Thromb Haemost 1999; 82(S 01): 73-75
DOI: 10.1055/s-0037-1615558
Commentaries
Schattauer GmbH

Ventricular Remodeling after Acute Myocardial Infarction

R. Dietz
1   From the Franz-Volhard-Klinik, Charité, Medizinische Fakultät der Humboldt-Universität zu Berlin, Germany
,
K. J. Osterziel
1   From the Franz-Volhard-Klinik, Charité, Medizinische Fakultät der Humboldt-Universität zu Berlin, Germany
,
R. Willenbrock
1   From the Franz-Volhard-Klinik, Charité, Medizinische Fakultät der Humboldt-Universität zu Berlin, Germany
,
D. C. Gulba
1   From the Franz-Volhard-Klinik, Charité, Medizinische Fakultät der Humboldt-Universität zu Berlin, Germany
,
R. v. Harsdorf
1   From the Franz-Volhard-Klinik, Charité, Medizinische Fakultät der Humboldt-Universität zu Berlin, Germany
› Author Affiliations
Further Information

Publication History

Publication Date:
14 December 2017 (online)

Summary

The term ventricular remodeling has been coined to describe the geometrical changes in size and shape of the left ventricle occurring after large myocardial infarcts.

We do not exactly know what initiates this process. Slipping of myofilaments following destruction of connective tissue – probably due to metalloproteinase activation – could be the initial event.

As a consequence, wall stress is increased triggering deleterious adaptation processes, such as

– intracardiac angiotensin II generation

– cardiac endothelin formation and release

– pro-apoptotic signals for cardiomyocytes

– hypertrophic signals for fibroblasts and cardiomyocytes

This cascade of events is not only observed in the process of remodeling following myocardial infarction but is also operating during the progression of heart failure.

Therapeutic principles therefore are similar in both conditions:

– reduction of wall stress (pharmacological or mechanical unloading of the heart)

– blockade of angiotensin II generation or of AT1-receptors (ACEinhibitors or AT1 antagonists)

– blockade of endothelin receptors (ETA-blockers)

– blockade of adrenergic receptors (preferably β1-adrenergic receptor blockers).

Better understanding of the molecular mechanisms of the remodeling process already has fueled the search for new therapeutic interventions (such as endothelin receptor blockers, aldosterone antagonists and growth hormone application). Continuous research in this field may be especially rewarding if we will succeed in identifying the very first step in the cascade.

 
  • References

  • 1 Sharpe N. Cardiac remodeling in congestive heart failure. In: Hospenpud JD, Greenberg BH. eds. Congestive Heart Failure. New York: Springer; 1994: 83-94.
  • 2 McKay RG, Pfeffer MA, Paternak RC, Markis JE, Come PC, Nakao S, Aldermann JD, Ferguson JJ, Safian RD, Grossmann W. Left ventricular remodeling after myocardial infarction: a corollary to infarction expansion. Circulation 1986; 74: 693-702.
  • 3 Gerdes AM, Capasso JM. Structural remodeling and mechanical dysfunction of cardiac myocytes in heart failure. J Mol Cell Cardiol 1995; 27: 849-56.
  • 4 Beltrami CA, Finato N, Rocco M, Feruglio GA, Puricelli C, Cigola E, Quaini F, Sonnenblick EH, Olivetti G, Anversa P. Structural basis of end-stage failure in ischemic cardiomyopathy in humans. Circulation 1994; 89: 151-63.
  • 5 Katz AM. Evolving concepts of heart failure: cooling furnace malfunctioning pump enlarging muscle II: hypertrophy and dilatation of the failing heart. J Cardiac Failure 1998; 467-81.
  • 6 Katz AM. Cardiomyopathy of overload: a major determinant of prognosis in congestive heart failure. N Eng J Med 1990; 322: 100-10.
  • 7 Mitchell GF, Lamas GA, Vaughan DE, Pfeffer MA. Left ventricular remodeling in the year after anterior myocardial infarction. A quantitative analysis of contractile segment lengths and ventricular shape. J Am Coll Cardiol 1992; 19: 1136-44.
  • 8 Francis GS, Benedict C, Johnstone DE, Kirlin P, Nicklas J, Liang C, Kubo SH, Rudin-Toretsky E, Yusuf S. Comparsion of neuroendocrine activation in patients with left ventricular dysfunction with and without congestive heart failure. Circulation 1990; 82 (5) 1724-9.
  • 9 Narula J, Haider N, Virmani R, DISalvo Th G, Kolodgie FD, Hajjar RJ, Schmidt U, Semigran MJ, Dec GW, Knaw BA. Apoptosis in Myocytes in End-Stage Heart Failure. New Engl J Med 1996; 17: 1182-9.
  • 10 Puri PL, Avantaggiati ML, Burgio VL, Chirillo P, Collepardo D, Natoli G, Balsano C, Levrero M. Reactive oxygen intermediates mediate angiotensin II-induced c-Jun/c-Fos heterodimer DNA binding activity and proliferative hypertrophic responses in myogenic cells. J Biol Chem 1995; 270: 22129-34.
  • 11 Sharma HS, van Heugten HAA, Goedbloed MA, Verdouw PD, Larners JMJ. Angiotensin II induced expression of transcription factors precedes increase in transforming growth factor p1 mRNA in neonatal cardiac fibroblasts. Biochem Biophys Res Commun 1994; 205: L 105-12.
  • 12 Latini R, Maggioni AP, Flather M. et al. ACE-inhibitor use in patients with myocardial infarction. Summary of evidence from clinical trials. Circulation 1995; 92: 313-7.
  • 13 Erlebacher JA, Weiss JL, Edton LW, Kallmann C, Weissfeldt ML, Bulkley BH. Late effects of acute infarction dilatation on heart size. A two-dimensional echocardiographic study. Am J Cardiol 1982; 49: 1120-6.
  • 14 Schieffer B, Wirger A, Meybrunn M, Seitz S, Holtz J, Riede UN, Drexler H. Comparative effects of chronic angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor blockade on cardiac remodeling after myocardial infarction in the rat. Circulation 1994; 89: 2273-82.
  • 15 Ventrimpont P, Pouleau JL, Wun CC, Ciampi A, Klein M, Sussex B, Arnold JMO, Moye L, Pfeffer M. Additive benefical effects of beta-blockers to angiotensin-converting enzyme inhibitors in the survival and ventricular enlargement (SAVE) study. J Am Coll Cardiol 1997; 29: 229-36.
  • 16 Zafeiridis A, Jeevanandam V, Houser SR, Margulies KB. Regression of left ventricular hypertrophy following left ventricular assist device support. Circulation 1998; 98: 656-62.
  • 17 Levin HR, Oz MC, Chen JM, Packer M, Rose EA, Burkhoff D. Reversal of chronic ventricular dilation in patients with end-stage cardiomyopathy by prolonged mechanical unloading. Circulation 1995; 91: 2717-20.
  • 18 Batista RJ, Santos JL, Takeshita N, Bocchino L, Lima PN, Cunha MA. Partial left ventriculectomy to improve left ventricular function in end-stage heart disease. J Card Surg 1996; 11: 96-7.
  • 19 Cittadini A, Grossmann JD, Napoli R. et al. Growth hormone attenuates early left ventricular remodeling and improves cardiac function in rats with large myocardial infarction. J Am Coll Cardiol 1997; 29: 1109-16.
  • 20 Osterziel K-J, Strohm O, Schuler J, Friedrich M, Hanlein D, Willenbrock R, Anker SD, Poole-Wilson PA, Ranke MB, Dietz R. Randomised, double-blind, placebo-controlled trial of human recombinant growth hormone in patients with chronic heart failure due to dilated cardiomyopathy. Lancet 1998; 351: 1233-7.