Τόμος 7 (1993) – Τεύχος 3 – Άρθρο 1 – Επιθεώρηση Κλινικής Φαρμακολογίας και Φαρμακοκινητικής-Διεθνής Έκδοση – Volume 7 (1993) – Issue 3 – Article 1 – Epitheorese Klinikes Farmakologias και Farmakokinetikes-International Edition

 

Title The diastolic and systolic function of hypertrophic myocardium
Author Constantine L. Papadopoulos

2nd Department of Cardiology, Aristotelian University of Thessaloniki, Greece

Citation Papadopoulos, C.L.: The diastolic and systolic function of hypertrophic myocardium, Epitheorese Klin. Farmakol. Farmakokinet. 7(3): 101-107 (1993)
Publication Date Received for publication: 25 October 1993

Accepted for publication: 5 November 1993

Full Text Language English
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Keywords Hypertrophic myocardium, diastolic function, systolic function.
Other Terms review article
Summary In cardiac overload, myocardial hypertrophy represents the most efficient long-term compensatory mechanism; hypertrophy leads lately to heart failure because several disorders are gradually grown up within the hypertrophied myocardium resulting initially in diastolic and eventually in systolic dysfunction. The increased consumption and the impaired regeneration of ATP result in a decrease in the available ATP. Small ATP deficits lead to allosteric transformation of many functional proteins thus impairing their contribution in the diastolic and systolic processes. The mechanical effects of the hypertrophic myocardium and the hyperplastic connective tissue affect adversely relaxation, as well. Severe ATP deficit results in myocardial asystole and necrosis. Down regulation of β1 adrenoceptors, alteration in proteinic composition, altered membrane assembly and reappearance of foetal proteins contribute to the impairment of the systolic function.
References 1.    Circ. Res. 51: 10-18 (19 Wangler R.D., Peters K.G., Marcus M.L. and Tomanes R.J.: Effects of duration and severity of arterial hypertension and cardiac hypertrophy on coronary vascular reserve

2.    Wearn J.T.: Morphological and funcional alterations of the coronary circulation. Harvey Lect. 35: 243-270 (1939-40)

3.    Roberts J.T. and Wearn J.T.: Quantitative changes in the capillary-muscle relationship in human hearts during normal growth and hypertrophy. Am. Heart J. 21: 617-633 (1941)

4.    Anversa P., Olivettei G., Melissari M. and Loud A.V.: Stereological measurement of cellular and subcellular hypertrophy and hyperplasia in the papillary muscle of adult. J. Med. Coll. Cardiol. 12: 781-795 (1980)

5.    Meerson F.Z.: On the mechanism of compensatory hyperfunction and insufficiency of the heart. Cor. Vasa 3: 161-177 (1961)

6.    Wollenberger A. and Schulze W.: Über das Volumenverhaltnis von Mitochiondrien zu Myofibrillen im chronisch überlasteten, hypertrophierten Herzen. Naturwissenschaften 7: 161-162 (1962)

7.    Robinowitz M.: Protein synthesis and turnover in normal and hypertrophied heart. Am. J. Cardiol. 31: 202-210 (1973)

8.    Page E. and McCalister L.P.: Quantitative electromicroscopic description of heart muscle cells. Application in normal hypertrophied and thyroxin-stimulated hearts. Am. Cardiol. 31: 172-181 (1973)

9.    Schultheiss H.P., Ullrich G., Schindler M., Schulze K. and Strauer B.E.: The effect of ACE inhibition on myocardial energy metabolism. Eur. Heart J. 11 (suppl.B): 116-122 (1990)

10.  Bashore T.M., Magorian D.J., Letterio J., Shaffer P. and Unverfeth D.V.: Histologic and biochemical correlates of left ventricular chamber dynamics in man. J. Am. Coll. Cardiol. 9: 734-742 (1987)

11.  Wexler L.F., Lorell B.H., Monomura S.I.: Enhanced sensitivity to hypoxia-induced diastolic dysfunction in pressure oveload left ventricular hypertrophy in the rat: Role of high energy phosphate depletion. Circ. Res. 62: 766-755 (1988)

12.  Peyton R.B., Jones R.N., Attarian D., Sink J.D. and Trigt P., Currie W.D. and Wechsler A.S.: Depressed high energy phosphate content in hypertrophied ventricles of animal and man. Ann. Surg. 196: 278-283 (1982)

13.  Swain J.L., Sabina R.L, Peyton R.B., et al: Derangements in myocardial purine and pyrimidine nucleotide metabolism in patients with coronary artery disease and left ventricular hypertrophy. Proc. Natl. Acad. Set. U.S.A. 79: 655-659 (1982)

14.  Shigekawa M., Cougherjy J.P. and Katz A.M.: Reaction mechanism of Ca²+ dependent ATP hydrolysis by skeletal muscle sarcoplasmic reticulum in the absence of added alkali metal salts. I. Characterization of steady state ATP hydrolysis and comparison with that in the presence of KCl. J. Biol Chem. 256: 1442-1450 (1978)

15.  Nakamura Y. and Tonomura Y.: The binding of ATP to the catalytic and the regulatory site of Ca²+, Mg²+-dependent ATPase of the sarcoplasmic reticulum. J. Bioeng. Biomed. 14: 3-7-318 (1982)

16.  DiPolo R.: The influence of nucleotides on calcium fluxes. 35: 2579-2582 (1976)

17.  Yamaguchi M, and Tonomura Y.: Binding of monovalent cations to Na+, K+-dependent ATPase purified from porcine kidney. N. Acceleration of transition from a K+-bound form to a Na+-bound form by binding of ATP to a regulatory size of the enzyme. J. Biochem (Tokyo) 88: 1377-1385 (1980)

18.  Kameyama M., Hescheler J., Hofman F. and Trautwein W.: Modulation of Ca current during the phosphorylation cycle in the guinea pig heart. Pflügers Arch., 407: 123-128 (1986)

19.  Smith J., Coronado R. and Meissner G.: Single channel measurements of the calcium release channel from sarcoplasmic reticulum. Activation by calcium and ATP and modulation by magnesium. J. Gen. Physiol. 88: 573-588 (1986)

20.  Spray D.C. and Bennett M.V.L.: Physiology and pharmacology of gap junctions. Annu. Rev. Physiol 47: 218-303 (1985)

21.  Casch W.H.: Congestive heart failure in patients with normal left ventricular systolic function: a manifestation of diastolic dysfunction. Herz 16: 22-32 (1991)

22.  Haneda T., Watson P.A. and Morgan H.E.: Elevated aortic pressure calcium uptake and protein synthesis in rat heart. J. Mol. Cell. Cardiol. 21 (suppl 1): 131-138 (1989)

23.  Simpson P.: Proto-oncogenes and cardiac hypertrophy. Annu. Rev. Physiol 51: 189-201 (1989)

24.  Linz W., Scholkens B., Lindpaintner K. and Ganten D.: Cardiac renin-angiotensin system. Am. J. Hypertens. 2: 307-310 (1989)

25.  Dzau B.J.: Cardiac renin-angiotensin system. Molecular and functional aspects. Am. J. Med. 84 (suppl 3A): 22-27 (1988)

26.  Komuro I., Kaida T., Shibazaki Y., Kurabayashi M., Katoh Y., Hoh E., Takaku F. and Yazaki Y.: Stretching cardiac myocytes stimulates protooncogene expression. J. Biol Chem. 265: 3595-3598 (1990)

27.  Cooper G., Kent R.L. and Mann D.L.: Load induction of cardiac hypertrophy. J. Mol. Cell. Cardiol 21 (suppl V): 11-30 (1989)

28.  Samuel J.L., Marotte F., Delcayre C. and Rappaport L.: Microtubule reorganization is related to rate of heart myocyte hypertrophy in rat. Am. J. Physiol. 251: H1118-1125 (1986)

29.  Komuro I., Kurabayashi M., Takaku F, and Yazaki Y.: Expression of cellular oncogenes in the myocardium during the development stage and pressure-overloaded hypertrophy of the rat heart. Circ. Res. 62: 1075-1079 (1988)

30.  Caspari P.G., Newcomb M., Gibson K. and Harris P.: Collagen in the normal and hypertrophied human ventricle. Cardiovasc. Res. 11: 554-558 (1977)

31.  Weber K.T., Janicki J.S., Schroff S.G., Pick R., Chen R.M. and Bashey R.I.: Collagen remodeling of the pressure-overloaded hypertrophied nonhuman primate myocardium. Circ. Res. 62: 757-765 (1988)

32.  Dalla-Volta S., Razzolini R., Scognamiglio R., Rubino A. and Chioin R.: Myocardial function in heart failure. Cardiology, 75: 8-18 (1988)

33.  Linzbach A.J.: Heart failure from the point of view of quantitative anatomy. Am. J. Cardiol 5: 370-382 (1960)

34.  Bean B.P., Nowocky M.C., Tsien R.W.: β-adrenergic modulation of the number of functional calcium channels in frog ventricular heart cells. Nature 307: 371-374 (1984)

35.  Toda M.: Mechanisms of the stimulation of Ca²+-dependent ATPase of cardiac sarcoplasmic reticulum by adenosine-3′,5′-monophosphate dependent protein kinase. J. Biol. Chem. 254: 319-324 (1979)

36.  Holroyde M.J., Howe E., Solazo R.J.: Modifications of calcium requirements for activation of cardiac myofibrillar ATPase by cyclic AMP-dependent phosphorylation. Biochem. Biophys. Acta 586: 62-70 (1979)

37.  Bristow M.R., Anderson F.L., Port J.D., Skerl L., Hershberger R.E., Larrabee P., O’Connell J.B., Renlund D.G., Vokmann K., Murray J., Feldman A.M.: Differences in β-adrenergic neuroeffector mechanisms in ischemic versus idiopathic dilated cardiomyopathy. Circulation 84: 1024-1039 (1991)

38.  Chen L.H., Vatner D.E., Vatner S.F., Hittinger L., Homey C.J.: Decreased Gs alpha mRNA levels accompany the fall in Gs and adenylyl cyclase activities in compensated left ventricular hypertrophy. In heart failure, only the impairment in adenylyl cyclase activation progresses. J. Clin. invest. 87: 293-298 (1991)

39.  Deitmer J.W., Ellis D.: Interactions between the regulation of the intracellular pH and sodium activity of sheep cardiac Purkinje fibers. J. Physiol. (Lond) 304: 471-488 (1980)

40.  Kamuro I., Shibazaki Y., Kurabayshi M., Takaku F. and Yazaki Y.: Molecular cloning of gene sequences from rat heart rapidly responsive to pressure overload. Circ. Res. 66: 979-985 (1990)

41.  Swynghedauw B.: Developmental and functional adaptation of contractile proteins in cardial and skeletal muscles. Physiol. Rev. 66: 710-771 (1986)

42.  Emerson G.P., Jr. and Bersten S.I.: Molecular genetics of myosin. Annu. Rev. Biochem. 56: 695- 726 (1987)

43.  Breitabart R.E., Andreadis A. and Nadal-Ginard B.: Alternative splicing: A ubiquitous mechanism for the generation of multiple protein isoforms from single genes. Anna Rev. Biochem. 65: 467-475 (1987)

44.  Van Cao A., Bouvenet P., Lorente P., Piqnica A., Slama R. and Schwartz K.: Alpha-myosin heavy chain isoform and atrial size in patients with various types of mitral valve dysfunction: a quantitative study. J. Am. Coll. Cardiol. 9: 1024-1030 (1987)

45.  Kurabayashi M., Komuro I., Tsuchimofchi J., Takaku F., and Yazaki Y.: Molecular cloning and characterization of human atrial and ventricular myosin alkali light chain cDNA clones J. Biol. Chem. 263: 13930-13936 (1988)

46.  Schneider M.D. and Parker T.G.: Cardiac myocytes as targets for the action of peptide growth factors. Circulation 81: 1443-14456 (1990)

47.  Komuro I., Kurabayashi M., Shibazaki Y., Takaku F. and Yazaki Y.: Molecular cloning and characterization of a Ca²+ + Mg²+-dependent adenosine triphosphatase from rat cardiac sarcoplasmic reticulum. Regulation of its expression by pressure overload and developmental stage. J. Clin. Invest. 83: 1102-1108 (1989)

48.  De la Bastie D., Levitsky D., Rappaport L., Mercadier J.J., Marotte F., Wisnewsky C., Brokovich V., Schwartz K. and Lompre A.M.: Function of the sarcoplasmic reticulum and expression of its Ca²+ ATPase gene in pressure-overloaded cardiac hypertrophy in the rat. Circ. Res. 66: 554-564 (1990)

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