(Circulation. 1996;94:2285-2296.)
© 1996 American Heart Association, Inc.
Articles |
Medical Therapy Can Improve the Biological Properties of the Chronically Failing Heart
A New Era in the Treatment of Heart Failure
the Department of Internal Medicine (Cardiology Division) (E.J.E.), The University of Texas Southwestern and Dallas VA Medical Centers; and the Division of Cardiology (M.R.B.), University of Colorado Health Science Center (Denver).
Abstract Myocardial failure has been considered to be an irreversible and progressive process characterized by ventricular enlargement, chamber geometric alterations, and diminished pump performance. However, more recent evidence has suggested that certain types of medical therapy may lead to retardation and even reversal of the cardiomyopathic process. In the failing heart, long-term neurohormonal/autocrine-paracrine activation results in abnormalities in myocyte growth, energy production and utilization, calcium flux, and receptor regulation that produce a progressively dysfunctional, mechanically inefficient heart. Interventions such as ACE inhibition and ß-blockade result in a reduction in the harmful long-term consequences of neurohormonal/autocrine-paracrine effects and retard the progression of left ventricular dysfunction or ventricular remodeling. Furthermore, in subjects with idiopathic dilated or ischemic cardiomyopathy, antiadrenergic therapy with ß-blocking agents appears to be able to partially reverse systolic dysfunction and ventricular remodeling. Although the precise mechanisms underlying this latter effect have not yet been elucidated, the general mechanism appears to be via improvement in the biological function of the cardiac myocyte. Such an improvement in the intrinsic defect(s) responsible for myocardial failure will likely translate into important clinical benefits.
Key Words: heart failure • remodeling • myocardial contraction
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G. W Moe and P. Armstrong Pacing-induced heart failure: a model to study the mechanism of disease progression and novel therapy in heart failure Cardiovasc Res, June 1, 1999; 42(3): 591 - 599. [Full Text] [PDF]
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P. H. Sugden Signaling in Myocardial Hypertrophy : Life After Calcineurin? Circ. Res., April 2, 1999; 84(6): 633 - 646. [Full Text] [PDF]
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H. P. Brunner-La Rocca, G. Vaddadi, and M. D. Esler Recent insight into therapy of congestive heart failure: focus on ACE inhibition and angiotensin-II antagonism J. Am. Coll. Cardiol., April 1, 1999; 33(5): 1163 - 1173. [Abstract] [Full Text] [PDF]
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D. J. Peterson, H. Ju, J. Hao, M. Panagia, D. C. Chapman, and I. M.C. Dixon Expression of Gi-2{alpha} and Gs{alpha} in myofibroblasts localized to the infarct scar in heart failure due to myocardial infarction Cardiovasc Res, March 1, 1999; 41(3): 575 - 585. [Abstract] [Full Text] [PDF]
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M. Bohm, S. Ettelbruck, M. Flesch, W. H van Gilst, A. Knorr, C. Maack, Y. M Pinto, M. Paul, A. C.H Teisman, and O. Zolk {beta}-Adrenergic signal transduction following carvedilol treatment in hypertensive cardiac hypertrophy Cardiovasc Res, October 1, 1998; 40(1): 146 - 155. [Abstract] [Full Text] [PDF]
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C. Communal, K. Singh, D. R. Pimentel, and W. S. Colucci Norepinephrine Stimulates Apoptosis in Adult Rat Ventricular Myocytes by Activation of the ß-Adrenergic Pathway Circulation, September 29, 1998; 98(13): 1329 - 1334. [Abstract] [Full Text] [PDF]
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M. R. Bristow Tumor Necrosis Factor-{alpha} and Cardiomyopathy Circulation, April 14, 1998; 97(14): 1340 - 1341. [Full Text] [PDF]
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H. Ju, S. Zhao, P. S. Tappia, V. Panagia, and I. M. C. Dixon Expression of Gq{alpha} and PLC-ß in Scar and Border Tissue in Heart Failure Due to Myocardial Infarction Circulation, March 10, 1998; 97(9): 892 - 899. [Abstract] [Full Text] [PDF]
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M. Nabauer and S. Kaab Potassium channel down-regulation in heart failure Cardiovasc Res, February 1, 1998; 37(2): 324 - 334. [Abstract] [Full Text] [PDF]
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P. P de Tombe Altered contractile function in heart failure Cardiovasc Res, February 1, 1998; 37(2): 367 - 380. [Abstract] [Full Text] [PDF]
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M. Gheorghiade and R. O. Bonow Chronic Heart Failure in the United States : A Manifestation of Coronary Artery Disease Circulation, January 27, 1998; 97(3): 282 - 289. [Full Text] [PDF]
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J E Sanderson, S K W Chan, C M Yu, L Y C Yeung, W M Chan, K Raymond, K W Chan, and K S Woo beta Blockers in heart failure: a comparison of a vasodilating beta blocker with metoprolol Heart, January 1, 1998; 79(1): 86 - 92. [Abstract] [Full Text] [PDF]
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D.-J. Choi, W. J. Koch, J. J. Hunter, and H. A. Rockman Mechanism of beta -Adrenergic Receptor Desensitization in Cardiac Hypertrophy Is Increased beta -Adrenergic Receptor Kinase J. Biol. Chem., July 4, 1997; 272(27): 17223 - 17229. [Abstract] [Full Text] [PDF]
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M. R. Bristow, E. M. Gilbert, W. T. Abraham, K. F. Adams, M. B. Fowler, R. E. Hershberger, S. H. Kubo, K. A. Narahara, H. Ingersoll, S. Krueger, et al. Carvedilol Produces Dose-Related Improvements in Left Ventricular Function and Survival in Subjects With Chronic Heart Failure Circulation, December 1, 1996; 94(11): 2807 - 2816. [Abstract] [Full Text]
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K. Swedberg, M. R. Bristow, J. N. Cohn, H. Dargie, M. Straub, C. Wiltse, T. J. Wright, and for the Moxonidine Safety and Efficacy (MOXSE) Inv Effects of Sustained-Release Moxonidine, an Imidazoline Agonist, on Plasma Norepinephrine in Patients With Chronic Heart Failure Circulation, April 16, 2002; 105(15): 1797 - 1803. [Abstract] [Full Text] [PDF]
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