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      Incidence and predictors of left ventricular thrombus formation following acute ST-segment elevation myocardial infarction: A serial cardiac MRI study

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          Abstract

          Aims

          Left ventricular (LV) thrombus is a complication of acute ST-segment elevation myocardial infarction (STEMI). We determined the incidence and predictors of LV thrombus formation using serial cardiac magnetic resonance (CMR) and two-dimensional echocardiography studies.

          Methods and results

          Two hundred and ten patients underwent CMR (median 4 days [IQR 3-7]) and transthoracic echocardiography (median 4 days [IQR 3-7]) early after STEMI presentation with serial follow-up CMR (median 55 days [IQR 46-64]) and echocardiography studies (median 54 days [IQR 45-64]) performed subsequently. The incidence of LV thrombus was 12.3% (26/210) by CMR and 6.2% (13/210) by two-dimensional echocardiography. Echocardiography had 50% sensitivity and 100% specificity for LV thrombus detection compared to CMR. LV thrombus was found in 23.6% of patients with anterior STEMI (22/93). Ischaemic stroke occurred in 1.4% of patients (3/210). Patients with LV thrombus had lower baseline LV ejection fraction (LVEF) (34.9% vs 47.4%, p < 0.001). Microvascular obstruction was more common in patients with LV thrombus (77% vs 39%, p < 0.001). Patients with LV thrombus had increased LV dimensions with larger LV end-diastolic (19 ml [IQR 9-44] vs 6 ml [IQR -4-18], p < 0.001) and end-systolic volumes (10 ml [IQR 0–22] vs -4 ml [IQR -12-4], p < 0.001).

          Conclusion

          CMR increases the detection of LV thrombi which standard echocardiography may underestimate. Serial studies post-STEMI may improve detection of LV thrombus, which is more prevalent in patients with anterior infarction, moderate LV dysfunction and adverse LV remodelling. This subgroup of patients may represent a high-risk group for targeted serial screening with CMR.

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          Most cited references17

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          2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation

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            Embolic potential, prevention and management of mural thrombus complicating anterior myocardial infarction: a meta-analysis.

            The management of mural thrombus complicating acute anterior myocardial infarction remains controversial in part because of the small size of studies on this topic. We performed a meta-analysis of published studies to address three questions: 1) What is the embolic risk of mural thrombi after myocardial infarction? 2) What is the impact of systemic anticoagulation in reducing the embolic risk of mural thrombi? 3) What is the impact of systemic anticoagulation, thrombolytic therapy and antiplatelet therapy in preventing mural thrombus formation? Studies were identified by a computerized and manual search and were included if they were published in manuscript form in the English-language literature. Pooling of data was performed by calculating the Mantel-Haenszel odds ratio and an event rate difference by the method of DerSimonian and Laird. The odds ratio for increased risk of emboli in the presence of echocardiographically demonstrated mural thrombus (11 studies, 856 patients) was 5.45 (95% confidence interval [CI] 3.02 to 9.83), and the event rate difference was 0.09 (95% CI 0.03 to 0.14). The odds ratio of anticoagulation versus no anticoagulation in preventing embolization (seven studies, 270 patients) was 0.14 (95% CI 0.04 to 0.52) with an event rate difference of -0.33 (95% CI -0.50 to -0.16). The odds ratio of anticoagulation versus control in preventing mural thrombus formation (four studies, 307 patients) was 0.32 (95% CI 0.20 to 0.52), and the event rate difference was -0.19 (95% CI -0.09 to -0.28). The odds ratio for thrombolytic therapy in preventing mural thrombus (six studies, 390 patients) was 0.48 (95% CI 0.29 to 0.79) with an event rate difference of -0.16 (95% CI 0.10 to -0.42), whereas for antiplatelet agents (two studies, 112 patients) the odds ratio was 1.43 (95% CI 0.04 to 56.8) with an event rate difference of 0.16 (95% CI -0.20 to 0.52). This analysis supports the hypotheses that 1) mural thrombus after myocardial infarction poses a significantly increased risk of embolization, 2) the risk of embolization is reduced by systemic anticoagulation, and 3) anticoagulation can prevent mural thrombus formation. Thrombolytic therapy may prevent mural thrombus formation, but evidence for a similar benefit of antiplatelet therapy is lacking.
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              Detection of left ventricular thrombus by delayed-enhancement cardiovascular magnetic resonance prevalence and markers in patients with systolic dysfunction.

              This study sought to assess the prevalence and markers of left ventricular (LV) thrombus among patients with systolic dysfunction. Prior studies have yielded discordant findings regarding prevalence and markers of LV thrombus. Delayed-enhancement cardiovascular magnetic resonance (DE-CMR) identifies thrombus on the basis of tissue characteristics rather than just anatomical appearance and is potentially highly accurate. Prevalence of thrombus by DE-CMR was determined in 784 consecutive patients with systolic dysfunction (left ventricular ejection fraction [LVEF] <50%) imaged between July 2002 and July 2004. Patients were recruited from 2 separate institutions: a tertiary-care referral center and an outpatient clinic. Comparison to cine-cardiovascular magnetic resonance (CMR) was performed. Follow-up was undertaken for thrombus verification via pathology evaluation or documented embolic event within 6 months after CMR. Clinical and imaging parameters were assessed to determine risk factors for thrombus. Among this at-risk population (age 60 +/- 14 years; LVEF 32 +/- 11%), DE-CMR detected thrombus in 7% (55 patients) and cine-CMR in 4.7% (37 patients, p < 0.005). Follow-up was consistent with DE-CMR as a better reference standard than cine-CMR, including 100% detection among 5 patients with thrombus verified by pathology (cine-CMR, 40% detection), and logistic regression analysis testing the contributions of DE-CMR and cine-CMR simultaneously, which showed that only the presence of thrombus by DE-CMR was associated with follow-up end points (p < 0.005). Cine-CMR generally missed small intracavitary and small or large mural thrombus. In addition to traditional indices such as low LVEF and ischemic cardiomyopathy, multivariable analysis showed that increased myocardial scarring, an additional parameter available from DE-CMR, was an independent risk factor for thrombus. In a broad cross section of patients with systolic dysfunction, thrombus prevalence was 7% by DE-CMR and included small intracavitary and small or large mural thrombus missed by cine-CMR. Prevalence increased with worse LVEF, ischemic etiology, and increased myocardial scarring.
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                Author and article information

                Contributors
                Journal
                Int J Cardiol Heart Vasc
                Int J Cardiol Heart Vasc
                International Journal of Cardiology. Heart & Vasculature
                Elsevier
                2352-9067
                04 July 2019
                September 2019
                04 July 2019
                : 24
                : 100395
                Affiliations
                [a ]Department of Cardiology, Liverpool Hospital, Sydney, New South Wales, Australia
                [b ]South Western Sydney Clinical School, The University of New South Wales, Sydney, New South Wales, Australia
                [c ]Department of Radiology, Liverpool Hospital, Sydney, New South Wales, Australia
                [d ]Department of Cardiology, Westmead Hospital, Sydney, New South Wales, Australia
                [e ]Westmead Clinical School, The University of Sydney, New South Wales, Australia
                Author notes
                [* ]Corresponding author at: Department of Cardiology, Westmead Hospital, Hawkesbury Road and Darcy Road, Westmead, NSW 2145, Australia. l.thomas@ 123456unsw.edu.au
                Article
                S2352-9067(19)30119-8 100395
                10.1016/j.ijcha.2019.100395
                6612928
                8f8c310c-fda3-4549-a4a1-3e948c5784ae
                © 2019 Published by Elsevier B.V.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 29 April 2019
                : 24 June 2019
                Categories
                Original Paper

                myocardial infarction,left ventricular thrombus
                myocardial infarction, left ventricular thrombus

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