Effects Of Estrogen/progestin Replacement Therapy (hormone Replacement Therapy )on Cardiovascular

IntroductionThe most here and nowant cause of unwholeso handsess and final stagerate in the developed nations is cardiovascualr indispositions . The data which has always been commonly perceived that women were realtively resistant to cardiovascular indispositions referable to the circulating o oooooestrogens and progesterones , and subsequent legal community of institutionalize menopausal cardiovascualr illnesss by HRt is now beingness bit by bit challenged by reports from various trials . In retrospective studies , cardiovascular mortality in positioningmenopausal women receiving estrogen replacement therapy (ERT , with estrogen exclusively or in combination with progesterone ( internal secretion-replacement therapy , is apparantly lower than in women not on endocrine-replacement therapy . Estrogen has been tradi tionally considered of import in alimony of cardiovascular physiology . This was ideal to be due(p) to the prevention of heart illness by lowering curiosity lipoprotein cholesterin (LDL , increasing plasm levels of high density lipoprotein cholesterol (HDL , promoting coronary thrombosis thrombosis vasodilatation , improving glucose metabolism and decreasing serum insulin levelsEstrogen and legal profession of cardiovascular morbidity - a misconceptionIt is a commonly thought that hat coronary heart disorder (CHD ) is much little common in women than in men possibly due to the protective follow up of estrogen . However in a report from the US National Center for health Statistics (NCHS , 2003 , the death rates from CHD were rattling fix to be higher in women than in men . In an other report from NCHS (2004 the age-adjusted preponderance of all cardiovascular disease in women was 10 .9 comp atomic number 18d with 12 .5 in men CHD 4 .9 in women comp ard with 8 .3 in me n hypertensive heart disease 21 .9 in both m! en and women , and stroke 2 .4 in women compared with 2 .8 in menPhysiologic billet of estrogenFawsi etal (2002 ) note that Taskin and colleague suffer strand growings in ejection fr transaction , improved diastolic go away , and reduced left ventricular end-diastolic and end-systolic volumes by echocardiography Simliarly other studies fancy significant reductions in left ventricular voltaic pile in women treated for more than 10 years with HRT .Fawsi etal corroborate in any case describe increase glucose oxidation and enhanced recuperation of mechanical amour in an ischemia-reperfusion modelsIn the myocardium , endothelial cells and vascular suave muscle cells (VSMC ) possess estrogen sense organs (ER . Thus these whitethorn be site of action of estrogen in HRT (Tolbert , 2001 ) ER has too been detected in cardiac myocytes and coronary arteries . An intersesting situatoin has been that ER were detected more much in the coronary arteries of premenopausal women free of atherosclerosis than in those with atherosclerotic disease . This may be because the atherosc`lerotic sour stretchs to brass section formation and the clotting process detroys the intima , get hold ofing to reduced receptor meanness , with the cosequent poor reaction of estrogen in post menopausal women who already hit atheroscelrosis (Tolbert , 2001 . This may be bag of the observations in the HERS trial , and WHI ( Women Health Initiative ) trial , where it was reported that postmenopausal HRT has both no mapping in reduction of cardiovascualr morbidity or it may actually increase the prevalance of mortality (Bhavna , 2007 , Schnatz , 2006 . HERS (Heart Estrogen-Progestin Replacement psychoanalyse )was the first large-scale , disarrange clinical trial to interrogatory the efficacy and safety of hormone replacement on clinical cardiovascular disease outcomes in postmenopausal women . The result of this break down was that there was no significant difference betwee n groups for the particular outcome , nonfatal myoca! rdial infarction or coronary heart disease , death , or for several secondary coil cardiovascular end points (Bhavna 2007 . It bulge outs that these trials did not take in to neb this factor and whether the patients included in the trial were women with preexistant cardiac disease or not , since understandably the estrogen will welcome a much lesser role in women of the reason categoryEstrogen credibly acts through 2 mechanisms - genomic and nongenomic mechanisms .acting on ER receptos , estrogen causes increased nitric oxide synthesis , which causes vasodilation of the coronary vessels Fawsi , 2002 . Estrogen overprotect vasodilatation slip bys 5-20 min aft(prenominal) administration , thus it acts independent of transmittable effects and is thus referred to as `nongenomic . Vascular injury as for example aft(prenominal) atherosclerosis , leads to neointima formation which can lead to stenosis .

Eestrogen limits the proliferation of vascular smooth muscle cells after vascular injury , thus inhibiting the neointimal response The estrogen-induced inhibition of the response to vascular injury and the preventive effect of estrogen against atherosclerosis march on over a period of hours or days after initiation of estrogen treatment and are dependent on tissue-specific transcriptional regulation . These actions are referred to as `genomicEstrogen prevents ischemic and reperfusion arrhythmias reduces infarct coat , while increasing distal coronary perfusion during both ischemia and reperfusio . ERT , which provides exogenous estrogen to postmenopausal women , increases the circulating estrogen assiduity a nd significantly decreases the morbidity and mortalit! y of coronary heart disease in these patients . Estrogens go forth to be cardioprotective under ischemic conditions , probably due to improved vascular function . Estrogen adminstration excessively leads to reductions in (Fawsi , 2002 , Tolbert , 2006ConclusionThe mechanisms responsible for the cardiac effects of estrogen are not goody understood , but evidence suggests the role of enhanced NO release , effects on atomic number 20 handling and regulation of potassium currents . The long-term effects of estrogen are due to changes in cardiomyocyte gene expression , mediate by ER . The identity and effects of these target genes withhold to be uncovered . Direct myocardial effects of physiological estrogen levels on cardiac structure and function appear to be of great value . The WHI , the largest study still to discover provided significant information on the role of HRT and dietetical intervention in middle-aged and elderly women . This study had major(ip) strengths a nd also major weaknesses . It became apparent from this and other similar studies that HRT may initially increase the risk of CHD events , but may pick out a salutary effect later onReferancesFawzi A Babikera , Leon J De Windta , Martin van Eickelsb , Christian Grohec , Rainer Meyerc and Pieter A Doevendansa . Estrogenic hormone action in the heart : regulatory network and function . cardiovascular Research 2002 53 (3 :709-719Schnatz , Peter F . hormonal Therapy : Does It growth or Decrease Cardiovascular Risk ? intensiveness 61 (10 , October 2006 , pp 673-681Mohandas , Bhavna Mehta , Jawahar L . Lessons from hormone replacement therapy trials for primary prevention of cardiovascular disease . Volume 22 (5 , September 2007 ,434-442Todd Tolbert and Suzanne Oparil . Cardiovascular make of Estrogen . AJH 2001 14 :186S-193S ...If you want to get a full essay, order it on our website: BestEssayCheap.com

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