Does increased lipoprotein (a) impair the effectiveness of thrombolysis with streptokinase?

Although lipoprotein (a) [Lp(a)] has been shown to interfere with thrombolysis in vitro, its effects on thrombolytic therapy in patients with acute myocardial infarction (MI) are not clear. The authors evaluated 32 male patients ages thirty-five to seventy-five (mean fifty-two +/- ten) with the diagnosis of acute MI who underwent thrombolytic therapy with 1,500,000 units of intravenous streptokinase. All patients underwent coronary angiography within seven days of the infarction from which the thrombolysis in myocardial infarction (TIMI) flow grades of the 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 that 6 patients (18.8%) had TIMI flow 0 to 1, and 26 patients (81.2%) had TIMI flow grade 2 or 3. The Lp(a) levels ranged from 0.1 to 60 mg/dL 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 lower in patients with high Lp(a) levels (P > 0.05), and there was no significant 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 correlation between the extent of coronary atherosclerosis and Lp(a) levels, Lp(a) is not a strong predictor of the outcome of thrombolytic therapy.