Viable Myocardium — the Place of Calcium Antagonists

Conference paper


The pathogenetic mechanism of myocardial hibernation has not been fully established. Wall motion abnormalities, occurring early after an acute myocardial infarction, may be reversible or permanent [1]. Thrombolytic therapy increases the probability of early reperfusion and may increase the probability of reversible dysfunction [2]. The infarcted segments may show resting hypoperfusion, despite a preserved viability, and functional recovery once perfusion is restored by bypass grafting or coronary angioplasty [3]. Because enhanced left ventricular function after revascularization is associated with improved survival [4], diagnostic procedures that identify reversible dyssynergy may provide significant prognostic information [5]. Recent studies have shown that the presence of both viable and ischemic myocardium detected by positron emission tomography (PET) is associated with increased incidence of cardiac events at follow-up. PET provides improved imaging capabilities compared with single photon emission computed tomography (SPECT) by correcting for photon attenuation and permitting the noninvasive measurement of regional myocardial blood flow in absolute terms or myocardial substrate utilization. Viable myocardium is identified on the basis of enhanced or preserved metabolic activity in underperfused and dysfunctional myocardial regions [6].


Positron Emission Tomography Single Photon Emission Compute Tomography Myocardial Blood Flow Viable Myocardium Wall Motion Abnormality 
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  1. 1.
    Wilson JL, Ramathan KB, Ingram LA, Mirvis DM (1988) Effects of residual stenosis on infarct size and regional transmural myocardial blood flow after reperfusion. Am Heart J: 1523–1529Google Scholar
  2. 2.
    Ress JCJ, Simoons ML, Van der Wall EE, Van Eeinge MJ, Vermeer F (1986) Long term improvement in global left ventricular function after early thrombolytic treatment in acute myocardial infarction: report of a randomized multicenter trial of intracoronary streptokinase in acute myocardial infarction. Br Heart J 56: 414–421CrossRefGoogle Scholar
  3. 3.
    Chatterjee K, Swan HJC, Parmely WW, Sustaita H, Marcus HS (1973) Influence of direct myocardial revascularization on left ventricular assynergy and function in patients with coronary heart disease. Circulation: 276–286Google Scholar
  4. 4.
    Alderman EL, Fisher LD, Litwin P, Kaiser GC, Myers WO (1983) Result of coronary artery surgery in patients with poor left vetricular function (CASS). Circulation 68: 785–795PubMedCrossRefGoogle Scholar
  5. 5.
    Dilsizian V, Bonow RO (1993) Current diagnostic techniques of assessing myocardial viability in patients with hibernating and stunned myocardium. Circulation 87: 1–20PubMedGoogle Scholar
  6. 6.
    Tillish JH, Brunken R, Marshall R, Schwaiger M, Mandelkorn M (1986) Reversibility of cardiac wall-motion abnormalities predicted by positron tomography. N Engl J Med 314: 884–888CrossRefGoogle Scholar
  7. 7.
    Ellis SG, Wynne J, Braunwald E, Henschke CI, Sandor T (1984) Response of reperfusion-salvaged, stunned myocardium to inotropic stimulation. Am Heart J 107: 13–19PubMedCrossRefGoogle Scholar
  8. 8.
    Mercier JC, Lando U, Kanmatsuse K, Ninomiya K, Meerbaum S (1982) Divergent effects of inotropic stimulation on the ischemic and severely depressed reperfused myocardium. Circulation 66: 397–400PubMedCrossRefGoogle Scholar
  9. 9.
    Smart SC, Sawada S, Ryan T, Segar D, Atheron L, Berkovitz K, Bourdillon PDV, Feigenbaum H (1993) Low-dose dobutamine echocardiography detects reversible dysfunction after thrombolytic therapy of acute myocardial infarction. Circulation 88: 405–415PubMedGoogle Scholar
  10. 10.
    Barilla F, Gheorghiade M, Alam M, Khaja F, Goldstein S (1991) Low-dose dobutamine in patients with acute myocardial infarction identifies viable but not contractile myocardium and predicts the magnitude of improvement in wall motion abnormalities in response to coronary revascularization. Am Heart J 12: 1522–1531CrossRefGoogle Scholar
  11. 11.
    McKay RG, Pfeffer MA, Pasternak RC (1986) Left ventricular remodeling after myocardial infarction: a corollary to infarct expansion. Circulation 74: 693–702PubMedCrossRefGoogle Scholar
  12. 12.
    Sharpe N, Smith H, Murphy J, Hannan S (1988) Treatment of patients with symptomless ventricular dysfunction after myocardial infarction. Lancet i: 256–259Google Scholar
  13. 13.
    Pouleur H, Van Eyll C, Gurne O, Rousseau F (1992) Analysis of the mechanism underlying the changes in left ventricular filling dynamics during oral nisoldipine therapy in patients with anterior myocardial infarction. Eur Heart J 13: 952–959PubMedGoogle Scholar
  14. 14.
    Bristow JD, Arai AE, Anselone Panteley GA (1991) Response to myocardial ischemia as a regulated process. Circulation 84: 2580–2587PubMedGoogle Scholar

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© Springer-Verlag Berlin Heidelberg 1999

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