Ad. Mbewu et al., SERUM LP(A) LIPOPROTEIN CONCENTRATION AND OUTCOME OF THROMBOLYTIC TREATMENT FOR MYOCARDIAL-INFARCTION, British Heart Journal, 71(4), 1994, pp. 316-321
Background-Lp(a) lipoprotein has structural homology with plasminogen
and has been shown to inhibit plasminogen activation in vitro. Objecti
ve-To determine whether the serum concentration of Lp(a) lipoprotein p
resent when streptokinase was given in acute myocardial infarction inf
luenced the outcome as judged by electrocardiographic methods. Patient
s and design-Serum Lp(a) lipoprotein concentration was measured in 135
consecutive patients admitted with a diagnosis of acute myocardial in
farction who received streptokinase treatment. Recovery from myocardia
l injury was assessed by the reduction in the sum of ST segment elevat
ion measured from the J point (STJ) in the electrocardiogram immediate
ly before streptokinase was given compared with that three hours later
. Results-The serum Lp(a) lipoprotein concentrations were measured wit
hin 12 hours of the onset of symptoms of myocardial infarction and wer
e higher than in healthy reference populations. Recovery from myocardi
al infarction could be assessed from the STJ in 116 patients (86% of t
he series). Those in whom it could not had bundle branch block, left v
entricular hypertrophy, did not survive three hours, or had started in
travenous nitrate treatment or some other clinical procedure before or
at the time the second electrocardiogram was to be recorded. Patients
with reductions in STJ after streptokinase that were > 4 mm (the medi
an decrease) had mean (range) serum Lp(a) lipoprotein concentrations o
f 41.0 (0.8-220) mg/dl and those with a smaller reduction in STJ had c
oncentrations of 29.1 (1.7-151) mg/dl. The difference was not statisti
cally significant. Conclusion-In this study Lp(a) lipoprotein concentr
ation did not significantly influence the outcome of thrombolytic trea
tment with streptokinase.