(Circulation. 1997;95:1755-1759.)
© 1997 American Heart Association, Inc.
Articles |
From the Cardiac Unit, Department of Medicine, Massachusetts General Hospital, Boston.
Correspondence to Herman K. Gold, MD, Ambulatory Care Center, Suite 480, Massachusetts General Hospital, Boston, Mass 02114. E-mail gold{at}olorin.mgh.harvard.edu
Background Coronary thrombus is composed of platelets and fibrin, and during thrombolytic treatment, reflow may be slowed by platelet deposition. It may be possible to initiate coronary reflow without exogenous plasminogen activators by blocking platelet aggregation while fibrin generation is impeded with heparin.
Methods and Results In 14 dogs, left anterior descending
coronary artery thrombosis was produced by
endothelial trauma and thrombin instillation in the
presence of stenosis distally. Reflow was monitored by flow
probe during treatment with (1) heparin, (2) heparin and aspirin, and
(3) heparin, aspirin, and intravenous 7E3. Eighty percent
of dogs treated with the third combination showed stable reflow (
25%
of prestenotic flow) in 50±9 minutes. In addition, 13 patients
were studied during intravenous administration of c7E3 10
minutes before primary angioplasty for acute myocardial infarction and
Thrombolysis In Myocardial Infarction (TIMI) grade 0 or 1
flow. Pretreatment included heparin and oral aspirin. Flow increased
during a 10-minute period by at least one TIMI grade in 11 (85%) of 13
and reached TIMI grade 2 or 3 in 7 (54%) of 13 patients. Average TIMI
grade flow increased from 0.31±0.5 to 1.54±0.8 (P<.001).
Thrombus length 10 minutes after c7E3 was 5.1±3.5 mm. All but 1
patient then underwent angioplasty. There were no complications.
Conclusions Coronary reflow can be initiated by intravenous 7E3 administration in the presence of heparin and aspirin. In human patients, this flow can be observed in 10 minutes without exogenous thrombolytic agents.
Key Words: 7E3 myocardial infarction platelet aggregation inhibitors reperfusion
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