Low dose‐eplerenone treatment decreases aortic stiffness in patients with resistant hypertension
Vascular damage is aggravated in animal models of hypertension with mineralocorticoid (MR) excess and in hypertensive patients with primary hyperaldosteronism. MR antagonism has shown to provide effective blood pressure (BP)‐control in patients with treatment resistant hypertension (TRH), but the co...
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Published in | The journal of clinical hypertension (Greenwich, Conn.) Vol. 19; no. 7; pp. 669 - 676 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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United States
John Wiley and Sons Inc
01.07.2017
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Abstract | Vascular damage is aggravated in animal models of hypertension with mineralocorticoid (MR) excess and in hypertensive patients with primary hyperaldosteronism. MR antagonism has shown to provide effective blood pressure (BP)‐control in patients with treatment resistant hypertension (TRH), but the concurrent effects on the vasculature have not been examined. In a randomized, double‐blinded, placebo‐controlled parallel‐group study, 51 patients with TRH received either eplerenone 50 mg or placebo for 6 months together with additional antihypertensives titrated to achieve a BP target of <140/90 mm Hg. Pulse wave velocity (PWV), augmentation index (AIx), augmentation pressure (AP), AP normalized to a heart rate of 75/min (AP@HR75), renal resistive index (RRI), intima‐media thickness (IMT) and urinary albumin excretion rate (UAER) were assessed before and after treatment. PWV was reduced only with eplerenone (from 11.3±3.6 to 9.8±2.6 m/s, P˂.001), but not with placebo (10.3±2.0 to 10.1±1.8 m/s, P=.60), despite similar reductions in BP (−35±20/−15±11 mm Hg vs −30±19/−13±7 mm Hg, n.s.). Further, reductions in AP and AP@HR75 were greater with eplerenone, while changes in AIx, RRI, IMT and UAER were similar. Our data show that eplerenone beneficially affects markers of arterial stiffness and wave reflection in patients with TRH, independently of BP lowering. These data add to the evidence that MR antagonism should be the preferred treatment option in TRH. |
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AbstractList | Vascular damage is aggravated in animal models of hypertension with mineralocorticoid (MR) excess and in hypertensive patients with primary hyperaldosteronism. MR antagonism has shown to provide effective blood pressure (BP)‐control in patients with treatment resistant hypertension (TRH), but the concurrent effects on the vasculature have not been examined. In a randomized, double‐blinded, placebo‐controlled parallel‐group study, 51 patients with TRH received either eplerenone 50 mg or placebo for 6 months together with additional antihypertensives titrated to achieve a BP target of <140/90 mm Hg. Pulse wave velocity (PWV), augmentation index (AIx), augmentation pressure (AP), AP normalized to a heart rate of 75/min (AP@HR75), renal resistive index (RRI), intima‐media thickness (IMT) and urinary albumin excretion rate (UAER) were assessed before and after treatment. PWV was reduced only with eplerenone (from 11.3±3.6 to 9.8±2.6 m/s, P˂.001), but not with placebo (10.3±2.0 to 10.1±1.8 m/s, P=.60), despite similar reductions in BP (−35±20/−15±11 mm Hg vs −30±19/−13±7 mm Hg, n.s.). Further, reductions in AP and AP@HR75 were greater with eplerenone, while changes in AIx, RRI, IMT and UAER were similar. Our data show that eplerenone beneficially affects markers of arterial stiffness and wave reflection in patients with TRH, independently of BP lowering. These data add to the evidence that MR antagonism should be the preferred treatment option in TRH. Vascular damage is aggravated in animal models of hypertension with mineralocorticoid (MR) excess and in hypertensive patients with primary hyperaldosteronism. MR antagonism has shown to provide effective blood pressure (BP)-control in patients with treatment resistant hypertension (TRH), but the concurrent effects on the vasculature have not been examined. In a randomized, double-blinded, placebo-controlled parallel-group study, 51 patients with TRH received either eplerenone 50 mg or placebo for 6 months together with additional antihypertensives titrated to achieve a BP target of <140/90 mm Hg. Pulse wave velocity (PWV), augmentation index (AIx), augmentation pressure (AP), AP normalized to a heart rate of 75/min (AP@HR75), renal resistive index (RRI), intima-media thickness (IMT) and urinary albumin excretion rate (UAER) were assessed before and after treatment. PWV was reduced only with eplerenone (from 11.3±3.6 to 9.8±2.6 m/s, P˂.001), but not with placebo (10.3±2.0 to 10.1±1.8 m/s, P=.60), despite similar reductions in BP (-35±20/-15±11 mm Hg vs -30±19/-13±7 mm Hg, n.s.). Further, reductions in AP and AP@HR75 were greater with eplerenone, while changes in AIx, RRI, IMT and UAER were similar. Our data show that eplerenone beneficially affects markers of arterial stiffness and wave reflection in patients with TRH, independently of BP lowering. These data add to the evidence that MR antagonism should be the preferred treatment option in TRH. Abstract Vascular damage is aggravated in animal models of hypertension with mineralocorticoid ( MR ) excess and in hypertensive patients with primary hyperaldosteronism. MR antagonism has shown to provide effective blood pressure ( BP )‐control in patients with treatment resistant hypertension ( TRH ), but the concurrent effects on the vasculature have not been examined. In a randomized, double‐blinded, placebo‐controlled parallel‐group study, 51 patients with TRH received either eplerenone 50 mg or placebo for 6 months together with additional antihypertensives titrated to achieve a BP target of <140/90 mm Hg. Pulse wave velocity ( PWV ), augmentation index ( AI x), augmentation pressure ( AP ), AP normalized to a heart rate of 75/min ( AP @ HR 75), renal resistive index ( RRI ), intima‐media thickness ( IMT ) and urinary albumin excretion rate ( UAER ) were assessed before and after treatment. PWV was reduced only with eplerenone (from 11.3±3.6 to 9.8±2.6 m/s, P ˂.001), but not with placebo (10.3±2.0 to 10.1±1.8 m/s, P =.60), despite similar reductions in BP (−35±20/−15±11 mm Hg vs −30±19/−13±7 mm Hg, n.s.). Further, reductions in AP and AP @ HR 75 were greater with eplerenone, while changes in AI x, RRI , IMT and UAER were similar. Our data show that eplerenone beneficially affects markers of arterial stiffness and wave reflection in patients with TRH , independently of BP lowering. These data add to the evidence that MR antagonism should be the preferred treatment option in TRH . Vascular damage is aggravated in animal models of hypertension with mineralocorticoid ( MR ) excess and in hypertensive patients with primary hyperaldosteronism. MR antagonism has shown to provide effective blood pressure ( BP )‐control in patients with treatment resistant hypertension ( TRH ), but the concurrent effects on the vasculature have not been examined. In a randomized, double‐blinded, placebo‐controlled parallel‐group study, 51 patients with TRH received either eplerenone 50 mg or placebo for 6 months together with additional antihypertensives titrated to achieve a BP target of <140/90 mm Hg. Pulse wave velocity ( PWV ), augmentation index ( AI x), augmentation pressure ( AP ), AP normalized to a heart rate of 75/min ( AP @ HR 75), renal resistive index ( RRI ), intima‐media thickness ( IMT ) and urinary albumin excretion rate ( UAER ) were assessed before and after treatment. PWV was reduced only with eplerenone (from 11.3±3.6 to 9.8±2.6 m/s, P ˂.001), but not with placebo (10.3±2.0 to 10.1±1.8 m/s, P =.60), despite similar reductions in BP (−35±20/−15±11 mm Hg vs −30±19/−13±7 mm Hg, n.s.). Further, reductions in AP and AP @ HR 75 were greater with eplerenone, while changes in AI x, RRI , IMT and UAER were similar. Our data show that eplerenone beneficially affects markers of arterial stiffness and wave reflection in patients with TRH , independently of BP lowering. These data add to the evidence that MR antagonism should be the preferred treatment option in TRH . |
Author | Reinold, Annemarie Schwarz, Thomas K. Kalizki, Tatjana Schneider, Andreas Schneider, Markus P. Schmieder, Roland E. Schmidt, Bernhard M.W. Raff, Ulrike |
AuthorAffiliation | 1 Department of Nephrology and Hypertension University Hospital of the Friedrich‐Alexander‐University Erlangen‐Nürnberg Erlangen Germany 2 Department of Nephrology and Hypertension Hannover Medical School Hannover Germany 3 Divisions of Nephrology and Intensive Care Medicine Department of Internal Medicine University Hospital Würzburg and Comprehensive Heart Failure Center Würzburg Germany |
AuthorAffiliation_xml | – name: 1 Department of Nephrology and Hypertension University Hospital of the Friedrich‐Alexander‐University Erlangen‐Nürnberg Erlangen Germany – name: 2 Department of Nephrology and Hypertension Hannover Medical School Hannover Germany – name: 3 Divisions of Nephrology and Intensive Care Medicine Department of Internal Medicine University Hospital Würzburg and Comprehensive Heart Failure Center Würzburg Germany |
Author_xml | – sequence: 1 givenname: Tatjana surname: Kalizki fullname: Kalizki, Tatjana organization: University Hospital of the Friedrich‐Alexander‐University Erlangen‐Nürnberg – sequence: 2 givenname: Bernhard M.W. surname: Schmidt fullname: Schmidt, Bernhard M.W. organization: Hannover Medical School – sequence: 3 givenname: Ulrike surname: Raff fullname: Raff, Ulrike organization: University Hospital of the Friedrich‐Alexander‐University Erlangen‐Nürnberg – sequence: 4 givenname: Annemarie surname: Reinold fullname: Reinold, Annemarie organization: University Hospital of the Friedrich‐Alexander‐University Erlangen‐Nürnberg – sequence: 5 givenname: Thomas K. surname: Schwarz fullname: Schwarz, Thomas K. organization: University Hospital of the Friedrich‐Alexander‐University Erlangen‐Nürnberg – sequence: 6 givenname: Markus P. surname: Schneider fullname: Schneider, Markus P. organization: University Hospital of the Friedrich‐Alexander‐University Erlangen‐Nürnberg – sequence: 7 givenname: Roland E. orcidid: 0000-0003-2356-5883 surname: Schmieder fullname: Schmieder, Roland E. email: Roland.Schmieder@uk-erlangen.de organization: University Hospital of the Friedrich‐Alexander‐University Erlangen‐Nürnberg – sequence: 8 givenname: Andreas surname: Schneider fullname: Schneider, Andreas organization: and Comprehensive Heart Failure Center |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28211216$$D View this record in MEDLINE/PubMed |
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Snippet | Vascular damage is aggravated in animal models of hypertension with mineralocorticoid (MR) excess and in hypertensive patients with primary hyperaldosteronism.... Abstract Vascular damage is aggravated in animal models of hypertension with mineralocorticoid ( MR ) excess and in hypertensive patients with primary... Vascular damage is aggravated in animal models of hypertension with mineralocorticoid ( MR ) excess and in hypertensive patients with primary... |
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SubjectTerms | Aged aldosterone aortic stiffness Arterial Stiffness Blood Pressure Determination - instrumentation Carotid Intima-Media Thickness - instrumentation Coronary Vasospasm - drug therapy Coronary Vasospasm - physiopathology Double-Blind Method Eplerenone Female Humans hypertension Hypertension - drug therapy Hypertension - physiopathology Male Middle Aged Mineralocorticoid Receptor Antagonists - administration & dosage Mineralocorticoid Receptor Antagonists - pharmacology Original Paper Prospective Studies Pulse Wave Analysis - instrumentation pulse wave velocity Serum Albumin, Human - urine Spironolactone - administration & dosage Spironolactone - analogs & derivatives Spironolactone - pharmacology Vascular Stiffness - drug effects |
Title | Low dose‐eplerenone treatment decreases aortic stiffness in patients with resistant hypertension |
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