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Circulation. 1990;81:1161-1172

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Circulation, Vol 81, 1161-1172, Copyright © 1990 by American Heart Association


ARTICLES

Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications

MA Pfeffer and E Braunwald
Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115.

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.


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Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function
Physiol Rev, October 1, 2007; 87(4): 1285 - 1342.
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Am. J. Physiol. Heart Circ. Physiol.Home page
K. Uemura, M. Li, T. Tsutsumi, T. Yamazaki, T. Kawada, A. Kamiya, M. Inagaki, K. Sunagawa, and M. Sugimachi
Efferent vagal nerve stimulation induces tissue inhibitor of metalloproteinase-1 in myocardial ischemia-reperfusion injury in rabbit
Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2254 - H2261.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
A. Severino, M. Campioni, S. Straino, F. N. Salloum, N. Schmidt, U. Herbrand, S. Frede, G. Toietta, G. Di Rocco, R. Bussani, et al.
Identification of Protein Disulfide Isomerase as a Cardiomyocyte Survival Factor in Ischemic Cardiomyopathy
J. Am. Coll. Cardiol., September 11, 2007; 50(11): 1029 - 1037.
[Abstract] [Full Text] [PDF]


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CirculationHome page
R. Beeri, C. Yosefy, J. L. Guerrero, S. Abedat, M. D. Handschumacher, R. E. Stroud, S. Sullivan, M. Chaput, D. Gilon, G. J. Vlahakes, et al.
Early Repair of Moderate Ischemic Mitral Regurgitation Reverses Left Ventricular Remodeling: A Functional and Molecular Study
Circulation, September 11, 2007; 116(11_suppl): I-288 - I-293.
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CirculationHome page
A. C. Shuros, R. W. Salo, V. G. Florea, J. Pastore, M. A. Kuskowski, Y. Chandrashekhar, and I. S. Anand
Ventricular Preexcitation Modulates Strain and Attenuates Cardiac Remodeling in a Swine Model of Myocardial Infarction
Circulation, September 4, 2007; 116(10): 1162 - 1169.
[Abstract] [Full Text] [PDF]


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J CARDIOVASC PHARMACOL THERHome page
D. Chen, R. Chang, B. Umakanthan, L. N. Stoletniy, and J. T. Heywood
Improvement of Cardiac Function Persists Long Term With Medical Therapy for Left Ventricular Systolic Dysfunction
Journal of Cardiovascular Pharmacology and Therapeutics, September 1, 2007; 12(3): 220 - 226.
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Am. J. Physiol. Heart Circ. Physiol.Home page
M. P. Chandler, E. E. Morgan, T. A. McElfresh, T. A. Kung, J. H. Rennison, B. D. Hoit, and M. E. Young
Heart failure progression is accelerated following myocardial infarction in type 2 diabetic rats
Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1609 - H1616.
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Am. J. Physiol. Heart Circ. Physiol.Home page
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.
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Am. J. Physiol. Heart Circ. Physiol.Home page
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.
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Am. J. Physiol. Heart Circ. Physiol.Home page
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.
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CirculationHome page
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.
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J Am Coll CardiolHome page
N. Cheung, D. A. Bluemke, R. Klein, A. R. Sharrett, F.M. A. Islam, M. F. Cotch, B. E.K. Klein, M. H. Criqui, and T. Y. Wong
Retinal Arteriolar Narrowing and Left Ventricular Remodeling: The Multi-Ethnic Study of Atherosclerosis
J. Am. Coll. Cardiol., July 3, 2007; 50(1): 48 - 55.
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Am. J. Physiol. Heart Circ. Physiol.Home page
H. Thibault, L. Gomez, E. Donal, G. Pontier, M. Scherrer-Crosbie, M. Ovize, and G. Derumeaux
Acute myocardial infarction in mice: assessment of transmurality by strain rate imaging
Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H496 - H502.
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J Am Coll CardiolHome page
J. E. Udelson, F. A. McGrew, E. Flores, H. Ibrahim, S. Katz, G. Koshkarian, T. O'Brien, M. W. Kronenberg, C. Zimmer, C. Orlandi, et al.
Multicenter, Randomized, Double-Blind, Placebo-Controlled Study on the Effect of Oral Tolvaptan on Left Ventricular Dilation and Function in Patients With Heart Failure and Systolic Dysfunction
J. Am. Coll. Cardiol., June 5, 2007; 49(22): 2151 - 2159.
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EuropaceHome page
S. Gizurarson, M. Lorentzon, T. Ramunddal, F. Waagstein, L. Bergfeldt, and E. Omerovic
Effects of complete heart block on myocardial function, morphology, and energy metabolism in the rat
Europace, June 1, 2007; 9(6): 411 - 416.
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Eur J Heart FailHome page
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.
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Arch Intern MedHome page
A. Abdel-Latif, R. Bolli, I. M. Tleyjeh, V. M. Montori, E. C. Perin, C. A. Hornung, E. K. Zuba-Surma, M. Al-Mallah, and B. Dawn
Adult Bone Marrow-Derived Cells for Cardiac Repair: A Systematic Review and Meta-analysis
Arch Intern Med, May 28, 2007; 167(10): 989 - 997.
[Abstract] [Full Text] [PDF]