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Circulation. 1993;87:755-763

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Circulation, Vol 87, 755-763, Copyright © 1993 by American Heart Association


ARTICLES

Progressive left ventricular dysfunction and remodeling after myocardial infarction. Potential mechanisms and early predictors

P Gaudron, C Eilles, I Kugler and G Ertl
Department of Medicine, Julius-Maximilians-University, Wurzburg, FRG.

BACKGROUND. Left ventricular enlargement and the development of chronic heart failure are potent predictors of survival in patients after myocardial infarction. Prospective studies relating progressive ventricular enlargement in individual patients to global and regional cardiac dysfunction and the onset of late chronic heart failure are not available. It was the aim of this study to define the relation between left ventricular dilatation and global and regional cardiac dysfunction and to identify early predictors of enlargement and chronic heart failure in patients after myocardial infarction. METHODS AND RESULTS. Left ventricular volumes, regional area shrinkage fraction in 18 predefined sectors (gated single photon emission computed tomography), global ejection fraction, and hemodynamics at rest and during exercise (supine bicycle, 50 W, 4 minutes, Swan-Ganz catheter) were assessed prospectively 4 days, 4 weeks, 6 months, and 1.5 and 3 years after first myocardial infarction. Seventy patients were assigned to groups with progressive, limited, or no dilatation. Patients without dilatation (n = 38) maintained normal volumes and hemodynamics until 3 years. With limited dilatation (n = 18), left ventricular volume increased up to 4 weeks after infarction and stabilized thereafter; depressed stroke volume was restored 4 weeks after infarction and then remained stable at rest. Wedge pressure during exercise, however, progressively increased. With progressive dilatation (n = 14), depressed cardiac and stroke indexes were also restored by 4 weeks but progressively deteriorated thereafter. Area shrinkage fraction as an estimate of regional left ventricular function in normokinetic sectors at 4 days gradually deteriorated during 3 years, but hypokinetic and dyskinetic sectors remained unchanged. Global ejection fraction fell after 1.5 years, whereas right atrial pressure, wedge pressure, and systemic vascular resistance increased. By multivariate analysis, ejection fraction and stroke index at 4 days, ventriculographic infarct size, infarct location, and Thrombolysis in Myocardial Infarction trial grade of infarct artery perfusion were significant predictors of progressive ventricular enlargement and chronic dysfunction. CONCLUSIONS. Almost 26% of patients may develop limited left ventricular dilatation within 4 weeks after first infarction, which helps to restore cardiac index and stroke index at rest and to preserve exercise performance and therefore remains compensatory. A somewhat smaller group (20%) develops progressive structural left ventricular dilatation, which is compensatory at first, then progresses to noncompensatory dilatation, and finally results in severe global left ventricular dysfunction. In these patients, depression of global ejection fraction probably results from impairment of function of initially normally contracting myocardium. Early predictors from multivariate analysis allow identification of patients at high risk for progressive left ventricular dilatation and chronic ventricular dysfunction within 4 weeks after acute infarction.


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CirculationHome page
Z. Mallat, I. Philip, M. Lebret, D. Chatel, J. Maclouf, and A. Tedgui
Elevated Levels of 8-iso-Prostaglandin F2{alpha} in Pericardial Fluid of Patients With Heart Failure : A Potential Role for In Vivo Oxidant Stress in Ventricular Dilatation and Progression to Heart Failure
Circulation, April 28, 1998; 97(16): 1536 - 1539.
[Abstract] [Full Text] [PDF]


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CirculationHome page
D. Fraccarollo, K. Hu, P. Galuppo, P. Gaudron, and G. Ertl
Chronic Endothelin Receptor Blockade Attenuates Progressive Ventricular Dilation and Improves Cardiac Function in Rats With Myocardial Infarction : Possible Involvement of Myocardial Endothelin System in Ventricular Remodeling
Circulation, December 2, 1997; 96(11): 3963 - 3973.
[Abstract] [Full Text]


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Cardiovasc ResHome page
K. McDonald, C. Chu, G. Francis, D. Judd, W. Carlyle, C. Toher, K. Hauer, and M. Hartman
The effect of delayed reperfusion following infarction in the rat on structural changes in viable myocardium
Cardiovasc Res, December 1, 1997; 36(3): 347 - 353.
[Abstract] [Full Text] [PDF]


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CirculationHome page
M. St. J. Sutton, M. A. Pfeffer, L. Moye, T. Plappert, J. L. Rouleau, G. Lamas, J. Rouleau, J. O. Parker, M. O. Arnold, B. Sussex, et al.
Cardiovascular Death and Left Ventricular Remodeling Two Years After Myocardial Infarction : Baseline Predictors and Impact of Long-term Use of Captopril: Information From the Survival and Ventricular Enlargement (SAVE) Trial
Circulation, November 18, 1997; 96(10): 3294 - 3299.
[Abstract] [Full Text]


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CirculationHome page
L. Bolognese, G. Cerisano, P. Buonamici, A. Santini, G. M. Santoro, D. Antoniucci, and P. F. Fazzini
Influence of Infarct-Zone Viability on Left Ventricular Remodeling After Acute Myocardial Infarction
Circulation, November 18, 1997; 96(10): 3353 - 3359.
[Abstract] [Full Text]


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CirculationHome page
M. A. Pfeffer, S. C. Greaves, J. M. O. Arnold, R. J. Glynn, F. S. LaMotte, R. T. Lee, F. J. Menapace Jr, E. Rapaport, P. M. Ridker, J.-L. Rouleau, et al.
Early Versus Delayed Angiotensin-Converting Enzyme Inhibition Therapy in Acute Myocardial Infarction : The Healing and Early Afterload Reducing Therapy Trial
Circulation, June 17, 1997; 95(12): 2643 - 2651.
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NEJMHome page
R. S. Vasan, M. G. Larson, E. J. Benjamin, J. C. Evans, and D. Levy
Left Ventricular Dilatation and the Risk of Congestive Heart Failure in People without Myocardial Infarction
N. Engl. J. Med., May 8, 1997; 336(19): 1350 - 1355.
[Abstract] [Full Text] [PDF]


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CirculationHome page
P. Dubach, J. Myers, G. Dziekan, U. Goebbels, W. Reinhart, P. Vogt, R. Ratti, P. Muller, R. Miettunen, and P. Buser
Effect of Exercise Training on Myocardial Remodeling in Patients With Reduced Left Ventricular Function After Myocardial Infarction : Application of Magnetic Resonance Imaging
Circulation, April 15, 1997; 95(8): 2060 - 2067.
[Abstract] [Full Text]


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CirculationHome page
K. T. Sun, J. Czernin, J. Krivokapich, Y.-K. Lau, M. Bottcher, G. Maurer, M. E. Phelps, and H. R. Schelbert
Effects of Dobutamine Stimulation on Myocardial Blood Flow, Glucose Metabolism, and Wall Motion in Normal and Dysfunctional Myocardium
Circulation, December 15, 1996; 94(12): 3146 - 3154.
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Arch Intern MedHome page
R. S. Vasan and D. Levy
The Role of Hypertension in the Pathogenesis of Heart Failure: A Clinical Mechanistic Overview
Arch Intern Med, September 9, 1996; 156(16): 1789 - 1796.
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NEJMHome page
J. N. Cohn
The Management of Chronic Heart Failure
N. Engl. J. Med., August 15, 1996; 335(7): 490 - 498.
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CirculationHome page
B. I. Jugdutt, M. I. Khan, S. J. Jugdutt, and G. E. Blinston
Effect of Enalapril on Ventricular Remodeling and Function During Healing After Anterior Myocardial Infarction in the Dog
Circulation, February 1, 1995; 91(3): 802 - 812.
[Abstract] [Full Text]


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Arch Intern MedHome page
R. J. Cody
Comparing Angiotensin-Converting Enzyme Inhibitor Trial Results in Patients With Acute Myocardial Infarction
Arch Intern Med, September 26, 1994; 154(18): 2029 - 2036.
[Abstract] [PDF]