Circulation, Vol 81, 1161-1172, Copyright © 1990 by American Heart Association
MA Pfeffer and E Braunwald
An acute myocardial infarction, particularly one that is large and
transmural, can produce alterations in the topography of both the infarcted
and noninfarcted regions of the ventricle. This remodeling can importantly
affect the function of the ventricle and the prognosis for survival. In the
early period, infarct expansion has been recognized by echocardiography as
a lengthening of the noncontractile region. The noninfarcted region also
undergoes an important lengthening that is consistent with a secondary
volume-overload hypertrophy and that can be progressive. The extent of
ventricular enlargement after infarction is related to the magnitude of the
initial damage to the myocardium and, although an increase in cavity size
tends to restore stroke volume despite a persistently depressed ejection
fraction, ventricular dilation has been associated with a reduction in
survival. The process of ventricular enlargement can be influenced by three
interdependent factors, that is, infarct size, infarct healing, and
ventricular wall stresses. A most effective way to prevent or minimize the
increase in ventricular size after infarction and the consequent adverse
effect on prognosis is to limit the initial insult. Acute reperfusion
therapy has been consistently shown to result in a reduction in ventricular
volume. The reestablishment of blood flow to the infarcted region, even
beyond the time frame for myocyte salvage, has beneficial effects in
attenuating ventricular enlargement. The process of scarification can be
interfered with during the acute infarct period by the administration of
glucocorticosteroids and nonsteroidal antiinflammatory agents, which result
in thinner infarcts and greater degrees of infarct expansion. Modification
of distending or deforming forces can importantly influence ventricular
enlargement. Even short-term augmentations in afterload have deleterious
long-term effects on ventricular topography. Conversely, judicious use of
nitroglycerin seems to be associated with an attenuation of infarct
expansion and long-term improvement in clinical outcome. Long-term therapy
with an angiotensin converting enzyme inhibitor can favorably alter the
loading conditions on the left ventricle and reduce progressive ventricular
enlargement as demonstrated in both experimental and clinical studies. With
the former therapy, this attenuation of ventricular enlargement was
associated with a prolongation in survival. The long-term clinical
consequences of long- term angiotensin converting enzyme inhibitor therapy
after myocardial infarction is currently being evaluated. Although studies
directed at attenuating left ventricular remodeling after infarction are in
the early stages, it does seem that this will be an important area in which
future research might improve long-term outcome after infarction.
ARTICLES
Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications
Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115.
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L. Gomez, H. Thibault, A. Gharib, J.-M. Dumont, G. Vuagniaux, P. Scalfaro, G. Derumeaux, and M. Ovize Inhibition of mitochondrial permeability transition improves functional recovery and reduces mortality following acute myocardial infarction in mice Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1654 - H1661. [Abstract] [Full Text] [PDF]
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J. T. Colston, S. D. de la Rosa, M. Koehler, K. Gonzales, R. Mestril, G. L. Freeman, S. R. Bailey, and B. Chandrasekar Wnt-induced secreted protein-1 is a prohypertrophic and profibrotic growth factor Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1839 - H1846. [Abstract] [Full Text] [PDF]
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T.-M. Lee, M.-S. Lin, and N.-C. Chang Inhibition of histone deacetylase on ventricular remodeling in infarcted rats Am J Physiol Heart Circ Physiol, August 1, 2007; 293(2): H968 - H977. [Abstract] [Full Text] [PDF]
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S. Erbs, A. Linke, V. Schachinger, B. Assmus, H. Thiele, K.-W. Diederich, C. Hoffmann, S. Dimmeler, T. Tonn, R. Hambrecht, et al. Restoration of Microvascular Function in the Infarct-Related Artery by Intracoronary Transplantation of Bone Marrow Progenitor Cells in Patients With Acute Myocardial Infarction: The Doppler Substudy of the Reinfusion of Enriched Progenitor Cells and Infarct Remodeling in Acute Myocardial Infarction (REPAIR-AMI) Trial Circulation, July 24, 2007; 116(4): 366 - 374. [Abstract] [Full Text] [PDF]
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Y. Wang, M. C. de Waard, A. Sterner-Kock, H. Stepan, H.-P. Schultheiss, D. J. Duncker, and T. Walther Cardiomyocyte-restricted over-expression of C-type natriuretic peptide prevents cardiac hypertrophy induced by myocardial infarction in mice Eur J Heart Fail, June 1, 2007; 9(6-7): 548 - 557. [Abstract] [Full Text] [PDF]
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