Are the Eutrophic Effects of Angiotensin Receptor Blockers Real?

Abstract

HomeHypertensionVol. 48, No. 4Are the Eutrophic Effects of Angiotensin Receptor Blockers Real? Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBAre the Eutrophic Effects of Angiotensin Receptor Blockers Real? Flávio Danni. Fuchs Flávio Danni. FuchsFlávio Danni. Fuchs Division of Cardiology, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil Search for more papers by this author Originally published21 Aug 2006https://doi.org/10.1161/01.HYP.0000238605.34864.9fHypertension. 2006;48:E18Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: August 21, 2006: Previous Version 1 To the Editor:In a laborious experimental study, Savoia et al1 concluded that the addition of valsartan but not atenolol to the antihypertensive treatment decreased the resistance artery media/lumen ratio of diabetic patients. On the basis of such a finding, the authors suggest that it may be preferable to achieve tight blood pressure (BP) control by using angiotensin receptor blockers in addition to other antihypertensive agents to improve vascular structure and reduce cardiovascular risk in diabetic hypertensive patients. I do believe that this advantage was not clearly demonstrated in this study, and even if it was done, it could not be extended to other antihypertensive agents.The lower efficacy of atenolol in terms of prevention of cardiovascular events was demonstrated repeatedly in elderly patients.2 At least in this age group, atenolol should not be used anymore as first-line therapy or as a comparison drug in clinical trials.3 Probably most of the lower efficacy of atenolol in this setting is attributable to a lower BP-lowering effect in this age group, a phenomenon evident in the first 6 months of the Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure Lowering Arm trial.3 In the experiment of Savoia et al,1 patients were ≈60 years old, on the average, in the atenolol group. The authors assumed that BP did not vary between groups at the end of the experiment, but the data suggest the contrary. Systolic BP was 4.8 mm Hg lower in the valsartan group, and pulse pressure 2.4 mm Hg. The absence of formal statistical significance may be secondary to a β error, in view of the small sample size of the experiment. Moreover, similar office BP values may conceal substantial differences in BP along the 24-hour period, as was shown in the Heart Outcomes Prevention Evaluation trial.4My main point, however, is related to the statistical analysis of this experiment. The analysis based on the within-group statistics in experiments with 2 groups is questionable. The right approach seems to be to perform a between-group comparison of changes of variation in the media/lumen ratio or any other parameter or to use the significance of F value for the group/time interaction in repeated measurements and the multiple factors ANOVA procedure. In addition, the groups differed substantially in terms of potential confounding variables, such as age (patients in the atenolol group were 4.5 years older, on average), baseline diabetes control (worst in the valsartan group), and mainly BP at the end of and presumably during the experiment. An ANCOVA procedure for changes (after minus before values) of the media/lumen ratio controlling for confounding is required in this case to identify an independent drug effect. And finally, media thickness was unchanged in both groups after the experiment, showing that the effect, if any, was restricted to arteriolar lumen (again a trend, not statistically significant), in accordance with the between-group difference in BP.These shortcomings cast doubt on the internal validity of this experiment, which does not support the preference for any type of antihypertensive agent to reach tight BP control in patients with diabetes. The importance of the BP versus eutrophic effects of antagonists of the renin–angiotensin system is still an open issue and requires further clinical and experimental investigations.DisclosuresNone.1 Savoia C, Touyz RM, Endemann DH, Pu Q, Ko EA, De Ciuceis C, Schiffrin EL. Angiotensin receptor blocker added to previous antihypertensive agents on arteries of diabetic hypertensive patients. Hypertension. 2006; 48: 271–277.LinkGoogle Scholar2 Carlberg B, Samuelsson O, Lindholm LH. Atenolol in hypertension: is it a wise choice? Lancet. 2004; 364: 1684–1689.CrossrefMedlineGoogle Scholar3 Fuchs FD, Gus M, Ribeiro JP. ASCOT-BPLA [letter]. Lancet. 2006; 367: 205.CrossrefGoogle Scholar4 Svensson P, Faire U, Sleight P, Yusuf S, Östergren J. Comparative effects of ramipril on ambulatory and office blood pressures: A HOPE substudy. Hypertension. 2001; 38: e28–e32.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Fuchs F (2018) Prevention and Treatment Essentials of Hypertension, 10.1007/978-3-319-63272-8_4, (101-145), . Savoia C, Touyz R and Schiffrin E (2006) Response to Are the Eutrophic Effects of Angiotensin Receptor Blockers Real?, Hypertension, 48:4, (E19-E19), Online publication date: 1-Oct-2006. October 2006Vol 48, Issue 4 Advertisement Article InformationMetrics https://doi.org/10.1161/01.HYP.0000238605.34864.9fPMID: 16923991 Originally publishedAugust 21, 2006 PDF download Advertisement SubjectsACE/Angiotensin Receptors/Renin Angiotensin SystemRemodelingSmooth Muscle Proliferation and Differentiation