Research Journal of Pharmacology and Pharmacodynamics

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Significance of Estrogen in Acute Coronary Syndrome


Affiliations
1 Shri Sarvajanik Pharmacy College, Mehsana-384001, Gujarat, India
2 Shri Sarvajanik Pharmacy College, Mehsana, India
3 L. M. College of Pharmacy, Ahmedabad, India
4 Care Institute of Medical Sciences, Ahmedabad, India
     

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Estrogen, a cardioprotective agent, potentiates acetylcholine-induced increase in coronary blood flow, decreases coronary endothelin-1 levels, reduces ischemia, enhances fibrinolysis, shifts markers of coagulation toward hypercoagulability, and increases blood levels of matrix metalloproteinase-9, involved in plaque disruption and inflammatory markers like interleukin-6 and C-reactive protein. Rates of cardiovascular disease in women tend to rise during menopause, when estrogen level decreases. Hormone replacement therapy (HRT) provides exogenous estrogen to encounter the deficiency of estrogen into body, which demonstrates favorable cardioprotective effects, if initiated few years within the onset of menopause. However, use of HRT is controversial in preventing progression of the diseases at the later stages; since it cannot repair the damage already occurred. The therapy reduces the progression rate of atherosclerosis in post-menopausal women, who are not suffering from cardiovascular disease. However, in patients with cardiovascular disease or risk factors, estrogen therapy enhances cardiac events.

Keywords

Estrogen, Hormone Replacement Therapy, Cardiovascular Disease, Menopause.
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  • Pifarre R, Scanlon P, editors. Evidence-based management of the acute coronary syndrome. Philadelphia: Hanley and Belfus, Inc; 2001.

  • La Vecchia C. Sex hormones and cardiovascular risk. Hum Reprod.7; 1992:162-7.

  • Li Xiang-Ping, Zhou Yan, Zhao Shui-Ping, Gao Mei, Zhou Qichang, Li Yan-Sheng. Effect of endogenous estrogen on endothelial function in women with coronary heart disease and its mechanism. Clinica Chimica Acta. 339; 2004: 183-8.

  • Rossouw JE. Hormones, genetic factors, and gender differences in cardiovascular disease. Cardiovasc Res. 53; 2002: 550.

  • Baker L, Meldrum KK, Wang M, Sankula R, Vanam R, Raiesdana A, et al. The Role of Estrogen in Cardiovascular Disease. Journal of Surgical Research.115; 2003: 325-44.

  • Williams JK, Adams MR, Klopfenstein HS. Estrogen modulates responses of atherosclerotic coronary arteries. Circulation. 81; 1990: 1680-7.

  • Herrington DM, Braden GA, Williams JK, Morgan TM. Endothelial-dependent coronary vasomotor responsiveness in postmenopausal women with and without estrogen replacement therapy. Am J Cardiol. 73; 1994: 951-2.

  • Barrett-Connor E, Grady D. Hormone replacement therapy, heart disease, and other considerations. Annu Rev Public Health. 19; 1998: 55 - 72.

  • Grady D, Herrington D, Bittner V, et al for the HERS Research Group. Cardiovascular disease outcomes during 6.8 years of hormone therapy: Heart and Estrogen/Progestin Replacement Study follow-up (HERS II). J Am Med Assoc. 288; 2002:49-57.

  • Li Xiang-Ping, Zhou Yan, Zhao Shui-Ping, Gao Mei, Zhou Qichang, Li Yan-Sheng. Effect of endogenous estrogen on inhibition of human vascular smooth muscle cell proliferation by estrogens. Mol. Cell. Endocrinol. 219; 2004: 17-26.

  • Simpson ER, et al. Aromatase expression in health and disease. Recent Prog. Horm. Res. 199, 52, 185-213.

  • Bruch, H.R. et al. Androstenedione metabolism in cultured human osteoblastlike cells. J. Clin. Endocrinol. Metab. 75; 1992: 101-5.

  • Bayard F, et al. Oestrogen biosynthesis, oestrogen metabolism and functional oestrogen receptors in bovine aortic endothelial cells. Ciba Found. Symp. 191; 1995: 122-32.

  • Sasano H, et al. Aromatase and sex steroid receptors in human vena cava. Endocr. J. 46; 1999: 233-42.

  • Naftolin F, et al. The formation of estrogens by central neuroendocrine tissues. Recent Prog. Horm. Res. 31; 1975: 295-319.

  • Liao JK. Endothelium and acute coronary syndromes. Clinical Chemistry. 44, 8(B); 1998: 1799-1808.

  • Green S, Walter P, Kumar V, Krust A, Bornert JM, Argos P, Chambon P. Human oestrogen receptor cDNA: sequence, expression and homology to v-erb-A. Nature. 320; 1986: 134-9.

  • Flouriot G, Brand H, Denger S, Metivier R, Kos M, Reid G, Sonntag-Buck V, Gannon F. Identification of a newisoform of the human estrogen receptor alpha (hER-α) that is encoded by distinct transcripts and that is able to repress hER-α activation function 1. EMBO J. 19; 2000: 4688-700.

  • Mendelsohn ME, Karas RH. The protective effects of estrogen on the cardiovascular system. N Engl J Med. 340; 1999: 1801-11.

  • Miller AP, Xing D, Feng W, Fintel M, Chen YF, Oparil S. Aged rats lose vasoprotective and anti-inflammatory actions of estrogen in injured arteries. Menopause. 14; 2007: 251-60.

  • Nakamura Y, Suzuki T, Miki Y, Tazawa C, Senzaki K, Moriya T, et al. Estrogen receptors in atherosclerotic human aorta:

  • Grady D, Rubin SM, Petitti DB, Fox CS, Black D, Ettinger B, Ernster VL, Cummings SR. Hormone therapy to prevent disease and prolong life in postmenopausal women. Ann. Intern. Med. 117; 1992: 1016-37.

  • Caulin-Glaser T, Watson CA, Pardi R, Bender JR. Effects of 17β-estradiol on cytokine-induced endothelial cell adhesion molecule expression. J. Clin. Invest. 98; 1996: 36-42.

  • Mendelsohn ME, Karas RH. The protective effects of estrogen on the cardiovascular system. N. Engl. J. Med. 340; 1999: 1801-11.

  • Hayashi T, Yamada K, Esaki T, et al. Estrogen increases endothelial nitric oxide by a receptor mediated system. Biochem Biophys Res Commun. 214; 1995: 847-55.

  • Hayashi T, Esaki T, Sumi D, et al. Modulating role of estradiol on arginase II expression in hyperlipidemic rabbits as an atheroprotective mechanism. ProcNatlAcadSci U S A. 103; 2006: 10485-90.

  • Razmara A, Sunday L, Stirone C, Wang XB, Krause DN, Duckles SP, Procaccio V. Mitochondrial effects of estrogen are mediated by estrogen receptor alpha in brain endothelial cells. J. Pharmacol. Exp. Ther. 325; 2008: 782-90.

  • Rosano GMC, Webb CM, Chierchia S, et al. Natural progesterone, but not medroxyprogesterone acetate, enhances the beneficial effect of estrogen on exercise-induced myocardial ischemia in postmenopausal women. J Am CollCardiol. 36; 2000: 2154-9.

  • Rosano GMC, Caixeta AM, Chierchia S, et al. Short-term antiischemic effect of 17-estradiol in postmenopausal women with coronary artery disease. Circulation. 96; 1997: 2837-41

  • Guetta V, Quyyumi AA, Prasad A, Panza JA, Waclawiw M, Cannon RO. The role of nitric oxide in coronary vascular effects of estrogen in postmenopausal women. Circulation. 96; 1997: 2795-801.

  • Webb CM, Ghatei MA, McNeill JG, Collins P. 17-Estradiol decreases endothelin-1 levels in the coronary circulation of postmenopausal women with coronary artery disease. Circulation. 102; 2000: 1617-22.

  • Vehkavaara S, Silveira A, Hakala-Ala-Pietilla T, et al. Effects of oral and transdermal estrogen replacement therapy on markers of coagulation, fibrinolysis, inflammation and serum lipids and lipoproteins in postmenopausal women. Thromb Haemost. 85; 2001: 619-25.

  • Zanger D, Yang BK, Ardans J, et al. Divergent effects of hormone therapy on serum markers of inflammation in postmenopausal women with coronary artery disease on appropriate medical management. J Am CollCardiol. 36; 2000: 1797-802.

  • Falk E. Pathogenesis of atherosclerosis. J Am CollCardiol. 47(8); 2006: C7-12.

  • Kannel WB. The Framingham Study: historical insight on the impact of cardiovascular risk factors in men versus women. J Gend Specif Med. 5; 2002: 27-37.

  • Clarkson TB. Estrogen effects on arteries vary with stage of reproductive life and extent of subclinical atherosclerosis progression. Menopause. 14; 2007: 373-84.

  • Hulley S, Grady D, Bush T, Furberg C, Herrington D, Riggs B, Vittinghoff E. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart diseasein postmenopausal women. Heart and Estrogen/progestin Replacement Study (HERS) Research Group. JAMA. 280; 1998: 605.

  • MacLennan AH. Hormone replacement therapy: a 2008 perspective. Obstetrics, Gynaecology and Reproductive Medicine. 19(1); 2008: 13-8.

  • Tackett AH, Bailey AL, Foody JM, Carolynpperson-Hansen JM, Ohman EM, Hochman JS, et al. Hormone Replacement Therapy among Postmenopausal Women Presenting with Acute endothelial function in women with coronary heart disease and its mechanism. Clinica Chimica Acta. 339; 2004: 183-8.

  • Antonicelli R, Olivieri F, Morichi V, Urbani E, Mais M. Prevention of cardiovascular events in early menopause: A possible role for hormone replacement therapy. International Journal of Cardiology. 130; 2008: 140-6.

  • Post WS, Goldschmidt-Clermont PJ, Wilhide CC, et al. Methylation of the estrogen receptor gene is associated with aging and atherosclerosis in the cardiovascular system. Cardiovasc Res. 43; 1999: 985-91.


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  • Significance of Estrogen in Acute Coronary Syndrome

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Authors

Varunkumar Babulal Suthar
Shri Sarvajanik Pharmacy College, Mehsana-384001, Gujarat, India
Jigna S. Shah
Shri Sarvajanik Pharmacy College, Mehsana, India
Parloop A. Bhatt
L. M. College of Pharmacy, Ahmedabad, India
Sizan B. Patel
Care Institute of Medical Sciences, Ahmedabad, India

Abstract


Estrogen, a cardioprotective agent, potentiates acetylcholine-induced increase in coronary blood flow, decreases coronary endothelin-1 levels, reduces ischemia, enhances fibrinolysis, shifts markers of coagulation toward hypercoagulability, and increases blood levels of matrix metalloproteinase-9, involved in plaque disruption and inflammatory markers like interleukin-6 and C-reactive protein. Rates of cardiovascular disease in women tend to rise during menopause, when estrogen level decreases. Hormone replacement therapy (HRT) provides exogenous estrogen to encounter the deficiency of estrogen into body, which demonstrates favorable cardioprotective effects, if initiated few years within the onset of menopause. However, use of HRT is controversial in preventing progression of the diseases at the later stages; since it cannot repair the damage already occurred. The therapy reduces the progression rate of atherosclerosis in post-menopausal women, who are not suffering from cardiovascular disease. However, in patients with cardiovascular disease or risk factors, estrogen therapy enhances cardiac events.

Keywords


Estrogen, Hormone Replacement Therapy, Cardiovascular Disease, Menopause.

References