Circulation, Vol 83, 739-746, Copyright © 1991 by American Heart Association
GB Habib, J Heibig, SA Forman, BG Brown, R Roberts, ML Terrin and R Bolli
BACKGROUND. The influence of coronary collateral vessels on infarct size in
humans remains controversial, partly because no previous study has examined
the impact of collaterals present at the onset of acute myocardial
infarction on infarct size. METHODS AND RESULTS. The present study used the
data base of the Thrombolysis in Myocardial Infarction (TIMI) Phase I trial
to correlate the presence or absence of angiographically documented
collaterals in the initial hours of myocardial infarct evolution with the
size of the infarct as assessed by serial measurements of serum creatine
kinase (CK). To avoid the confounding effects of reperfusion on enzymatic
estimates of infarct size, this report is limited to those 125 patients who
failed to recanalize at 90 minutes after administration of tissue
plasminogen activator or streptokinase. Patients with angiographically
documented collaterals (group A, n = 51) had significantly lower values of
peak serum CK than patients without collaterals (group B, n = 74) (1,877
+/- 216 versus 2,661 +/- 212 IU/l, respectively [mean +/- SEM], p = 0.004).
Similarly, CK-derived infarct size estimates were significantly lower in
group A than in group B (20.6 +/- 2.5 versus 31.4 +/- 2.8 CK gram
equivalents, p = 0.001). The infarct size observed in patients with
collaterals was less for anterior infarctions as well as for infarctions of
other locations; thus, the beneficial effects of collaterals were
independent of the site of the infarct. In 65 of the 125 patients who
failed to reperfuse, left ventricular ejection fraction (LVEF) was assessed
by contrast ventriculography both at initial cardiac catheterization
(before thrombolytic therapy) and at hospital discharge. Among the patients
who had both studies, global LVEF tended to increase from pretreatment to
hospital discharge in group A (from 50.6 +/- 1.8% to 53.4 +/- 1.8%, p =
0.10) but decreased in group B patients (from 50.3 +/- 1.8% to 47.8 +/-
1.7%, p = 0.02). At hospital discharge, global LVEF was greater in patients
with coronary collaterals (53.5 +/- 1.7% versus 49.6 +/- 1.7%, p = 0.01).
CONCLUSIONS. The results demonstrate that, in patients in whom thrombolytic
therapy fails to induce reperfusion, the presence of coronary collateral
vessels at the onset of myocardial infarction is associated with limitation
of infarct size as assessed enzymatically and with improved ventricular
function on discharge as assessed by LVEF.
ARTICLES
Influence of coronary collateral vessels on myocardial infarct size in humans. Results of phase I thrombolysis in myocardial infarction (TIMI) trial. The TIMI Investigators
Section of Cardiology, Baylor College of Medicine, Houston, Tex.
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