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

IntroductionThe most here and nowant cause of morbidity and final stagerate in the developed nations is cardiovascualr indispositions . The data which has always been commonly perceived that women were realtively tolerant to cardiovascular diseases referable to the circulating o estrogens and progesterones , and subsequent ginmill of institutionalize menopausal cardiovascualr diseases by HRt is now being bit by bit challenged by reports from various trials . In retrospective studies , cardiovascular mortality in postmenopausal 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 HRT . Estrogen has been traditionally considered of import in maintenance of cardiovascular physiology . This was ideal to be due(p) to the prevention of heart disease by lowering curiosity lipoprotein cholesterin (LDL , increasing plasma levels of high density lipoprotein cholesterol (HDL , promoting coronary 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 disease (CHD ) is much little common in women than in men possibly due to the protective action of estrogen . However in a report from the US National Center for health Statistics (NCHS , 2003 , the death rates from CHD were actually fix to be higher in women than in men . In another 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 compared with 8 .3 in men hypertensive heart disease 21 .9 in both men 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 found increases in ejection fraction , 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 mass in women treated for more than 10 years with HRT .Fawsi etal corroborate in any case reported increased 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 receptors (ER . Thus these whitethorn be site of action of estrogen in HRT (Tolbert , 2001 ) ER has also been detected in cardiac myocytes and coronary arteries . An intersesting situatoin has been that ER were detected more frequently 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 plaque formation and the clotting process detroys the intima , leading to reduced receptor meanness , with the cosequent poor reaction of estrogen in post menopausal women who already hit atheroscelrosis (Tolbert , 2001 . This may be basis of the observations in the HERS trial , and WHI ( Women Health Initiative ) trial , where it was reported that postmenopausal HRT has both no role 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 , randomized 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 between groups for the particular outcome , nonfatal myocardial 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 flier this factor and whether the patients included in the trial were women with preexistant cardiac disease or not , since understandably the estrogen will have a much lesser role in women of the precedent 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 generate vasodilatation slip bys 5-20 min aft(prenominal) administration , thus it acts independent of genetic effects and is thus referred to as `nongenomic . Vascular injury as for example after 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 occur 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 size , while increasing distal coronary perfusion during both ischemia and reperfusio . ERT , which provides exogenous estrogen to postmenopausal women , increases the circulating estrogen concentration and significantly decreases the morbidity and mortality of coronary heart disease in these patients . Estrogens appear to be cardioprotective under ischemic conditions , probably due to improved vascular function . Estrogen adminstration also leads to reductions in (Fawsi , 2002 , Tolbert , 2006ConclusionThe mechanisms responsible for the cardiac effects of estrogen are not fully understood , but evidence suggests the role of enhanced NO release , effects on calcium handling and regulation of potassium currents . The long-term effects of estrogen are due to changes in cardiomyocyte gene expression , arbitrate by ER . The identity and effects of these target genes retain 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 encounter provided significant information on the role of HRT and dietetical intervention in middle-aged and elderly women . This study had major(ip) strengths and also major weaknesses . It became apparent from this and other similar studies that HRT may initially increase the risk of CHD events , but may have 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 Increase 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 Effects of Estrogen . AJH 2001 14 :186S-193S ...If you want to get a full essay, order it on our website: Ordercustompaper.com

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