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P Lem

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Left ventricular thrombosis and arterial embolism after thrombolysis in acute anterior myocardial infarction: predictors and effects of adjunctive antithrombotic therapy.

The prevalence of left ventricular (LV) thrombosis and incidence of arterial embolism after acute anterior myocardial infarction (AAMI) treated with streptokinase 1.5 x 10(6) IU intravenously was studied in 136 patients enrolled consecutively in five cardiological centres. Adjunctive antithrombotic therapy was administered according to the routine of each centre. Thrombus formation was studied by two-dimensional echocardiography, and events of arterial embolism recorded. LV thrombosis was found in 37 (27.2%) of the patients. In a subgroup of 53 patients receiving post-thrombolytic therapy with acetylsalicylic acid only, a thrombus developed in 14 (26.4%). The thrombus prevalence among patients given high-dose heparin was significantly lower than among those receiving either low-dose heparin or no heparin (4/30 vs 33/106, P = 0.045). Logistic regression analysis suggested that severe LV wall motion abnormality (P < 0.001) and avoidance of treatment with high-dose heparin (P = 0.023) were independent predictors of LV thrombus formation. Only one patient (0.7%) suffered arterial embolism (ischaemic stroke). In conclusion, LV thrombosis is frequent after thrombolytic therapy for AAMI, and impaired LV wall motion represents an independent predisposing factor. Low-dose heparin and acetylsalicylic acid seem less effective for LV thrombus prophylaxis than high-dose heparin. The incidence of arterial embolism is low.

Age Factors

Adverse effect of warfarin in acute myocardial infarction: increased left ventricular thrombus formation in patients not treated with high-dose heparin.

In a prospective non-randomized study, 229 patients with a verified first acute anterior myocardial infarction (AAMI) underwent echocardiography before discharge in order to study left ventricular (LV) thrombus formation. Antithrombotic therapy was given according to the routine of each centre. Patients receiving high-dose heparin had few LV thrombi, irrespective of warfarin therapy (6/32 vs 3/25, P ns). In patients not given heparin, however, a significantly higher prevalence of LV thrombi was found in a subgroup of patients treated with warfarin as compared to those who did not receive warfarin (8/13 vs 17/68, P 0.02). A similar, but non-significant difference was observed in patients given low-dose heparin (42% vs 27%, P ns). Within the non-heparin and low-dose heparin groups, age, infarct size, occurrence of Q-wave infarction, congestive heart failure and LV wall motion impairment did not differ between those treated or not treated with warfarin. In conclusion, high-dose heparin seems effective in the prevention of LV thrombosis irrespective of warfarin therapy after AAMI. The start of warfarin therapy in patients not receiving heparin was, however, associated with an increased prevalence of LV thrombosis.

Administration, Oral

Left ventricular thrombosis and arterial embolism in acute anterior myocardial infarction.

To study left ventricular thrombus (LVT) formation and arterial embolism (AE), 106 consecutive patients with a first acute anterior myocardial infarction (AAMI) underwent two-dimensional echocardiography before discharge. Repeated assessments for detection of AE were performed. Patients were non-randomly allocated to either no heparin, low-dose heparin or high-dose heparin. LVT was found in 25 (26.9%) of 93 patients with technically satisfactory echocardiograms. Left ventricular (LV) wall motion impairment (P = 0.0017) and treatment with either heparin or low-dose heparin (P = 0.0019) were independent predictors of LVT formation. AE, all strokes, occurred in 10 patients (9.4%) and was strongly associated with high age (P = 0.0013). In conclusion, LVT and AE are frequent complications to AAMI. LV wall motion impairment predisposes for LVT and low-dose heparin seems not to prevent these complications.

Adult

[Gold lung].

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Acute Disease