Summary
Changes of ischemic myocardium following coronary occlusion, including active and passive functions, and adaptive changes of non-ischemic surviving myocardium have been summarized under the term “left ventricular remodeling” post myocardial infarction. An increase in left ventricular volume may be a consequence, and associated with an adverse prognosis. Although left ventricular dilatation may increase stroke volume and, thus, be compensatory at first, in about one-fifth of patients it ultimately results in progressive dysfunction and heart failure. Major determinants of this process are time, infarct size, infarct location, global left ventricular function assessed 4 days after infarction by radionuclide ejection fraction and right heart catheter (stroke volume), and morphology of the infarct-associated coronary artery.
The surviving myocardium hypertrophies and may also dilate structurally. Depression of left ventricular ejection fraction chronically after the infarct is due to deterioration of wall motion of chamber segments initially classified normal by radionuclide analysis. Biochemical changes may also occur, including reduction of phosphocreatine, prolongation of time to peak Cai 2+, and changes in myosin isoforms. Systemic or local humoral factors may be involved in these changes, however, clear evidence is still lacking. Perfusion of surviving myocardium may be altered under various conditions due to morphologic and functional changes of coronary vasculature. Successful prevention of heart failure and death by angiotensin converting enzyme inhibitors in asymptomatic patients with left ventricular dysfunction post-myocardial infarction has supported the pathophysiologic concepts of remodeling.
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References
Anversa P, Beghi C, Kikkawa Y, Olivetti G (1986) Myocardial infarction in rats. Infarct size, myocyte hypertrophy, and capillary growth. Circ Res 58: 26–37
Cigarroa RG, Lange RA, Hillis LD (1989) Prognosis after acute myocardial infarction in patients with and without residual anterograde coronary blood flow. Am J Cardiol 64: 155–160
Drexler H, Hablawetz BS, Lu W, Riede U, Christes A (1992) Effects of inhibition of nitric oxide formation of regional blood flow in experimental myocardial infarction. Circulation 86: 255–262
Drexler H, Hanze J, Finckh M, Lu W, Just H, Lang RE (1989) Atrial natriuretic peptide in a rat model of cardiac failure. Circulation 79: 620–633
Eaton LW, Weiss JL, Bulkley BH, Garrison JB, Weisfeldt ML (1979) Regional cardiac dilatation after acute myocardial infarction. N Engl J Med 300: 57–62
Erlenbacher JA, Weiss JL, Eaton LW, Kallman C, Weisfeldt ML, Bulkley BH (1982) Late effects of acute infarct dilation on heart size: A two-dimensional echocardiagraphic study. Am J Cardiol 49: 1120–1126
Ertl G, Just H, Lang K (1976) Herzrhythmusstörungen in der chronischen Phase des Myokardinfarktes. Dtsch Med Wschr 101: 845–849
Franz MR, Cima R, Wang D, Profitt D, Kurz R (1992) Electrophysiological effects of myocardial stretch and mechanical determinants of stretch-activated arrhythmias. Circulation 86: 968–978
Gaudron P, Ellies C, Ertl G, Kochsiek K (1990) Early remodelling of the left ventricle in patients with myocardial infarction. Eur Heart J ll:( Suppl B ), 139–146
Gaudron P, Eilles C, Ertl G, Kochsiek K (1992) Compensatory and noncompensatory left ventricular dilatation after myocardial infarction: Time course and hemodynamic consequences at rest and during exercise. Am Heart J 123: 377–385
Gaudron P, Eilles C, Kugler I, Ertl G (1993) Progressive left ventricular dysfunction and remodelling following myocardial infarction: Potential mechanisms and early predictors. Circulation 87: 755–763
Gaudron PJ, Eilles Ch, Neuser D, Ertl G, Kochsiek K (1988) Plasma ANP in patients with acute myocardial infarction: time course, relation to infarct size, central hemodynamics and left ventricular volume. Circulation 78 (Suppl EE): II–63
Ginzton LE, Conant R, Rodrigues DM, Laks MM (1989) Functional significance of hypertrophy of the noninfarcted myocardium after myocardial infarction in humans. Circulation 80: 816–822
Gülch RW, Jacob R (1988) Geometric and muscle physiological determinants of cardiac stroke volume as evaluated on the basis of model calculation. Basic Res Cardiol 83: 476 - 485
Han H, Neubauer S, Gaudron P, Hu K, Ertl G (1992) Effects of Leukotriene D4 and its specific antagonist L-660,711 in isolated rat heart after myocardial infarction. J Moll Cell Cardiol 24 (Suppl V): 51
Hirai T, Fujita M, Nakajima H, Asanoi H, Yamanishi K, Ohno A, Sasayama S (1989) Importance of collateral circulation for prevention of left ventricular aneurysm formation in acute myocardial infarction. Circulation 79: 791–796
Hirsch AT, Talsness CE, Schunkert H, Paul M, Dzau VJ (1991) Tissue-specific activation of cardiac angiotensin converting enzyme in experimental heart failure. Circulation Research 69: 475–482
Hort W (1965) Ventrikeldilatation und Muskelfaserdehnung als früheste morphologische Befunde beim Herzinfarkt. Virchows Arch Path Anat 339: 71–82
Hu K, Gaudron P, Bahner U, Palkovits M, Ertl G (1991) Atrial natriuretic factor (ANF) in brain areas of rats post myocardial infarction (MI). Eur Heart J 12 (Suppl): 702
Jeremy RW, Hackworthy RA, Bautovich G, Hutton BF, Harris PJ (1987) Infarct artery perfusion and changes in left ventricular volume in the month after acute myocardial infarction. J Am Coll Cardiol 9: 989–995
Karam R, Healy BP, Wicker P (1990) Coronary reserve is depressed in postmyocardial infarction reactive cardiac hypertrophy. Circulation 81: 238–246
Kostuk WJ, Kazamias TM, Gander MP, Simon AL, Ross J (1973) Left ventricular size after acute myocardial infarction. Serial changes and their prognostic significance. Circulation 47: 1174–1179
Kowey PR, Friehling TD, Sewter J, Wu Y, Sokil A, Paul J, Nocella J (1991) Electrophysiological effects of left ventricular hypertrophy. Effect of calcium and potassium channel blockade. Circulation 83: 2067–2076
Lavie CJ, O’Keefe JH, Chesebro JH, Clements IP, Gibbons RJ (1990) Prevention of late ventricular dilatation after acute myocardial infarction by successful thrombolytic reperfusion. Am J Cardiol 66: 31–36
Leung W-H, Lau C-P (1992) Effects of severity of the residual stenosis of the infarct related coronary artery on left ventricular dilation and function after acute myocardial infarction. J Am Coll Cardiol 20: 307–313
Linzbach AJ, Linzbach M (1951) Die Herzdilatation. Klin Wochenschr 29: 621–630
Litwin SE, Litwin CM, Raya TE, Warner AL, Goldman S (1991) Contractility and stiffness of noninfarcted myocardium after coronary ligation in rats. Effects of chronic angiotensin converting enzyme inhibition. Circulation 83: 1028–1037
Litwin SE, Morgan JP (1992) Captopril enhances intracellular calcium handling and ß-adrenergic responsiveness of myocardium from rats with postinfarction failure. Circulation Research 71: 797–807
Marino P, Zanolla L, Zardini P (1989) on behalf of the Gruppo Italiano per lo Studio della Streptochinasi nell Infarto Miocardico (GISSI): 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 14: 1149–1158
Mendez RE, Pfeffer JM, Ortola FV, Bloch KD, Anderson S, Seidman JG, Brenner BM (1987) Atrial natriuretic peptide transcription, storage, and release in rats with myocardial infarction. Am J Physiol 253: H1449–H1455
Mercadier JJ, Bouveret P, Gorza L, Schiaffino S, Clark WA, Zak R, Swynghedauw B, Schwartz K (1983) Myosin isoenzymes in normal and hypertrophied human ventricular myocardium. Circ Res 53: 52–62
Mercadier JJ, Lompre AM, Wisnewsky C, Samuel JL, Bercovici J, Swynghedauw B, Schwartz K (1981) Myosin isoenzymic changes in several models of rat cardiac hypertrophy. Circ Res 49: 525–532
Neubauer S, Horn M, Gaudron P, Hu K, Laser M, Voll J, Tian R, Ingwall J, Ertl G (1991) Susceptibility of chronically infarcted rat heart to hypoxia and reoxygenation. A 31P-NMR study. Circulation 84 (Suppl H): 275
Pfeffer JM, Pfeffer MA, Fletcher PJ, Braunwald E (1991) Progressive ventricular remodeling in rat with myocardial infarction. Am J Physiol 260: H1406–H1414
Pfeffer MA, Braunwald E, Moye LA, Basta L, Brown EJ, Cuddy TE, Davis BR, Geltmann EM, Goldman S, Flaker GC, Klein M, Lamas GA, Packer M, Rouleau J, Rouleau JL, Rutherford J, Wertheimer JH, Hawkins CM (1992) on Behalf of the SAVE Investigators: Effect of Captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 327: 669–677
Reimer KA, Lowe JE, Rasmussen MM, Jennings RB (1977) The Wavefront phenomenon of ischemic cell death. 1. Myocardial infarct size vs duration of coronary occlusion in dogs. Circulation 56: 786–794
Swedberg K, Held P, Kjekshus J, Rasmussen K, Ryden L, Wedel H (1992) on Behalf of the CONSENSUS II Study Group: Effects of the early administration of enalapril on mortality in patients with acute myocardial infarction. N Engl J Med 327: 678–684
The SOLVD Investigators: Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med 327: 685–691
Thollon C, Kreher P, Charlon V, Rossi A (1989) Hypertrophy induced alteration of action potential and effects of the inhibition of angiotensin converting enzyme by Perindopril in infarcted rat hearts. Cardiovasc Res 23: 224–230
Tian R, Gaudron P, Hu K, Han H, Neubauer S, Ertl G (1991) Pressure-Volume Relation and Oxygen Consumption in Isolated Rat Hearts with Chronic Myocardial Infarction. Eur Heart J 12 (Suppl): 133
Topol EJ, Califf RM, Vandormael M, Grines CL, George BS, Sanz ML, Wall T, O’Brien M, Schwaiger M, Aguirre FV, Young S, Popma JJ, Sigmon KN, Lee KL, Ellis SG (1992) A randomized trial of late reperfusion therapy for acute myocardial infarction. Circulation 85: 2090–2099
Tsunoda K, Hodsman GP, Sumithran E, Johnston CI (1986) Atrial natriuretic peptide in chronic heart failure in the rat: A correlation with ventricular dysfunction. Circ Res 59: 256–261
Villari B, Piscione F, Bonaduce D, Golino P, Lanzillo T, Condorelli M, Chiariello M (1990) Usefulness of late coronary thrombolysis (recombinant tissue-type plasminogen activator) in preserving left ventricular function in acute myocardial infarction. Am J Cardiol 66: 1281–1286
Waris EK, Siitonen L, Himanka E (1966) Heart size and prognosis in myocardial infarction. Am Heart J 71: 187–195
Warren SE, Royal HD, Markis JE, Grossman W, McKay RG (1988) Time course of left ventricular dilatation after myocardial infarction: Influence of infarct-related artery and success of coronary thrombolysis. J Am Coll Cardiol 11: 12–19
Weber KT, Janicki JS (1989) Angiotensin and the remodelling of the myocardium. Br J Clin Pharmac 28: 141S–150S
White HD, Norris RM, Brown MA, Brandt PWT, Whitlock RML, Wild CJ (1987) Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction. Circulation 76: 44–51
Wolf R, Nötges A, Sinn R, Lichtlen PR (1991) Einfluß koronarer Kollateralgefäße auf den Verlauf der linksventrikulären Dilatation nach Myokardinfarkt. Z Kardiol 8: 614–621
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© 1993 Dr. Dietrich Steinkopff Verlag GmbH & Co. KG, Darmstadt
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Ertl, G., Gaudron, P., Hu, K. (1993). Ventricular remodeling after myocardial infarction. Experimental and clinical studies. In: Grobecker, H., Heusch, G., Strauer, B.E. (eds) Angiotensin and the Heart. Steinkopff. https://doi.org/10.1007/978-3-642-72497-8_9
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