Copyright © 2004 by the European Society of Cardiology.
Preclinical research
The sequential changes in myocardial thickness and thickening which occur during acute transmural infarction, infarct reperfusion and the resultant expression of reperfusion injury
a Department of Cardiology, University Hospital Gasthuisberg, Catholic University of Leuven, Herestraat 49, B-3000 Leuven, Belgium
b Medical Image Computing, Department of Electrical Engineering, Catholic University of Leuven, Leuven, Belgium
c Department of Physics, Catholic University of Leuven, Leuven, Belgium
d Department of Pathology, Catholic University of Leuven, Leuven, Belgium
Received February 12, 2003;
revised December 22, 2003;
accepted January 12, 2004
* Corresponding author. Tel.: +32-16-34-75-68; fax: +32-16-34-34-67
E-mail address: Jan.Dhooge{at}uz.kuleuven.ac.be
See page 714 for the editorial comment on this article1
This paper was guest edited by Prof. G. Maurer, Vienna, Austria
Abstract
Aim Successful primary PTCA (with TIMI 3 reflow) in patients with acute transmural infarction has been observed to result in an immediate abnormal increase in wall thickness associated with persisting abnormal post-systolic thickening. To understand the sequential changes in regional deformation during: (i) the development of acute transmural infarction, (ii) upon TIMI grade 3 infarct reperfusion and (iii) during the subsequent expression of reperfusion injury the following correlative experimental study was performed in a pure animal model in which there was no distal dispersion of thrombotic material causing either no reflow or secondary microvascular obstruction.
Methods In 10 closed-chest pigs, a 90 min PTCA circumflex occlusion was used to induce a transmural infarction. This was followed by 60 min of TIMI 3 infarct reperfusion. M-mode ultrasound data from the "at risk" posterior wall infarct segment and from a control remote non-ischemic septal segment were acquired at standardized time intervals. Changes in regional deformation (end-diastolic (EDWT), end-systolic (ESWT) and post-systolic (PSWT) wall thickness, end-systolic strain (
) and post-systolic strain (
)) were measured.
Results In this pure animal model of acute transmural infarction/infarct reperfusion (with no pre-existing intra-luminal thrombus), the induced changes in wall thickness and thickening were complex. During prolonged occlusion, after an initial acute fall in ESWT, there was no further change in systolic deformation to indicate the progression of ischaemia to infarction. Both transmurally infarcted and reperfused-infarcted myocardium retained post-systolic thickening indicating that this parameter, taken in isolation, is not a consistent marker of segmental viability and, in this regard, should be interpreted only in combination with other indices of segmental function. The most striking abnormality induced by reperfusion was an immediate increase in EDWT which then increased logarithmically over a 60 min period as reperfusion injury was further expressed. 
did not change significantly during reperfusion. Histology confirmed the wall thickness changes on reperfusion to be due to massive extra-cellular oedema.
Conclusions The identification of an acute increase in regional wall thickness in a reperfused infarct zone by cardiac ultrasound following primary PTCA might be used in patients to both identify successful infarct reperfusion and to monitor the presence, extent and resolution of the oedema associated with reperfusion injury.
Key Words: Viability • Post-systolic thickening • Myocardial infarction • Infarct reperfusion • Reperfusion injury • Echocardiography
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