Gender (dis)advantages in cardiac remodeling; Female gender, myocardial remodelling and cardiac function
Many studies have shown that women with MI are usually diagnosed late during the course, are often misdiagnosed at first, are less likely to receive optimal medical care, and in many series their crude mortality is higher than men. This has lead to the idea that women are disadvantaged. Indeed they are disadvantaged if they are diagnosed late and if they are treated less aggressively (social disadvantage). The question whether they are biologically disadvantaged on the other hand is still debated. It is indeed plausible that female gender is protective toward adverse remodeling after MI.
After an insult (i.e. ischemia, infarct, pressure overload) the heart attempts to compensate by remodeling which usually entails hypertrophy of the walls and enlargement of cavity. This process although initially beneficial in maintaining an adequate cardiac output eventually leads to unfavorable outcome. It has been described that females (humans and animals) tend to have a prevalent hypertrophic response rather than dilatation of the cavity and this associated with preserved contractile function and overall better outcome. There may indeed be a gender-dependent difference in the pathway dominating the remodeling process. Several candidate molecules have been proposed but no definite data are available. An increased resistance to apoptosis in females is suggested.
The role of estrogens in gender-related differences in cardiac care is also complex. Estrogens play a major role in the difference in incidence of ischemic heart disease. As a general rule, premenopausal women have a more favorable lipid profile and are relatively protected from atherosclerosis which is however lost as time goes by after menopause. Estrogens however do not explain other differences in the outcome. The differences in remodeling seem to persist even when the role of circulating estrogens is limited (post-menopausal). The plot thickens as it has been shown that estrogens are not only produced in the ovaries which undergo failure at menopause but also in other organs such as the heart. Myocardial synthesis of estrogens has been demonstrated, and it remains not completely clear how it is affected by menopause. It is indeed possible that although the circulating levels of estrogens are low, the tissue levels may still be higher than men and mediate the beneficial effects. The data on this topic is scattered and inconclusive, and further studies are necessary.
Notes to editors:
This study was presented at the ESC Congress 2007 in Vienna
The European Society of Cardiology (ESC)
The ESC represents nearly 53,000 cardiology professionals across Europe and the Mediterranean. Its mission is to reduce the burden of cardiovascular disease in Europe.
The ESC achieves this through a variety of scientific and educational activities including the coordination of: clinical practice guidelines, education courses and initiatives, pan-European surveys on specific disease areas and the ESC Annual Congress, the largest medical meeting in Europe. The ESC also works closely with the European Commission and WHO to improve health policy in the EU.
The ESC comprises 3 Councils, 5 Associations, 19 Working Groups,
50 National Cardiac Societies and an ESC Fellowship Community
(Fellow, FESC; Nurse Fellow, NFESC). For more information on ESC
Initiatives, Congresses and Constituent Bodies see www.escardio.org.
European Society of Cardiology, The European Heart House 2035 Route des Colles, B.P. 179 - Les Templiers, Sophia Antipolis F-06903 France
About the Author(s)
Antonio Abbate, MD
Assistant Professor of Medicine
Department of Internal Medicine
Division of Cardiology - VCU Pauley Heart Center
Virginia Commonwealth University
Richmond, VA 23298
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