Although lipoprotein (a) [Lp(a)] has been shown to interfere with thro
mbolysis in vitro, its effects on thrombolytic therapy in patients wit
h acute myocardial infarction (MI) are not clear. The authors evaluate
d 32 male patients ages thirty-five to seventy-five (mean fifty-two +/
-ten) with the diagnosis of acute MI who underwent thrombolytic therap
y with 1,500,000 units of intravenous streptokinase. All patients unde
rwent coronary angiography within seven days of the infarction from wh
ich the thrombolysis in myocardial infarction (TIMI) flow grades of th
e infarct-related artery, coronary scores, and ejection fraction were
determined. Anterior MI was found in 19 patients (59.4%), inferior MI
in 12 (37.5%), and posterolateral MI in 1 patient (3.1%). They found t
hat 6 patients (18.8%) had TIMI flow 0 to 1, and 26 patients (81.2%) h
ad TIMI flow grade 2 or 3. The Lp(a) levels ranged from 0.1 to 60 mg/d
L with a mean of 8.6 +/- 17 mg/dL. Eight (25%) of the patients had Lp(
a) levels above 30 mg/dL. The TIMI flow rates were not found to be low
er in patients with high Lp(a) levels (P > 0.05), and there was no sig
nificant correlation between the TIMI flow rates and the Lp(a) levels
(r=0.28). There was a good correlation between coronary scores and Lp(
a) levels (r=0.87). They conclude that although there is a good correl
ation between the extent of coronary atherosclerosis and Lp(a) levels,
Lp(a) is not a strong predictor of the outcome of thrombolytic therap
y.