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Highlights of the January issue

Mancia, Giuseppea,b

doi: 10.1097/HJH.0000000000002301
EDITOR'S CORNER
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aUniversità Milano-Bicocca, Milano

bPoliclinico di Monza, Monza, Italy

Correspondence to Prof Giuseppe Mancia, P.za dei Daini, 4, 20126 Milano, Italy. Tel: +39 3474327142; e-mail: giuseppe.mancia@unimib.it

The first issue of the Journal of Hypertension in 2020 includes two meta-analyses and a document of a Group of investigators and clinicians appointed by the Lancet to work on the improvement of the standards for blood pressure (BP) measuring devices around the world. Monticone et al. (pp. 3–12) review the available data on renal damage in patients with a primary aldosteronism of more than an 8-year duration. In a meta-analysis of 46 studies for a total of more than 6000 patients, primary aldosteronism was associated with an increased incidence and a more severe proteinuria compared with a control group of almost 10 000 patients with no aldosteronism-dependent hypertension. This suggests that, when generated by excessive aldosterone levels, hypertension is accompanied by a greater degree of renal damage than when it is due to other causes and mechanisms. Significantly, 1 year after medical or surgical treatment, the primary aldosteronism group exhibited a clear-cut reduction of urinary protein excretion, which implies that, even after a long term, the adverse influences of aldosterone on the kidney remain at least in part reversible with treatment. Kollias et al. (pp. 13–20) report the results of a large meta-analysis (more than 65 000 patients) on the prognostic role of office BP values in patients with atrial fibrillation and anticoagulant treatment. The authors emphasize that the methods by which office BP was measured were markedly heterogeneous and not standardized in most studies. Yet, and despite the notoriously lower accuracy of classical BP measurements in patients with atrial fibrillation, office BP exhibited a predictive value for the risk of stroke and systemic embolism, although not for major haemorrhagic events and all-cause mortality. The Lancet Commission on Hypertension (pp. 21–29) addresses the problem of the large use of BP measuring devices which have not been tested for accuracy according to established scientific standards. This includes not only office but also home devices as well as devices based on new technologies (e.g. cuffless sensors) whose accuracy is uncertain. Strong emphasis is placed on the urgent need to release adequate validating protocols and precise device testing and standardization procedures, in the meantime discouraging use of untested instruments even when based on new potentially interesting principles. The fight against hypertension, that is the first cause of death and burden of disease worldwide, cannot be effectively conducted without proper identification of the presence and extent of BP elevations and treatment-dependent reductions.

Two articles of the January issue are devoted to the epidemiology, and three to diagnostic aspects of hypertension. Yeung et al. (pp. 38–44) made use of the genetic material that was found to be related to glycated hemoglobin (HbA1c) in a large genome association study (n = 123 665) to investigate the relationship of HbA1c with the development of hypertension in the even larger UK Biobank database (n = 376 644). HbA1c was associated with the risk of new hypertension, and in some analyses also with actual BP values. This is ‘per se’ not new because the greater risk of diabetic patients to develop hypertension has been known for years. The study of Yeung et al. however, provides evidence that the diabetes–hypertension relationship has a genetic basis, and not just an origin from the progressive structural and functional small vessels abnormalities produced by the chronically deranged glucose metabolism. Further considerations on this issue can be found in the Editorial Commentary of Redon and Grau-Perez (pp. 30–32). In addition, converse evidence on this important issue is provided by Holtrop et al. (pp. 45–51) who show patients with resistant hypertension to have a significantly greater risk (+48%) of new onset type 2 diabetes mellitus than controls. According to the authors this suggests that resistant hypertension may represent a risk factor for the development of diabetes, although it remains to be clarified which diabetogenic features of resistant hypertension may be responsible, that is sympathetic hyperactivity or the high diuretic doses normally used in these patients.

Muiesan et al. (pp. 52–58) provide a detailed description of the prevalence, demography and clinical characteristics of patients admitted to the Emergency Department of the Brescia Hospital for an acute BP rise. Emphasis is placed on the high prevalence of organ damage and previous events exhibited by these patients as well as on the high rate of the inappropriate treatment strategies employed. Further interesting comments on this often overlooked aspect of hypertension are provided in the Editorial Commentary of Tocci et al. (pp. 33–34). Lamar et al. (pp. 59–64) report that, in about 1000 old patients, decision-making was influenced by BP values, a further compelling reason to try to improve their overall accuracy. Grandjean et al. (pp. 65–72) show that, in more than 11 000 patients, the combination of N-terminal-pro hormone BNP with the voltage of the R wave in lead aVL (RaVL) can stratify cardiovascular risk with an accuracy that outweighs the well known stratification based on echocardiographic calculation of left ventricular (LV) mass index. To obtain an echocardiogram is often far from being easy in medical practice and thus data in favour of a simplification of the diagnostic procedures are good news. This may especially be the case for stratification of cardiovascular risk which is still unfrequent in clinical practice.

The following six articles focus on organ damage. Perilhão et al. (pp. 73–81) report that, in spontaneously hypertensive rats, training lowered BP and that this was accompanied by an improvement of cardiac function and a reduction of cardiac structural abnormalities (including the amount of collagen in the cardiac walls) compared with sedentary animals. Hu et al. (pp. 82–94) show that both in-vitro and in-vivo shear stress (induced by a β2-dependent receptor signal) can improve the re-endothelialization capacity (i.e. cell proliferation) of endothelial progenitor cells from healthy individuals. This might help restoring vascular structure after vascular injuries. Park et al. (pp. 95–101) find that, in a Korean population, serum carbohydrate antigen was positively and independently associated with arterial stiffness and the degree of coronary artery calcification. Bello et al. (pp. 102–110) show that prevalence of cardiac damage (abnormal LV geometry) was related with the absolute awake and asleep SBP values rather than with the day-night BP changes. The importance of determining whether the well known protective effect of nocturnal BP on the risk of cardiovascular outcomes is related to BP dipping from the daytime awake values or the lower nocturnal absolute BP has been recently emphasized by a number of studies, which have also argued that these two variables may not change in parallel. That is, if daytime BP is high, even a marked BP dipping may not prevent a high nocturnal BP and vice versa. Hwang et al. (pp. 111–117) show that in young healthy individuals even a moderate alcohol consumption can lead to aortic stiffening. This is not surprising because alcohol increases sympathetic activity (in the study of Hwang et al. suggested by an increase of urinary norepinephrine) which has been found to increase large and medium artery stiffness possibly via contraction of smooth muscle cells (and increase of elastic modulus) in the vessel wall. Significantly, this occurs also with binge drinking, which is in line with the position of the recent European Hypertension guidelines that do not make a difference between the adverse consequences of binge and chronic drinking. Soulat et al. (pp. 118–126) report that global and segmental pulse wave velocity can be accurately assessed by 4D flow MRI, confirming and extending the evidence that this approach, and bioimaging in general, can provide information not only on large vessel structure but also on its function, in this case mechanical properties.

The remaining articles deal with pregnancy (two articles) and treatment (four articles). As far as pregnancy is concerned Mo et al. (pp. 127–132) provides a detailed description of the BP changes in the weeks preceding gestational hypertension, and shows that their magnitude bears a clear relationship with the onset of this condition. Weber-Schoendorfer et al. (pp. 133–141) report the greater risk of fetotoxicity of AT1 antagonists compared with angiotensin-converting enzyme-inhibitors, based on information available from the data-bases of six teratology information services. This is of considerable interest, although of limited relevance to practice, because both blockers of the renin–angiotensin system must not be prescribed in pregnant women as well as in women with child-bearing potential in whom no contraceptives are used. This issue is further discussed in the Editorial Commentary of Stabouli (pp. 35–37).

The four final articles on antihypertensive treatment address a variety of issues. Rea et al. (pp. 142–149) provide evidence from the large Lombardy data-bases that men are more adherent to antihypertensive drugs than women. This is not in line with a number of previous studies which reported the opposite to be the case. The present results, however, are based on a high number of individuals studied in a real-life setting, which make the conclusion robust. Del Pinto et al. (pp. 150–158) show that in treated hypertensive adults with vitamin D deficiency mean BP was slightly but significantly greater than in those with normal serum vitamin D levels, the difference extending to the percentage of people with treatment-related BP control. Braconnier et al. (pp. 159–166) provide the interesting observation that, in healthy participants to a cross-over designed study, high and low-sodium diets were associated with, respectively, higher and lower sodium contents in muscle tissues (23 Na MRI) and sweat (ionophoretic collection), the muscle and sweat sodium contents also exhibiting the expected relationship with plasma renin activity and aldosterone. These results expand basic knowledge on this matter. They also extend the potential means by which sodium intake can be measured in observational studies, in addition to the often criticized urinary sample measurements. Finally, Bokrantz et al. (pp. 167–175) provide a very large data-base on the association between exposure to different antihypertensive drugs and hip fracture (about 60 000 individuals and 2600 fractures). Compared with nondrug users, thiazide diuretics (alone or in combination) were accompanied by a reduction in the risk of fractures while the opposite was the case for loop diuretics (+23%). The readers will forgive me if I add that this is in line with a article published by our group in which elderly individuals from the general population starting treatment with a loop diuretic exhibited a significant increase in risk of hospitalization for hip fractures (which we attributed to excessive BP falls) during the 30 days after the beginning of treatment. These data emphasize the importance of providing information on treatment tolerability in real life settings, and not just in trials in which doctors’ expertise and close patients’ follow-up may minimize or mask some important treatment-related side effects.

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There are no conflicts of interest.

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