Trends in Cardiovascular Medicine
Volume 16, Issue 8 , Pages 285-291 , November 2006

Heart Hypertrophy During Pregnancy: A Better Functioning Heart?

  • Mansoureh Eghbali

      Affiliations

    • Department of Anesthesiology, Division of Molecular Medicine, David Geffen School of Medicine at University of California–Los Angeles, Los Angeles, CA 90095-7115, USA
  • ,
  • Yibin Wang

      Affiliations

    • Department of Anesthesiology, Division of Molecular Medicine, David Geffen School of Medicine at University of California–Los Angeles, Los Angeles, CA 90095-7115, USA
    • Department of Medicine, David Geffen School of Medicine at University of California–Los Angeles, Los Angeles, CA 90095-7115, USA
  • ,
  • Ligia Toro

      Affiliations

    • Department of Anesthesiology, Division of Molecular Medicine, David Geffen School of Medicine at University of California–Los Angeles, Los Angeles, CA 90095-7115, USA
    • Department of Molecular and Medical Pharmacology, David Geffen School of Medicine at University of California–Los Angeles, Los Angeles, CA 90095-7115, USA
    • Brain Research Institute, David Geffen School of Medicine at University of California–Los Angeles, Los Angeles, CA 90095-7115, USA
  • ,
  • Enrico Stefani

      Affiliations

    • Department of Anesthesiology, Division of Molecular Medicine, David Geffen School of Medicine at University of California–Los Angeles, Los Angeles, CA 90095-7115, USA
    • Department of Physiology, David Geffen School of Medicine at University of California–Los Angeles, Los Angeles, CA 90095-7115, USA
    • Brain Research Institute, David Geffen School of Medicine at University of California–Los Angeles, Los Angeles, CA 90095-7115, USA
    • Corresponding Author InformationAddress correspondence to: Dr. Enrico Stefani, Department of Anesthesiology, University of California–Los Angeles School of Medicine, BH-520A CHS, Box 957115, Los Angeles, CA 90095-7115, USA. Tel.: (+1) 310-794-7808; fax: (+1) 310-825-6649.

References 

  1. Adams JW, Sakata Y, Davis MG, et al. Enhanced Galphaq signaling: a common pathway mediates cardiac hypertrophy and apoptotic heart failure. Proc Natl Acad Sci U S A. 1998;95:10140–10145
  2. An WF, Bowlby MR, Betty M, et al. Modulation of A-type potassium channels by a family of calcium sensors. Nature. 2000;403:553–556
  3. Aoyagi T, Fujii AM, Flanagan MF, et al. Maturation-dependent differences in regulation of sarcoplasmic reticulum Ca(2+) ATPase in sheep myocardium in response to pressure overload: a possible mechanism for maturation-dependent systolic and diastolic dysfunction. Pediatr Res. 2001;50:246–253
  4. Babiker FA, Lips D, Meyer R, et al. Estrogen receptor beta protects the murine heart against left ventricular hypertrophy. Arterioscler Thromb Vasc Biol. 2006;26:1524–1530
  5. Booz GW. Putting the brakes on cardiac hypertrophy: exploiting the NO–cGMP counter-regulatory system. Hypertension. 2005;45:341–346
  6. Cantor EJ, Babick AP, Vasanji Z, et al. A comparative serial echocardiographic analysis of cardiac structure and function in rats subjected to pressure or volume overload. J Mol Cell Cardiol. 2005;38:777–786
  7. Capuano V, Ruchon Y, Antoine S, et al. Ventricular hypertrophy induced by mineralocorticoid treatment or aortic stenosis differentially regulates the expression of cardiac K+ channels in the rat. Mol Cell Biochem. 2002;237:1–10
  8. Carabello BA. Concentric versus eccentric remodeling. J Card Fail. 2002;8:S258–S263
  9. Castoria G, Migliaccio A, Bilancio A, et al. PI3-kinase in concert with Src promotes the S-phase entry of oestradiol-stimulated MCF-7 cells. EMBO J. 2001;20:6050–6059
  10. Chizzonite RA, Everett AW, Clark WA, et al. Isolation and characterization of two molecular variants of myosin heavy chain from rabbit ventricle. Change in their content during normal growth and after treatment with thyroid hormone. J Biol Chem. 1982;257:2056–2065
  11. Daniels SR, Meyer RA, Liang YC, et al. Echocardiographically determined left ventricular mass index in normal children, adolescents and young adults. J Am Coll Cardiol. 1988;12:703–708
  12. DeBosch B, Treskov I, Lupu TS, et al. Akt1 is required for physiological cardiac growth. Circulation. 2006;113:2097–2104
  13. De Windt LJ, Lim HW, Bueno OF, et al. Targeted inhibition of calcineurin attenuates cardiac hypertrophy in vivo. Proc Natl Acad Sci U S A. 2001;98:3322–3327
  14. Dorn GW, Force T. Protein kinase cascades in the regulation of cardiac hypertrophy. J Clin Invest. 2005;115:527–537
  15. Eghbali M, Deva R, Alioua A, et al. Molecular and functional signature of heart hypertrophy during pregnancy. Circ Res. 2005;96:1208–1216
  16. Esposito G, Prasad SV, Rapacciuolo A, et al. Cardiac overexpression of a G(q) inhibitor blocks induction of extracellular signal-regulated kinase and c-Jun NH(2)-terminal kinase activity in in vivo pressure overload. Circulation. 2001;103:1453–1458
  17. Gealekman O, Abassi Z, Rubinstein I, et al. Role of myocardial inducible nitric oxide synthase in contractile dysfunction and beta-adrenergic hyporesponsiveness in rats with experimental volume-overload heart failure. Circulation. 2002;105:236–243
  18. Gowda RM, Khan IA, Mehta NJ, et al. Cardiac arrhythmias in pregnancy: clinical and therapeutic considerations. Int J Cardiol. 2003;88:129–133
  19. Guo W, Jung WE, Marionneau C, et al. Targeted deletion of Kv4.2 eliminates I(to,f) and results in electrical and molecular remodeling, with no evidence of ventricular hypertrophy or myocardial dysfunction. Circ Res. 2005;97:1342–1350
  20. Hainsey T, Csiszar A, Sun S, et al. Cyclosporin A does not block exercise-induced cardiac hypertrophy. Med Sci Sports Exerc. 2002;34:1249–1254
  21. Hansson M, Forsgren S. Expression of brain natriuretic peptide in the rat heart studies during heart growth and in relation to sympathectomy. Microsc Res Tech. 2004;64:30–42
  22. Harris IS, Zhang S, Treskov I, et al. Raf-1 kinase is required for cardiac hypertrophy and cardiomyocyte survival in response to pressure overload. Circulation. 2004;110:718–723
  23. Hart G. Cellular electrophysiology in cardiac hypertrophy and failure. Cardiovasc Res. 1994;28:933–946
  24. Hart G. Exercise-induced cardiac hypertrophy: a substrate for sudden death in athletes?. Exp Physiol. 2003;88:639–644
  25. Hayakawa Y, Chandra M, Miao W, et al. Inhibition of cardiac myocyte apoptosis improves cardiac function and abolishes mortality in the peripartum cardiomyopathy of Galpha(q) transgenic mice. Circulation. 2003;108:3036–3041
  26. Iemitsu M, Maeda S, Jesmin S, et al. Activation pattern of MAPK signaling in the hearts of trained and untrained rats following a single bout of exercise. J Appl Physiol. 2006;101:151–163
  27. Iemitsu M, Maeda S, Miyauchi T, et al. Gene expression profiling of exercise-induced cardiac hypertrophy in rats. Acta Physiol Scand. 2005;185:259–270
  28. Iemitsu M, Miyauchi T, Maeda S, et al. Physiological and pathological cardiac hypertrophy induce different molecular phenotypes in the rat. Am J Physiol Regul Integr Comp Physiol. 2001;281:R2029–R2036
  29. Jankowski M, Rachelska G, Donghao W, et al. Estrogen receptors activate atrial natriuretic peptide in the rat heart. Proc Natl Acad Sci U S A. 2001;98:11765–11770
  30. Jankowski M, Wang D, Mukaddam-Daher S, et al. Pregnancy alters nitric oxide synthase and natriuretic peptide systems in the rat left ventricle. J Endocrinol. 2005;184:209–217
  31. Jiang QS, Huang XN, Yang GZ, et al. Cardiac hypertrophy induced by prostaglandin F(2alpha) may be mediated by calcineurin signal transduction pathway in rats. Sheng Li Xue Bao. 2005;57:742–748
  32. Kaab S, Dixon J, Duc J, et al. Molecular basis of transient outward potassium current downregulation in human heart failure: a decrease in Kv4.3 mRNA correlates with a reduction in current density. Circulation. 1998;98:1383–1393
  33. Kato T, Muraski J, Chen Y, et al. Atrial natriuretic peptide promotes cardiomyocyte survival by cGMP-dependent nuclear accumulation of zyxin and Akt. J Clin Invest. 2005;115:2716–2730
  34. Kim H, Laing M, Muller W. c-Src-null mice exhibit defects in normal mammary gland development and ERalpha signaling. Oncogene. 2005;24:5629–5636
  35. Kiriazis H, Sato Y, Kadambi VJ, et al. Hypertrophy and functional alterations in hyperdynamic phospholamban-knockout mouse hearts under chronic aortic stenosis. Cardiovasc Res. 2002;53:372–381
  36. Kovacic B, Ilic D, Damsky CH, et al. c-Src activation plays a role in endothelin-dependent hypertrophy of the cardiac myocyte. J Biol Chem. 1998;273:35185–35193
  37. Lebeche D, Kaprielian R, Del Monte F, et al. In vivo cardiac gene transfer of Kv4.3 abrogates the hypertrophic response in rats after aortic stenosis. Circulation. 2004;110:3435–3443
  38. Lee JK, Nishiyama A, Kambe F, et al. Down regulation of voltage-gated K(+) channels in rat heart with right ventricular hypertrophy. Am J Physiol. 1999;277:H1725–H1731
  39. Li ZB, Gao YQ, Tang ZS. Differential expression of cardiac immediate early and late response gene in exercise-induced and hypertensive cardiac hypertrophic remodeling. Sheng Li Xue Bao. 1998;50:551–556
  40. Liao Y, Asakura M, Takashima S, et al. Celiprolol, a vasodilatory beta-blocker, inhibits pressure overload-induced cardiac hypertrophy and prevents the transition to heart failure via nitric oxide-dependent mechanisms in mice. Circulation. 2004;110:692–699
  41. Lim HW, De Windt LJ, Steinberg L, et al. Calcineurin expression, activation, and function in cardiac pressure-overload hypertrophy. Circulation. 2000;101:2431–2437
  42. MacCarthy PA, Shah AM. Impaired endothelium-dependent regulation of ventricular relaxation in pressure-overload cardiac hypertrophy. Circulation. 2000;101:1854–1860
  43. Magga J, Marttila M, Mantymaa P, et al. Brain natriuretic peptide in plasma, atria, and ventricles of vasopressin- and phenylephrine-infused conscious rats. Endocrinology. 1994;134:2505–2515
  44. Miyamoto T, Takeishi Y, Takahashi H, et al. Activation of distinct signal transduction pathways in hypertrophied hearts by pressure and volume overload. Basic Res Cardiol. 2004;99:328–337
  45. Molkentin JD. Calcineurin–NFAT signaling regulates the cardiac hypertrophic response in coordination with the MAPKs. Cardiovasc Res. 2004;63:467–475
  46. Nerbonne JM, Kass RS. Molecular physiology of cardiac repolarization. Physiol Rev. 2005;85:1205–1253
  47. Panou FK, Kafkas NV, Michelakakis NA, et al. Effect of different AV delays on left ventricular diastolic function and ANF levels in DDD paced hypertensive patients during daily activity and exercise. Pacing Clin Electrophysiol. 1999;22:635–642
  48. Patten RD, Pourati I, Aronovitz MJ, et al. 17beta-estradiol reduces cardiomyocyte apoptosis in vivo and in vitro via activation of phospho-inositide-3 kinase/Akt signaling. Circ Res. 2004;95:692–699
  49. Petrich BG, Wang Y. Stress-activated MAP kinases in cardiac remodeling and heart failure; new insights from transgenic studies. Trends Cardiovasc Med. 2004;14:50–55
  50. Pluim BM, Zwinderman AH, Van der LA, et al. The athlete's heart. A meta-analysis of cardiac structure and function. Circulation. 2000;101:336–344
  51. Ro A, Frishman WH. Peripartum cardiomyopathy. Cardiol Rev. 2006;14:35–42
  52. Ropero AB, Eghbali M, Minosyan TY, et al. Heart estrogen receptor alpha: distinct membrane and nuclear distribution patterns and regulation by estrogen. J Mol Cell Cardiol. 2006;41:496–510
  53. Schannwell CM, Zimmermann T, Schneppenheim M, et al. Left ventricular hypertrophy and diastolic dysfunction in healthy pregnant women. Cardiology. 2002;97:73–78
  54. Skavdahl M, Steenbergen C, Clark J, et al. Estrogen receptor-beta mediates male–female differences in the development of pressure overload hypertrophy. Am J Physiol Heart Circ Physiol. 2005;288:H469–H476
  55. Song LS, Pi Y, Kim SJ, et al. Paradoxical cellular Ca2+ signaling in severe but compensated canine left ventricular hypertrophy. Circ Res. 2005;97:457–464
  56. Sopontammarak S, Aliharoob A, Ocampo C, et al. Mitogen-activated protein kinases (p38 and c-Jun NH2-terminal kinase) are differentially regulated during cardiac volume and pressure overload hypertrophy. Cell Biochem Biophys. 2005;43:61–76
  57. Su X, Brower G, Janicki JS, et al. Differential expression of natriuretic peptides and their receptors in volume overload cardiac hypertrophy in the rat. J Mol Cell Cardiol. 1999;31:1927–1936
  58. Szymanska G, Stromer H, Silverman M, et al. Altered phosphorylation of sarcoplasmic reticulum contributes to the diminished contractile response to isoproterenol in hypertrophied rat hearts. Pflugers Arch. 1999;439:1–10
  59. Takeishi Y, Huang Q, Abe J, et al. Src and multiple MAP kinase activation in cardiac hypertrophy and congestive heart failure under chronic pressure-overload: comparison with acute mechanical stretch. J Mol Cell Cardiol. 2001;33:1637–1648
  60. Takimoto K, Li D, Hershman KM, et al. Decreased expression of Kv4.2 and novel Kv4.3 K+ channel subunit mRNAs in ventricles of renovascular hypertensive rats. Circ Res. 1997;81:533–539
  61. Tomaselli GF, Marban E. Electrophysiological remodeling in hypertrophy and heart failure. Cardiovasc Res. 1999;42:270–283
  62. Van Eickels M, Grohe C, Cleutjens JP, et al. 17beta-estradiol attenuates the development of pressure-overload hypertrophy. Circulation. 2001;104:1419–1423
  63. Van Natta TL, Ralphe JC, Mascio CE, et al. Ontogeny of vascular growth factors in perinatal sheep myocardium. J Soc Gynecol Investig. 2004;11:503–510
  64. Wang X, Bdel-Rahman AA. Estrogen modulation of eNOS activity and its association with caveolin-3 and calmodulin in rat hearts. Am J Physiol Heart Circ Physiol. 2002;282:H2309–H2315
  65. Weiner CP, Lizasoain I, Baylis SA, et al. Induction of calcium-dependent nitric oxide synthases by sex hormones. Proc Natl Acad Sci U S A. 1994;91:5212–5216
  66. Wilkins BJ, Dai YS, Bueno OF, et al. Calcineurin/NFAT coupling participates in pathological, but not physiological, cardiac hypertrophy. Circ Res. 2004;94:110–118
  67. Woods RL. Cardioprotective functions of atrial natriuretic peptide and B-type natriuretic peptide: a brief review. Clin Exp Pharmacol Physiol. 2004;31:791–794
  68. Wu CH, Liu JY, Wu JP, et al. 17beta-estradiol reduces cardiac hypertrophy mediated through the up-regulation of P13K/Akt and the suppression of calcineurin/NF-AT3 signaling pathways in rats. Life Sci. 2005;78:347–356
  69. Yamazaki T, Yazaki Y. Molecular basis of cardiac hypertrophy. Z Kardiol. 2000;89:1–6
  70. Zhang T, Brown JH. Role of Ca2+/calmodulin-dependent protein kinase II in cardiac hypertrophy and heart failure. Cardiovasc Res. 2004;63:476–486
  71. Zhang TT, Cui B, Dai DZ. Down-regulation of Kv4.2 and Kv4.3 channel gene expression in right ventricular hypertrophy induced by monocrotaline in rat. Acta Pharmacol Sin. 2004;25:226–230
  72. Zobel C, Kassiri Z, Nguyen TT, et al. Prevention of hypertrophy by overexpression of Kv4.2 in cultured neonatal cardiomyocytes. Circulation. 2002;106:2385–2391

PII: S1050-1738(06)00113-7

doi: 10.1016/j.tcm.2006.07.001

Trends in Cardiovascular Medicine
Volume 16, Issue 8 , Pages 285-291 , November 2006