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J Am Coll Cardiol, 2010; 55:1057-1065, doi:10.1016/j.jacc.2009.09.065
© 2010 by the American College of Cardiology Foundation
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STATE-OF-THE-ART PAPER

Sex-Related Differences in Myocardial Remodeling

Maddalena Piro, MD, PhD*,*, Roberta Della Bona, MD*, Antonio Abbate, MD, PhD*,{dagger}, Luigi M. Biasucci, MD* and Filippo Crea, MD*

* Catholic University of the Sacred Heart, Rome, Italy
{dagger} VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, Virginia

Manuscript received February 13, 2009; revised manuscript received July 27, 2009, accepted September 1, 2009.

* Reprint requests and correspondence: Dr. Maddalena Piro, Catholic University of the Sacred Heart, Department of Cardiology, Largo A. Gemelli 8, Rome 00168, Italy (Email: prmarilena{at}tiscali.it).

Sex has a profound impact on myocardial remodeling, which is defined as the molecular and cellular events after an injury to the myocardium (i.e., necrosis, pressure overload, volume overload, and aging) leading to a change in shape, dimension, and function of cardiac chambers. Indeed, experimental studies and post-mortem and observational clinical studies suggest the presence of important differences in myocardial remodeling between females and males in response to different types of injures including aging, pressure and volume overload, and myocardial infarction. Interestingly, the remodeling process appears to be more favorable in women versus men; women are more likely to present heart failure with preserved systolic function and are at greater risk for low output syndrome acutely. These differences between men and women are widely held to be related to sex hormones such as estrogen, although the molecular effects of estrogen on ventricular cardiomyocytes are incompletely understood. In this review, we summarize the evidence supporting these notions and discuss the underlying mechanisms and the clinical implications.

Key Words: sex • myocardial remodeling • estrogen • cardiomyopathy

Abbreviations and Acronyms
  ANF = atrial natriuretic factor
  EF = ejection fraction
  EPC = endothelial progenitor cell
  ER = estrogen receptor
  IGF = insulin growth factor
  LV = left ventricle/ventricular
  LVH = left ventricular hypertrophy
  MI = myocardial infarction
  mRNA = messenger ribonucleic acid
  MSC = mesenchymal stem cell
  SHR = spontaneously hypertensive rat


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