Left ventricular topographic alterations in the completely healed rat infarct caused by early and late coronary artery reperfusion

Topographic changes in the completely healed (6 weeks) left ventricle of the rat, caused by early (30 minutes) and delayed (90 minutes) coronary artery reperfusion, were examined. With early reperfusion the extent of the scar, as a percentage of left ventricular (LV) circumference, was reduced compa...

Full description

Saved in:
Bibliographic Details
Published inThe American heart journal Vol. 116; no. 6; pp. 1508 - 1513
Main Authors Hale, Sharon L, Kloner, Robert A
Format Journal Article
LanguageEnglish
Published New York, NY Mosby, Inc 01.12.1988
Elsevier
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Topographic changes in the completely healed (6 weeks) left ventricle of the rat, caused by early (30 minutes) and delayed (90 minutes) coronary artery reperfusion, were examined. With early reperfusion the extent of the scar, as a percentage of left ventricular (LV) circumference, was reduced compared to the extent of the scar in rats with permanent occlusion (27 ± 3% vs 42 ± 2%, p < 0.01). Early reperfusion also preserved LV topography by preventing dilation of the LV cavity and thinning of the healed free wall. Late reperfusion (90 minutes) did not reduce the extent of the scar (35 ± 3% vs 42 ± 2% of LV circumference, p = NS) or prevent dilation of the LV cavity compared with permanent occlusion. However, the healed free wall/noninfarcted septum ratio was significantly greater in rats with late reperfusion than in those with permanent occlusion (0.98 ± 0.06 vs 0.73 ± 0.07, p < 0.05). Thus early reperfusion completely inhibited scar thinning and dilation of the LV cavity, maintaining normal LV topography. Late reperfusion, too late to reduce infarct size, still contributed to improved healing of the myocardium by resulting in a thicker scar.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0002-8703
1097-6744
DOI:10.1016/0002-8703(88)90736-3