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Myocardial Viability: Stunning and Hibernation

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Cardiac Positron Emission Tomography

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 166))

Abstract

Myocardial stunning is defined as a transient postischemic myocardial dysfunction, occurring during full reperfusion after a short episode of non-lethal ischemia. This phenomenon was first recognized by Heyndrickx et al.1 and termed “myocardial stunning” by Braunwald and Kloner.2 The initial description of stunning i.e. a total coronary occlusion of only 5 to 15 minutes that was not associated with detectable myocardial necrosis, resulted in impairment of ventricular systolic function that lasted for several hours following reperfusion. Since then, myocardial stunning has been demonstrated experimentally under a variety of conditions and in many different animal species. Several of these conditions become extremely important for a better understanding of the clinical relevance of myocardial stunning. At first there is the problem of “peri-infarction stunning”. It has been well established that during prolonged coronary artery occlusion only a variable fraction of the area at risk will become necrotic.3 A “border zone” of myocardial tissue, adjacent to necrotic myocardium will survive mainly due to collateral flow, and myocardial stunning can be demonstrated in this border zone after delayed reperfusion of the blocked vessel.4Therefore, the akinetic area related to infarction can easy be overestimated in the early reperfusion phase: at this stage differentiation between viable and necrotic tissue cannot be made on the basis of regional function studies alone. Second, not only regional ischemia will result in stunning upon reperfusion but also global ischemia or anoxia. This finding has important implications because it explains why hearts of patients undergoing cardiac surgery are very often dysfunctional in the early period of reperfusion after cross clamping of the aorta despite cardioplegic protection. A third important circumstance under which stunning can be demonstrated is that stunning also occurs in the presence of partial coronary stenosis instead of complete occlusion followed by reperfusion.5 Obviously relative ischemia due to imbalance between oxygen supply and demand can induce stunning as well as a complete occlusion of the coronary vessel. This observation is important because it explains why transient coronary spasm may result in regional myocardial dysfunction.

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References

  1. Heyndrickx GR, Millard RW, Mc Ritchie RJ et al. Regional myocardial functional and electrophysiological alterations after brief coronary artery occlusion in conscious dogs. J Clin Invest 1975;56:978–85.

    Article  PubMed  CAS  Google Scholar 

  2. Braunwald E, Kloner RA. The stunned myocardium: Prolonged, postischemic ventricular dysfunction. Circulation 1982;66:1146–9.

    Article  PubMed  CAS  Google Scholar 

  3. Flameng W, Lesaffre E, Vanhaecke J. Determinants of infarct size in non-human primates. Basic Res Cardiol 1990;85:392–403.

    Article  PubMed  CAS  Google Scholar 

  4. Ellis SG, Henschke CI, Sandor T et al. Time course of functional and biochemical recovery of myocardium salvaged by reperfusion. J Am Coll Cardiol 1983;1:1047–55.

    Article  PubMed  CAS  Google Scholar 

  5. Thaulow E, Guth BD, Heusch G et al. Characteristics of regional myocardial stunning after exercise in dogs with chronic coronary stenosis. Am J Physiol 1989;257:H113–9.

    PubMed  CAS  Google Scholar 

  6. Flameng W, Vanhaecke J, Borgers M. Histology of the postischaemic myocardium and its relation to left ventricular function. Br J Anaesth 1988;60:145–225.

    Article  Google Scholar 

  7. Vanhaecke J, Flameng W, Borgers M, Jang IK, VandeWerf F, Degeest H. Evidence for decreased coronary flow reserve in viable postischemic myocardium. Circ Res 1990;67:1201–11.

    Article  PubMed  CAS  Google Scholar 

  8. Flameng W, Andres J, Ferdinande P, Mattheussen M, Van Belle H. Mitochondrial function in myocardial stunning. J Mol Cell Cardiol 1991;23:1–11.

    Article  PubMed  CAS  Google Scholar 

  9. Greenfield RA, Swain JL. Disruption of myofibrillar energy use: mechanisms that may contribute to postischemic dysfunction in stunned myocardium. Circulation 1985;72(Suppl 3):68.

    Google Scholar 

  10. Schaper W, Buchwald A, Hoffmeister HM, Ito BR. “Stunned myocardium” is a problem of energy utilization and not of energy supply. Circulation 1985;72(Suppl 3):119.

    Google Scholar 

  11. Ito BR, Tate H, Schaper W. Calcium induced increases in regional contractile function before and after transient coronary occlusion in dog. Circulation 1985;72(Suppl 3):68.

    Google Scholar 

  12. Bolli R. Mechanism of myocardial “Stunning”. Circulation 1990;82:723–38.

    Article  PubMed  CAS  Google Scholar 

  13. Kaplan P, Hendrikx M, Mattheussen M, Mubagwa K, Flameng W. Effect of ischemia and reperfusion on sarcoplasmic reticulum calcium uptake. Circ Res 1992;71:1123–30.

    Article  PubMed  CAS  Google Scholar 

  14. Mattheussen M, Mubagwa K, Rusy BF, Van Aken H, Flameng W. Potentiated state contractions in isolated hearts: effects of ischemia and reperfusion. Am J Physiol 1993;264:H1663–73.

    PubMed  CAS  Google Scholar 

  15. Kusuoka H, Koretsune Y, Chacko VP, Weisfeldt ML, Marban E. Excitation-contraction coupling in postischemic myocardium: Does failure of activator Ca2+ transients underlie “Stunning”? Circ Res 1990;66:1268–76.

    Article  PubMed  CAS  Google Scholar 

  16. Flameng W, Van der Vusse J, Borgers M. Methods for assessing preservation techniques-Invasive techniques. In: Engelman R, Levitsky L, editors. Handbook of clinical cardioplegia. Mount Kisco, New York: Futura Publishing Company, 1982:63–80.

    Google Scholar 

  17. Flameng W, Sergeant P, Vanhaecke J, Suy R. Emergency coronary bypass grafting for evolving myocardial infarction: effects on infarct size and left ventricular function. J Thorac Cardiovasc Surg 1987;94:124–31.

    PubMed  CAS  Google Scholar 

  18. Robertson WS, Feigenbaum H, Armstrong WF, Dillon JC, O’Donnell J, McHenry PW. Exercise echocardiography: a clinical practical addition in the evaluation of coronary artery disease. J Am Coll Cardiol 1983;6:1085–9.

    Article  Google Scholar 

  19. Camici P, Araiyo LI, Spinks T et al. Increased uptake of 18F-fluorodeoxyglucose in postischemic myocardium of patients with exercise-induced angina. Circulation 1986;74:81–8.

    Article  PubMed  CAS  Google Scholar 

  20. Renkin J, Wyns W, Ladha Z, Col J. Reversal of segmental hypkinesis by coronary angioplasty in patients with unstable angina, persistent T wave inversion, and left anterior descending coronary artery stenosis. Additional evidence for myocardial stunning in humans. Circulation 1990;82:913–21.

    Article  PubMed  CAS  Google Scholar 

  21. Rahimtoola SH. A perspective on three large multicenter randomized clinical trials of coronary bypass surgery for chronic stable angina. Circulation 1985;72(Suppl V): 123–5.

    Google Scholar 

  22. Rahimtoola SH. The hibernating myocardium. Am Heart J 1989;117:211–21.

    Article  PubMed  CAS  Google Scholar 

  23. Flameng W, Wouters L, Sergeant P et al. Multivariate analysis of angiographic, histologic and electrocardiographic data in patients with coronary heart disease. Circulation 1984;70:7–17.

    Article  PubMed  CAS  Google Scholar 

  24. Flameng W, Suy R, Schwarz F et al. Ultrastructural correlates of left ventricular contraction abnormalities in patients with chronic ischemie heart disease: determinants of reversible segmental asynergy. Am Heart J 1981; 102:846–57.

    Article  PubMed  CAS  Google Scholar 

  25. Flameng W, Vanhaecke J, Van Belle H, Borgers M, De Beer L, Mimen J. Relation between coronary artery stenosis and myocardial purine metabolism, histology and regional functions in humans. J Am Coll Cardiol 1987;9:1235–42.

    Article  PubMed  CAS  Google Scholar 

  26. Borgers M, Thone F, Wouters L, Ausma J, Shivalkar B, Flameng W. Structural correlates of regional myocardial dysfunction in patients with critical coronary artery stenosis: Chronic Hibernation? Cardiovasc Pathol 1993;2:237–45.

    Article  Google Scholar 

  27. Shivalkar B, Borgers M, Maes A, Mortelmans L, Flameng W. Low regional function associated with high metabolism predicts functional recovery after coronary bypass surgery. Circulation 1994;90, 4:1–251.

    Google Scholar 

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© 1995 Springer Science+Business Media Dordrecht

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Flameng, W., Shivalkar, B., Borgers, M. (1995). Myocardial Viability: Stunning and Hibernation. In: van der Wall, E.E., Blanksma, P.K., Niemeyer, M.G., Paans, A.M.J. (eds) Cardiac Positron Emission Tomography. Developments in Cardiovascular Medicine, vol 166. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-0023-6_2

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  • DOI: https://doi.org/10.1007/978-94-011-0023-6_2

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-4014-3

  • Online ISBN: 978-94-011-0023-6

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