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Hypertension-related organ damage and cardiovascular risk

Zanchetti, Alberto

doi: 10.1097/HJH.0000000000000388

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 Milano, Italy. Tel: +39 02 50320484; e-mail:

Different aspects of hypertension-related organ damage and cardiovascular disease are the topics of a consistent number of articles in the present issue of the Journal of Hypertension.

Methodologies for evaluating microvascular structure in man are reviewed by Virdis et al. (pp. 2120–2129) on behalf of the Italian Society of Arterial Hypertension with a critical comparison of invasive approaches, substantially based on micromyography of biopsied small arteries, and noninvasive approaches, such as capillaroscopy and evaluation of the retinal vascular bed by scanning laser Doppler flowmeter. About the latter innovative methodology new supportive data are presented by an important article by Harazny et al. (pp. 2246–2252), reporting the results of two studies, a methodological one on the reliability of this technique for evaluating the pulsatility in the retinal circulation of man and a second one showing significant differences in pulsatile retinal capillary flow and structural parameters between patients with hypertension grades 1 and 2 and those with treatment-resistant hypertension.

Two studies have investigated arterial stiffness by pulse wave velocity (PWV) to provide clinically useful information. Fodor et al. (pp. 2238–2245) show that arterial stiffness is higher in patients with atherosclerotic renovascular hypertension than in patients with essential hypertension with similar levels of brachial blood pressure, and that treatment of renovascular hypertension fails to reduce PWV. Nilsson et al. (pp. 2152–2157) have explored the relationships between arterial stiffness, measured by PWV and cognitive function in a sample of the Malmö Diet and Cancer Study, and found an inverse association, which was markedly nonlinear, however, with individuals in the top decentile (PWV >13.8) explaining the association.

In a large Danish population-based setting Seven et al. (pp. 2231–2237) have studied the relations of 5-year changes in weight with blood pressure and insulin changes, and found that weight loss and, in particular, avoidance of weight gain play a role in reducing blood pressure and in prevention of hypertension. However, none of the insulin variables investigated were significantly associated with blood pressure, and the authors conclude that the role of insulin in hypertension may be smaller than previously thought. The relative impact of hypertension and obesity on coronary heart disease has been investigated by Rhéaume et al. (pp. 2224–2230) in a large population-based cohort representative of a contemporary European population. They find that abdominal obesity and hypertension have both independent and additive contributions to coronary heart disease risk.

If blood pressure has a role in the development of coronary disease, the reverse may also be true, as suggested by an article by Campbell et al. (pp. 2158–2165), who report that there is a J-curve relationship between the cardiovascular risk marker amino-terminal-pro-B-type natriuretic peptide (NT-proBNP) and DBP, but the association is explained by clinical variables, such as age and coronary heart disease rather than by blood pressure-lowering treatment. In an accompanying editorial, Rubattu and Volpe (pp. 2142–2143) develop on the implications that these data may have in explaining the increased cardiovascular risk often found with low DBP more by concomitant cardiovascular disease than by an effect of excessive blood pressure reduction.

Among the various consequences of coronary heart disease Radaelli et al. (pp. 2261–2266) describe a profound alteration of both heart rate and blood pressure variability similar to that occurring in chronic heart failure, but independent of myocardial infarction and left ventricular dysfunction, presumably ascribed to reduced baroreflex function. Finally, Raff et al. (pp. 2267–2276) report the results of a prespecified echocardiographic substudy of the Randomized Olmesartan And Diabetes MicroAlbuminuria Prevention (ROADMAP) trial, showing that the angiotensin receptor blocker olmesartan, compared with placebo, substantially delayed the development of left ventricular remodelling, as indicated by Cornell voltage QRS duration product, in type 2 diabetes.

A number of articles are focused on renal injury and sodium reabsorption. Sharkovska et al. (pp. 2211–2223) find that in a mouse model of type 2 diabetic nephropathy treatment with the dipeptidylpeptidase-4 inhibitor linagliptin delayed progression of renal damage in a glucose and blood pressure independent manner probably owing to attenuation of podocyte injury and inhibition of myofibroblast transformation. The incidental finding that the therapeutic use of the vascular endothelial growth factor antagonist sunitinib could induce hypertension has stimulated interest in its possible effects on renal vascular resistance and renal sodium reabsorption. In a rat model, Grisk et al. (pp. 2199–2210) report that sunitinib treatment caused an increase in renal vascular resistance and in renal sodium reabsorption, and that only the renal vascular effect, but not the increased sodium reabsorption, was prevented by Rho kinase inhibition, suggesting a direct action of sunitinib on the renal collecting duct. White et al. (pp. 2253–2260) have studied urinary sodium excretion separately during day and night, to assess the relative contribution of hypertension and obstructive sleep apnoea (OSA) on higher night-time than day-time urinary sodium excretion, and report that in hypertensive patients OSA exacerbates the reversal of the normal circadian sodium excretion pattern by increasing nocturnal urine sodium excretion, possibly via its blood pressure-elevating action. However, OSA does not affect nocturnal urine sodium excretion in normotensive individuals. Finally, Calò et al. (pp. 2109–2119) review the mechanisms by which angiotensin II signalling is involved in hypertension and related cardiovascular damage via insight provided by human models of endogenous angiotensin II signalling antagonism, the Bartter's and Gitelman's syndromes, conditions presenting themselves with a constellation of clinical findings that can be considered as the opposite of hypertension.

Two other articles in the current issue of the journal present data on important epidemiological problems. Liang et al. (pp. 2130–2141) have made a comprehensive survey and meta-analysis of studies investigating the role of air pollution, as signalled by exposure to PM2.5, on blood pressure, and find that exposure to PM2.5 had a statistically significant impact on blood pressure and the magnitude of the effect was such as to potentially have substantial clinical implications. Owing to conflicts in available evidence, Dratva et al. (pp. 2146–2151) have investigated the association of parity and blood pressure in a large (2837 individuals) women cohort, and report differential effects of parity on BP in older versus younger women: reduction in blood pressure in women younger than 40 years and increased blood pressure in women 60 years or older. As the authors remark, their finding cannot at the moment distinguish between mechanisms related to aging and birth cohort effects.

As obvious in a condition such as hypertension, defined by blood pressure measurements, problems related to blood pressure measurement are the objective of active research. In this issue, Holland and Lewis (pp. 2166–2170) report the results of a survey they had carried out in a variety of medical wards to observe measurement of blood pressure in patients confined to bed, observing a total lack of standardization and a failure to adhere to principles of measurement established for office blood pressure. The authors recommend that a task force be commissioned to develop universal guidelines for this important part of clinical assessment. Sheppard et al. (pp. 2171–2178) approach the important practical problem whether home blood pressure can be predicted by clinic blood pressure in such a way that the more laborious ambulatory or home measurements can be limited to only a number of patients and conclude that multiple SBP measurements in a single clinic in patients with treated hypertension appear to reasonably predict those unlikely to have a large white-coat or masked effect. In an accompanying commentary, Boivin and Fay (pp. 2144–2145) take issue with these conclusions, maintaining that out-of-office blood pressure measurement can hardly be avoided if the white-coat and masked effects must be avoided.

Recent progress in the genomics of hypertension has renovated interest in blood pressure heritability studies, especially when populations studied for a 25-year-period, such as in the Gubbio population study, are available. In this population Bonati et al. (pp. 2179–2187) have found not only a strong to moderate heritability of SBP and (to a lesser degree) DBP at baseline, but also of blood pressure variation over time (slope of blood pressure changes with age). They also report that shared environment exert a significant influence, but to a smaller extent. Environmental factors have been studied by Zhang et al. (pp. 2188–2198) in adult male rats. These authors have investigated the role of epigenetic mechanisms in the effects exerted by extrauterine growth restriction on pulmonary vascular endothelial function, and conclude that epigenetic dysregulation is a strong mechanism for propagating the cellular memory of early postnatal events, influencing the long-term susceptibility to pulmonary hypertension.

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Conflicts of interest

There are no conflicts of interest.

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