Cardiac hypertrophy: A risk factor for QT-prolongation and cardiac sudden death

Toxicologic Pathology

Volumn 34, Issue 1, 2006, Pages 58-66

  Kang, Y ^a  

^a University of Louisville School of Medicine   (United States)

Author keywords

Arrhythmia; Cardiac hypertrophy; Cardiac sudden death; Heart failure; Maladaptive response; QT prolongation; Signaling pathway

Indexed keywords

ADENYLATE KINASE; ANGIOTENSIN; BETA 1 ADRENERGIC RECEPTOR; CALCINEURIN; CALCIUM; DOXORUBICIN; ENDOTHELIN RECEPTOR; G PROTEIN COUPLED RECEPTOR; GLYCOGEN SYNTHASE KINASE 3; GUANINE NUCLEOTIDE BINDING PROTEIN; MITOGEN ACTIVATED PROTEIN KINASE; MYOCYTE ENHANCER FACTOR 2; PHOSPHATIDYLINOSITOL 3 KINASE; POTASSIUM CHANNEL; PROTEIN KINASE C; SODIUM CHANNEL; TRANSCRIPTION FACTOR; TRANSCRIPTION FACTOR AP 1; TRANSCRIPTION FACTOR GATA 1; TRANSCRIPTION FACTOR GATA 2; TRANSCRIPTION FACTOR GATA 3; TRANSCRIPTION FACTOR GATA 4; TRANSCRIPTION FACTOR GATA 5; TRANSCRIPTION FACTOR GATA 6;

ADAPTATION; CARDIOVASCULAR RISK; GAP JUNCTION; GENE EXPRESSION; GENOMICS; HEART ARRHYTHMIA; HEART FAILURE; HEART HYPERTROPHY; HEART MUSCLE FIBROSIS; HEART MUSCLE ISCHEMIA; HEART VENTRICLE HYPERTROPHY; HOMEOSTASIS; NONHUMAN; PRIORITY JOURNAL; PROTEIN MOTIF; PROTEOMICS; PURKINJE FIBER; QT INTERVAL; QT PROLONGATION; REVIEW; SIGNAL TRANSDUCTION; STRESS; SUDDEN DEATH; TORSADE DES POINTES;

ADAPTATION, PHYSIOLOGICAL; ANIMALS; CARDIOMEGALY; CAUSE OF DEATH; DEATH, SUDDEN, CARDIAC; DISEASE MODELS, ANIMAL; HUMANS; LONG QT SYNDROME; RISK FACTORS;

ANIMALIA;

EID: 33644645746     PISSN: 01926233     EISSN: 15331601     Source Type: Journal    
DOI: 10.1080/01926230500419421     Document Type: Review

References (75)

1. Abas, L., Bogoyevitch, M. A., and Guppy, M. (2000). Mitochondrial ATP production is necessary for activation of the extracellular-signal-regulated kinases during ischaemia/reperfusion in rat myocyte-derived H9c2 cells. Biochem J 349, 119-26.
2. Adams, J. W., Sakata, Y., Davis, M. G., Sah, V. P., Wang, Y., Liggett, S. B., Chien, K. R., Brown, J. H., and Dorn, G. W. (1998). Enhanced Galphaq signaling: a common pathway mediates cardiac hypertrophy and apoptotic heart failure. Proc Natl Acad Sci USA 95, 10140-15.
3. Akhter, S. A., Luttrell, L. M., Rockman, H. A., Iaccarino, G., Lefkowitz R. J., and Koch, W. J. (1998). Targeting the receptor-Gq interface to inhibit in vivo pressure overload myocardial hypertrophy. Science 280, 574-7.
4. Arad, M., Moskowitz, I. P., Patel, V. V., Ahmad, F., Perez-Atayde, A. R., Sawyer, D. B., Walter, M., Li, G. H., Burgon, P. G., Maguire, C. T., Stapleton, D., Schmitt, J. P., Guo, X. X., Pizard, A., Kupershmidt, S., Roden, D. M., Berul, C. I., Seidman, C. E., and Seidman, J. G. (2003). Transgenic mice overexpressing mutant PRKAG2 define the cause of Wolff-Parkinson-White syndrome in glycogen storage cardiomyopathy. Circulation 107, 2850-6.
5. Bennett, P. B., Yazawa, K., Makita, N., and George, A. L., Jr. (1995). Molecular mechanism for an inherited cardiac arrhythmia. Nature 376, 683-5.
6. Berenji, K., Drazner, M. H., Rothermel, B. A., and Hill, J. A. (2005). Does load-induced ventricular hypertrophy progress to systolic heart failure? Am J Physiol Heart Circ Physiol 289, H8-H16.
7. Bisognano, J. D., Weinberger, H. D., Bohlmeyer, T. J., Pende, A., Raynolds, M. V., Sastravaha, A., Roden, R., Asano, K., Blaxall, B. C., Wu, S. C., Communal, C., Singh, K., Colucci, W., Bristow, M. R., and Port, D. J. (2000). Myocardial-directed overexpression of the human beta(1)-adrenergic receptor in transgenic mice. J Mol Cell Cardiol 32, 817-30.
8. Black, B. L., and Olson, E. N. (1998). Transcriptional control of muscle development by myocyte enhancer factor-2 (MEF2) proteins. Annu Rev Cell Dev Biol 14, 167-96.
9. Brand, T., Sharma, H. S., Fleischmann, K. E., Duncker, D. J., McFalls, E. O., Verdouw, P. D., and Schaper, W. (1992). Proto-oncogene expression in porcine myocardium subjected to ischemia and reperfusion. Circ Res 71, 1351-60.
10. Buck, E. D., Lachnit, W. G., and Pessah, I. N. (1999). Mechanisms of delta-hexachlorocyclohexane toxicity: I. Relationship between altered ventricular myocyte contractility and ryanodine receptor function. J Pharmacol Exp Ther 289 477-85.
11. Cheng, T. H., Shih, N. L., Chen, S. Y., Wang, D. L., and Chen, J. J. (1999). Reactive oxygen species modulate endothelin-I-induced c-fos gene expression in cardiomyocytes. Cardiovasc Res 41, 654-62.
12. Cheng, W., Li, B., Kajstura, J., Li, P., Wolin, M. S., Sonnenblick, E. H., Hintze, T. H., Olivetti, G., and Anversa, P. (1995). Stretch-induced programmed myocyte cell death. J Clin Invest 96, 2247-59.
13. de Simone, G. (2003). Left ventricular geometry and hypotension in endstage renal disease: a mechanical perspective. J Am Soc Nephrol 14, 2421-7.
14. Delaughter, M. C., Taffet, G. E., Fiorotto, M. L., Entman, M. L., and Schwartz, R. J. (1999). Local insulin-like growth factor I expression induces physiologic, then pathologic, cardiac hypertrophy in transgenic mice. FASEB J 13, 1923-9.
15. Depre, C., and Taegtmeyer, H. (2000). Metabolic aspects of programmed cell survival and cell death in the heart. Cardiovasc Res 45, 538-48.
16. Diamond, M. I., Miner, J. N., Yoshinaga, S. K., and Yamamoto, K. R. (1990). Transcription factor interactions: selectors of positive or negative regulation from a single DNA element. Science 249, 1266-72.
17. Dorn, G. W., and Force, T. (2005). Protein kinase cascades in the regulation of cardiac hypertrophy. J Clin Invest 115, 527-37.
18. Eghbali, M., Deva, R., Alioua, A., Minosyan, T. Y., Ruan, H., Wang, Y., Toro, L., and Stefani, E. (2005). Molecular and functional signature of heart hypertrophy during pregnancy. Circ Res 96, 1208-16.
19. Esposito, G., Rapacciuolo, A., Naga Prasad, S. V., Takaoka, H., Thomas, S. A., Koch, W. J., and Rockman, H. A. (2002). Genetic alterations that inhibit in vivo pressure-overload hypertrophy prevent cardiac dysfunction despite increased wall stress. Circulation 105, 85-92.
20. Evans, T., Reitman, M., and Felsenfeld, G. (1988). An erythrocyte-specific DNA-binding factor recognizes a regulatory sequence common to all chicken globin genes. Proc Natl Acad Sci USA 85, 5976-80.
21. Evens, T. (1997). Regulation of cardiac gene expression by GATA-4/5/6. Trends Cardiovasc Med 7, 75-83.
22. Francis, G. S., and Chu, C. (1995). Compensatory and maladaptive responses to cardiac dysfunction. Curr Opin Cardiol 10, 260-7.
23. Frenneaux, M. P. (2004). Assessing the risk of sudden cardiac death in a patient with hypertrophic cardiomyopathy. Heart 90, 570-5.
24. Frey, N., and Olson, E. N. (2003). Cardiac hypertrophy: the good, the bad, and the ugly. Annu Rev Physiol 65, 45-79.
25. He, S. Y., Matoba, R., Sodesaki, K., Fujitani, N., and Ito, Y. (1996). Morphological and morphometric investigation of cardiac lesions after chronic administration of methamphetamine in rats. Nippon Hoigaku Zasshi 50, 63-71.
26. Hill, J. A., Karimi, M., Kutschke, W., Davisson, R. L., Zimmerman, K., Wang, Z., Kerber, R. E., and Weiss, R. M. (2000). Cardiac hypertrophy is not a required compensatory response to short-term pressure overload. Circulation 101, 2863-9.
27. Ho, P. D., Zechner, D. K., He, H., Dillmann, W. H., Glembotski, C. C., and McDonough, P. M. (1998). The Raf-MEK-ERK cascade represents a common pathway for alteration of intracellular calcium by Ras and protein kinase C in cardiac myocytes. J Biol Chem 273, 21730-5.
28. Holtz, J. (1993). Pathophysiology of heart failure and the renin-angiotensin-system. Basic Res Cardiol 88 (Suppl 1), 183-201.
29. Jalili, T., Takeishi, Y., and Walsh, R. A. (1999). Signal transduction during cardiac hypertrophy: the role of G alpha q, PLC beta I, and PKC. Cardiovasc Res 44, 5-9.
30. Joshi, A., Dimino, T., Vohra, Y., Cui, C., and Yan, G. X. (2004). Preclinical strategies to assess QT liability and torsadogenic potential of new drugs: the role of experimental models. J Electrocardiol 37 (Suppl). 7-14.
31. Kahan, T., and Bergfeldt, L. (2005). Left ventricular hypertrophy in hypertension: its arrhythmogenic potential. Heart 91, 250-6.
32. Kang, Y. J., Zhou, Z. X., Wang G, W., Buridi, A., and Klein, J. B. (2000). Suppression by metallothionein of doxorubicin-induced cardiomyocyte apoptosis through inhibition of p38 mitogen-activated protein kinases. J Biol Chem 275, 13690-8.
33. Kass, D. A., Saavedra, W. F., and Sabbah, H. N. (2004). Reverse remodeling and enhanced inotropic reserve from the cardiac support device in experimental cardiac failure. J Card Fail 10, S215-9.
34. Kozhevnikov, D. O., Yamamoto, K., Robotis, D., Restivo, M., and El Sherif, N. (2002). Electrophysiological mechanism of enhanced susceptibility of hypertrophied heart to acquired torsade de pointes arrhythmias: tridimensional mapping of activation and recovery patterns. Circulation 105, 1128-34.
35. Lenczowski, J. M., Dominguez, L., Eder, A. M., King, L. B., Zacharchuk, C. M., and Ashwell J. D. (1997). Lack of a role for Jun kinase and AP-1 in Fas-induced apoptosis. Mol Cell Biol 17, 170-81.
36. Marsin, A. S., Bertrand, L., Rider, M. H., Deprez, J., Beauloye, C., Vincent, M. F., Van den, B. G., Carling, D., and Hue, L. (2000). Phosphorylation and activation of heart PFK-2 by AMPK has a role in the stimulation of glycolysis during ischaemia. Curr Biol 10, 1247-55.
37. Matsui, T., Li, L., Wu, J. C., Cook, S. A., Nagoshi, T., Picard, M. H., Liao, R., and Rosenzweig, A. (2002). Phenotypic spectrum caused by transgenic overexpression of activated Akt in the heart. J Biol Chem 277, 22896-901.
38. McMahon, S. B., and Monroe, J. G. (1992). Role of primary response genes in generating cellular responses to growth factors. FASEB J 6, 2707-15.
39. Molkentin, J. D., Lu, J. R., Antos, C. L., Markham, B., Richardson, J., Robbins, J., Grant, S. R., and Olson E. N. (1998). A calcineurin-dependent transcriptional pathway for cardiac hypertrophy. Cell 93, 215-28.
40. Neubauer, S., Horn, M., Cramer, M., Harre, K., Newell, J. B., Peters, W., Pabst, T., Ertl, G., Hahn, D., Ingwall, J. S., and Kochsiek, K. (1997). Myocardial phosphocreatine-to-ATP ratio is a predictor of mortality in patients with dilated cardiomyopathy. Circulation 96, 2190-6.
41. Newton, A. C. (1995). Protein kinase C: Structure, function, and regulation. J Biol Chem 270, 28495-8.
42. Orkin, S. H. (1992). GATA-binding transcription factors in hematopoietic cells. Blood 80, 575-81.
43. Paradis, P., MacLellan, W. R., Belaguli, N. S., Schwartz, R. J., and Schneider, M. D. (1996). Serum response factor mediates AP-1-dependent induction of the skeletal alpha-actin promoter in ventricular myocytes. J Biol Chem 271, 10827-33.
44. Peters, A., Liu, E., Verrier, R. L., Schwartz, J., Gold, D. R., Mittleman, M., Baliff, J., Oh, J. A., Allen, G., Monahan, K., and Dockery, D. W. (2000). Air pollution and incidence of cardiac arrhythmia. Epidemiology 11, 11-17.
45. Piano, M. R. (1994). Cellular and signaling mechanisms of cardiac hypertrophy. J Cardiovasc Nurs 8, 1-26.
46. Pu, W. T., Ma, Q., and Izumo, S. (2003). NFAT transcription factors are critical survival factors that inhibit cardiomyocyte apoptosis during phenylephrine stimulation in vitro. Circ Res 92, 725-731.
47. Puceat, M., and Vassort, G. (1996). Signalling by protein kinase C isoforms in the heart. Mol Cell Biochem 157, 65-72.
48. Rao, A., Luo, C., and Hogan, P. G. (1997). Transcription factors of the NFAT family: regulation and function. Annu Rev Immunol 15, 707-747.
49. Rooney, J. W., Hodge, M. R., McCaffrey, P. G., Rao, A., and Glimcher, L. H. (1994). A common factor regulates both Th1- and Th2-specific cytokine gene expression. EMBO J 13, 625-33.
50. Rosen M. R. (1995). Cardiac arrhythmias and antiarrhythmic drugs: recent advances in our understanding of mechanism. J Cardiovasc Electrophysiol 6, 868-79.
51. Russell, R. R., III, Bergeron, R., Shulman, G. I., and Young, L. H. (1999). Translocation of myocardial GLUT-4 and increased glucose uptake through activation of AMPK by AICAR. Am J Physiol 277, H643-H649.
52. Schoenmakers, M., Ramakers, C., van Opstal, J. M., Leunissen, J. D., Londono, C., and Vos, M. A. (2003). Asynchronous development of electrical remodeling and cardiac hypertrophy in the complete AV block dog. Cardiovasc Res 59, 351-9.
53. Schreiner, K. D., Kelemen, K., Zehelein, J., Becker, R., Senges, J. C., Bauer, A., Voss, F., Kraft, P., Katus, H. A., and Schoels, W. (2004). Biventricular hypertrophy in dogs with chronic AV block: effects of cyclosporin A on morphology and electrophysiology. Am J Physiol Heart Circ Physiol 287, H2891-80.
54. Shier, W. T., and DuBourdieu, D. J. (1992). Sodium- and calcium-dependent steps in the mechanism of neonatal rat cardiac myocyte killing by ionophores. I. The sodium-carrying ionophore, monensin. Toxicol Appl Pharmacol 116, 38-46.
55. Shioi, T., Kang, P. M., Douglas, P. S., Hampe, J., Yballe, C. M., Lawitts, J., Cantley, L. C., and Izumo, S. (2000). The conserved phosphoinositide 3-kinase pathway determines heart size in mice. EMBO J 19, 2537-18.
56. Shioi, T., McMullen, J. R., Kang, P. M., Douglas, P. S., Obata, T., Franke, T. F., Cantley. L. C., and Izumo, S. (2002). Akt/protein kinase B promotes organ growth in transgenic mice. Mol Cell Biol 22, 2799-809.
57. Sleight, P. (1996). Calcium antagonists during and after myocardial infarction. Drugs 51, 216-25.
58. Splawski, I., Shen J., Timothy, K. W., Lehmann, M. H., Priori, S., Robinson, J. L., Moss, A. J., Schwartz, P. J., Towbin, J. A., Vincent, G. M., and Keating, M. T. (2000). Spectrum of mutations in long-QT syndrome genes. KVLQT1, HERG, SCN5A, KCNE1, and KCNE2. Circulation 102, 1178-85.
59. Stemmer, P. M., and Klee, C. B. (1994). Dual calcium ion regulation of calcineurin by calmodulin and calcineurin B. Biochemistry 33, 6859-66.
60. Sugden, P. H., and Clerk, A. (1998). "Stress-responsive" mitogen-activated protein kinases (c-Jun N-terminal kinases and p38 mitogen-activated protein kinases) in the myocardium. Circ Res 83, 345-52.
61. Swynghedauw, B. (1999). Molecular mechanisms of myocardial remodeling. Physiol Rev 79, 215-62.
62. Swynghedauw, B., Baillard, C., and Milliez, P. (2003). The long QT interval is not only inherited but is also linked to cardiac hypertrophy. J Mol Med 81, 336-15.
63. Symanski, J. D., and Gettes, L. S. (1993). Drug effects on the electrocardiogram. A review of their clinical importance. Drugs 46, 219-48.
64. Tan, Y., Rouse, J., Zhang, A., Cariati, S., Cohen, P., and Comb, M. J. (1996). FGF and stress regulate CREB and ATF-1 via a pathway involving p38 MAP kinase and MAPKAP kinase-2. EMBO J 15, 4629-42.
65. ten Eick, R. E., Whalley, D. W., and Rasmussen, H. H. (1992). Connections: heart disease, cellular electrophysiology, and ion channels. FASEB J 6, 2568-80.
66. + mobilization during excitation-contraction in cultured cardiac myocytes exposed to antimony. Toxicol Appl Pharmacol 146, 104-15.
67. van Empel, V. P., and De Windt, L. J. (2004). Myocyte hypertrophy and apoptosis: A balancing act. Cardiovasc Res 63, 487-99.
68. Wang, X. Z., and Ron. D. (1996). Stress-induced phosphorylation and activation of the transcription factor CHOP (GADD153) by p38 MAP Kinase. Science 272, 1347-9.
69. Wang, Y., Huang, S., Sah, V. P., Ross, J., Jr., Brown J. H., Han J., and Chien, K. R. (1998). Cardiac muscle cell hypertrophy and apoptosis induced by distinct members of the p38 mitogen-activated protein kinase family. J Biol Chem 273, 2161-8.
70. Wettschureck, N., Rutten, H., Zywietz, A., Gehring, D., Wilkie, T. M., Chen, J., Chien, K. R., and Offermanns, S. (2001). Absence of pressure overload induced myocardial hypertrophy after conditional inactivation of Galphaq/Galpha11 in cardiomyocytes. Nat Med 7, 1236-10.
71. Wollert, K. C., Heineke, J., Westermann, J., Ludde M., Fiedler, B., Zierhut, W., Laurent, D., Bauer, M. K., Schulze-Osthoff K., and Drexler, H. (2000). The cardiac Fas (APO-1/CD95) Receptor/Fas ligand system: relation to diastolic wall stress in volume-overload hypertrophy in vivo and activation of the transcription factor AP-1 in cardiac myocytes. Circulation 101, 1172-8.
72. Wollnik, B., Schroeder, B. C., Kubisch, C., Esperer, H. D., Wieacker, P., and Jentsch, T. J. (1997). Pathophysiological mechanisms of dominant and recessive KVLQT1 K+ channel mutations found in inherited cardiac arrhythmias. Hum Mol Genet 6, 1943-9.
73. Yamamoto, M., Ko, L. J., Leonard, M. W., Beug, H., Orkin, S. H., and Engel, J. D. (1990a). Activity and tissue-specific expression of the transcription factor NF-E1 multigene family. Genes Dev 4, 1650-2.
74. Yin, T., Sandhu, G., Wolfgang, C. D., Burrier, A., Webb, R. L., Rigel, D. F., and Hai T., Whelan, J. (1997). Tissue-specific pattern of stress kinase activation in ischemic/reperfused heart and kidney. J Biol Chem 272, 19943-50.
75. Zou, Y., Hiroi, Y., Uozumi, H., Takimoto, E., Toko, H., Zhu W., Kudoh, S., Mizukami, M., Shimoyama, M., Shibasaki, F., Nagai R., Yazaki, Y., and Komuro, I. (2001). Calcineurin plays a critical role in the development of pressure overload-induced cardiac hypertrophy. Circulation 104, 97-101.