The October issue of the Journal of Hypertension includes reviews on different aspects of hypertension: aortic stiffness in old hypertensive patients, immune disorders in hypertension and heart failure, polypill treatment with antihypertensive and lipid-lowering drugs, cardiovascular effects of exposure to passive smoking and BP-lowering effects of exercise training. Onuh and Qiu (pp. 1871–1877) review recent progress on the factors responsible for aortic stiffening (metabolic alterations, neuroendocrine derangements, inflammation and their interaction) in the light of the possibility that large artery stiffening can be the main cause of hypertension in the elderly. Rai et al. (pp. 1878--1889) review the observations supporting that cellular immunity plays an important role in the initiation and progression of the vascular alterations that are found in hypertension and heart failure. Description is made of the monocyte, macrophage and cytokine infiltrates that have been shown to occur in animals and humans with a chronic blood pressure (BP) elevation, as well as of their association with degradation and fibrosis of the cardiac and vascular wall structure. Special attention is devoted to the role played by effector T-cell infiltrates. Coca et al. (pp. 1890--1898) discuss the advantages of the polypill for the treatment of hypertension, that is improved adherence to the treatment regimen with special attention to polypills that include antihypertensive agents, a lipid-lowering drug and low dose aspirin, which makes them suitable for secondary cardiovascular prevention in people with a history of cardiovascular events. Skipina et al. (pp. 1899--1908) review the studies that have addressed the cardiovascular effects of passive smoking and conclude that there is consistent evidence of its association with a chronic hypertensive state. The review also points out, however, that much more needs to be done in this area, with particular regard to the possible association between passive smoking and hypertension-related organ damage. Finally, Oliver-Martínes et al. (pp. 1909--1918) provide a meta-analysis of the studies that have addressed the BP-lowering effect of strength exercise training of moderate intensity. All types of training were associated with a BP reduction, particularly when there was no concomitant antihypertensive drug assumption and the exercise sessions were held three to seven times per week. Somewhat surprisingly, isometric exercises were more effective than dynamic exercises, although for both types of exercise, the BP-lowering effect became no longer significant after the training programme exceeded a 20-week duration. Exercise is regularly included among the lifestyle measures to be implemented in order to normalize BP when the BP elevation is modest or to help the BP-lowering effect of antihypertensive drugs when the BP increase is more marked. More information appears to be desirable on several aspects of this intervention, including the persistence of the effect over the long-term.
The following two articles are consensus documents on primary aldosteronism of the Working Group on Endocrine Hypertension of the European Society of Hypertension. The former article (Mulatero et al., pp. 1919–1928) focuses on the epidemiology and diagnosis of this condition, whereas the latter (pp. 1929--1936) deals exhaustively with its complications and treatment options. The point is made that primary aldosteronism is an underdiagnosed condition that represents a frequent cause of secondary hypertension with a high rate of complications and a significant contribution to hypertension-related morbidity and mortality. Both articles discuss the future directions of research in this field, an issue further addressed by the accompanying Editorial Commentary of Funder (pp. 1937--1939).
The next five articles deal with pregnancy (two articles) and hypertension in children and adolescents (three articles). Muijsers et al. (pp. 1948--1954) show that, compared with women without a history of early onset preeclampsia, women with a history of early onset preeclampsia exhibited higher high-sensitive cardiac troponin I levels, a further increase characterizing those with hypertension. Data were obtained 9–10 years after pregnancy, which justifies the suggestion that high-sensitive cardiac troponin I levels may represent a persistent marker of preeclampsia-generated cardiac damage. Orabona et al. (pp. 1955--1963) report that normotensive women with a pregnancy complicated by foetal growth restriction show, 6 months to 4 years later, evidence of cardiac dysfunction at speckle-tracing echocardiography, similarly to women with pregnancies complicated by preeclampsia. Thus, not only preeclampsia but also other pregnancy-related complications may lead to subclinical cardiac damage that may require close observation and perhaps treatment. Viering et al. (pp. 1964--1970) and Salazar-Tortosa et al. (pp. 1971--1979) address the genetic predisposition to children's renovascular hypertension and adolescents’ cardiovascular disease. In 37 children from a tertiary referral centre, exome sequencing was found to rarely identify the cause of renovascular hypertension, suggesting that nongenetic factors may play a more important role. Several individual polymorphisms and a haplotype of ADIPOQ gene were found to be significantly associated with risk factors for cardiovascular disease (lipids, risk score, weight, height, leptin, insulin, skinfold thickness and so on) in European adolescents, which provides evidence of a genetic predisposition. Both articles emphasize that in young individuals, genetic studies are rare and more information would thus be desirable. Ntineri et al. (pp. 1980--1988) show that, although values differed according to the calculation methods, in 136 adolescents (mean age 17 years), central 24-h mean BP was more closely associated with cardiac (left ventricular mass) and carotid (intima-media thickness) alterations than peripheral 24-h mean BP. These are important findings because so far evidence on the prognostic superiority of central vs. peripheral BP is limited, and data are especially scanty in young people in whom a peripheral BP elevation is accompanied by normal central BP values. Further comments on these findings and, more in general on the central-peripheral BP discrepancies in young people can be found in the Editorial Commentary of Grillo et al. (pp. 1940--1942).
The next eight articles all focus on the mechanistic and clinical aspects of hypertension-related organ damage. Skrabal et al. (pp. 1989--1999) describe a method that allows pulse wave velocity, and thus arterial stiffness, to be measured automatically during routine 12-channel ECG registration adapted to provide plethysmographic signals from the extremities and body composition from sequential multifrequency impedance measurements. Should, as it is concluded by Skrabal et al. (pp. 1989--1999), the measurements be sufficiently accurate and reproducible, this may facilitate acquisition of data that are important for assessment of organ damage in untreated and treated hypertensive individuals. Tomiyama et al. (pp. 2000–2007) show that at variance from isolated systolic or systo-diastolic hypertension, isolated diastolic hypertension is associated with no arterial stiffening but with an augmented wave reflection, which according to the authors may be the expression of isolated vascular damage. The Editorial Commentary of Ghiadoni (pp. 1943--1944) further addresses the nature of this condition that is seen mainly in young individuals and on which prognostic and therapeutic data are limited. Zanoli et al. (pp. 2008--2017) describe an increase of aortic pulse wave velocity, and thus large artery stiffness, in 86 consecutive patients with Crohn's disease compared with age-matched controls. There was also an association between pulse wave velocity and anxiety or depression, two well known characteristics of this disease, which according to the authors’ speculations, might reflect a vascular extension of the Crohn's inflammation as well as ‘brain-gut-vascular’ involvement via the sympathetic nervous system. Inflammation is also suggested to be a factor responsible for the results reported by Pietropaoli et al. (pp. 2018--2027) in 5396 adults from the NHANES database, in whom gingival bleeding caused by gingivitis and unstable periodontitis was independently associated with a 2.6 mmHg increase of SBP as well as with an increased risk of uncontrolled hypertension. Zhang et al. (pp. 2028--2035) show a relationship between carotid intima-media thickness and hypertensive retinopathy as diagnosed by the Keith-Wagener-Barker classification. Although this classification only provides semiquantitative data, this justifies the conclusion that there is a parallelism between structural changes of large and small vessels in hypertension. Pichler et al. (pp. 2036--2042) report that in patients with hypertensive heart disease, the extent of magnetic resonance derived cardiac fibrosis rather precisely mirrored left atrial diameter, left ventricular mass, left ventricular posterior wall thickness, left end-diastolic volume and even longitudinal strain, indicating a close connection between cardiac tissue fibrosis and structural or functional cardiac alterations. Molecular biomarkers of fibrosis were only marginally associated with myocardial strain and showed no association at all with cardiac magnetic resonance quantification of fibrosis, which leaves the significance of these measures uncertain. Yoo et al. (pp. 2043--2049) describe an association of BP lability, as identified by orthostatic hypotension or an increase of the standard deviation of nocturnal BP mean values, with a reduced volume of deep grey matter structures (magnetic resonance) in early nondemented patients with Parkinson's disease. This is in line with the multiple demonstration that short-term BP variability may adversely affect vital organ structure, leading in the long-term to an increased risk of cardiovascular events. Of course, the possibility of reversed causality, that is that brain structural alterations may alter BP control and cause an increased BP lability, should also be considered, although the choice of patients with early disease and no dementia makes this explanation unlikely. Mancia et al. (pp. 2050--2058) show that in the large number of high cardiovascular risk patients of the ONTARGET and TRANSCEND trials, visit-to-visit SBP variability had only a modest adverse effect on the risk of renal function deterioration, which in contrast showed a consistent and much greater increase with the increase of on-treatment mean BP values. This mirrors the results obtained in the same patients for the risk of cardiovascular outcomes, both studies favouring the conclusion that in patients treated with antihypertensive drugs visit-to-visit BP variations are prognostically less important than the average BP value during a long-term treatment period.
The final article of the October issue (Leite-Santos et al., pp. 2059--2073) focuses on the agreement and disagreement between hypertension guidelines as well as on the adaptability of internationally known guidelines to local medical realities, populations and environments. Among the eight guidelines selected by the authors as high quality, recommendations were frequently consistent, but disagreement was by no means marginal also on issues of major clinical relevance, such as BP threshold and target for drug treatment. Disagreement was more common among less selected guidelines and even high-quality guidelines scored low in the applicability domain, with a possible negative effect on their local adaptability. A further interesting insight into the multiple complex problems of the making of guidelines is provided by the Editorial Commentary of Steichen (pp. 1945--1947).
Conflicts of interest
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