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17beta-estradiol reduces endothelin-1 release in women with ischaemic left ventricular dysfunction

Session Poster Session 1

Speaker Giuseppe M C Rosano

Event : Heart Failure 2016

  • Topic : valvular, myocardial, pericardial, pulmonary, congenital heart disease
  • Sub-topic : Pulmonary Hypertension
  • Session type : Poster Session

Authors : G M C Rosano (Rome,IT), O Gebara (Sao Paulo,BR), M Wajngarten (Sao Paulo,BR), JC Aldrighi (Sao Paulo,BR), JAF Ramires (Sao Paulo,BR)

Authors:
G M C Rosano1 , O Gebara2 , M Wajngarten2 , JC Aldrighi2 , JAF Ramires2 , 1San Raffaele Pisana Hospital IRCCS - Rome - Italy , 2Instituto do Coracao FMUSP - Sao Paulo - Brazil ,

Citation:
European Journal of Heart Failure Abstracts Supplement ( 2016 ) 18 ( Supplement 1 ), 44

Objectives: To assess whether acute administration of 17ß-estradiol influences pacing-induced cardiac release of endothelin-1 in female menopausal patients with ischaemic left ventricular dysfunction. Background: Endothelin-1 is a potent vasoactive peptide, estrogens decrease plasma levels of endothelin-1 and improve stress-induced myocardial ischemia in menopausal women with coronary artery disease. Methods. Thirty-two postmenopausal women with angiographically proven coronary artery were screened to enter a double blinded, placebo-controlled study. Selected were those with left ventricular dysfunction (LVEF <40%). Patients were sampled into the coronary sinus and aorta for endothelin-1 at baseline and after incremental pacing. After baseline study patients were randomized to receive either sublingual 17ß-estradiol (1 mg) or placebo and underwent the sampling protocol 20 minutes thereafter. Results: The time of onset of myocardial ischemia during pacing (AST > 1mm) was significantly increased by 17ß-estradiol (223+21 versus 296+15 seconds; The coronary sinus plasma levels of endothelin-1 were significantly reduced by estradiol administration but not by placebo, at each step of pacing protocol. The maximum reduction of endothelin-1 levels after E2 administration was noted at peak pacing (-0.19; -0.08, -0.3; 95% CI) while no changes were noted in patients allocated to placebo (-0.002; -0.06, -0.01; 95% CI). Similarly, aorto-coronary sinus difference was also significantly influenced by estradiol administration but not by placebo. Conclusion: Acute administration of 17ß-estradiol reduces pacing-induced cardiac release of endothelin-1 in postmenopausal women with ischaemic left ventricular dysfunction.

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