title: Regression of myocardial hypertrophy after aortic valve replacement: faster in women?
abstract: BACKGROUND
  In patients with aortic stenosis, pressure overload induces cardiac hypertrophy and fibrosis. Female sex and estrogens influence cardiac remodeling and fibrosis in animal models and in men. Sex differences and their molecular mechanisms in hypertrophy regression after aortic valve replacement have not yet been studied.
  
  
  RESULTS
  We prospectively obtained preoperative and early postoperative echocardiography in 92 patients, 53 women and 39 men, undergoing aortic valve replacement for isolated aortic stenosis. We analyzed in a subgroup of 10 patients matrix gene expression in left ventricular (LV) biopsies. In addition, we determined the effect of 17β-estradiol on collagen synthesis in isolated rat cardiac fibroblasts. Preoperatively, women and men had similar ejection fraction. Similar percentages of women and men had increased LV diameters (37% and 38%). Women more frequently exhibited LV hypertrophy than men (women: 86%; men: 56%; P<0.01). Postoperatively, increased LV diameters persisted in 34% of men but only in 12% of women (P<0.023). LV hypertrophy reversed more frequently in women than in men, leading to a similar prevalence of LV hypertrophy after surgery (women: 45%; men: 36%). In surgical biopsies, men had significantly higher collagen I and III and matrix metalloproteinase 2 gene expression than women. In isolated rat cardiac fibroblasts, 17β-estradiol significantly increased collagen I and III gene expressions in male cells but decreased it in female cells.
  
  
  CONCLUSIONS
  Women adapt to pressure overload differently from men. Less fibrosis before surgery may enable faster regression after surgery.
authors.affiliation: Deutsches Herzzentrum Berlin, Berlin, Germany.
authors.forename: George
authors.initials: G
authors.lastname: Petrov
authors.forename: Vera
authors.initials: V
authors.lastname: Regitz-Zagrosek
authors.forename: Elke
authors.initials: E
authors.lastname: Lehmkuhl
authors.forename: Thomas
authors.initials: T
authors.lastname: Krabatsch
authors.forename: Anne
authors.initials: A
authors.lastname: Dunkel
authors.forename: Michael
authors.initials: M
authors.lastname: Dandel
authors.forename: Elke
authors.initials: E
authors.lastname: Dworatzek
authors.forename: Shokoufeh
authors.initials: S
authors.lastname: Mahmoodzadeh
authors.forename: Carola
authors.initials: C
authors.lastname: Schubert
authors.forename: Eva
authors.initials: E
authors.lastname: Becher
authors.forename: Hannah
authors.initials: H
authors.lastname: Hampl
authors.forename: Roland
authors.initials: R
authors.lastname: Hetzer
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D001021:Aortic Valve / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D001024:Aortic Valve Stenosis / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D002478:Cells, Cultured; D004958:Estradiol / Q000378:metabolism / Q000494:pharmacology; D004967:Estrogens / Q000378:metabolism / Q000494:pharmacology; D016326:Extracellular Matrix Proteins / Q000096:biosynthesis*; D005260:Female; D005347:Fibroblasts / Q000378:metabolism* / Q000473:pathology; D005786:Gene Expression Regulation; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009124:Muscle Proteins / Q000096:biosynthesis*; D011446:Prospective Studies; D019736:Prostheses and Implants; D051381:Rats; D017208:Rats, Wistar; D012727:Sex Characteristics; D012737:Sex Factors
chemical_list: D004967:Estrogens; D016326:Extracellular Matrix Proteins; D009124:Muscle Proteins; D004958:Estradiol