G. Rousseau et al., IMPORTANCE OF PLATELETS IN MYOCARDIAL INJURY AFTER REPERFUSION IN THEPRESENCE OF RESIDUAL CORONARY STENOSIS IN DOGS, The American heart journal, 125(6), 1993, pp. 1553-1563
Residual coronary stenosis is common after successful thrombolysis for
acute infarction. We investigated the role of platelets and the influ
ence of a residual critical stenosis during early reperfusion in survi
val of reperfused myocardium. The left anterior descending coronary ar
tery was occluded for 90 minutes and reperfused for 6 hours in 5 group
s of dogs, 3 with a residual critical stenosis (groups 1 through 3) an
d 2 without (groups 4 and 5). Thrombocytopenia was produced by an anti
serum in groups 2, 3, and 5; group 3 was also made neutropenic by anot
her antiserum. Platelets (groups 1 and 4) and neutrophils (groups 1, 2
, 4, and 5) labeled with indium 111 were reinjected at occlusion. Coll
ateral flow was estimated with radioactive microspheres and was statis
tically similar among groups. Infarct size (percentage of area at risk
), revealed by triphenyltetrazolium, was more severe (49.4% +/- 4.0%;
p < 0.05) with stenosis (group 1) than without stenosis (group 4: 29.5
% +/- 4.6%). Platelet depletion reduced infarct size in group 2 (28.6%
+/- 6.3%; p < 0.05 vs group 1) with stenosis, but not in group 5 with
out stenosis (24.5% +/- 6.2% vs group 4: 29.5% +/- 4.6%). Neutropenia
(group 3) did not decrease infarct size in thrombocytopenic dogs. Neut
rophil accumulations in reperfused myocardium were similar among group
s, but platelets accumulated in greater numbers in reperfused infarcts
with stenosis (group 1: 338,581 +/- 52,857/gm; p < 0.05) than without
stenosis (group 4: 153,445 +/- 23,949/gm). Therefore a critical steno
sis at reperfusion compromises myocardial salvage and increases infarc
t size by means of a platelet-mediated mechanism.