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Highlights of the May issue

Mancia, Giuseppe

doi: 10.1097/HJH.0000000000002117
EDITOR'S CORNER
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Università Milano-Bicocca, Milan, Italy

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

The May issue of the Journal of Hypertension starts with three reviews on the epidemiological, diagnostic and treatment aspects of high blood pressure (BP). Hamoen et al. (pp. 865–877) provide an overview of the studies which analyzed the ability of different multivariable models to predict in children the risk of adulthood hypertension. Several models are reported to possess a predictive value, the BP and BMI of the children being the most common individual predictors. According to the authors, however, limited information on performance, lack of external validation and other drawbacks make the practical value of all models unclear, emphasizing the need for additional studies. De Becker et al. (pp. 878–883) review the environmental and genetic factors responsible for a rise in serum uric acid as well as for its adverse epidemiological consequences, in particular an increased risk of hypertension and of renal structural and functional abnormalities. Emphasis is placed on the fact that, largely because of dietary factors and metabolic abnormalities, hyperuricemia affects one out of five adults, justifying the recommendation to implement lifestyle changes that may keep serum uric acid within the normal range, especially in young hypertensive patients or normotensive individuals with metabolic problems or hypertensive parents. Katsi et al. (pp. 884–901) provide a detailed overview of the evidence that links antineoplastic chemotherapy with the development of hypertension. Several classes of antineoplastic drugs (endothelial growth factor inhibitors, proteasome inhibitors, cisplatin derivatives) as well as radiotherapy appear to be associated with either new onset hypertension or with a clinically significant BP increase in patients with previous BP control by treatment. Attention is directed to the need to take this phenomenon into serious consideration by appropriate antihypertensive treatment measures, also to reduce other chemotherapy-related inconveniences, such as cardiotoxicity, which carries greater adverse consequences in patients with a higher cardiac afterload.

Few original articles address diagnostic aspects of hypertension. Asayama et al. (pp. 905–916) summarize, in a Consensus Document co-authored by experts from Asia, Europe and the USA, the evidence validating home nocturnal BP measurements vis-à-vis the traditional measurements obtained by ambulatory BP monitoring, including the detection of the nondipping pattern. Given the prognostic importance of nocturnal hypotension, this represents an important finding, which will favour the assessment of nighttime BP in clinical practice. It will also allow to replicate nocturnal BP measurements within patients, which will cope with the problem of the limited dipping/nondipping reproducibility, that is, the fact that many patients diagnosed as dippers on one occasion become nondippers on the next occasion or vice versa. Stabouli et al. (pp. 917–922) assessed the ability of the simplified BP classifications provided by US and European pediatric guidelines to properly identify children's and adolescents’ high BP levels in a cohort of approximately 3000 Greek individuals. Although the performance of all classifications was reasonably good, false positive results were by no means uncommon, emphasizing that use of these tables requires attention not to overlook individuals eligible for further BP evaluation. Cremer et al. (pp. 923–927) show that in elderly hypertensive patients, use of home BP measurements in both the sitting and the standing position is associated with a much more common detection of orthostatic hypotension than measuring BP in the office environment only (37% vs. 15%). This is of obvious clinical relevance because in older patients, orthostatic hypotension is associated with a higher incidence of injurious falls as well as with an overall greater adverse prognosis. Börschel et al. (pp. 928–934) show that in more than 15 000 individuals from the population-based Guthenberg Health Study, atrial fibrillation was associated with peripheral vascular abnormalities, such as a reduced flow-mediated dilatation, a higher brachial artery diameter and an abnormal pulse pressure amplitude. The association, however, disappeared after adjustment for age and classical risk factors, indicating no direct connection between this arrhythmia and peripheral vascular damage.

Three original articles of the May issue deal with the epidemiology of hypertension. Ishida et al. (pp. 935–941) show that, in 1344 participants with no hypertension at baseline, the ankle–brachial index value was independently associated, over a 47-month follow-up, with the yearly change of SBP as well as with the incidence of hypertension. This links this measure of large artery structural alterations with the time-related increase of BP. Courand et al. (pp. 942–948) report that in the OLD-HTA Lyon cohort of hypertensive individuals, dizziness did not have any clear prognostic significance except for vertigo, which was associated with a risk of fatal stroke that was more than twice that seen in patients without dizziness or with dizziness other than vertigo. Mariampillai et al. (pp. 949–955) report that in apparently healthy men an increase of SBP greater than 180 mmHg during bicycle exercise was associated with an increase in the risk of coronary disease, regardless the resting BP values and the concomitance of classical coronary risk factors. The importance of this finding lies not only in the unusually long follow-up of the patients (28 years), but also in the fact that this finding clearly scores in favour of the prognostic value of exercise BP, thereby challenging the position taken by several hypertension guidelines, which do not consider exercise BP as a useful addition to resting BP measurements in the diagnosis of hypertension and the quantification of cardiovascular risk.

The subsequent seven articles address the mechanistic determinants of organ damage (four articles), and pre-eclampsia (three articles). Zieff et al. (pp. 956–963) report the results of a study in which various measures of brachial artery stiffness were collected with the arm above, below or at the heart level. All measures showed a clear-cut relationship with the arm position, emphasizing that, because stiffness is highly pressure dependent, measurements need to standardize this factor to properly compare values between and within studies. Li et al. (pp. 964–971) show that the atherosclerotic lesions induced in a common carotid artery of mice by placing a collar around the vessel exhibited a greater stability if the animals were previously given melatonin, an effect at least in part explained by the effects of the drug on vascular smooth muscle cells. Hu et al. (pp. 972–984) show, also in mice, that the endothelial repair that followed carotid artery injury was enhanced by hydrogen sulfide (a gasotransmitter involved in vascular homeostasis), due to an increased mobilization of nitric oxide from endothelial progenitor cells. Olson et al. (pp. 985–996) describe the protective effect (reduction of oxidative stress and BP) of transgenic overexpression of glutathione s-transferase μ-type 1 in the SHRSP rat. Finally, Melton et al. (pp. 997–1011), Raio et al. (pp. 1012–1017) and Marozio et al. (pp. 1018–1022) address the mechanisms responsible and/or predictive of preeclampsia with a number of interesting results. Namely, that the increase of C-reactive protein and arterial stiffness in preeclamptic women depend on genetic factors but also on factors such as inflammation, whose measurement may perhaps offer additional markers of the development of this condition.

Six articles of this issue of the Journal deal with treatment of hypertension. Hohneck et al. (pp. 1023–1031) show that in patients with stable coronary heart disease reducing heart rate by ivabradine is accompanied by a reduction of arterial stiffness and an increase of endothelium-dependent vasodilation. This provides a pathophysiological background to the data that show heart rate to be an independent predictor of cardiovascular outcomes, an observation previously made by experimental and human studies that showed arterial distensibility to directly relate to heart rate changes by pacing. Kjellberg et al. (pp. 1032–1039) show that in 421 consecutive patients admitted to the stroke unit for an acute cerebrovascular event SBP decreased steeply over the first 2 days, with no difference between different stroke types and no effect of age. There was also no relationship between the SBP decrease and the antihypertensive treatment administered over the first 7 days after the acute event. This expands previous findings and further emphasizes the difficulties posed by this varying poststroke BP pattern to the studies that aim at assessing the effect of BP-lowering interventions on patient outcome. Smith et al. (pp. 1040–1047) report that patients with resistant hypertension frequently exhibit neurocognitive impairment, the reduced performance being worse in those with low aerobic fitness, more deranged microvascular function and a worse cerebral or metabolic cardiovascular risk profile. Overgaauw et al. (pp. 1048–1057) show that, among patients admitted to the emergency department for a hypertensive emergency or urgency, nonadherence to antihypertensive treatment is a frequent finding. Rueda-Ochoa et al. (pp. 1058–1069) provide a post hoc analysis of the SPRINT data which shows that, although intense BP-lowering treatment reduced the risk of the primary outcome in the early treatment phase the benefit was subsequently lost in many patients, e.g. women, blacks, patients with chronic kidney diseases and very elderly individuals in whom the outcome reduction was outnumbered by an increase of serious adverse effects. As emphasized in the Editorial Commentary of Kjeldsen et al. (pp. 902–904), this adds ammunition to those who hold a critical view of the conclusion that the lower BP target achieved in the trial is invariably beneficial. Sarma et al. (pp. 1070–1076) provide evidence that in almost 700 men with type 1 diabetes who did not use antihypertensive medications and had no erectile dysfunction at baseline, a 16-year follow-up revealed the risk of erectile dysfunction to be independently related to the SBP value, which argues in favour of the potential benefit of early BP control.

The last two articles deal with the diagnosis and treatment of primary aldosteronism. Takeda et al. (pp. 1077–1082) report the results obtained in about 2000 patients with primary aldosteronism in whom adrenal vein sampling was performed during the administration (bolus, infusion or bolus and infusion) of ACTH. ACTH loading decreased the lateralization indices and had no effect on outcomes, questioning its usefulness as a diagnostic procedure. Kishimoto et al. (pp. 1083–1095) describes the effect of a 12-week administration of eplerenone in patients with idiopathic hyperaldosteronism. The drug decreased the aldosterone–renin ratio and had some favourable effect on microvascular and macrovascular functions without reducing, however, BP, which is compatible with the possibility that direct vascular effects of a reduced concentration of tissue aldosterone were involved.

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Conflicts of interest

There are no conflicts of interest.

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