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Myocardium stunned

Przyklenk, K. and Kloner, R.A. (1986). Superoxide dismutase plus catalase improve contractile function in the canine model of the stunned myocardium. Circ. Res. 58, 148-156. [Pg.72]

Bolli, R, Patel, B.S., Jeroudi, M.O., Lai, E.K. and McCay, P.B. (1988). Demonstration of free radical generation in stunned myocardium of intact dogs with the use of the spin trap a-phenyl-N-ferr-butyl nitrone. J. Clin. Invest. 82, 476-485. [Pg.274]

Ascher, E.K. Stauffer, J-C.E. and Gaasch, W.H. Coronary artery spasm, cardiac arrest, transient electrocardiographic Q waves and stunned myocardium in cocaine-associated acute myocardial infarction. [Pg.337]

Figure 2.6 illustrates stunned myocardium with normal resting perfusion but a severe stress induced perfusion defect that indicates severe ischemia in the distribution of the RCA and the LAD proximal to the first septal perforator. Metabolic imaging with FDG is not necessary, since resting perfusion is normal without scar with a left ventricular ejection fraction (LVEF) of 30% thereby indicating stunned myocardium that normalized after bypass surgery. This patient with severe stress induced ischemia and reduced LV function characteristic of stunned myocardium contrasts with the patient of Fig. 2.2 with severe ischemia but normal LV function and no stunning. [Pg.20]

Figure 2.7 also illustrates stunned myocardium with resting perfusion and resting metabolic uptake of FDG in a patient with congestive heart failure, diabetes, and a LVEF of 10% where stress was not... [Pg.20]

Fig. 2.6 Positron emission tomography (PET) scan showing stunned myocardium with normal resting perfusion but a severe stress induced perfusion defect that indicates severe... Fig. 2.6 Positron emission tomography (PET) scan showing stunned myocardium with normal resting perfusion but a severe stress induced perfusion defect that indicates severe...
For patients with chronic CAD, nuclear imaging is essential for addressing the following major clinical issues (i) detection of ischemic myocardium, (ii) differentiation between viable hibernating or stunned myocardium and scar tissue in mechanically dysfunctional regions, and (ill) risk stratification for future major adverse events. Such information provides the basis for percutaneous coronary intervention (PCI) or coronary artery bypass (CAB) surgery and assessing their outcomes based on detection of residual ischemia and recovery of contractile function. [Pg.21]

Braunwald E, Kloner RA. The stunned myocardium prolonged, postischemic ventricular dysfunction. Circulation 1982 66 1146-1149... [Pg.32]

At present, angiogenic therapy using bone marrow MNCs is performed worldwide in patients with treatment-resistant ischemic limbs. Moreover, angiogenic therapy using autologous bone marrow MNCs injected into stunned (hibernated) myocardium is performed in several institutions, and the number of trial centers is also increasing very fast. [Pg.292]

RuettenH, Badorff C, IhlingC, Zeiher AM, Dimmeler S. Inhibition of caspase-3 improves contractile recovery of stunned myocardium, independent of apoptosis-inhibitory effects. J Am Coll Cardiol 2001 38 2063-2070. [Pg.42]

Conflicting views exist in the literature on the cardioprotective effect of PBN. By far the most detailed investigation on this subject came from pioneering studies by Bolli and coworkers [104-110], These investigators reported a causal relationship between production of PBN adducts and the post-ischemic functional recovery of stunned myocardium afforded by PBN in canine models. However, another report on the lack of cardioprotection by PBN in a canine model has recently appeared [132]. Hearse and Tosaki [114,115] have previously shown that PBN inhibits the development of arrhythmias in a rat model however, the concentrations of PBN used in that study were too low to be acting as a radical scavenger. It is plausible that some hitherto unknown pharmacologic property of PBN could have been responsible for the observed antiarrhythmic effect. [Pg.353]

In isolated perfused hearts, ventricular dysfunction may be due to myocardial stunning or lethal cell injury. In the Langendorff perfused ischemic rat hearts, ATP concentrations decrease rapidly to 60% in the first minute, with a rapid secondary decrease by 13 min due to contracture (33). Recovery from stunned to normal myocardium requires 24-48 h in the in vivo reperfused heart with coronary artery occlusion of 2-20 min (34). Dobrinina et al. (11) showed that neutral liposomes preserved liver integrity in rats subjected to hepatotropic poisons by non-specific mechanisms. However, histochemical infarct size data do not support this hypothesis in the myocardium (Fig. 3b). [Pg.317]

S.J. Kim, C. Depre and S. Vatner, Novel mechanisms mediating stunned myocardium, Heart Failure Reviews 8, 143-153 (2003). [Pg.67]

H. Kusuoka, J.K. Porterfield, H.F. Weisman, M.L. Weisfeldtand and E. Marban, Pathophysiology and pathogenesis of stunned myocardium. Depressed Ca2+ activation of contraction as a consequence of reperfusion-induced cellular calcium overload in ferret hearts, J. Clin. Invest. 79(3), 950-961 (1987). [Pg.68]

W.D. Gao, Y. Liu and E. Marban, Mechanism of decreased myofilament Ca2 responsiveness in stunned rat ventricular myocardium relative roles of soluble cytosolic factors versus structural alterations, Circ. Res. 78, 455 165 (1996). [Pg.68]

J.A. Fallavollita and J.M. Canty Jr, Differential 18F-2-deoxyglucose uptake in viable dysfunctional myocardium with normal resting perfusion evidence for chronic stunning in pigs, Circulation 99(21), 2798-2805 (1999). [Pg.68]

J. Jansen, P. Gres, C. Umschlag, F.R. Heinzel, H. Degenhardt, K.D. Schluter, G. Heusch and R. Schulz, Parathyroid hormone-related peptide improves contractile function of stunned myocardium in rats and... [Pg.95]

C. M. Ballantyne, M. S. Verani, H. D. Short, C. Hyatt, G. P. Noon, Delayed recovery of severely stunned myocardium with the support of a left ventricular assist device after coronary artery bypass graft surgery, J Am Coll Cardiol 10, 710-712 (1987). [Pg.190]

Z. Yao, G. J. Gross, Glibenclamide antagonizes adenosine A, rcccptor-mediatcd cardioprotection in stunned canine myocardium, Circulation 88,235-44 (1993). [Pg.191]


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See also in sourсe #XX -- [ Pg.265 ]




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