no direct effect on the prevalence of cardiovascular disease even after seven decades since exposure. On the basis of a prospective study of a Kaiser Permanente cohort, Black et al. (pp. 1860–1867) have found that women with prehypertension prior to or early in pregnancy were significantly more likely to develop any hypertensive disorder in pregnancy or gestational diabetes mellitus. In another prospective cohort study of an African American population (Jackson Heart Study), McMullan et al. (pp. 1939–1946) find that loss of nocturnal blood pressure dipping but not morning blood pressure surge are associated with decline in glomerular filtration rate and increased risk of developing chronic kidney disease. Another article is focused on patients with chronic kidney disease; in a randomized controlled study Barden et al. (pp. 1947–1953) have observed that an 8-week diet supplementation with n-3 fatty acid reduces plasma 20-hydroxyeicosatetraenoic (20-HETE) in patients with chronic kidney disease and this associates with blood pressure reduction. In an accompanying editorial comment, Zoccali et al. (pp. 1764–1766) remark that reduction in 20-HETE levels may be a fundamental step mediating the hypotensive effect of n-3 fatty acids and suggest that focusing attention on this ecosanoid may have far-reaching implications in hypertension and chronic kidney disease.

Another group of articles focuses on obesity, insulin resistance, and diabetes. Two articles have investigated diet-induced obesity in animal models. Sastre et al. (pp. 1819–1830) have observed that aerobic exercise training increases nitrergic innervation function and decreases sympathetic innervation function in mesenteric arteries from rats with high fat diet-induced obesity. Toral et al. (pp. 1831–1844) report that proliferator-activated receptors-β/δ activation prevents obesity and exerts protective effects on hypertension and endothelial dysfunction in mice with high fat diet-induced obesity. In a 17-year follow-up study of 100 healthy young men, Skårn et al. (pp. 1845–1852) have investigated stability over time of clamp-derived insulin sensitivity and found baseline sensitivity had no significant correlation with values at follow-up, but that family history of hypertension and baseline triglycerides were significantly associated with future insulin sensitivity. Ushigome et al. (pp. 1853–1859) have performed a retrospective cohort study of patients with type 2 diabetes mellitus to investigate the relationship of progression of diabetic nephropathy with home SBP, and conclude that morning SBP lower than 120 mmHg were associated with the lowest progression of diabetic nephropathy. The implications of these observations for treatment recommendations are discussed by Coca and Doménech (pp. 1758–1760), who remark that the posthoc nonrandomized nature of this study makes it not robust enough to change guidelines on SBP targets for diabetic nephropathy, but should encourage researchers to design and perform appropriate randomized clinical trials.

The advantages of home blood pressure measurement are further illustrated in this issue by the publication of an Australian Expert Consensus Statement on this topic, which recommends that, when feasible, home blood pressure should be considered for routine use in the clinical management of hypertension (pp. 1721–1728). In another article dealing on blood pressure measurement techniques, Tokitsu et al. (pp. 1780–1790) find that bilateral measurement of brachial arterial pressure shows that interarm blood pressure differences were significantly higher in patients with coronary artery disease than in patients without.

The research group headed by Alan Y. Deng publishes the results of a further study on genetics of rat models of human polygenic hypertension with the identification of two candidate genes for two quantitative trait loci, which epistatically attenuate hypertension (Chauvet et al., pp. 1791–1801). Kiando et al. (pp. 1802–1810) have investigated the genetics of fibromuscular dysplasia, concluding for genetic heterogeneity and the unlikely existence of a major gene for this disease. As fibromuscular disease is often associated with renovascular hypertension, another article on renovascular hypertension published in the current issue of the Journal may be mentioned here: Goupil et al. (pp. 1931–1938) in a retrospective survey of patients with at least 60% renal artery stenosis and renal venous renin measurements report that positive stimulated lateralization ratios of renal venous renin positively associated with benefit from angioplasty.

Three studies are focused on hypertension-associated cardiac changes: Tadic et al. (pp. 1954–1961) describe the relationship between left ventricular deformation and different geometric patterns according to an updated classification; Szelényi et al. (pp. 1962–1969) have explored the mechanism of reduced longitudinal left ventricular function in hypertensive patients with normal ejection fraction; and Hung et al. (pp. 1922–1930) report that in aldosterone producing adenoma excess aldosterone induces cardiac diastolic dysfunction, which is reversible after surgery.

Finally, an article deals with an interesting pathophysiological aspect, namely, the intracranial pressure-cerebral hemodynamic interplay during prolonged apneas in healthy individuals (Wszedybyl-Winklewska et al., pp. 1811–1818); apnea was found to be associated with intracerebral pressure swings, closely reflecting changes in end-tidal CO2, heart rate, and peripheral blood pressure.

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