LIPOPROTEIN(A) LEVELS IN PATIENTS WITH MYOCARDIAL-INFARCTION TREATED WITH ANISTREPLASE - NO PREDICTION OF EFFICACY BUT INVERSE CORRELATION WITH PLASMINOGEN ACTIVATION IN NON-PATENCY
J. Brugemann et al., LIPOPROTEIN(A) LEVELS IN PATIENTS WITH MYOCARDIAL-INFARCTION TREATED WITH ANISTREPLASE - NO PREDICTION OF EFFICACY BUT INVERSE CORRELATION WITH PLASMINOGEN ACTIVATION IN NON-PATENCY, International journal of cardiology, 45(2), 1994, pp. 109-113
The aim of this study was to investigate whether failure of thrombolyt
ic treatment might be due to inhibition of fibrinolysis by high lipopr
otein(a) levels. Fifty-eight patients with acute myocardial infarction
were treated intravenously within 4 h after onset of symptoms with an
istreplase (30 units) and heparin (30 000 IU/24 h). Blood samples for
measurement of coagulation parameters were taken before and 1.5 h afte
r treatment. Coronary angiography was performed after 48 h. Levels of
lipoprotein(a) were measured 6 months after discharge from hospital. T
he patency rate was 74% (43/58). Median lipoprotein(a) levels were not
different between the patients with a patent and those with a non-pat
ent vessel (10 and 8 mg/dl, respectively), however, in patients with a
non-patent infarct-related vessel, a significant inverse correlation
was found between the lipoprotein(a) level and the decrease of plasmin
ogen in the first 1.5 h after treatment. It is concluded that high lip
oprotein(a) levels, although not directly associated with a poor outco
me of anistreplase therapy, might contribute to insufficient fibrinoly
sis in patients with a non-patent infarct-related vessel.