(Circulation. 2000;102:470.)
© 2000 American Heart Association, Inc.
Clinical Cardiology: New Frontiers |
Left Ventricular Hypertrophy
Pathogenesis, Detection, and Prognosis
From the Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass (B.H.L.), and the Department of Medicine, Baylor College of Medicine, and Veterans Affairs Medical Center, Houston, Tex
Correspondence to Beverly H. Lorell, MD, Cardiology Division, Beth Israel Deaconess Medical Center, Boston, MA 02215.
Key Words: hypertrophy • diastole • heart failure • hypertension
When the heart faces a hemodynamic burden, it can do the following to compensate: (1) use the Frank-Starling mechanism to increase crossbridge formation; (2) augment muscle mass to bear the extra load; and (3) recruit neurohormonal mechanisms to increase contractility. The first mechanism is limited in its scope, and the third is deleterious as a chronic adjustment. Thus, increasing mass assumes a key role in the compensation for hemodynamic overload. This increase in mass is due to the hypertrophy of existing myocytes rather than hyperplasia, because cardiomyocytes become terminally differentiated soon after birth. In response to pressure overload in conditions such as aortic stenosis or hypertension, the parallel addition of sarcomeres causes an increase in myocyte width, which in turn increases wall thickness. This remodeling results in concentric hypertrophy (increase in ratio of wall thickness/chamber dimension).
According to LaPlace’s Law, the load on any region of the
myocardium is given as follows: (pressurexradius)/(2xwall
thickness); thus, an increase in pressure can be offset by an increase
in wall thickness. Because systolic stress (afterload) is a
major determinant of ejection performance, the normalization of
systolic stress helps maintain a normal ejection fraction even
when needing to generate high levels of systolic
pressure.1 Volume overload in conditions such as chronic
aortic regurgitation, mitral
regurgitation, or anemia engenders myocyte lengthening
by sarcomere replication in series and an increase in
ventricular volume. This pattern of eccentric
hypertrophy (cavity dilatation with a decrease in ratio of
wall thickness/chamber dimension) is also initially
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R. Dash, A. G Schmidt, A. Pathak, M. J Gerst, D. Biniakiewicz, V. J Kadambi, B. D Hoit, W. T Abraham, and E. G Kranias Differential regulation of p38 mitogen-activated protein kinase mediates gender-dependent catecholamine-induced hypertrophy Cardiovasc Res, March 1, 2003; 57(3): 704 - 714. [Abstract] [Full Text] [PDF]
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W. Nadruz Jr, C. B. Kobarg, S. S. Constancio, P. D.C. Corat, and K. G. Franchini Load-Induced Transcriptional Activation of c-jun in Rat Myocardium: Regulation by Myocyte Enhancer Factor 2 Circ. Res., February 7, 2003; 92(2): 243 - 251. [Abstract] [Full Text] [PDF]
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S. Pikkarainen, H. Tokola, R. Kerkela, T. Majalahti-Palviainen, O. Vuolteenaho, and H. Ruskoaho Endothelin-1-specific Activation of B-type Natriuretic Peptide Gene via p38 Mitogen-activated Protein Kinase and Nuclear ETS Factors J. Biol. Chem., January 31, 2003; 278(6): 3969 - 3975. [Abstract] [Full Text] [PDF]
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E. O. Weinberg, M. Mirotsou, J. Gannon, V. J. Dzau, R. T. Lee, and R. E. Pratt Sex dependence and temporal dependence of the left ventricular genomic response to pressure overload Physiol Genomics, January 15, 2003; 12(2): 113 - 127. [Abstract] [Full Text] [PDF]
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E. van Rooij, P. A. Doevendans, C. C. de Theije, F. A. Babiker, J. D. Molkentin, and L. J. De Windt Requirement of Nuclear Factor of Activated T-cells in Calcineurin-mediated Cardiomyocyte Hypertrophy J. Biol. Chem., December 6, 2002; 277(50): 48617 - 48626. [Abstract] [Full Text] [PDF]
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R. Kerkela, S. Pikkarainen, T. Majalahti-Palviainen, H. Tokola, and H. Ruskoaho Distinct Roles of Mitogen-activated Protein Kinase Pathways in GATA-4 Transcription Factor-mediated Regulation of B-type Natriuretic Peptide Gene J. Biol. Chem., April 12, 2002; 277(16): 13752 - 13760. [Abstract] [Full Text] [PDF]
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O. F Bueno, E. van Rooij, J. D Molkentin, P. A Doevendans, and L. J De Windt Calcineurin and hypertrophic heart disease: novel insights and remaining questions Cardiovasc Res, March 1, 2002; 53(4): 806 - 821. [Abstract] [Full Text] [PDF]
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K. C. Wollert, B. Fiedler, S. Gambaryan, A. Smolenski, J. Heineke, E. Butt, C. Trautwein, S. M. Lohmann, and H. Drexler Gene Transfer of cGMP-Dependent Protein Kinase I Enhances the Antihypertrophic Effects of Nitric Oxide in Cardiomyocytes Hypertension, January 1, 2002; 39(1): 87 - 92. [Abstract] [Full Text] [PDF]
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M.H. Yacoub A novel strategy to maximize the efficacy of left ventricular assist devices as a bridge to recovery Eur. Heart J., April 1, 2001; 22(7): 534 - 540. [PDF]
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K. Haghighi, A. G. Schmidt, B. D. Hoit, A. G. Brittsan, A. Yatani, J. W. Lester, J. Zhai, Y. Kimura, G. W. Dorn II, D. H. MacLennan, et al. Superinhibition of Sarcoplasmic Reticulum Function by Phospholamban Induces Cardiac Contractile Failure J. Biol. Chem., June 22, 2001; 276(26): 24145 - 24152. [Abstract] [Full Text] [PDF]
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J. C. Braz, O. F. Bueno, L. J. De Windt, and J. D. Molkentin PKC{alpha} regulates the hypertrophic growth of cardiomyocytes through extracellular signal-regulated kinase1/2 (ERK1/2) J. Cell Biol., March 4, 2002; 156(5): 905 - 919. [Abstract] [Full Text] [PDF]
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B. D. Rosen, T. Edvardsen, S. Lai, E. Castillo, L. Pan, M. Jerosch-Herold, S. Sinha, R. Kronmal, D. Arnett, J. R. Crouse III, et al. Left Ventricular Concentric Remodeling Is Associated With Decreased Global and Regional Systolic Function: The Multi-Ethnic Study of Atherosclerosis Circulation, August 16, 2005; 112(7): 984 - 991. [Abstract] [Full Text] [PDF]
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