In order to study the effects of residual stenosis on myocardial salvage, we created
99
% coronary stenosis with or without contrast washout delay at reperfusion in six groups of dogs. In Group A (n=8), the artery was occluded for 1h before being fully reperfused. In Group B (n=
9
), the artery was occluded for 1h, then subjected to
6
h of
99
% stenosis without contrast washout delay. In Group C (n=8), the artery was occluded for 1h, followed by 1 week of
99
% stenosis without contrast washout delay. In Group D (n=10). again the artery was occluded for 1h, then subjected to
6
h of
99
% stenosis with contrast washout delay. In Group
E
(n=8). the artery was occluded for
7
h, then fully reperfused for 1 week. Finally, in Group
F
(n=8). the occlusion lasted for a full week. All dogs were sacrificed 1 week after occlusion. In Group A, myocardial creatine phosphokinase activity (CK) in the inner layer was 43.8±12.
5
% that of non-infarcted myocardium. Myocardial CK in Group B (46.
5
±
7
.4%) was little different but in Group C it dropped to 26.
6
±8.4%, suggesting that
99
% residual stenosis is not deleterious if it is continued for
6
h or less but that it will result in considerable depletion of myocardial CK, if it is sustained for 1 week. In Group D, myocardial CK dropped markedly to 11.3±3.
7
%, little different from that for either Group
E
(13.3±2.
6
%) or Group
F
(
9
.3±3.3%). This suggests that contrast washout de-lay following
99
% stenosis is not beneficial to myocardial salvage. Infarct size, as determined using triphenyl tetrazolium chloride as a stain was smallest for Group A (
6
.8±3.
6
%) and largest for Group
F
(62.
6
±
9
.8%). Group B showed smaller infarct size (13.2±3.
7
%) than did either Group D (27.0±
5
.
5
%) or Group
E
(25.3±
6
.3%). From this. we came to the conclusion that
99
% residual stenosis without contrast washout delay is not deleterious provided it is sustained for
6
h or less.
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