919-12 Transient Wall Motion Abnormalities Following Rotational Coronary Atherectomy are Reflective of Myocardial Stunning More than Microinfarction
Gordon S. HugginsMichael WilliamsJane YangCharles J. DowRoger J. HajjarMichael PicardIgor F. Palacios
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Stunning
Myocardial Stunning
Transient (computer programming)
Myocardiai stunning is a mechanical dysfunction that persists after reperfusion of previously ischemic tissue in the absence of irreversible damage including myocardial necrosis. Myocardial stunning is an unfavorable phenomenon that is manifest during reperfusion and is caused mostly by events associated with reperfusion. This dysfunction and the accompanying contractile abnormalities delay the benefits of reperfusion therapy.
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Myocardial Stunning
Myocardial reperfusion
Myocardial Reperfusion Injury
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Myocardial Stunning
Coronary occlusion
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Recent studies suggest that the hydroxyl radical (.OH) plays a pathogenetic role in postischemic ventricular dysfunction (myocardial "stunning"). This concept, however, is predicated exclusively on results obtained in anesthetized open-chest preparations, which are subject to the confounding influence of many unphysiological conditions and in which both myocardial stunning and free radical generation are greatly exaggerated. The lack of supporting evidence in more physiological animal models represents a major limitation of the .OH hypothesis of stunning. Furthermore, concern has been raised that myocardial stunning may be a period of "rest" necessary for full recovery, so that attenuation of the early phase of stunning by antioxidant therapy may have subsequent detrimental effects on the resting function and/or on the return of myocardial contractile reserve. To address these issues, in phase 1 of this study conscious unsedated dogs undergoing a 15-minute coronary artery occlusion received an intravenous infusion of normal saline (n = 22), of the .OH scavenger N-2-mercaptopropionyl glycine (MPG, n = 17), or of the iron chelator desferrioxamine (DF, n = 14). Compared with control dogs, the dogs treated with MPG or DF exhibited significantly greater postischemic wall thickening throughout the first 6 hours of reperfusion; the total deficit of wall thickening during this time interval was reduced 50% by MPG and 50% by DF. The magnitude of this beneficial effect was a function of the severity of ischemia, so that the dogs with the lowest collateral flows had the greatest improvement of wall thickening. The accelerated recovery produced by MPG and DF in the first 6 hours was not followed by any deterioration of resting wall thickening at 24 or 48 hours. Furthermore, in dogs treated with MPG or DF, the increase in wall thickening elicited by maximal inotropic stimulation (isoproterenol or dopamine) was similar before stunning and shortly after resting wall thickening had normalized (24 or 48 hours after reflow); thus, despite the fact that most of the early postischemic dysfunction had been eliminated by antioxidant therapy, there was no subsequent impairment of either resting function or contractile reserve. In phase 2, production of free radicals (measured with the spin trap alpha-phenyl N-tert-butyl nitrone) was markedly (> 80%) inhibited by the same doses of MPG and DF that attenuated stunning in phase 1.(ABSTRACT TRUNCATED AT 400 WORDS)
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Free radical scavenger
Coronary occlusion
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This article describes clinical situations in which stunning occurs and updates previous reviews on the topic. Stunning following angioplasty, angina and exercise-induced ischemia, infarction, and after cardiac surgery are described. In addition, newer concepts regarding stunning, including neurogenic stunned myocardium, are discussed. Left atrial stunning following cardioversion is a recently recognized phenomenon with important clinical implications, but differs from the original concept of post-ischemic stunning.
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Myocardial Stunning
Stunning
Hibernating myocardium
Phospholamban
Cardioprotection
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Recent studies suggest that the hydroxyl radical (.OH) plays a pathogenetic role in postischemic ventricular dysfunction (myocardial stunning). This concept, however, is predicated exclusively on results obtained in anesthetized open-chest preparations, which are subject to the confounding influence of many unphysiological conditions and in which both myocardial stunning and free radical generation are greatly exaggerated. The lack of supporting evidence in more physiological animal models represents a major limitation of the .OH hypothesis of stunning. Furthermore, concern has been raised that myocardial stunning may be a period of rest necessary for full recovery, so that attenuation of the early phase of stunning by antioxidant therapy may have subsequent detrimental effects on the resting function and/or on the return of myocardial contractile reserve. To address these issues, in phase 1 of this study conscious unsedated dogs undergoing a 15-minute coronary artery occlusion received an intravenous...
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Myocardial Stunning
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Myocardial Stunning
Hibernating myocardium
Hibernation
Ventricular Function
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Myocardial Stunning
Hibernating myocardium
Coronary occlusion
Collateral circulation
Coronary anatomy
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Abstract Over the past two decades, we have challenged the belief that transient ischemia is benign with little functional sequelae following resolution of ischemia. The phenomenon of prolonged postischemic contractile dysfunction, or of myocardial stunning, has been developed and is under investigation using multiple experimental and clinical models. Classifications of myocardial stunning have been suggested and include single and multiple reversible ischemic episodes, partially reversible episodes, and global ischemia. More challenging is the understanding of the mechanisms of myocardial stunning, including free radical protection, excitation-contraction uncoupling, altered calcium flux, microvascular dysfunction, and impaired energy production and use. Finally, advances have been made in the clinical arena, including development of new more sensitive technologies to detect dysfunction, and development of potentially important therapies, including free radical scavengers, adenosine-regulating agents, and calcium channel blockers. In this brief overview, we focus on myocardial stunning, including a historical perspective of coronary occlusion, and definition, classification, and clinical implications of myocardial stunning.
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