Circulation. 2002;105:85-92
doi: 10.1161/hc0102.101365
doi: 10.1161/hc0102.101365
(Circulation. 2002;105:85.)
© 2002 American Heart Association, Inc.
Basic Science Reports |
Genetic Alterations That Inhibit In Vivo Pressure-Overload Hypertrophy Prevent Cardiac Dysfunction Despite Increased Wall Stress
From the Departments of Medicine (G.E., A.R., S.V.N.P., H.T., H.A.R.) and Surgery (W.J.K.), Duke University Medical Center, Durham, NC, and the Department of Pharmacology, University of Pennsylvania, Philadelphia (S.A.T.).
Correspondence to Howard A. Rockman, MD, Department of Medicine, Duke University Medical Center, DUMC 3104, Durham, NC, 27710. E-mail h.rockman{at}duke.edu
Background— A long-standing hypothesis has been that hypertrophy is compensatory and by normalizing wall stress acts to maintain normal cardiac function. Epidemiological data, however, have shown that cardiac hypertrophy is associated with increased mortality, thus casting doubt on the validity of this hypothesis.
Methods and Results— To determine whether cardiac hypertrophy is necessary to preserve cardiac function, we used 2 genetically altered mouse models that have an attenuated hypertrophic response to 8 weeks of pressure overload. End-systolic wall stress (
es) obtained by sonomicrometry after 1 week of pressure overload showed complete normalization of es in pressure-overloaded wild-type mice (287±39 versus sham, 254±34 g/cm2), whereas the blunted hypertrophic response in the transgenic mice was inadequate to normalize es (415±81 g/cm2, P<0.05). Remarkably, despite inadequate normalization of es, cardiac function as measured by serial echocardiography showed little deterioration in either of the pressure-overloaded genetic models with blunted hypertrophy. In contrast, wild-type mice with similar pressure overload showed a significant increase in chamber dimensions and progressive deterioration in cardiac function. Analysis of downstream signaling pathways in the late stages of pressure overload suggests that phosphoinositide 3-kinase may play a pivotal role in the transition from hypertrophy to heart failure.
Conclusions— These data suggest that under conditions of pressure overload, the development of cardiac hypertrophy and normalization of wall stress may not be necessary to preserve cardiac function, as previously hypothesized.
Key Words: contractility • hypertrophy • heart failure • receptors, adrenergic, beta • signal transduction
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B. S. Scopacasa, V. P. A. Teixeira, and K. G. Franchini Colchicine attenuates left ventricular hypertrophy but preserves cardiac function of aortic-constricted rats J Appl Physiol, April 1, 2003; 94(4): 1627 - 1633. [Abstract] [Full Text] [PDF]
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C. Morisco, J. Sadoshima, B. Trimarco, R. Arora, D. E. Vatner, and S. F. Vatner Is treating cardiac hypertrophy salutary or detrimental: the two faces of Janus Am J Physiol Heart Circ Physiol, April 1, 2003; 284 (4): H1043 - H1047. [Full Text] [PDF]
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 J. M. Colomer, L. Mao, H. A. Rockman, and A. R. Means Pressure Overload Selectively Up-Regulates Ca2+/Calmodulin-Dependent Protein Kinase II in Vivo Mol. Endocrinol., February 1, 2003; 17(2): 183 - 192. [Abstract] [Full Text] [PDF]
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 I. Sjaastad, J A. Wasserstrom, and O. M Sejersted Heart failure - a challenge to our current concepts of excitation-contraction coupling J. Physiol., January 1, 2003; 546(1): 33 - 47. [Abstract] [Full Text] [PDF]
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S. Nemoto, G. DeFreitas, D. L. Mann, and B. A. Carabello Effects of changes in left ventricular contractility on indexes of contractility in mice Am J Physiol Heart Circ Physiol, December 1, 2002; 283(6): H2504 - H2510. [Abstract] [Full Text] [PDF]
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M. A. Sussman, A. McCulloch, and T. K. Borg Dance Band on the Titanic: Biomechanical Signaling in Cardiac Hypertrophy Circ. Res., November 15, 2002; 91(10): 888 - 898. [Abstract] [Full Text] [PDF]
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J. R. Keys, E. A. Greene, W. J. Koch, and A. D. Eckhart Gq-Coupled Receptor Agonists Mediate Cardiac Hypertrophy Via the Vasculature Hypertension, November 1, 2002; 40(5): 660 - 666. [Abstract] [Full Text] [PDF]
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R. Nishio, S. Sasayama, and A. Matsumori Left ventricular pressure-volume relationship in a murine model of congestive heart failure due to acute viral myocarditis J. Am. Coll. Cardiol., October 16, 2002; 40(8): 1506 - 1514. [Abstract] [Full Text] [PDF]
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C. Indolfi, E. Di Lorenzo, C. Perrino, A. M. Stingone, A. Curcio, D. Torella, A. Cittadini, L. Cardone, C. Coppola, L. Cavuto, et al. Hydroxymethylglutaryl Coenzyme A Reductase Inhibitor Simvastatin Prevents Cardiac Hypertrophy Induced by Pressure Overload and Inhibits p21ras Activation Circulation, October 15, 2002; 106(16): 2118 - 2124. [Abstract] [Full Text] [PDF]
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D. Fatkin and R. M. Graham Molecular Mechanisms of Inherited Cardiomyopathies Physiol Rev, October 1, 2002; 82(4): 945 - 980. [Abstract] [Full Text] [PDF]
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J. Kim, A. D. Eckhart, S. Eguchi, and W. J. Koch beta -Adrenergic Receptor-mediated DNA Synthesis in Cardiac Fibroblasts Is Dependent on Transactivation of the Epidermal Growth Factor Receptor and Subsequent Activation of Extracellular Signal-regulated Kinases J. Biol. Chem., August 23, 2002; 277(35): 32116 - 32123. [Abstract] [Full Text] [PDF]
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B. J Wilkins and J. D Molkentin Calcineurin and cardiac hypertrophy: Where have we been? Where are we going? J. Physiol., May 15, 2002; 541(1): 1 - 8. [Abstract] [Full Text] [PDF]
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J. A. Hill, B. Rothermel, K.-D. Yoo, B. Cabuay, E. Demetroulis, R. M. Weiss, W. Kutschke, R. Bassel-Duby, and R. S. Williams Targeted Inhibition of Calcineurin in Pressure-overload Cardiac Hypertrophy. PRESERVATION OF SYSTOLIC FUNCTION J. Biol. Chem., March 15, 2002; 277(12): 10251 - 10255. [Abstract] [Full Text] [PDF]
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 S.V. NAGA PRASAD, J. NIENABER, and H.A. ROCKMAN G-Protein-coupled Receptor Function in Heart Failure Cold Spring Harb Symp Quant Biol, January 1, 2002; 67(0): 439 - 444. [Abstract] [PDF]
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M. Sano and M. D. Schneider Still Stressed Out but Doing Fine: Normalization of Wall Stress Is Superfluous to Maintaining Cardiac Function in Chronic Pressure Overload Circulation, January 1, 2002; 105(1): 8 - 10. [Full Text] [PDF]
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M. Suzuki, K. M. Carlson, D. A. Marchuk, and H. A. Rockman Genetic Modifier Loci Affecting Survival and Cardiac Function in Murine Dilated Cardiomyopathy Circulation, April 16, 2002; 105(15): 1824 - 1829. [Abstract] [Full Text] [PDF]
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