Cardiac Remodeling and Its Prevention

  • Scott D. Solomon
  • Marc A. Pfeffer


Cardiac chambers have the capacity to alter (remodel) their size and configuration in response to a chronic change in their hemodynamic load. Whether across or within species, the mass and volume of the ventricular chambers maintain a close relationship with the required external work. The changes in chamber volume and mass that accompany normal growth provide the most striking example of the heart’s intrinsic capacity to remodel in response to the insidious alterations in demand that take place as a consequence of body growth. Under pathologic conditions of chronic pressure or volume overload, the chamber remodels in direct relation to the imposed hemodynamic burden. The mass increase is attributable to both myocyte hypertrophy and growth of nonmyocyte interstitial components. However, the manner of rearrangement of these additional contractile tissues can lead to either an eccentric (chamber volume > mass) or a concentric (chamber mass > volume) pattern of ventricular growth. Although remodeling in response to a pathologic condition can in one sense be considered adaptive because it permits the restoration of pump function in the face of an imposed hyperfunctional condition, the extent of ventricular remodeling is nevertheless an important marker for poor prognosis.


Cardiac Resynchronization Therapy Wall Stress Cardiac Remodel Ventricular Remodel Ventricular Enlargement 
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  1. 1.
    Holt J, Rhode E, Kines H: Ventricular volumes and body weight in mammals. Am J Physiol 1968, 215: 704–715.PubMedGoogle Scholar
  2. 2.
    Grossman W, Carabello BA, Gunther S, et al Ventricular wall stress and the development of cardiac hypertrophy and failure. In Perspectives in Cardiovascular Research: Myocardial Hypertrophy and Failure,vol 7. Edited by Alpert NR. New York: Raven Press; 1993:1–15.Google Scholar
  3. 3.
    Hutchins GM, Bulkley BH: Infarct expansion versus extension: two different complications of acute myocardial infarction. Am J Cardiol 1978, 41: 1127–1132.PubMedCrossRefGoogle Scholar
  4. 4.
    Erlebacher JA, Weiss JL, Weisfeldt ML, et al Early dilation of the infarcted segment in acute transmural myocardial infarction: role of infarct expansion in acute left ventricular enlargement. J Am Coll Cardiol 1984, 4:201–208.Google Scholar
  5. 5.
    Jugdutt BI, Michorowski BL: Role of infarct expansion in rupture of the ventricular septum after acute myocardial infarction: a two-dimensional echocardiographic study. Clin Cardiol 1987, 10: 641–652.PubMedCrossRefGoogle Scholar
  6. 6.
    Hammermeister KE, DeRouen TA, Dodge HT: Variables predictive of survival in patients with coronary disease: selection by univariate and multivariate analyses from the clinical, electrocardiographic, exercise, arteriographic, and quantitative angiographie evaluations. Circulation 1979, 59: 421–430.PubMedCrossRefGoogle Scholar
  7. 7.
    White HD, Norris RM, Brown MA, et al Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction. Circulation 1987, 76:44–51.Google Scholar
  8. 8.
    Meizlish JL, Berger HJ, Plankey M, et al Functional left ventricular aneurysm formation after acute anterior transmural myocardial infarction: incidence, natural history, and prognostic implications. N Engl J Med 1984, 311:1001–1006.Google Scholar
  9. 9.
    Lamas GA, Vaughan DE, Pfeffer MA: Left ventricular thrombus formation after first anterior wall acute myocardial infarction. Am J Cardiol 1988, 62: 31–35.PubMedCrossRefGoogle Scholar
  10. 10.
    Pfeffer JM, Pfeffer MA, Fletcher PJ, et al Progressive ventricular remodeling in rat with myocardial infarction. Am J Physiol 1991, 29 (suppl H):1406–1414.Google Scholar
  11. 11.
    Gaudron P, Eilles C, Kugler I, et al Progressive left ventricular dysfunction and remodeling after myocardial infarction: potential mechanisms and early predictors. Circulation 1993, 87:755–763.Google Scholar
  12. 12.
    Solomon SD, Glynn RJ, Greaves S, et al Recovery of ventricular function after myocardial infarction in the reperfusion era: the healing and early afterload reducing therapy study. Ann Intern Med 2001, 134:451–458.Google Scholar
  13. 13.
    Pfeffer JM: Progressive ventricular dilatation in experimental myocardial infarction and its attenuation by angiotensin converting enzyme inhibition. Am J Cardiol 1991, 68: 17D - 25D.PubMedCrossRefGoogle Scholar
  14. 14.
    Solomon SD, St. John Sutton M, Lamas GA, et al. for the Survival and Ventricular Enlargement (SAVE) Investigators: Ventricular remodeling does not accompany the development of heart failure in diabetic patients after myocardial infarction. Circulation 2002, 106: 1251–1255.PubMedCrossRefGoogle Scholar
  15. 15.
    Capasso J, Zhang P, Anversa P: Heterogeneity of ventricular remodeling after acute myocardial infarction in rats. Am J Physiol 1992, 262 (suppl H): 486–495.Google Scholar
  16. 16.
    White HD, Norris RIVI, Brown MA, et al Effect of intravenous streptokinase on left ventricular function and early survival after acute myocardial infarction. N Engl J Med 1987, 317:850–855.Google Scholar
  17. 17.
    Marino P, Zanolla L, Zardini P: Effect of streptokinase on left ventricular modeling and function after myocardial infarction: the GISSI (Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardico) Trial. J Am Coll Cardiol 1989, 14: 1149–1158.PubMedCrossRefGoogle Scholar
  18. 18.
    Braunwald E: Myocardial reperfusion, limitation of infarct size, reduction of left ventricular dysfunction, and improved survival: should the paradigm by expanded? Circulation 1989, 79: 441 444.Google Scholar
  19. 19.
    Kim C, Braunwald E: Potential benefits of late reperfusion of infarcted myocardium: the open artery hypothesis. Circulation 1993, 88: 2426–2436.PubMedCrossRefGoogle Scholar
  20. 20.
    Pfeffer JM, Pfeffer MA, Braunwald E: Influence of chronic captopril therapy on the infarcted left ventricle of the rat. Cire Res 1985, 57: 84–95.CrossRefGoogle Scholar
  21. 21.
    Pfeffer MA, Pfeffer JM, Steinberg C, Finn P: Survival after an experimental myocardial infarction: beneficial effects of long-term captopril therapy. Circulation 1985, 72: 406–412.PubMedCrossRefGoogle Scholar
  22. 22.
    Pfeffer MA, Lamas GA, Vaughan DE, et al Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction. N Engl J Med 1988, 319:80–86.Google Scholar
  23. 23.
    Sharpe N: Early preventive treatment of left ventricular dysfunction following myocardial infarction: optimal timing and patient selection. Am J Cardiol 1991, 68 (suppl D): 64–69.CrossRefGoogle Scholar
  24. 24.
    Mitchell GF, Lamas GA, Vaughan DE, et al Left ventricular remodeling in the year following first anterior myocardial infarction: a quantitative analysis of contractile segment lengths and ventricular shape. J Am Coll Cardiol 1992, 19:1136–1144.Google Scholar
  25. 25.
    Konstam M, Kronenberg M, Rousseau M, et al Effects of the angiotensin converting enzyme inhibitor enalapril on the longterm progression of left ventricular dilatation in patients with asymptomatic systolic dysfunction. Circulation 1993, 88:2277–2283.Google Scholar
  26. 26.
    St. John Sutton M, Pfeffer M, Plappert T, et al Quantitative two dimensional echocardiographic measurements are major predictors of adverse cardiovascular events following acute myocardial infarction: the protective effects of captopril. Circulation 1994, 89:68–75.Google Scholar
  27. 27.
    Pfeffer MA, Greaves SC, Arnold JMO, et al Early versus delayed angiotensin-converting enzyme inhibition therapy in acute myocardial infarction: the Healing and Early Afterload Reducing Therapy Trial. Circulation 1997, 95:2643–2651.Google Scholar
  28. 28.
    Mahmarian JJ, Moyé LA, Chinoy DA, et al Transdermal nitroglycerin patch therapy improves left ventricular function and prevents remodeling after acute myocardial infarction: results of a multicenter prospective randomized, double-blind, placebo-controlled trial. Circulation 1998, 97:2017–2024.Google Scholar
  29. 29.
    Lowes BD, Gill EA, Abraham WT, et al Effect of carvedilol on left ventricular mass, chamber geometry and mitral regurgitation in chronic heart failure. Am J Cardiol 1999, 83:1201–1205.Google Scholar
  30. 30.
    Lindsey ML, Gannon J, Aikawa M, et al Selective matrix metalloproteinase inhibition reduces left ventricular remodeling but does not inhibit angiogenesis after myocardial infarction. Circulation 2002,105:753–832.Google Scholar
  31. 31.
    St. John Sutton MG, Plappert T, Abraham WT, et al. for the Multicenter InSync Randomized Clinical Evaluation (MIRACLE) Study Group: Effect of cardiac resynchronization therapy on left ventricular size and function in chronic heart failure. Circulation 2003, 107: 1985–1990.CrossRefGoogle Scholar
  32. 32.
    Jain M, DerSimonian H, Brenner DA, et al Cell therapy attenuates deleterious ventricular remodeling and improves cardiac performance after myocardial infarction. Circulation 2001, 103:1920–1927.Google Scholar
  33. 33.
    Fraccarollo D, Galuppo P, Hildemann S, et al Additive improvement of left ventricular remodeling and neurohormonal activation by aldosterone receptor blockade with eplerenone and ACE inhibition in rats with myocardial infarction. JAnm Coll Cardiol 2003, 42:1666–1673.Google Scholar

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© Springer Science+Business Media New York 2005

Authors and Affiliations

  • Scott D. Solomon
  • Marc A. Pfeffer

There are no affiliations available

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