Abstract

HomeHypertensionVol. 63, No. 6Clinical Implications Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBClinical Implications Originally published1 Jun 2014https://doi.org/10.1161/HYPERTENSIONAHA.114.03613Hypertension. 2014;63:1137Eligibility for Renal Denervation (page 1319)Based on the SYMPLICITY studies and Conformité Européenne certification, renal denervation is currently applied as a novel treatment of resistant hypertension in Europe. However, information on the proportion of patients with resistant hypertension qualifying for renal denervation after a thorough workup and treatment adjustment remains scarce. This issue of Hypertension includes a study that aimed to investigate the proportion of patients eligible for renal denervation and the reasons for noneligibility at 11 expert centers participating in the European Network COordinating Research on renal Denervation in treatment-resistant hypertension (ENCOReD). The analysis included 731 patients. After careful screening and treatment adjustment at hypertension expert centers, only ≈40% of patients referred for renal denervation, mostly by specialists, were eligible for the procedure. The main reasons of noneligibility were normalization of blood pressure after treatment adjustment (46.9%), unsuitable renal arterial anatomy (17.0%), and previously undetected secondary causes of hypertension (11.1%). Our findings highlight that hypertension centers with a record in clinical experience and research should remain the gatekeepers before renal denervation is considered. Moreover, assuming that renal denervation would be efficacious in a large number of patients with a variety of conditions may be overly optimistic. This groundless belief might well explain why SYMPLICITY HTN-3 failed to reach its primary end point for efficacy.Download figureDownload PowerPointEstrogen Receptor-β and Intracranial Aneurysm Rupture (page 1339)Clinical observations suggest that postmenopausal women have a higher incidence of aneurysmal subarachnoid hemorrhage than premenopausal women. In addition, hormone replacement regimens that contain estrogen seem to reduce the risk for subarachnoid hemorrhage in postmenopausal women. These clinical observations led to the hypothesis that estrogen may protect against the development of intracranial aneurysm rupture (subarachnoid hemorrhage) in postmenopausal women. In this issue of Hypertension, Tada et al sought to establish the causal relationship between estrogen treatment and the prevention of aneurysmal rupture in postmenopausal mice. They used a mouse model of intracranial aneurysm. This model recapitulates the key features of human intracranial aneurysms, including spontaneous rupture. In ovariectomized female mice, estrogen significantly reduced the rupture rates. The protective effect of estrogen seemed to occur through the activation of estrogen receptor-β, a predominant subtype of estrogen receptor in human intracranial aneurysms and cerebral arteries. Estrogen’s unwanted effects are often attributed to its agonistic activity without tissue specificity. Selective estrogen receptor modulators can exert agonistic or antagonistic actions on estrogen receptor subtypes in a tissue-specific fashion. Findings from this study may become the basis for testing selective estrogen receptor modulators with a favorable tissue and receptor subtype specificity profile for the prevention of the growth and rupture of intracranial aneurysms in humans, particularly in postmenopausal women.Download figureDownload PowerPointCardiometabolic Risk at 5 Years (page 1326)The time immediately before and after birth may be a sensitive period related to programming cardiometabolic risk. The present prospective study, performed in children born at term after a noncomplicated pregnancy, shows that birth weight and postnatal weight gain exert independent influences on cardiometabolic parameters at 5 years of age. Although birth weight influenced the metabolic parameters, insulin levels, homeostatic model assessment index, and postnatal weight gain influenced both metabolic parameters and blood pressure values. Throughout the study, systolic blood pressure was related to weight gain, and at 5 years the heaviest children had the highest systolic blood pressure. Moreover, the highest values of insulin, homeostatic model assessment index, and triglycerides were related to both weight gain and current weight. Interestingly, small for gestational age children had the highest values of fasting insulin and homeostatic model assessment index and the lowest high-density lipoprotein. Therefore, it stands to reason that subjects smaller at birth who gain more weight have more risk for metabolic alterations, a fingerprint of early subtle adaptations in the glucose-insulin metabolism. Furthermore, a clustering of higher blood pressure values, insulin levels, and uric acid levels has been observed early in life, indicating the potential for increased cardiometabolic risk later on. This information provides a window of opportunity for intervention to avoid an unbalanced weight gain and to reduce the potential increment of cardiometabolic risk later in life.Download figureDownload PowerPoint Previous Back to top Next FiguresReferencesRelatedDetails June 2014Vol 63, Issue 6 Advertisement Article InformationMetrics © 2014 American Heart Association, Inc.https://doi.org/10.1161/HYPERTENSIONAHA.114.03613 Originally publishedJune 1, 2014 PDF download Advertisement

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