Left ventricular thrombus in anterior acute myocardial infarction after thrombolysis. A GISSI-2 connected study.

C Vecchio, F Chiarella, G Lupi, P Bellotti… - Circulation, 1991 - Am Heart Assoc
C Vecchio, F Chiarella, G Lupi, P Bellotti, S Domenicucci
Circulation, 1991Am Heart Assoc
BACKGROUND Streptokinase reduces the incidence of left ventricular thrombosis after
acute myocardial infarction. However, it is unknown whether a similar effect can be obtained
with different thrombolytic agents and whether subcutaneous calcium heparin can have an
additional efficacy. METHODS AND RESULTS To compare the effects of two different
thrombolytic agents combined or not with heparin on the incidence and features of left
ventricular thrombi and their related embolic events, we performed a GISSI-2 ancillary …
BACKGROUND
Streptokinase reduces the incidence of left ventricular thrombosis after acute myocardial infarction. However, it is unknown whether a similar effect can be obtained with different thrombolytic agents and whether subcutaneous calcium heparin can have an additional efficacy.
METHODS AND RESULTS
To compare the effects of two different thrombolytic agents combined or not with heparin on the incidence and features of left ventricular thrombi and their related embolic events, we performed a GISSI-2 ancillary echocardiographic study (the first echocardiogram obtained within 48 hours of symptoms onset and the second before hospital discharge) that enrolled 180 consecutive patients (mean age, 63 +/- 11 years, 142 men) with a first anterior acute myocardial infarction. Patients were randomized into four groups of treatment: recombinant tissue-type plasminogen activator (rt-PA) (n = 47), rt-PA plus heparin (n = 45), streptokinase (n = 39), and streptokinase plus heparin (n = 49). Left ventricular thrombosis was observed in 51 of 180 patients (28%). No significant differences were found concerning the incidence of thrombi in the four treatment groups. Mural shape of left ventricular thrombi was found more frequently than the protruding shape (71% versus 29% at the first examination, 64% versus 36% at the second), particularly in heparin-treated patients (93% versus 7% at first examination, 70% versus 30% at the second). Only one embolic event (0.5%) occurred during the hospitalization.
CONCLUSIONS
We conclude that 1) the rate of left ventricular thrombi does not differ in patients with acute myocardial infarction treated either with streptokinase or rt-PA, 2) subcutaneous heparin, when begun 12 hours after intravenous thrombolysis, does not appear to further reduce the occurrence of thrombi but seems to influence the shape of left ventricular thrombi, and 3) during the predischarge period, embolic events are rare in patients treated by thrombolysis.
Am Heart Assoc