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Obesity and other aspects of hypertension

Zanchetti, Alberto

doi: 10.1097/HJH.0000000000000517
EDITOR'S CORNER

Istituto Auxologico Italiano and Centro Interuniversitario di Fisiologia Clinica e Ipertensione, Università di Milano, Milan, Italy

Correspondence to Professor 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/alberto.zanchetti@auxologico.it

A consistent group of papers in the present issue of the Journal of Hypertension is focused on the elusive problem of the relationship of obesity with hypertension and mortality. A consensus document of the two major scientific societies in the field – the European Association for the Study of Obesity and the European Society of Hypertension – approaches this elusive evidence, calling attention on the fact that there is a latency of decades between obesity onset and overt cardiovascular complications, and suggests risk estimation and management should not be based only on short-term risk (normally 10 years), but on over lifetime cardiovascular risk (pp. 425–434). A short-term alternative may be development of organ damage, on the assumption that this is an early step in the cardiovascular disease continuum, leading later on to diminished survival. In support of this hypothesis, Sabbatini et al. review available evidence on the association of adipokines, such as adiponectin, leptin and resistin, with arterial stiffness, which is a proven predictor of cardiovascular events (pp. 435–444). On the contrary, Tanamas et al. (pp. 542–545), analyzing prospective data from the Framingham Heart Study, found that the mechanism by which excess adiposity may increase blood pressure is primarily immediate, and long-term exposure to obesity does not further increase the risk of developing hypertension beyond the level of BMI attained. On the basis of another epidemiological study, using an adolescent subsample of a UK birth cohort, nonalcoholic fatty liver disease was not associated with higher central or peripheral blood pressure, once confounding for adiposity was taken into account (Patel et al., pp. 546–553).

A number of papers in the current issue deal with mechanisms of vascular and organ changes in hypertension. Two methodological studies by Segers et al. (pp. 554–563) and by Borlotti et al. (pp. 564–574) investigate mechanisms of pressure and flow aortic waves in a model of normal and coarctated aorta and, respectively, in the canine aorta. In an accompanying editorial, Westerhof and Westerhof (pp. 458–460) review the current debate on the validity of the reservoir-wave paradigm and conclude that data comparing the arterial information obtainable from the reservoir-wave paradigm, and the Windkessel and classical wave travel analyses are largely awaited. Mynard et al. (pp. 461–464), in an additional commentary, also cast doubt on the validity of the reservoir-wave model and call attention on a more complete model recently described. In another methodological paper, Bollache et al. (pp. 575–583) show the usefulness of phase-contrast cardiovascular magnetic resonance and carotid applanation tonometry in estimating aortic characteristic impedance, as complementary to the estimation of aortic geometry and stiffness.

Functional aspects of conduit and resistance arteries have been reviewed by Montero et al. (pp. 445–453) in a systematic search for articles evaluating smooth muscle function in the brachial artery or resistance arteries in older versus young healthy individuals. They show that aging reduces smooth muscle function, both in conduit and resistance arteries. In Chinese patients with type 2 diabetes, Li et al. (pp. 482–490) found that serum uric acid was closely associated with hypertension and metabolic syndrome, but, though carotid atherosclerosis was obviously associated with hypertension and metabolic syndrome, serum uric acid levels were not associated with carotid atherosclerosis.

Molecular and genetic mechanisms of hypertensive renal damage have been investigated by Skogstrand et al. (pp. 584–596), combining work in animal models of hypertension and in humans. Vink et al. (pp. 597–604) have used blood oxygen level-dependent MRI (BOLD-MRI) to determine noninvasively the renal oxygenation in humans, and Ratto et al. (pp. 605–611) report that left ventricular dilatation appears to be an independent predictor of subclinical renal damage. Shim et al. (pp. 612–620) found that an exaggerated blood pressure response to exercise is accompanied by a variable degree of left ventricular dysfunction, the association with arterial stiffening contributing to left ventricular function deterioration. Hypertension is also associated with a high susceptibility to increased blood pressure responses to noise exposure according to Chang et al. (pp. 634–643). In a large cohort of diabetic and nondiabetic patients with stable angina and total occlusion of at least one major coronary artery, Shen et al. (pp. 621–626) report that in diabetic, but not in nondiabetic patients, the incidence of poor collateralization was related to DBP in a U-shaped pattern, with the optimal collateralization in the 80–90-mmHg range.

Other areas of hypertension are dealt with by papers in the current issue of the Journal. An epidemiological paper focuses on prevalence and control of hypertension in Bangladesh, a world region in which little information on hypertension was so far available (Rahman et al., pp. 465–472). Another study (Cooper et al., pp. 473–481) investigates whether higher blood pressure in persons of African descent in the United States is attributable to genetic factors common to an African-origin population or to environmental exposures such as racial discrimination, and finds that African-origin populations with lower social status in multiracial societies, such as in the United States and South Africa, experience more hypertension than anticipated on anthropometric and socio-economic risk factors.

Davis et al. (pp. 499–506) report that an auscultatory hybrid sphygmomanometer is more accurate than an automatic oscillometric device in pregnancy when compared with a mercury sphygmomanometer. In a 5-year prospective study of a large cohort of hypertensive patients, Gavish and Bursztyn (pp. 491–498) found that systolic and diastolic 24-h variability, when related to heart period variability, are powerful independent predictors of all-cause mortality. These interesting data are commented by Angeli et al. (pp. 454–457), who review the different indices of blood pressure variability that have been proposed to improve cardiovascular risk stratification and prognosis.

A group of papers are focused on therapeutic aspects. Frenkel et al. (pp. 627–633) have explored the mechanisms by which thiazide diuretics may induce hyponatraemia. Chang et al. (pp. 634–643) have investigated the claim that treatment with angiotensin-converting enzyme inhibitors (ACEIs) might decrease the risk of pneumonia by following up patients receiving ACEIs or losartan for 5 years in the Taiwan's National Insurance Database, and reported treatment with ACEIs was not associated with a lower risk of pneumonia incidence and mortality as compared with losartan. Sakhuja et al. (pp. 644–652) have calculated how much the prevalence of uncontrolled hypertension diminishes in the National Health and Nutrition Examination Survey 2011–2012 by using the new blood pressure targets suggested by the Joint National Committee-8 guidelines and the European Society of Hypertension–European Society of Cardiology guidelines. Laurent et al. (pp. 653–662) report promising results from the use of a combination of perindopril and amlodipine.

Finally, a number of papers deal with pathophysiological issues: Krause et al. (pp. 515–524) have investigated whether arginase contributes to endothelial dysfunction in rats with chronic intermittent hypoxia; Ding et al. (pp. 525–533) have found that lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) affects autophagy and toll-like receptor (TLR4) expression in the brain of hypertensive mice; Fedorova et al. (pp. 534–541) report that plasma marinobufagenin is directly related to 24-h blood pressures, and a high-salt diet is accompanied by increased plasma marinobufagenin and marked salt sensitivity, but all these patterns are sex-specific, being present in men only.

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