The embolic storm: dramatic peripheral complications of left ventricular thrombosis after myocardial infarction (original) (raw)
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Acute myocardial infarction, intraventricular thrombus and risk of systemic embolism
Biomedical Papers
The development of left ventricular thrombus (LVT) is a well-known and serious complication of acute myocardial infarction (AMI) due to the risk of systemic arterial embolism (SE), which is variable in its clinical picture and has potentially serious consequences depending on the extent of target organ damage. SE results in an increase in mortality and morbidity in these patients. LVT is one of the main causes of the development of ischaemic cardio-embolic cardiovascular events (CVE) after MI and the determination of the source of cardiac embolus is crucial for the initiation of adequate anticoagulant therapy in secondary prevention. Echocardiography holds an irreplaceable place in the diagnosis of LVT, contrast enhancement provides higher sensitivity. The gold standard for LVT diagnosis is cardiac magnetic resonance imaging, but it is not suitable as a basic screening test. In patients with already diagnosed LVT, it is necessary to adjust antithrombotic therapy by starting warfarin anticoagulation for at least 6 months with the need for echocardiographic follow-up to detect thrombotic residues. The effect of prophylactic administration of warfarin in high-risk patients after anterior AMI does not outweigh the risk of severe bleeding complications and does not result in a decrease in mortality and morbidity. At the present time, there is not enough evidence to use direct oral anticoagulants in this indication.
Congestive Heart Failure, 2001
The contribution of cardiac ultrasound in assessment of the embolic potential of left ventricular thrombi after anterior acute myocardial infarction was verified in a prospective study of serial echocardiograms (mean, 18.9 examinations per patient) obtained over a long-term period (1-72 months; mean, 38±12). The study population comprised 222 patients (162 men; age, 64±11 years) with a first anterior acute myocardial infarction, treated with thrombolysis (group A) or receiving no antithrombolic therapy (group B). Embolism occurred in a total of 12 patients (11 with a left ventricular thrombus; p<0.005) and was more frequent in group B (10 patients; p<0.04). Predictors of embolism were the absence of thrombolysis, detection of a left ventricular thrombus, protrusion or mobility of the thrombus, and morphologic changes in the thrombus over time. Patients in group A had a lower incidence of each of these predictors, and a higher thrombus resolution rate. An appropriate echocardiographic protocol is crucial to assessment of the embolic potential of left ventricular thrombi after anterior acute myocardial infarction and may help to identify candidates for aggressive antithrombotic therapy. (CHF. 2001;7:250-255)
Journal of Internal Medicine, 1995
Objectives. To examine the incidence of left ventricular thrombus in patients with anterior myocardial infarction, with and without streptokinase treatment. To identify predictors of thrombus development. Design. Consecutive patients prospectively studied during the hospitalized period. Echocardiography was performed within 3 days of admission and before discharge. Setting. Umei University Hospital, a teaching hospital in Northern Sweden. Subjects. Ninety-nine patients with anterior myocardial infarction of whom 74 were treated with streptokinase. Main outcome measures. Left ventricular thrombus and left ventricular segmental myocardial function. Results. During the hospital stay, a thrombus developed in 46% (95% confidence interval [CI], 3 5 5 7 %) of the patients in the thrombolysis group and in 40% (95% CI, 21-59%) of the patients in the non-thrombolysis group. No difference in left ventricular segmental myocardial function was found between the thrombolysis and non-thrombolysis groups at hospital discharge. No embolic events were observed. The occurrence of a left ventricular thrombus at hospital discharge was significantly associated with previous myocardial infarction, peak enzyme levels, left ventricular global and segmental dysfunction and an increased dose of peroral diuretics or use of parenteral diuretics. In a multiple logistic regression model, left ventricular segmental dysfunction was the most important predictor of left ventricular thrombus. Conclusion. Thrombolytic treatment with streptokinase does not prevent the development of a left ventricular thrombus but the risk of embolic complications is low. The left ventricular segmental myocardial score can be used to assess the risk of thrombus development, also, after thrombolysis.
Heart, 1988
Risk factors for systemic embolisation in patients with ventricular thrombi caused by an acute myocardial infarction were studied in 150 consecutive patients with an infarction of the anterior wall. Serial echocardiograms were performed 2-10 days after the acute event and patients were followed up for three months. Anticoagulation treatment was started only after the detection of thrombi. Of the 55 patients in whom a thrombus developed, 15 (27%) had peripheral emboli between 6-62 days; but only two (2%) of 95 patients without thrombus had emboli. Among 15
Left ventricular thrombus formation after first anterior wall acute myocardial infarction
The American Journal of Cardiology, 1988
The characteristics of the left ventricle and coronary arteries associated with left ventricular (LV) thrombus in patients with recent anterior acute myocardial infarction were defined. Of 77 patients studied, 35 (46%) had LV thrombi. The presence of LV thrombus was not correlated to the extent of coronary artery disease. The frequency of LV thrombus progressively increased with groups of increasing wall motion abnormality as determined by the extent of akinesia and dyskinesia (%AD) (%AD 0 to 14, thrombus present in 3 of 16 [19%], %AD 15 to 29, thrombus in 8 of 27 [30%]; %AD greater than or equal to 30%, thrombus in 24 of 34 [71%]; p less than 0.001) and with increasingly severe degrees of early ventricular shape change (normal or mildly abnormal contour, 16% with thrombus; moderately abnormal contour, 36% with thrombus; severely abnormal contour, 70% with thrombus; p less than 0.001). Patients with thrombi had higher diastolic (249 +/- 55 vs 225 +/- 48 ml; p less than 0.05) and systolic (158 +/- 48 vs 120 +/- 45 ml; p less than 0.001) volumes than patients without thrombi, respectively. A stepwise discriminant analysis identified ejection fraction, extent of early shape change and LV end-diastolic pressure as independent correlates of LV thrombus after acute myocardial infarction.
Left ventricular thrombosis in acute transmural myocardial infarction
Postgraduate Medical Journal, 1988
Summary To determine the incidence and natural history of left ventricular thrombosis in acute transmural myocardial infarction we performed serial two-dimensional echocardiography in 51 patients. Seventeen patients had inferior infarcts. None of these developed left ventricular thrombosis. The remaining 34 patients had anterior infarcts. Ten of these developed left ventricular thrombus at an average of 4 +/- 2 days after admission. All patients with left ventricular thrombosis had apical akinesia or dyskinesia. Patients with anterior myocardial infarction and akinesia or dyskinesia of the apex are at high risk of developing left ventricular thrombosis. Peak aspartate aminotransferase and lactate dehydrogenase enzyme activity were of little value in identifying this high risk group.