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Highlights of the July issue

Mancia, Giuseppe

doi: 10.1097/HJH.0000000000002144
EDITOR'S CORNER
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Università Milano-Bicocca, Milan, Italy

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

The July issue of the Journal of Hypertension starts with three meta-analyses. Cuspidi et al. (pp. 1312–1319) looked at the alterations of echocardiographic left ventricular geometry in prehypertension. In a total of 14 453 untreated individuals (6 studies) in whom blood pressure (BP) fit the definition of this condition the risk of a left ventricular abnormality was almost twice as large as that of normotensive individuals (n = 60 949), this being the case also when concentric remodelling, eccentric and concentric hypertrophy were separately analysed. Current hypertension guidelines only recommend drug treatment in a subgroup of individuals laying in the upper portion of the prehypertension BP range (patients with a high normal BP and a high or very high cardiovascular risk), but the evidence that in this condition structural cardiac changes with adverse prognostic significance are common suggests that a more interventional attitude deserves further discussion. López-Valenciano et al. (pp. 1320–1333) show that in 492 patients from 16 randomized trials, isometric resistance training lowered systolic BP by more than 5 mmHg, which is a respectable antihypertensive effect for a non-pharmacological treatment approach. This scores against the view that, because of its marked acute pressor effect, isometric exercise is not the ideal type of exercise for patients with hypertension. Piperidou et al. (pp. 1334–1343) report that, in 17 540 patients with type 2 diabetes made available by 15 randomized trials, administration of sodium-glucose-cotransporter (SGLT-2) inhibitors was associated with a pronounced reduction (−25%) of urinary protein excretion compared to placebo or an active control, the antiproteinuric effect being, as it may be expected, greater in patients with a greater baseline proteinuria. This extends information of the renal protection of these drugs, an effect that may, at least in part, depend on their ability to lower BP because BP reductions have a major renal protective effect. In the meta-analysis of Piperidou et al. systolic BP was more than 4 mmHg lower in patients treated with SGLT2-inhibitors than in controls.

The following five papers deal with the epidemiological aspects of hypertension. Rojek et al. (pp. 1350–1358) report that long-term exposure to aircraft noise was associated with a clear-cut increase of office (about 8 mmHg) systolic BP as well as with a small but significant increase in night-time BP, suggesting not only that that noise-related stress is pressogenic but also that it interferes with the BP effects of nocturnal sleep, which are notoriously protective for the cardiovascular system. Interestingly, there was also a noise-related increase of large artery stiffness, which may have passively originated from the BP increase (because of the relationship between arterial stiffness and BP levels) but also on sympathetic modulation and structural modifications of the vessel walls.Indeed, previous evidence is available that sympathetic activity exerts a stiffening influence on large and middle size arteries, independently on BP and possibly related to contraction of smooth muscle fibers in the middle layer of the vessels. Zoccali et al. (pp. 1359–1365) report that in patients with predialytic chronic kidney disease plasma concentration of neuropeptide Y is an independent predictor of cardiovascular outcomes, the predictive ability being stronger in younger than in older patients. Yamagishi et al. (pp. 1366–1371) show an association between BP and cardiovascular mortality in a large cohort (n = 27 728) of Japanese men and women, healthy at the start and followed for about 20 years. An interesting aspect of this study is that the association was seen in both untreated and treated individuals, although in the latter optimal or normal BP values were accompanied by a greater risk of mortality than high normal BP values, that is, by a J curve phenomenon. Ponto et al. (pp. 1372–1383) provide evidence from the Gutenberg Retinal Vein Occlusion study of an important association of retinal vein occlusion with cardiovascular risk factors such as hypertension, dyslipidemia, hyperhomocysteinemia and high levels of factor VIII both when collectively ad when individually considered. Eze et al. (pp. 1384–1392) report on the association between malaria and hypertension, an issue whose mechanistic rationale has recently been discussed in a number of papers. In a randomly selected cohort of about 1000 Ivorian individuals, however, the malaria-hypertension association was seen in participants with an elevation of body temperature, but not in those in whom body temperature was normal. The complexity of this issue and the need of studies of a longitudinal rather than only cross-sectional nature is further addressed by the editorial commentary of Volpe and Battistoni. Finally, two papers focus on the modifications of the hypertension prevalence originating from the lower BP threshold for the definition of hypertension of the 2017 ACC/AHA compared to the 2018 ESC/ESH guidelines. Analysing the results of a Spanish survey, Gijón-Conde et al. (pp. 1393–1400) show that, compared to the European guidelines, adoption of the ACC/AHA guidelines would increase the number of adult Spanish hypertensive patients by 5.3 million, with a 1.4 million increase of the candidates to antihypertensive treatment. Along the same line, Poudel et al. (pp. 1401–1410) show that the lower BP threshold for the definition of hypertension recommended by recent guidelines would result in a substantial increase in all hypertension phenotypes: white-coat, masked, sustained, uncontrolled, and day or night hypertension. This represents a considerable increase in the economic burden associated with a BP elevation, which may justify the search for less expensive treatment strategies, including a more effective implementation of lifestyle changes which have so far been plagued by the problem of a very low adherence.

Four papers of the July issue of the Journal of Hypertension deal with BP variability. Yu et al. (pp. 1411–1418) report that in a large number of Chinese patients with type 2 diabetes (n = 12 630) visit-to-visit BP variability was a risk factor for diabetic nephropathy, which confirms previous data from the ADVANCE and other studies. An additional interesting contribution of the study of Yu et al., however, is that diabetic nephropathy was more effectively predicted by the combined use of visit-to-visit BP variability and mean BP, in line with what has been recently reported for cardiovascular outcome in the high cardiovascular risk population of the ONTARGET-TRANSCEND trials. Palatini et al. (pp. 1419–1426) show that 24-h BP variability independently predicted cardiovascular events in young-to-middle age individuals screened for stage 1 hypertension, in whom its addition improved the prediction provided by other ambulatory BP indices. This expands previous evidence on the prognostic role of short-term BP variability to people in which event-based studies are made difficult by the low event rate, a problem that in the Palatini's study was in part overcome by a remarkably long (>15 years) follow-up. Ye et al. (pp. 1427–1436) describe the results of a study on the normotensive people of the Osahama population in whom an isolated elevation of morning BP was accompanied by left ventricular hypertrophy while Head et al. (pp. 1437–1447) report an association, limited to the female study component, between the morning BP surge and the risk of cardiovascular outcomes. This adds evidence in favour of the adverse prognostic value of the morning BP surge, although the issue remains somewhat controversial not only because of the negative conclusions of other studies but also because of the difficulty to precisely assess the slope of the BP rise from the sleep to the awake state when only few BP values collected at considerable time intervals are available.

The following eight papers address diagnostic aspects (four papers) and secondary hypertension (four papers). On the diagnostic side Soulat et al. (pp. 1448–1454) describe the measurement of brachial and central pulse pressure values during MRI examinations, an improvement of data acquisition that can improve the quantification of aortic distensibility. Tan et al. (pp. 1455–1462) show that carotid ultrasonography allows to identify an increased volume of the carotid body, which in their study was strongly associated with hypertension, but also present in other conditions, such as heart failure, smoking, pulmonary disease, etc. A carotid body hyperactivity has been implicated in the increased sympathetic drive that characterizes many hypertensive individuals, which makes the observation of Tan et al. intriguing and worthy of further studies. One of these studies might try to correlate the increased carotid body volume detected by echocardiography with the sympathetic activity measured by microneurography or other methods to determine whether the structural carotid body abnormality translates into greater reflex sympathetic influences. Wang et al. (pp. 1463–1466) provide the important observation that, in the 3233 patients with intracerebral haemorrhage of the INTERACT trial, a high admission BP was more closely associated with factors indicating an activation of the sympathetic nervous system (eg heart rate) than with the hematoma location or the mass effect. Horjus et al. (pp. 1467–1474) show that in more than 3600 women the plasma creatine kinase activity measured in early pregnancy was associated with the BP values throughout the pregnancy duration as well as with the occurrence of gestational hypertension. This extends to pregnancy the relationship of hypertension with plasma creatine kinase described for the general population and it also increases the number of potential measurements that may help prediction and thus alert against gestational problems.

The four papers on secondary hypertension deal all with the adrenal gland. Tatsi et al. (pp. 1475–1481) report a novel mutation in the glucocorticoid receptor gene (NR3C1) as a cause of severe glucocorticoid resistance in a young woman with signs of mineralocorticoid excess, androgen excess and hypertensive encephalopathy, in whom high doses of dexamethasone (14 mg/day) successfully controlled BP and symptoms. The case is commented, in both its specific and more general aspects, by Funder (pp. 1347–1349). Araos et al. (pp. 1482–1492) report on the role of dendritic cells for some of the effects of mineralocorticoid receptor activation, such as cardiovascular fibrosis. Nagasawa et al. (pp. 1493–1499) provide an analysis of a large number of patients with primary aldosteronism (n = 2122), which supports use of ACTH-stimulated adrenal venous sampling to minimize the confounding effect of treatment with blockers of the renin-angiotensin-aldosterone system (often not discontinuable for safety reasons) for the diagnostic value of the laterality index and the prediction of the effect of adrenalectomy. Wu et al. (pp. 1500–1512) evaluate the methodological quality and implementability of guidelines for the management of primary aldosteronism. The quality of the 12 guidelines examined is described as mostly poor and discrepant in general and even on specific clinical problems, leading to the advice to develop and adhere, in the future, to better diagnostic and treatment recommendations.

Finally, two papers address treatment aspects. Katabami et al. (pp. 1513–1520) compared the effect of unilateral adrenalectomy and medical treatment by mineralocorticoid receptor antagonists in 339 patients with primary aldosteronism. Over a 6-month follow-up, clinical and biochemical outcomes were better in surgically treated patients, adrenalectomy thus being regarded as the better option than continuing drug use. Desjardins et al. (pp. 1521–1528) show that, as reported in the past, 1) kidney transplantation can quickly improve the marked aortic stiffening associated with chronic kidney disease and 2) this may not just be the consequence of the reduced BP of the transplanted patients but perhaps also of a modification of the intrinsic mechanical properties of the aorta that leads to destiffening. A disappointing observation, however, is that the early destiffening was followed by a later large artery restiffening that the authors suggest to be due to an activation of the immune system of the kidney recipients that adversely affected the arterial wall structure.

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