Effect of reperfusion on left ventricular regional remodeling strains after myocardial infarction.
BACKGROUND
Reperfusion therapy for myocardial infarction is currently the most effective means for limiting early and late mortality. We sought to elucidate how reperfusion influences remodeling strains in the infarct, borderzone, and remote myocardial regions. Understanding the effects of reperfusion on regional remodeling will help to evaluate and optimize emerging treatments for patients who do not achieve effective reperfusion after myocardial infarction.


METHODS
An ovine infarct model (n = 13) was used to assess the effect of 1 hour of ischemia followed by reperfusion on regional and global myocardial geometry, function, and perfusion using sonomicrometry, echocardiography, and microspheres. Thirteen additional animals were assessed chronically (8 weeks) with echocardiography and postmortem analysis after either reperfusion (n = 5) or untreated infarction (n = 8).


RESULTS
During ischemia the area at risk thinned, stretched, and became dyskinetic. The normally perfused borderzone also stretched, and contraction decreased by 40% during ischemia. Reperfusion increased area at risk wall thickness and reduced area at risk stretching but did not restore contractile function. Borderzone stretching was reduced and contractile function improved by reperfusion. Contractile function of remote regions was also improved with reperfusion. Ventricular dilatation after ischemia was reversed within 180 minutes of reperfusion. Chronically, reperfusion significantly improved global remodeling when compared with nonreperfused controls. Reperfused animals had thicker infarcts and akinetic rather than dyskinetic apical segments.


CONCLUSIONS
Reperfusion acutely increases area at risk wall thickness, reduces area at risk and borderzone stretching, and improves borderzone and remote function. Reperfusion increases mature scar thickness and improves chronic global remodeling. These beneficial effects of reperfusion result primarily from reduced infarct expansion (stretching).
Sakamoto
Hiroaki
H
Harrison Department of Surgical Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-4283, USA.
Parish
Landi M
LM
Hamamoto
Hirotsugu
H
Ryan
Liam P
LP
Eperjesi
Thomas J
TJ
Plappert
Theodore J
TJ
Jackson
Benjamin M
BM
St John-Sutton
Martin G
MG
Gorman
Joseph H
JH
Gorman
Robert C
RC
D000818:Animals; D003326:Coronary Circulation; D004452:Echocardiography; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000473:pathology; D012756:Sheep; D013314:Stress, Mechanical; D013599:Systole; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling