© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Distribution of myocardial injury and its relation to epicardial ST-segment change after coronary occlusion in the dog
Head, Section of Cardiology, Rikshospitalet, Pilestredet 32, 0027 Oslo, Norway
* Tel.: +47-22-86-8365; fax: +47-22-86-8357 john.kjekhus{at}klinmed.uio.no
KEYWORDS ECG; Infarction; Ischemia
From 1969 to 1970 I was a fortunate Fogarty research fellow in Professor Eugene Braunwalds Department at UCSD on the Pacific brim in sunny San Diego.
While John Glenn stepped down on the moon we discussed MJRU-projects. My particular undertaking was to develop methods to assess infarct size in order to examine the effect of interventions designed to prevent development of myocardial injury following an acute coronary occlusion. Together with Professor Burton Sobel, a large number of candidates for marker of myocardial injury was tested in order to determine the evolving infarct size. Of all enzymes and cellular constituents tested, creatinekinase (CK) was best in show [1]. Myocardial depletion of CK was shown to be a useful determinant of the extent and magnitude of myocardial necrosis. In the present study we demonstrated that myocardial CK depletion 24 h after coronary occlusion correlated well to regional myocardial flow as measured with microsphere technique (Fig. 1). The late Peter Maroko developed epicardial ST mapping as a semi-quantitative reflection of acutely induced myocardial ischemia [2]. The present study documented that early ST-segment elevation correlated with the ultimate depletion of myocardial CK from myocardial samples from the site of epicardial electrocardiograms. The study also documented that the magnitude of necrosis always was larger in sub-endocardial than in sub-epicardial samples with respect to the extent of CK depletion in the dog heart, demonstrating the excess vulnerability of myocardial tissue to ischemia in the sub-endocardial regions of the left ventricular wall (Fig. 2).
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) and sub-endocardial biopsies (
) from dog hearts 24 h after ligation of left anterior descending coronary artery. Local blood flow was estimated by the distribution of radioactively labelled microspheres in the same biopsy. The regression line (least squares method) characterizing the relationship between the depression of myocardial CPK activity and reduction in blood flow 24 h after corornary artery occlusion is represented.
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We also had in our hands a chance to demonstrate ischemic preconditioning of the myocardium, but unfortunately we were too focused on the ischemia and the subsequent myocardial damage to pay attention to the significance of the need for repeated coronary occlusions before the initial high ST-segment elevation stabilised and became reproducible.
Assessment of infarct size became an important tool to study pharmacological interventions on infarct evolution with β-blockers [2], inotropic drugs [2], free fatty acids [3] and revascularisation in dogs [4] and subsequently in patients.
Based on these interventional studies, β-blocker therapy and revascularisation became effective routine treatment in patients with acute coronary occlusion. The technique also enabled us to define the very short time window effective for treatment for infarct reduction [1,4]. The entrepreneurial activities and scientific results created in the atmosphere of the MIRU-research laboratories was forever valued by a young Norwegian who took the opportunity to spend his wandering years in San Diego at the relentless pace of the Pacific waves in the background. It was a great time for which I am forever grateful to the Fogarty Institution.
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 Top References |
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- Kjekshus J.K., Sobel B.E. Depressed myocardial creatine phosphokinase activity following experimental myocardial infarction in rabbit. Circ Res (1970) 27:403–414.
[Abstract/Free Full Text] - Maroko P.R., Kjekshus J.K., Sobel B.E., et al. Factors influencing infarct size following experimental coronary artery occlusion. Circulation (1971) 43:67–82.
[Abstract/Free Full Text] - Kjekshus J.K., Mjras O.D. Effect of inhibition of lipolysis on infarct size after experimental coronary artery occlusion. J Clin Invest (1973) 52:1770–1778.[Web of Science][Medline]
- Maroko P.R., Libby P., Ginks W.R., et al. Coronary artery reperfusion. I. Early effects on local myocardial function and the extent of myocardial necrosis. J Clin Invest (1972) 51:2710–2716.[Web of Science][Medline]
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