© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
"Myocardial stunning"
remaining questions1
aExperimental Cardiology, Thoraxcenter, Erasmus University Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, Netherlands
bDepartment of Pathophysiology, University of Essen, Essen, Germany
cFondazione Clinica del Lavoro, Brescia, Italy
dHospital General Universitairi, Vall d'Hebron, Barcelona, Spain
eDepartment of Biochemistry, University of Bologna, Bologna, Italy
* Corresponding author. Tel.: +31-10-408-8029; fax: +31-10-436-5607; e-mail: verdouw@tch.fgg.eur.nl
Received 12 December 1997; accepted 19 February 1998
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1 What is stunning and why is it important? |
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The pivotal importance of myocardial perfusion for the maintenance of myocardial contractile function was already recognized some 60 years ago [1], but the functional and metabolic consequences of brief as well as long coronary artery occlusions have become unravelled only in the last twenty years. Until the mid seventies, coronary artery occlusions of different duration were used to describe the transition of reversible to irreversible damage [2, 3]. It was more or less assumed that function of ischaemic myocardium would recover almost instantaneously upon reperfusion or did not recover completely because myocardium had become infarcted due to the long duration of occlusion (>30 min). In the seventies, the technology became available to determine regional myocardial function by sonomicrometry and using this technique Heyndrickx et al. [4]described that in awake dogs following a 15 min coronary artery occlusion recovery of regional myocardial contractile function was not immediate as
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2 What are the most pressing questions about myocardial stunning? |
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2.1 What are the remaining controversies of established triggers and modulators of myocardial stunning?
2.1.1 Oxygen-derived free radicals
2.1.2 Ca2+
2.1.3 How do free radicals and Ca2+ produce stunning?
2.1.4 Angiotensin converting enzyme and prostacyclin
2.2 Do we know all the triggers?
2.3 What are the controversies regarding abnormalities in excitation-contraction coupling?
2.3.1 Decreased Ca2+-transients or decreased myofilament responsiveness to calcium?
2.4 Is vascular stunning related to myocardial stunning?
2.5 Can we discard alterations in metabolism as a cause for myocardial stunning?
2.6 Is inotropic reserve of stunned myocardium normal?
2.7 Is recruitment of inotropic reserve harmful?
2.8 Is there a relation between stunning and ischaemic preconditioning?
2.9 Does stunning contribute to hibernation?
2.10 What is the clinical importance of myocardial stunning?
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3 Conclusion |
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