Circulation Research, Vol 57, 84-95, Copyright © 1985 by American Heart Association
ARTICLES |
JM Pfeffer, MA Pfeffer and E Braunwald
To determine whether the relationship between infarct size and ventricular performance, volume, and compliance could be altered favorably, captopril was administered to rats for 3 months following coronary artery ligation. Baseline left and right ventricular and systemic arterial pressures and aortic blood flow, and maximal stroke volume and cardiac indices attained during a volume loading, were measured. Passive pressure-volume relations of the left ventricle were determined, and the slopes of segments of this relation were analyzed to characterize ventricular chamber stiffness. In untreated rats, left ventricular end-diastolic pressure progressively rose (from 5-28 mm Hg) as a function of infarct size, whereas, in captopril-treated rats, filling pressure remained within normal limits (5 +/- 1 mm Hg) in all but those with extensive infarcts. Chronic captopril therapy reduced baseline mean arterial pressure and total peripheral resistance, yet maintained cardiac and stroke outputs in rats both with and without infarcts. In untreated rats, maximal pumping ability progressively declined with increasing infarct size, whereas, in captopril-treated rats, peak stroke volume index remained within normal limits in all but those with extensive infarcts. The in vitro left ventricular volumes of captopril-treated rats were significantly less than those of untreated rats. The maintenance of forward output from a lesser dilated left ventricle yielded an index of ejection fraction for treated rats with moderate and large infarcts that was significantly elevated compared with that of untreated rats with infarcts of comparable size. Left ventricular chamber stiffness, which fell as infarct size increased in untreated rats, was normalized by chronic captopril therapy. Thus, captopril attenuated the left ventricular remodeling (dilation) and deterioration in performance that were observed in rats with chronic myocardial infarction.
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M. A. Pfeffer ACE Inhibitors in Acute Myocardial Infarction : Patient Selection and Timing Circulation, June 9, 1998; 97(22): 2192 - 2194. [Full Text] [PDF] |
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N. J. Brown and D. E. Vaughan Angiotensin-Converting Enzyme Inhibitors Circulation, April 14, 1998; 97(14): 1411 - 1420. [Abstract] [Full Text] [PDF] |
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D. Grimm, D. Elsner, H. Schunkert, M. Pfeifer, D. Griese, G. Bruckschlegel, F. Muders, G. A.J Riegger, and E. P Kromer Development of heart failure following isoproterenol administration in the rat: role of the renin-angiotensin system Cardiovasc Res, January 1, 1998; 37(1): 91 - 100. [Abstract] [Full Text] [PDF] |
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R. G Schoemaker, P. R Saxena, and E. A.J Kalkman Low-dose aspirin improves in vivo hemodynamics in conscious, chronically infarcted rats Cardiovasc Res, January 1, 1998; 37(1): 108 - 114. [Abstract] [Full Text] [PDF] |
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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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I. S. Anand, D. Liu, S. S. Chugh, A. J.C. Prahash, S. Gupta, R. John, F. Popescu, and Y. Chandrashekhar Isolated Myocyte Contractile Function Is Normal in Postinfarct Remodeled Rat Heart With Systolic Dysfunction Circulation, December 2, 1997; 96(11): 3974 - 3984. [Abstract] [Full Text] |
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T. E. Raya, M. Gaballa, P. Anderson, and S. Goldman Left ventricular function and remodeling after myocardial infarction in aging rats Am J Physiol Heart Circ Physiol, December 1, 1997; 273(6): H2652 - H2658. [Abstract] [Full Text] [PDF] |
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T. Nishikimi, T. Horio, T. Sasaki, F. Yoshihara, S. Takishita, A. Miyata, H. Matsuo, and K. Kangawa Cardiac Production and Secretion of Adrenomedullin Are Increased in Heart Failure Hypertension, December 1, 1997; 30(6): 1369 - 1375. [Abstract] [Full Text] |
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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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T. A. Fischer, P. L. McNeil, R. Khakee, P. Finn, R. A. Kelly, M. A. Pfeffer, and J. M. Pfeffer Cardiac Myocyte Membrane Wounding in the Abruptly Pressure-Overloaded Rat Heart Under High Wall Stress Hypertension, November 1, 1997; 30(5): 1041 - 1046. [Abstract] [Full Text] |
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M. Flesch, F. Schiffer, O. Zolk, Y. Pinto, S. Rosenkranz, C. Hirth-Dietrich, G. Arnold, M. Paul, and M. Bohm Contractile Systolic and Diastolic Dysfunction in Renin-Induced Hypertensive Cardiomyopathy Hypertension, September 1, 1997; 30(3): 383 - 391. [Abstract] [Full Text] |
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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. [Abstract] [Full Text] |
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E. O. Weinberg, M. A. Lee, M. Weigner, K. Lindpaintner, S. P. Bishop, C. R. Benedict, K. K. L. Ho, P. S. Douglas, E. Chafizadeh, and B. H. Lorell Angiotensin AT1 Receptor Inhibition : Effects on Hypertrophic Remodeling and ACE Expression in Rats With Pressure-Overload Hypertrophy due to Ascending Aortic Stenosis Circulation, March 18, 1997; 95(6): 1592 - 1600. [Abstract] [Full Text] |
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P. Mulder, B. Devaux, V. Richard, J.-P. Henry, M.-C. Wimart, E. Thibout, B. Mace, and C. Thuillez Early Versus Delayed Angiotensin-Converting Enzyme Inhibition in Experimental Chronic Heart Failure: Effects on Survival, Hemodynamics, and Cardiovascular Remodeling Circulation, March 4, 1997; 95(5): 1314 - 1319. [Abstract] [Full Text] |
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Y. Kagaya, R. J. Hajjar, J. K. Gwathmey, W. H. Barry, and B. H. Lorell Long-term Angiotensin-Converting Enzyme Inhibition With Fosinopril Improves Depressed Responsiveness to Ca2+ in Myocytes From Aortic-Banded Rats Circulation, December 1, 1996; 94(11): 2915 - 2922. [Abstract] [Full Text] |
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E. J. Eichhorn and M. R. Bristow Medical Therapy Can Improve the Biological Properties of the Chronically Failing Heart: A New Era in the Treatment of Heart Failure Circulation, November 1, 1996; 94(9): 2285 - 2296. [Abstract] [Full Text] |
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A. Simonini, C. S. Long, G. A. Dudley, P. Yue, J. McElhinny, and B. M. Massie Heart Failure in Rats Causes Changes in Skeletal Muscle Morphology and Gene Expression That Are Not Explained by Reduced Activity Circ. Res., July 1, 1996; 79(1): 128 - 136. [Abstract] [Full Text] |
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B. I. Jugdutt, M. J. Joljart, and M. I. Khan Rate of Collagen Deposition During Healing and Ventricular Remodeling After Myocardial Infarction in Rat and Dog Models Circulation, July 1, 1996; 94(1): 94 - 101. [Abstract] [Full Text] |
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