759
EDITORIALS
Left ventricular thrombosis and stroke following myocardial infarction Increased interest in left ventricular thrombosis over the past ten years is largely due to the development of two-dimensional echocardiography, which has a diagnostic sensitivity and specificity of approximately 90%.12 Although echocardiography has some limitations--eg, imaging of the cardiac apex may be difficult-this technique has been used to study the frequency of left ventricular thrombi following myocardial infarction in fourteen recent studies. In the five largest,3-7 with a total of 463 patients, thrombi were detected in 28-37%, with a mean frequency of 31-5%. Left ventricular thrombus formation is much less common with inferior infarction than with anterior infarction (0-5% with a mean of
3-2%).6-9 The risk of cerebral embolism in
patients
with
proven left ventricular thrombi is less well defined. At
least
published studies addressed this but question,2,6-16 individually they were small and the reported risk varied from 0 to 35%. A reasonable estimate of the risk of cerebral embolism can be obtained by combining these studies. Of the 444 patients with echocardiographically diagnosed left ventricular thrombus, 69 (15-5%) sustained a cerebral embolic event during follow-up for up to two years. The risk of embolism was greatly increased when the thrombus appeared mobile or protruded into the left Can left ventricular ventricular cavity. 11,14,15 thrombosis after myocardial infarction be prevented? If so, will this result in fewer cerebral embolic events? Early controlled studies of the effects of anticoagulation on the development of left ventricular thrombus following myocardial infarction gave conflicting results. 17-20 Although these trials tended to be small and lacking in statistical power, the overall trend was in favour of active therapy-41 left ventricular thrombi in 95 control patients (43 %)vs 26 thrombi in 86 treated patients (30%). Two studies published in 1989 were large enough to detect a clinically important benefit from anticoagulation.3,4 In both studies the anticoagulant regimen was heparin twelve
12 500 units every 12 hours. Turpie et al4 compared this high-dose regimen with low-dose heparin in 221 patients and found that the frequency of left ventricular thrombus formation was reduced significantly from 32 % to 11 %. Cerebrovascular accidents were reported in 4 patients in the low-dose group compared with 1 patient in the high-dose group, but the difference was not significant. In the SCATI study,3 a subgroup of 200 patients with first anterior myocardial infarctions were studied by echocardiography before discharge. Left ventricular thrombi were found in 36 5% of controls, who received no anticoagulants, compared with 17-7% of the heparin-treated patients (p
EDITORIALS
Left ventricular thrombosis and stroke following myocardial infarction Increased interest in left ventricular thrombosis over the past ten years is largely due to the development of two-dimensional echocardiography, which has a diagnostic sensitivity and specificity of approximately 90%.12 Although echocardiography has some limitations--eg, imaging of the cardiac apex may be difficult-this technique has been used to study the frequency of left ventricular thrombi following myocardial infarction in fourteen recent studies. In the five largest,3-7 with a total of 463 patients, thrombi were detected in 28-37%, with a mean frequency of 31-5%. Left ventricular thrombus formation is much less common with inferior infarction than with anterior infarction (0-5% with a mean of
3-2%).6-9 The risk of cerebral embolism in
patients
with
proven left ventricular thrombi is less well defined. At
least
published studies addressed this but question,2,6-16 individually they were small and the reported risk varied from 0 to 35%. A reasonable estimate of the risk of cerebral embolism can be obtained by combining these studies. Of the 444 patients with echocardiographically diagnosed left ventricular thrombus, 69 (15-5%) sustained a cerebral embolic event during follow-up for up to two years. The risk of embolism was greatly increased when the thrombus appeared mobile or protruded into the left Can left ventricular ventricular cavity. 11,14,15 thrombosis after myocardial infarction be prevented? If so, will this result in fewer cerebral embolic events? Early controlled studies of the effects of anticoagulation on the development of left ventricular thrombus following myocardial infarction gave conflicting results. 17-20 Although these trials tended to be small and lacking in statistical power, the overall trend was in favour of active therapy-41 left ventricular thrombi in 95 control patients (43 %)vs 26 thrombi in 86 treated patients (30%). Two studies published in 1989 were large enough to detect a clinically important benefit from anticoagulation.3,4 In both studies the anticoagulant regimen was heparin twelve
12 500 units every 12 hours. Turpie et al4 compared this high-dose regimen with low-dose heparin in 221 patients and found that the frequency of left ventricular thrombus formation was reduced significantly from 32 % to 11 %. Cerebrovascular accidents were reported in 4 patients in the low-dose group compared with 1 patient in the high-dose group, but the difference was not significant. In the SCATI study,3 a subgroup of 200 patients with first anterior myocardial infarctions were studied by echocardiography before discharge. Left ventricular thrombi were found in 36 5% of controls, who received no anticoagulants, compared with 17-7% of the heparin-treated patients (p
