The cellular pathophysiology of progression to heart failure

Current Opinion in Cardiology

Volumn 11, Issue 3, 1996, Pages 237-244

  Wagoner, Lynne E ^a   Walsh, Richard A ^a  

^a UNIVERSITY OF CINCINNATI MEDICAL CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSINE TRIPHOSPHATASE (CALCIUM); BETA ADRENERGIC RECEPTOR; CALCIUM; CARRIER PROTEIN; PHOSPHOLAMBAN; PHOSPHOTRANSFERASE; SODIUM;

CALCIUM CELL LEVEL; CONGESTIVE HEART FAILURE; CYTOLOGY; HEART CONTRACTION; HEART MUSCLE CELL; HEART VENTRICLE HYPERTROPHY; HUMAN; MOLECULAR BIOLOGY; MORBIDITY; MORTALITY; PRIORITY JOURNAL; REVIEW; SARCOPLASMIC RETICULUM; SODIUM CELL LEVEL;

ACTION POTENTIALS; ADENOSINE TRIPHOSPHATASES; ANIMALS; BETA-ADRENERGIC RECEPTOR KINASE; CALCIUM; CALCIUM-BINDING PROTEINS; CATIONS; CATS; CYCLIC AMP-DEPENDENT PROTEIN KINASES; CYTOSKELETON; CYTOSOL; DOGS; GENE EXPRESSION; GUINEA PIGS; HEART FAILURE, CONGESTIVE; HUMANS; MICE; MUSCLE FIBERS; MYOCARDIUM; RECEPTORS, ADRENERGIC, BETA; SODIUM;

EID: 0029976708     PISSN: 02684705     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001573-199605000-00003     Document Type: Review

References (33)

1. Inoko M, Kihara Y, Moril I, Fujiwara H, Sasayama S: Transition from compensatory hypertrophy to dilated, failing left ventricles in Dahl salt-sensitive rats. Am J Physiol 1994, 267:H2471-H2482.
2. ++ coronary perfusion. J Mol Cell Cardiol 1995, 27:2009-2013.
3. Bing OHL: Hypothesis: Apoptosis may be a mechanism for the transition to heart failure with chronic pressure overload. J Mol Cell Cardiol 1994, 26:943-948.
4. Arai M, Matsui H, Periasamy M: Sarcoplasmic reticulum gene expression in cardiac hypertrophy and heart failure. Circ Res 1994, 74:555-564.
5. Field LJ: Transgenic mice in cardiovascular research. Annu Rev Physiol 1993, 55:97-114.
6. Robbins J: Gene targeting: the precise manipulation of mammalian genome. Circ Res 1993, 73:3-9.
7. Kitsis RN, Scheuer J: Functional significance of alterations in cardiac contractile protein isoforms. Clin Cardiol 1996, 19:9-18.
8. Naqvi RU, MacLeod KT: Effect of hypertrophy on mechanisms of relaxation in isolated cardiac myocytes from guinea pig. Am J Physiol 1994, 267:H1851-H1861.
9. Pieske B, Kretschmann B, Meyer M, Holubarsch C, Weirich J, Posival H, Miniami K, Just H, Hasenfuss G: Alterations in intracellular calcium handling associated with the inverse force-frequency relation in human dilated cardiomyopathy. Circulation 1995, 92:1169-1178. This critical analysis demonstrates the fundamental difference in force-frequency relationship between normal and cardiomyopathic human heart tissue.
10. Gunteski-Hamblin AM, Song G, Walsh RA, Frenzke M, Boivin GP, Dorn GW, Kaetzel MA, Horseman ND, Dedman JR: Annexin VI overexpression targeted to heart alters cardiomyocyte function in transgenic mice. Am J Physiol 1996, 270:H1091-H1100.
11. i in pressure-overloaded guinea pig heart. Am J Hypertens 1995, 8:934-943.
12. + ATPase in left ventricular hypertrophy: pharmacological consequences. Eur Heart J 1995, 16(suppl C):20-23.
13. Lompre AM, Anger M, Levitsky D: Sarco(endo)plasmic reticulum calcium pumps in the cardiovascular system: function and gene expression. J Mol Cell Cardiol 1994, 26:1109-1121.
14. 2+-ATPase protein concentration of isolated myocytes in pressure-overload hypertrophy [abstract]. Circulation 1994, 90(suppl 1):I-633.
15. ++ transport and mechanics in compensated pressure-overload hypertrophy and congestive heart failure. Circ Res 1995, 77:759-764.
16. Williams RE, Kass DA, Kawagoe Y, Pak P, Tunin RS, Shah R, Hwang A, Feldman AM: Endomyocardial gene expression during development of pacing tachycardia-induced heart failure in the dog. Circulation 1994, 75:615-623.
17. Kadambi VJ, Ponniah S, Harrer JM, Hoit BD, Dorn GW, Walsh RA, Kranias EG: Cardiac specific overexpression of phospholamban alters calcium kinetics and resultant cardiomyocyte mechanics in transgenic mice. J Clin Invest 1996, 97:533-539. This important study of transgenic overexpression of phospholamban showed that stoichiometry between phospholamban and SR ATPase is less than unity. It also showed the resultant effects on isolated cardiomyocyte mechanics and calcium transients.
18. Luo W, Grupp IL, Harrer J, Ponniah S, Grupp G, Duffy JJ, Doetschman T, Kranias EG: Targeted ablation of the phospholamban gene is associated with markedly enhanced myocardial contractility and loss of β-agonist stimulation. Circ Res 1994, 75:401-409.
19. ++-ATPase of cardiac sarcoplasmic reticulum are critical for functional association with phospholamban. J Biol Chem 1994, 269:22929-22932.
20. Hoit BD, Khoury SF, Kranias EG, Ball N, Walsh RA: In vivo echocardiographic detection of enhanced left ventricular function in gene-targeted mice with phospholamban deficiency. Circ Res 1995, 77:632-637. The first in vivo demonstration of the capacity to analyze left ventricular performance in normal and genetically engineered mice noninvasively using transthoracic and Doppler echocardiography.
21. Koss KL, Ponniah S, Jones WK, Grupp IL, Kranias EG: Differential phospholamban gene expression in murine cardiac compartments: molecular and physiological analyses. Circ Res 1995, 77:342-353.
22. Movsesian MA, Karimi M, Green K, Jones LR: Ca(2+)-transporting ATPase, phospholamban, and calsequestrin levels in nonfailing and failing human myocardium. Circulation 1994, 90:653-657.
23. ++-ATPase in failing and nonfailing human myocardium. Circ Res 1994, 75:434-442.
24. ++-ATPase activity of cardiac sarcoplasmic reticulum from dilated cardiomyopathy patients compared with patients with nonfailing hearts. Circulation 1995, 92:3220-3228. Controversial and careful analysis of the role of altered calcium-cycling proteins in human cardiomyopathic congestive heart failure.
25. Bohm M, Reiger B, Schfwinger RHG, Erdmann E: cAMP concentrations, cAMP dependent protein kinase activity, and phospholamban in non-failing and faiing myocardium. Cardiovasc Res 1994, 28:1713-1719.
26. del Monte F, O'Gara P, Poole-Wilson PA, Yacoub M, Harding SE: Cell geometry and contractile abnormalities of myocytes from failing human left ventricle. Cardiovasc Res 1995, 30:281-290.
27. Hoit BD, Shao Y, Gabel M, Walsh RA: Disparate effects of early pressure overload hypertrophy on velocity-dependent and force-dependent indices of ventricular performance in the conscious baboon. Circulation 1995, 91:1213-1220.
28. Vatner DE, Sato N, Kiuchi K, Shannon RP, Vatner SF: Decrease in myocardial ryanodine receptors and altered excitation-contraction coupling early in the development of heart failure. Circulation 1994, 90:1423-1430. Excellent demonstration of alterations in the ryanodine receptor and resultant functional changes in the paced tachycardia model of congestive heart failure.
29. 1-2 levels in rat hearts associated with impaired heart function after myocaridal infarction. Am J Physiol 1995, 269:H1073-H1079.
30. Ping P, Hammond HK: Diverse G protein and β-adrenergic receptor mRNA expression in normal and failing porcine hearts. Am J Physiol 1994, 267:H2079-H2085.
31. Koch WJ, Rockman HA, Samama P, Hamilton RA, Bond RA, Milano CA, Lefkowitz RJ: Cardiac function in mice overexpressing the β-adrenergic receptor kinase or a βARK inhibitor. Science 1995, 92:1350-1353. Definitive study of the in vivo role of β-adrenergic receptor kinase in β-adrenergic receptor coupling using transgenic analysis.
32. Tsutsui H, Tagawa H, Kent RL, McCollam P, Ishibara K, Nagatsu M, Cooper GI: Role of microtubules in contractile dysfunction of hypertrophied cardiocytes. Circulation 1994, 90:533-555.
33. Collins JF, Pawloski-Dahm C, Davis MG, Ball N, Dorn GW, Walsh RA: The role of the cytoskeleton in left ventricular pressure overload hypertrophy and failure. J Mol Cell Cardiol 1996, in press.