Cardiovascular Drugs and Therapy

, Volume 8, Supplement 2, pp 297–304 | Cite as

The ever expanding spectrum of ischemic left ventricular dysfunction

  • Lionel H. Opie
Article
Received:
Accepted:

Summary

Ischemic left ventricular (LV) dysfunction includes a number of discrete entities, such as acute LV failure in angina, acute myocardial infarction, and ischemic cardiomyopathy. Recently, new entities have arisen to expand the spectrum of ischemic LV function. These include postinfarct diastolic dysfunction, stunning, hibernation, and preconditioning. The tantalizing possibility exists that several of these states can coexist. There are widely differing underlying pathophysiologic states. I ence it is not easy to be dogmatic about whether a given group of therapeutic agents, such as the calcium antagonists, may be beneficial in ischemic LV dysfunction. Nonetheless, there is experimental evidence that calcium antagonists may benefit the specific entity of stunning and clinical evidence that they benefit postinfarct ischemic LV diastolic dysfunction. These agents, as a group, should be evaluated in reperfusion and postinfarct dysfunctional syndromes.

Key words

ischemia left ventricular dysfunction diastolic dysfunction systolic dysfunction stunning hibernation postinfarct 
This is a preview of subscription content, log in to check access.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Jennings RB. Myocardial ischemia—observations, definitions and speculations.J Mol Cell Cardiol 1970;1:345–349.Google Scholar
  2. 2.
    Opie LH. Effects of regional ischemia on metabolism of glucose and fatty acids. Relative rates of aerobic and anaerobic energy production during myocardial infarction and comparison with effects of anoxia.Circ Res 1976;38(Suppl I):152–174.Google Scholar
  3. 3.
    Hearse DJ, Braimbridge MV, Jynge P.Protection of the Ischemic Myocardium: Cardioplegia. New York: Raven Press, 1981:22–23.Google Scholar
  4. 4.
    Opie LH. Cardiac metabolism—emergence, decline, and resurgence. Part I.Cardiovasc Res 1992;26:721–733.Google Scholar
  5. 5.
    Bourdillon PD, Lorell BH, Mirsky I, Paulus WJ, Wynne J, Grossman W. Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man.Circulation 1983;67:316–323.Google Scholar
  6. 6.
    Opie LH. Reperfusion injury and its pharmacological modification.Circulation 1989;80:1049–1062.Google Scholar
  7. 7.
    Opie LH, Coetzee WA. Role of calcium ions in reperfusion arrhythmias. Relevance to pharmacological intervention.Cardiovasc Drugs Ther 1988;2:623–636.Google Scholar
  8. 8.
    Saman S, Coetzee WA, Opie LH. Inhibition by stimulated ischemia or hypoxia of delayed afterdepolarizations provoked by cyclic AMP: Significance for ischemic and reperfusion-arrhythmias.J Mol Cell Cardiol 1988;20:91–95.Google Scholar
  9. 9.
    Poole-Wilson PA, Harding DP, Bourdillon PDV, Tones MA. Calcium out of control.J Mol Cell Cardiol 1984;16:175–187.Google Scholar
  10. 10.
    Ehring T, Bohm M, Heusch G. The calcium antagonist nisoldipine improves the functional recovery of reperfused myocardium only when given before ischemia.J Cardiovasc Pharmacol 1992;20:63–74.Google Scholar
  11. 11.
    Dennis SC, Coetzee WA, Cragoe EJ, Opie LH. Effects of proton buffering and of amiloride derivatives on reperfusion arrhythmias in isolated rat hearts: Possible evidence for an arrhythmogenic role of Na+-H+ exchange.Circ Res 1990;66:1156–1159.Google Scholar
  12. 12.
    Heyndrickx GR, Millard RW, McRitchie RJ, Maroko PR, Vatner SF. Regional myocardial function and electrophysiological alterations after brief coronary occlusion in conscious dogs.J Clin Invest 1975;56:978–985.Google Scholar
  13. 13.
    Heyndrickx GR, Baig H, Nellens P, Leusen I, Fishbein MC, Vatner SF. Depression of regional blood flow and wall thickening after brief coronary occlusions.Am J Physiol 1978;234:H653-H659.Google Scholar
  14. 14.
    Braunwald E, Kloner RA. The stunned myocardium: Prolonged, postischemic ventricular dysfunction.Circulation 1982;66:1146–1149.Google Scholar
  15. 15.
    Braunwald E. Stunning of the myocardium. An update.Cardiovasc Drugs Ther 1991;5:849–852.Google Scholar
  16. 16.
    Bolli R. Mechanism of myocardial “stunning.”Circulation 1990;82:723–738.Google Scholar
  17. 17.
    Lavallee M, Cox D, Patrick TA, Vatner SF. Salvage of myocardial function by coronary artery reperfusion 1, 2, and 3 hours after occlusion in conscious dogs.Circ Res 1983;53:235–247.Google Scholar
  18. 18.
    Bolli R. Myocardial “stunning” in man.Circulation 1992;86:1671–1692.Google Scholar
  19. 19.
    Schartl M and the DEFIANT Research Group. Calcium antagonists in the treatment early after myocardial infarction.J Cardiovasc Pharmacol 1992;20(Suppl 5):S79-S81.Google Scholar
  20. 20.
    Natale E, Ricci R, Tubaro M, Milazzotto F. Diastolic ventricular dysfunction in noncomplicated acute myocardial infarction: The influence of gallopamil.J Cardiovasc Pharmacol 1992;20(Suppl 7):S48-S56.Google Scholar
  21. 21.
    Bourdillon PD, Broderick TM, Williams ES, et al. Early recovery of regional left ventricular function after reperfusion in acute myocardial infarction assessed by serial two-dimensional echocardiography.Am J Cardiol 1989;63:641–646.Google Scholar
  22. 22.
    Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the Survival and Ventricular Enlargement Trial.N Engl J Med 1992;327:669–677.Google Scholar
  23. 23.
    SOLVD Investigators. Effect of enalapril on mortality and the developement of heart failure in asymptomatic patients with reduced left ventricular fractions.N Engl J Med 1992;327:685–691.Google Scholar
  24. 24.
    Bolognesi R, Cucchini F, Manca C, Ferrari R. Effects of verapamil and nifedipine on rate of left ventricular relaxation in coronary arterial disease patients.Int J Cardiol 1987;14:333–341.Google Scholar
  25. 25.
    Ferlinz J, Easthope JL, Aronow WS. Effects of verapamil on myocardial performance in coronary disease.Circulation 1979;59:313–319.Google Scholar
  26. 26.
    Rodrigues EA, Lahiri A, Raftery EB. Improvement in left ventricular diastolic function in patients with stable angina after chronic treatment with verapamil and nicardipine.Eur Heart J 1987;8:624–629.Google Scholar
  27. 27.
    Nishimura RA, Schwartz RS, Holmes DR, Tajik AJ. Failure of calcium channel blockers to improve ventricular relaxation in humans.J Am Coll Cardiol 1993;21:182–188.Google Scholar
  28. 28.
    Brunken RC, Armbrecht JJ. Detection of hibernating myocardium with positron emission tomography. In: Zipes DP, Rowlands DJ, eds.Progress in Cardiology. Philadelphia: Lea and Febiger, 1990:161–179.Google Scholar
  29. 29.
    Uren NG, Camici PG. Hibernation and myocardial ischemia: Clinical detection by positron emission tomography. In: Opie LH, ed.Stunning, Hibernation, and Calcium in Myocardial Ischemia and Reperfusion. Boston: Kluwer Academic, 1992:202–215.Google Scholar
  30. 30.
    Pouleur H, van Eyll C, Gurne O, Rousseau MF. Effects of prolonged nisoldipine administration on the “hibernating” myocardium.J Cardiovasc Pharmacol 1992;20(Suppl 5):S73-S78.Google Scholar
  31. 31.
    Vanoverschelde J-L, Wijns W, Depre C, et al. Mechanisms of chronic regional post-ischemic dysfunction in humans. New insights from the study of noninfarcted collateral-dependent myocardium.Circulation 1993;87:1513–1523.Google Scholar
  32. 32.
    Zhao M, Zhang H. Robinson TF, Factor SM, Sonnenblick EH, Eng C. Profound structural alterations of the extracellular collagen matrix in postischemic dysfunction (“stunned”) but viable myocardium.J Am Coll Cardiol 1987;10:1322–1334.Google Scholar
  33. 33.
    Lawson CS, Downey JM. Preconditioning: State of the art myocardial protection.Cardiovasc Res 1993;27:542–550.Google Scholar
  34. 34.
    Nicklas JM, Becker LC, Bulkley BH. Effects of repeated brief coronary occlusion on regional left ventricular function and dimension in dogs.Am J Cardiol 1985;56:473–478.Google Scholar
  35. 35.
    Kent RL, Uboh CE, Thompson EW, et al. Biochemical and structural correlates in unloaded and reloaded cat myocardium.J Mol Cell Cardiol 1985;17:153–165.Google Scholar
  36. 36.
    Agostoni PG, De Cesare N, Doria E, Polese A, Tamborini G, Guazzi MD. Afterload reduction: A comparison of captopril and nifedipine in dilated cardiomyopathy.Br Heart J 1986;55:391–399.Google Scholar
  37. 37.
    Goldstein RE, Bocuzzi SJ, Cruess D, Nattal S, the Adverse Experience Committee, and the Multicenter Diltiazem Post-infarction Research Group. Diltiazem increases late-onset congestive heart failure in post infarction patients with early reduction in ejection fraction.Circulation 1991;83:52–60.Google Scholar
  38. 38.
    Setaro JF, Zaret BL, Schulman DS, Black HR, Soufer R. Usefulness of verapamil for congestive heart failure associated with abnormal left ventricular diastolic filling and normal left ventricular systolic performance.Am J Cardiol 1990;66:981–986.Google Scholar
  39. 39.
    Pouleur H, Rousseau MF, van Eyll C, Melin J, Youngblood M, Salim Y, for the SOLVD Investigators. Cardiac mechanics during development of heart failure.Circulation 1993;87(Suppl IV):IV14-IV20.Google Scholar
  40. 40.
    Hansen JF and the Danish Study Group on Verapamil in Myocardial Infarction. Treatment with verapamil during and after an acute myocardial infarction: A review based on the Danish Verapamil Infarction Trials I and II.J Cardiovasc Pharmacol 1991;18(Suppl 6):S20-S25.Google Scholar

Copyright information

© Kluwer Academic Publishers 1994

Authors and Affiliations

  • Lionel H. Opie
    • 1
  1. 1.Medical Research Council Ischaemic Heart Disease Research UnitUniversity of Cape Town Medical School, ObservatoryCape TownSouth Africa

Personalised recommendations