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Direct oral anticoagulants (DOAC) versus vitamin K antagonist in left ventricular thrombus: An updated meta‐analysis
research-article
Author(s):
Dhan B. Shrestha
1 ,
Sagun Dawadi
2
,
,
Bishal Dhakal
2 ,
Jurgen Shtembari
1 ,
Toralben Patel
3 ,
Rafae Shaikh
4 ,
George M. Bodziock
5 ,
Ghanshyam Shantha
5 ,
Cory R. Trankle
4 ,
Nimesh K. Patel
4
Publication date (Electronic):
24 November 2023
Journal:
Health Science Reports
Publisher:
John Wiley and Sons Inc.
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Abstract
Background and Aims
Current clinical guidelines for treating left ventricular thrombus (LVT) are limited by inadequate evidence to inform the comparative efficacy of oral anticoagulants. In this meta‐analysis, we aimed to compare the efficacy and safety of direct oral anticoagulants (DOAC) to vitamin K antagonists (VKA) in patients with LVT.
Methods
Four standard databases were searched for relevant literature comparing the efficacy and safety between DOAC and VKA for LVT treatment, published before August 19, 2023. Both the randomized controlled trials and observational studies were included in the analysis. The outcomes of interest were the resolution of LVT, all‐cause mortality, stroke, systemic embolism, and bleeding. Data from the selected studies were extracted and analyzed using RevMan 5.4 using odds ratio.
Results
Among 3959 studies from the database search and bibliography review, 33 were included in the analysis. LVT resolution was observed in 72.59% in the DOAC group versus 67.49% in the VKA group (odds ratio [OR]: 1.28, confidence interval [CI]: 1.07–1.53). Mortality was lower in the DOAC group (11.71% vs. 18.56%) (OR: 0.60, CI: 0.36–1.00; borderline statistical significance). Likewise, bleeding events (9.60% vs. 13.19%) (OR: 0.65, CI: 0.52–0.81) and stroke (7.54% vs. 11.04%) (OR: 0.71, CI: 0.53–0.96) were also significantly lower in the DOAC group.
Related collections
Most cited references47
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The Cochrane Collaboration’s tool for assessing risk of bias in randomised trials
Flaws in the design, conduct, analysis, and reporting of randomised trials can cause the effect of an intervention to be underestimated or overestimated. The Cochrane Collaboration’s tool for assessing risk of bias aims to make the process clearer and more accurate
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The PRISMA 2020 statement: an updated guideline for reporting systematic reviews
The Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) statement, published in 2009, was designed to help systematic reviewers transparently report why the review was done, what the authors did, and what they found. Over the past decade, advances in systematic review methodology and terminology have necessitated an update to the guideline. The PRISMA 2020 statement replaces the 2009 statement and includes new reporting guidance that reflects advances in methods to identify, select, appraise, and synthesise studies. The structure and presentation of the items have been modified to facilitate implementation. In this article, we present the PRISMA 2020 27-item checklist, an expanded checklist that details reporting recommendations for each item, the PRISMA 2020 abstract checklist, and the revised flow diagrams for original and updated reviews. In order to encourage its wide dissemination this article is freely accessible on BMJ, PLOS Medicine, Journal of Clinical Epidemiology and International Journal of Surgery journal websites. Systematic reviews serve many critical roles. They can provide syntheses of the state of knowledge in a field, from which future research priorities can be identified; they can address questions that otherwise could not be answered by individual studies; they can identify problems in primary research that should be rectified in future studies; and they can generate or evaluate theories about how or why phenomena occur. Systematic reviews therefore generate various types of knowledge for different users of reviews (such as patients, healthcare providers, researchers, and policy makers) [1, 2]. To ensure a systematic review is valuable to users, authors should prepare a transparent, complete, and accurate account of why the review was done, what they did (such as how studies were identified and selected) and what they found (such as characteristics of contributing studies and results of meta-analyses). Up-to-date reporting guidance facilitates authors achieving this [3]. The Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) statement published in 2009 (hereafter referred to as PRISMA 2009) [4–10] is a reporting guideline designed to address poor reporting of systematic reviews [11]. The PRISMA 2009 statement comprised a checklist of 27 items recommended for reporting in systematic reviews and an “explanation and elaboration” paper [12–16] providing additional reporting guidance for each item, along with exemplars of reporting. The recommendations have been widely endorsed and adopted, as evidenced by its co-publication in multiple journals, citation in over 60,000 reports (Scopus, August 2020), endorsement from almost 200 journals and systematic review organisations, and adoption in various disciplines. Evidence from observational studies suggests that use of the PRISMA 2009 statement is associated with more complete reporting of systematic reviews [17–20], although more could be done to improve adherence to the guideline [21]. Many innovations in the conduct of systematic reviews have occurred since publication of the PRISMA 2009 statement. For example, technological advances have enabled the use of natural language processing and machine learning to identify relevant evidence [22–24], methods have been proposed to synthesise and present findings when meta-analysis is not possible or appropriate [25–27], and new methods have been developed to assess the risk of bias in results of included studies [28, 29]. Evidence on sources of bias in systematic reviews has accrued, culminating in the development of new tools to appraise the conduct of systematic reviews [30, 31]. Terminology used to describe particular review processes has also evolved, as in the shift from assessing “quality” to assessing “certainty” in the body of evidence [32]. In addition, the publishing landscape has transformed, with multiple avenues now available for registering and disseminating systematic review protocols [33, 34], disseminating reports of systematic reviews, and sharing data and materials, such as preprint servers and publicly accessible repositories. To capture these advances in the reporting of systematic reviews necessitated an update to the PRISMA 2009 statement. Summary points • To ensure a systematic review is valuable to users, authors should prepare a transparent, complete, and accurate account of why the review was done, what they did, and what they found • The PRISMA 2020 statement provides updated reporting guidance for systematic reviews that reflects advances in methods to identify, select, appraise, and synthesise studies • The PRISMA 2020 statement consists of a 27-item checklist, an expanded checklist that details reporting recommendations for each item, the PRISMA 2020 abstract checklist, and revised flow diagrams for original and updated reviews • We anticipate that the PRISMA 2020 statement will benefit authors, editors, and peer reviewers of systematic reviews, and different users of reviews, including guideline developers, policy makers, healthcare providers, patients, and other stakeholders Development of PRISMA 2020 A complete description of the methods used to develop PRISMA 2020 is available elsewhere [35]. We identified PRISMA 2009 items that were often reported incompletely by examining the results of studies investigating the transparency of reporting of published reviews [17, 21, 36, 37]. We identified possible modifications to the PRISMA 2009 statement by reviewing 60 documents providing reporting guidance for systematic reviews (including reporting guidelines, handbooks, tools, and meta-research studies) [38]. These reviews of the literature were used to inform the content of a survey with suggested possible modifications to the 27 items in PRISMA 2009 and possible additional items. Respondents were asked whether they believed we should keep each PRISMA 2009 item as is, modify it, or remove it, and whether we should add each additional item. Systematic review methodologists and journal editors were invited to complete the online survey (110 of 220 invited responded). We discussed proposed content and wording of the PRISMA 2020 statement, as informed by the review and survey results, at a 21-member, two-day, in-person meeting in September 2018 in Edinburgh, Scotland. Throughout 2019 and 2020, we circulated an initial draft and five revisions of the checklist and explanation and elaboration paper to co-authors for feedback. In April 2020, we invited 22 systematic reviewers who had expressed interest in providing feedback on the PRISMA 2020 checklist to share their views (via an online survey) on the layout and terminology used in a preliminary version of the checklist. Feedback was received from 15 individuals and considered by the first author, and any revisions deemed necessary were incorporated before the final version was approved and endorsed by all co-authors. The PRISMA 2020 statement Scope of the guideline The PRISMA 2020 statement has been designed primarily for systematic reviews of studies that evaluate the effects of health interventions, irrespective of the design of the included studies. However, the checklist items are applicable to reports of systematic reviews evaluating other interventions (such as social or educational interventions), and many items are applicable to systematic reviews with objectives other than evaluating interventions (such as evaluating aetiology, prevalence, or prognosis). PRISMA 2020 is intended for use in systematic reviews that include synthesis (such as pairwise meta-analysis or other statistical synthesis methods) or do not include synthesis (for example, because only one eligible study is identified). The PRISMA 2020 items are relevant for mixed-methods systematic reviews (which include quantitative and qualitative studies), but reporting guidelines addressing the presentation and synthesis of qualitative data should also be consulted [39, 40]. PRISMA 2020 can be used for original systematic reviews, updated systematic reviews, or continually updated (“living”) systematic reviews. However, for updated and living systematic reviews, there may be some additional considerations that need to be addressed. Where there is relevant content from other reporting guidelines, we reference these guidelines within the items in the explanation and elaboration paper [41] (such as PRISMA-Search [42] in items 6 and 7, Synthesis without meta-analysis (SWiM) reporting guideline [27] in item 13d). Box 1 includes a glossary of terms used throughout the PRISMA 2020 statement. PRISMA 2020 is not intended to guide systematic review conduct, for which comprehensive resources are available [43–46]. However, familiarity with PRISMA 2020 is useful when planning and conducting systematic reviews to ensure that all recommended information is captured. PRISMA 2020 should not be used to assess the conduct or methodological quality of systematic reviews; other tools exist for this purpose [30, 31]. Furthermore, PRISMA 2020 is not intended to inform the reporting of systematic review protocols, for which a separate statement is available (PRISMA for Protocols (PRISMA-P) 2015 statement [47, 48]). Finally, extensions to the PRISMA 2009 statement have been developed to guide reporting of network meta-analyses [49], meta-analyses of individual participant data [50], systematic reviews of harms [51], systematic reviews of diagnostic test accuracy studies [52], and scoping reviews [53]; for these types of reviews we recommend authors report their review in accordance with the recommendations in PRISMA 2020 along with the guidance specific to the extension. How to use PRISMA 2020 The PRISMA 2020 statement (including the checklists, explanation and elaboration, and flow diagram) replaces the PRISMA 2009 statement, which should no longer be used. Box 2 summarises noteworthy changes from the PRISMA 2009 statement. The PRISMA 2020 checklist includes seven sections with 27 items, some of which include sub-items (Table 1). A checklist for journal and conference abstracts for systematic reviews is included in PRISMA 2020. This abstract checklist is an update of the 2013 PRISMA for Abstracts statement [54], reflecting new and modified content in PRISMA 2020 (Table 2). A template PRISMA flow diagram is provided, which can be modified depending on whether the systematic review is original or updated (Fig. 1). Table 1 PRISMA 2020 item checklist Section and topic Item # Checklist item Location where item is reported Title Title 1 Identify the report as a systematic review. Abstract Abstract 2 See the PRISMA 2020 for Abstracts checklist (Table 2). Introduction Rationale 3 Describe the rationale for the review in the context of existing knowledge. Objectives 4 Provide an explicit statement of the objective(s) or question(s) the review addresses. Methods Eligibility criteria 5 Specify the inclusion and exclusion criteria for the review and how studies were grouped for the syntheses. Information sources 6 Specify all databases, registers, websites, organisations, reference lists and other sources searched or consulted to identify studies. Specify the date when each source was last searched or consulted. Search strategy 7 Present the full search strategies for all databases, registers and websites, including any filters and limits used. Selection process 8 Specify the methods used to decide whether a study met the inclusion criteria of the review, including how many reviewers screened each record and each report retrieved, whether they worked independently, and if applicable, details of automation tools used in the process. Data collection process 9 Specify the methods used to collect data from reports, including how many reviewers collected data from each report, whether they worked independently, any processes for obtaining or confirming data from study investigators, and if applicable, details of automation tools used in the process. Data items 10a List and define all outcomes for which data were sought. Specify whether all results that were compatible with each outcome domain in each study were sought (e.g. for all measures, time points, analyses), and if not, the methods used to decide which results to collect. 10b List and define all other variables for which data were sought (e.g. participant and intervention characteristics, funding sources). Describe any assumptions made about any missing or unclear information. Study risk of bias assessment 11 Specify the methods used to assess risk of bias in the included studies, including details of the tool(s) used, how many reviewers assessed each study and whether they worked independently, and if applicable, details of automation tools used in the process. Effect measures 12 Specify for each outcome the effect measure(s) (e.g. risk ratio, mean difference) used in the synthesis or presentation of results. Synthesis methods 13a Describe the processes used to decide which studies were eligible for each synthesis (e.g. tabulating the study intervention characteristics and comparing against the planned groups for each synthesis (item #5)). 13b Describe any methods required to prepare the data for presentation or synthesis, such as handling of missing summary statistics, or data conversions. 13c Describe any methods used to tabulate or visually display results of individual studies and syntheses. 13d Describe any methods used to synthesise results and provide a rationale for the choice(s). If meta-analysis was performed, describe the model(s), method(s) to identify the presence and extent of statistical heterogeneity, and software package(s) used. 13e Describe any methods used to explore possible causes of heterogeneity among study results (e.g. subgroup analysis, meta-regression). 13f Describe any sensitivity analyses conducted to assess robustness of the synthesised results. Reporting bias assessment 14 Describe any methods used to assess risk of bias due to missing results in a synthesis (arising from reporting biases). Certainty assessment 15 Describe any methods used to assess certainty (or confidence) in the body of evidence for an outcome. Results Study selection 16a Describe the results of the search and selection process, from the number of records identified in the search to the number of studies included in the review, ideally using a flow diagram (see Fig. 1). 16b Cite studies that might appear to meet the inclusion criteria, but which were excluded, and explain why they were excluded. Study characteristics 17 Cite each included study and present its characteristics. Risk of bias in studies 18 Present assessments of risk of bias for each included study. Results of individual studies 19 For all outcomes, present, for each study: (a) summary statistics for each group (where appropriate) and (b) an effect estimate and its precision (e.g. confidence/credible interval), ideally using structured tables or plots. Results of syntheses 20a For each synthesis, briefly summarise the characteristics and risk of bias among contributing studies. 20b Present results of all statistical syntheses conducted. If meta-analysis was done, present for each the summary estimate and its precision (e.g. confidence/credible interval) and measures of statistical heterogeneity. If comparing groups, describe the direction of the effect. 20c Present results of all investigations of possible causes of heterogeneity among study results. 20d Present results of all sensitivity analyses conducted to assess the robustness of the synthesised results. Reporting biases 21 Present assessments of risk of bias due to missing results (arising from reporting biases) for each synthesis assessed. Certainty of evidence 22 Present assessments of certainty (or confidence) in the body of evidence for each outcome assessed. Discussion Discussion 23a Provide a general interpretation of the results in the context of other evidence. 23b Discuss any limitations of the evidence included in the review. 23c Discuss any limitations of the review processes used. 23d Discuss implications of the results for practice, policy, and future research. Other information Registration and protocol 24a Provide registration information for the review, including register name and registration number, or state that the review was not registered. 24b Indicate where the review protocol can be accessed, or state that a protocol was not prepared. 24c Describe and explain any amendments to information provided at registration or in the protocol. Support 25 Describe sources of financial or non-financial support for the review, and the role of the funders or sponsors in the review. Competing interests 26 Declare any competing interests of review authors. Availability of data, code, and other materials 27 Report which of the following are publicly available and where they can be found: template data collection forms; data extracted from included studies; data used for all analyses; analytic code; any other materials used in the review. Table 2 PRISMA 2020 for abstracts checklista Section and topic Item # Checklist item Title Title 1 Identify the report as a systematic review. Background Objectives 2 Provide an explicit statement of the main objective(s) or question(s) the review addresses. Methods Eligibility criteria 3 Specify the inclusion and exclusion criteria for the review. Information sources 4 Specify the information sources (e.g. databases, registers) used to identify studies and the date when each was last searched. Risk of bias 5 Specify the methods used to assess risk of bias in the included studies. Synthesis of results 6 Specify the methods used to present and synthesise results. Results Included studies 7 Give the total number of included studies and participants and summarise relevant characteristics of studies. Synthesis of results 8 Present results for main outcomes, preferably indicating the number of included studies and participants for each. If meta-analysis was done, report the summary estimate and confidence/credible interval. If comparing groups, indicate the direction of the effect (i.e. which group is favoured). Discussion Limitations of evidence 9 Provide a brief summary of the limitations of the evidence included in the review (e.g. study risk of bias, inconsistency and imprecision). Interpretation 10 Provide a general interpretation of the results and important implications. Other Funding 11 Specify the primary source of funding for the review. Registration 12 Provide the register name and registration number. aThis abstract checklist retains the same items as those included in the PRISMA for Abstracts statement published in 2013 [54], but has been revised to make the wording consistent with the PRISMA 2020 statement and includes a new item recommending authors specify the methods used to present and synthesise results (item #6) Fig. 1 PRISMA 2020 flow diagram template for systematic reviews. The new design is adapted from flow diagrams proposed by Boers [55], Mayo-Wilson et al. [56] and Stovold et al. [57] The boxes in grey should only be completed if applicable; otherwise they should be removed from the flow diagram. Note that a “report” could be a journal article, preprint, conference abstract, study register entry, clinical study report, dissertation, unpublished manuscript, government report or any other document providing relevant information We recommend authors refer to PRISMA 2020 early in the writing process, because prospective consideration of the items may help to ensure that all the items are addressed. To help keep track of which items have been reported, the PRISMA statement website (http://www.prisma-statement.org/) includes fillable templates of the checklists to download and complete (also available in Additional file 1). We have also created a web application that allows users to complete the checklist via a user-friendly interface [58] (available at https://prisma.shinyapps.io/checklist/ and adapted from the Transparency Checklist app [59]). The completed checklist can be exported to Word or PDF. Editable templates of the flow diagram can also be downloaded from the PRISMA statement website. We have prepared an updated explanation and elaboration paper, in which we explain why reporting of each item is recommended and present bullet points that detail the reporting recommendations (which we refer to as elements) [41]. The bullet-point structure is new to PRISMA 2020 and has been adopted to facilitate implementation of the guidance [60, 61]. An expanded checklist, which comprises an abridged version of the elements presented in the explanation and elaboration paper, with references and some examples removed, is available in Additional file 2. Consulting the explanation and elaboration paper is recommended if further clarity or information is required. Journals and publishers might impose word and section limits, and limits on the number of tables and figures allowed in the main report. In such cases, if the relevant information for some items already appears in a publicly accessible review protocol, referring to the protocol may suffice. Alternatively, placing detailed descriptions of the methods used or additional results (such as for less critical outcomes) in supplementary files is recommended. Ideally, supplementary files should be deposited to a general-purpose or institutional open-access repository that provides free and permanent access to the material (such as Open Science Framework, Dryad, figshare). A reference or link to the additional information should be included in the main report. Finally, although PRISMA 2020 provides a template for where information might be located, the suggested location should not be seen as prescriptive; the guiding principle is to ensure the information is reported. Discussion Use of PRISMA 2020 has the potential to benefit many stakeholders. Complete reporting allows readers to assess the appropriateness of the methods, and therefore the trustworthiness of the findings. Presenting and summarising characteristics of studies contributing to a synthesis allows healthcare providers and policy makers to evaluate the applicability of the findings to their setting. Describing the certainty in the body of evidence for an outcome and the implications of findings should help policy makers, managers, and other decision makers formulate appropriate recommendations for practice or policy. Complete reporting of all PRISMA 2020 items also facilitates replication and review updates, as well as inclusion of systematic reviews in overviews (of systematic reviews) and guidelines, so teams can leverage work that is already done and decrease research waste [36, 62, 63]. We updated the PRISMA 2009 statement by adapting the EQUATOR Network’s guidance for developing health research reporting guidelines [64]. We evaluated the reporting completeness of published systematic reviews [17, 21, 36, 37], reviewed the items included in other documents providing guidance for systematic reviews [38], surveyed systematic review methodologists and journal editors for their views on how to revise the original PRISMA statement [35], discussed the findings at an in-person meeting, and prepared this document through an iterative process. Our recommendations are informed by the reviews and survey conducted before the in-person meeting, theoretical considerations about which items facilitate replication and help users assess the risk of bias and applicability of systematic reviews, and co-authors’ experience with authoring and using systematic reviews. Various strategies to increase the use of reporting guidelines and improve reporting have been proposed. They include educators introducing reporting guidelines into graduate curricula to promote good reporting habits of early career scientists [65]; journal editors and regulators endorsing use of reporting guidelines [18]; peer reviewers evaluating adherence to reporting guidelines [61, 66]; journals requiring authors to indicate where in their manuscript they have adhered to each reporting item [67]; and authors using online writing tools that prompt complete reporting at the writing stage [60]. Multi-pronged interventions, where more than one of these strategies are combined, may be more effective (such as completion of checklists coupled with editorial checks) [68]. However, of 31 interventions proposed to increase adherence to reporting guidelines, the effects of only 11 have been evaluated, mostly in observational studies at high risk of bias due to confounding [69]. It is therefore unclear which strategies should be used. Future research might explore barriers and facilitators to the use of PRISMA 2020 by authors, editors, and peer reviewers, designing interventions that address the identified barriers, and evaluating those interventions using randomised trials. To inform possible revisions to the guideline, it would also be valuable to conduct think-aloud studies [70] to understand how systematic reviewers interpret the items, and reliability studies to identify items where there is varied interpretation of the items. We encourage readers to submit evidence that informs any of the recommendations in PRISMA 2020 (via the PRISMA statement website: http://www.prisma-statement.org/). To enhance accessibility of PRISMA 2020, several translations of the guideline are under way (see available translations at the PRISMA statement website). We encourage journal editors and publishers to raise awareness of PRISMA 2020 (for example, by referring to it in journal “Instructions to authors”), endorsing its use, advising editors and peer reviewers to evaluate submitted systematic reviews against the PRISMA 2020 checklists, and making changes to journal policies to accommodate the new reporting recommendations. We recommend existing PRISMA extensions [47, 49–53, 71, 72] be updated to reflect PRISMA 2020 and advise developers of new PRISMA extensions to use PRISMA 2020 as the foundation document. Conclusion We anticipate that the PRISMA 2020 statement will benefit authors, editors, and peer reviewers of systematic reviews, and different users of reviews, including guideline developers, policy makers, healthcare providers, patients, and other stakeholders. Ultimately, we hope that uptake of the guideline will lead to more transparent, complete, and accurate reporting of systematic reviews, thus facilitating evidence based decision making. Box 1 Glossary of terms Systematic review—A review that uses explicit, systematic methods to collate and synthesise findings of studies that address a clearly formulated question [43] Statistical synthesis—The combination of quantitative results of two or more studies. This encompasses meta-analysis of effect estimates (described below) and other methods, such as combining P values, calculating the range and distribution of observed effects, and vote counting based on the direction of effect (see McKenzie and Brennan [25] for a description of each method) Meta-analysis of effect estimates—A statistical technique used to synthesise results when study effect estimates and their variances are available, yielding a quantitative summary of results [25] Outcome—An event or measurement collected for participants in a study (such as quality of life, mortality) Result—The combination of a point estimate (such as a mean difference, risk ratio, or proportion) and a measure of its precision (such as a confidence/credible interval) for a particular outcome Report—A document (paper or electronic) supplying information about a particular study. It could be a journal article, preprint, conference abstract, study register entry, clinical study report, dissertation, unpublished manuscript, government report, or any other document providing relevant information Record—The title or abstract (or both) of a report indexed in a database or website (such as a title or abstract for an article indexed in Medline). Records that refer to the same report (such as the same journal article) are “duplicates”; however, records that refer to reports that are merely similar (such as a similar abstract submitted to two different conferences) should be considered unique. Study—An investigation, such as a clinical trial, that includes a defined group of participants and one or more interventions and outcomes. A “study” might have multiple reports. For example, reports could include the protocol, statistical analysis plan, baseline characteristics, results for the primary outcome, results for harms, results for secondary outcomes, and results for additional mediator and moderator analyses Box 2 Noteworthy changes to the PRISMA 2009 statement • Inclusion of the abstract reporting checklist within PRISMA 2020 (see item #2 and Box 2). • Movement of the ‘Protocol and registration’ item from the start of the Methods section of the checklist to a new Other section, with addition of a sub-item recommending authors describe amendments to information provided at registration or in the protocol (see item #24a-24c). • Modification of the ‘Search’ item to recommend authors present full search strategies for all databases, registers and websites searched, not just at least one database (see item #7). • Modification of the ‘Study selection’ item in the Methods section to emphasise the reporting of how many reviewers screened each record and each report retrieved, whether they worked independently, and if applicable, details of automation tools used in the process (see item #8). • Addition of a sub-item to the ‘Data items’ item recommending authors report how outcomes were defined, which results were sought, and methods for selecting a subset of results from included studies (see item #10a). • Splitting of the ‘Synthesis of results’ item in the Methods section into six sub-items recommending authors describe: the processes used to decide which studies were eligible for each synthesis; any methods required to prepare the data for synthesis; any methods used to tabulate or visually display results of individual studies and syntheses; any methods used to synthesise results; any methods used to explore possible causes of heterogeneity among study results (such as subgroup analysis, meta-regression); and any sensitivity analyses used to assess robustness of the synthesised results (see item #13a-13f). • Addition of a sub-item to the ‘Study selection’ item in the Results section recommending authors cite studies that might appear to meet the inclusion criteria, but which were excluded, and explain why they were excluded (see item #16b). • Splitting of the ‘Synthesis of results’ item in the Results section into four sub-items recommending authors: briefly summarise the characteristics and risk of bias among studies contributing to the synthesis; present results of all statistical syntheses conducted; present results of any investigations of possible causes of heterogeneity among study results; and present results of any sensitivity analyses (see item #20a-20d). • Addition of new items recommending authors report methods for and results of an assessment of certainty (or confidence) in the body of evidence for an outcome (see items #15 and #22). • Addition of a new item recommending authors declare any competing interests (see item #26). • Addition of a new item recommending authors indicate whether data, analytic code and other materials used in the review are publicly available and if so, where they can be found (see item #27). Supplementary Information Additional file 1. PRISMA 2020 checklist. Additional file 2. PRISMA 2020 expanded checklist.
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Left ventricular thrombus formation after acute myocardial infarction
Ronak Delewi, Felix Zijlstra, Jan Piek (2012)
Cardiovascular disease remains the leading cause of death in western society. Mortality from acute myocardial infarction (AMI) has decreased since the introduction of primary percutaneous coronary intervention (PCI), which has proved to be superior to thrombolytic therapy by demonstrating lower mortality rates and reduced clinical adverse events. Nevertheless, postinfarct complications still lead to morbidity and mortality in a large number of patients. One of the most feared complications is the occurrence of thromboembolic events (mostly cerebrovascular accidents) due to left ventricular (LV) thrombus formation. The risk of LV thrombus formation is highest during the first 3 months following acute myocardial infarction, but the potential for cerebral emboli persists in the large population of patients with chronic LV dysfunction. Since these thromboembolic events are usually unheralded by warning signs of transient cerebral ischaemia, the only truly satisfactory medical approach is adequate management of these high risk groups. This article discusses the incidence, diagnosis and management of LV thrombus formation after an AMI. Pathogenesis of LV thrombus The combination of blood stasis, endothelial injury and hypercoagulability, often referred to as Virchow's triad, is a prerequisite for in vivo thrombus formation. In the presence of LV thrombus formation after AMI, the three components of this triad can also be recognised (figure 1). LV regional wall akinesia and dyskinesia result in blood stasis, often recognised on two dimensional echocardiography by the occurrence of spontaneous LV contrast. Prolonged ischaemia leads to subendocardial tissue injury with inflammatory changes. Finally, patients with an acute coronary syndrome display a hypercoagulable state with, for example, increased concentrations of prothrombin, fibrinopeptide A, and von Willebrand factor, and decreased concentrations of the enzyme responsible for cleaving von Willebrand factor (ADAMTS13).w1 w2 This triad can result in the formation of LV thrombus composed of fibrin, red blood cells, and platelets. Figure 1 The three components of the Virchow's triad in left ventricular thrombus formation. ACS, acute coronary syndrome; LV, left ventricular. LV thrombus can occur within 24 h after AMI. One study performing serial echocardiographic studies showed that about 90% of thrombi are formed at a maximum of 2 weeks after the index event.w3 However, some patients develop a new LV thrombus after discharge, often in association with worsening LV systolic function. Spontaneous or anticoagulant induced resolution is relatively common in LV thrombus formation after AMI. Thrombus seems to disappear more often in patients with apical akinesia than those with apical aneurysm or dyskinesia.1 It has been speculated that LV thrombus plays a positive role in the acutely infarcted myocardium, by offering mechanical support to the infarcted myocardium and therefore protecting against LV rupture.w4 The thrombus becomes firmly attached to its site of origin, enhancing the underlying myocardial scar, limiting potential infarct expansion, and partially restoring the thickness of the myocardial wall. As a consequence, bulging is reduced, resulting in a more effective myocardial contraction. Often, however, expansion of the infarct zone occurs very early after infarction, before the thrombus has time to organise and is able to prevent formation of LV aneurysm and myocardial rupture. Incidence Early data from the prethrombolytic and thrombolytic eras suggest that in the setting of AMI, LV thrombus was present in 7–46% of patients, most frequently in acute anterior or apical myocardial infarction.2–4 w3–w5 Differences in diagnostic techniques, timing of examination and use of antithrombotic treatment cause substantial variation in the reported frequency of thrombus from different series. In addition, it should be noted that the incidence as reported in autopsy studies is consistently higher compared with clinical studies, probably due to better accuracy but also due to patient selection. Nowadays the reported incidence is lower. This is probably due to (1) more aggressive anticoagulation therapies in the acute phase (eg, the use of heparin, bivalirudin), (2) smaller infarctions, and (3) improved LV remodelling. Although the use of ACE inhibitors is also thought to be associated with improved LV remodelling, the GISSI-3 study found no difference in LV thrombus rates between patients who did and did not receive lisinopril.5 There are limited data on the exact frequency of LV thrombus in PCI treated AMI patients. Two studies found LV thrombus formation in 5.4% and 7.1% of patients with acute anterior wall myocardial infarctions.w6 w7 However, these studies were retrospective, non-serial and only assessed LV thrombus formation at a single point in time and during the early phase of recovery after myocardial infarction. In the latter study a follow-up echocardiography was performed at 1–3 months, showing LV thrombus in an additional 8% of the patients.w7 Solheim et al reported a similar incidence of 15% in the first 3 months in a selected group of AMI patients treated by primary PCI.6 So, the timing of LV thrombus assessment is crucial, as assessment too soon after the onset of myocardial infarction will probably lead to failure to detect the thrombus in a significant percentage of patients. Clinical factors contributing to LV thrombus formation Risk factors for the development of LV thrombus are consistently irrespective of infarct treatment and include large infarct size, severe apical asynergy (ie, akinesis or dyskinesis), LV aneurysm, and anterior MI.2 5–8 w6 This is consistent with an increased contribution of at least two of the three components of Virchow's triad, namely a larger area of blood stasis as well as an increased area of injured subendocardium. In a study of more than 8000 patients with ST elevation myocardial infarction (STEMI), LV thrombus was found in 427 patients (5.1%). This incidence is relatively low compared to other studies, probably because of the exclusion of high risk patients with severe LV dysfunction. Patients with anterior AMI had a higher incidence of LV thrombus compared to patients with AMI at other regions (11.5% vs 2.3%, p<0.0001). The incidence of LV thrombus was also higher in patients with an ejection fraction ≤40% (10.5% vs 4%, p<0.0001). In patients with an anterior AMI and an ejection fraction ≤40% this percentage was as high as 17.8%.5 Thrombus formation is not exclusively located apically; approximately 11% occurs at the septal wall and 3% at the inferoposterior wall.4 The prevalence of thrombus in non-anterior myocardial infarction increases when inferior necrosis extends towards the posterolateral wall. In such cases the prevalence is similar to that observed in anterior wall AMIs of comparable extension.w5 Thrombi can also be found in small apical infarcts, with good global systolic function.w3 The presence of thrombi is significantly related to the region of most severe functional impairment and/or the region with myocardial enhancement (ie, infarction or scarring).7 LV thrombus appears earlier in the course of the disease when initial ejection fraction ≤40%, in the presence of multivessel coronary artery disease, or a high peak creatine kinase value.w8 There is conflicting evidence with respect to the influence of β-blockers. Several studies have reported a higher frequency of thrombus development in patients treated with β-blockers which could be related to the negative inotropic action of these drugs and thus increased blood stasis. In particular, in a randomised study, Johannessen et al reported an increased occurrence of thrombus in patients with anterior AMI after oral β-blocker therapy.w9 Turpie et al reported similar results after treatment with β-blockers in a large population of patients with AMI.9 The GISSI-2 study, however, observed the same rate of LV thrombi in patients with or without atenolol.10 It has been demonstrated that mitral regurgitation prevents thrombus formation in patients with dilated cardiomyopathy.w10 The protective effect of mitral regurgitation may be the consequence of augmented early diastolic flow velocities at the mitral annulus level, as well through the entire length of the left ventricle, protecting the LV cavity from a stagnant, thrombogenic blood flow pattern. In addition, studies suggest abnormal flow profiles are associated with the presence of an LV thrombus.11 w11 However, to date no studies have demonstrated the same association in patients with AMI. There have been few studies on the use of biomarkers in the setting of LV thrombus formation. It could be postulated that factors involved in the coagulation cascade could serve as biomarkers to identify patients at increased risk for LV thrombus development. Data presented at the European Society of Cardiology in 2011 demonstrated higher soluble tissue factor and d-dimer concentrations in patients with LV thrombus formation.w12 Another study observed mildly elevated anticardiolipin antibody levels in patients with LV thrombus formation after AMI.w13 Whether these factors are indeed capable of predicting LV thrombus formation needs to be evaluated. Diagnostic modalities to detect LV thrombus Radionuclide based techniques In 39 series using radionuclide ventriculography, a so-called ‘square left ventricle’ was reported to be associated with LV thrombus.w14 The use of indium-111 labelled platelets is much better documented. It provides excellent specificity (95%) in identifying LV thrombus, and its sensitivity was reported to be 70% compared with transthoracic echocardiography (TTE).w15 It is not applied widely though because it is time consuming and expensive, not universally available, and involves radiation exposure. Furthermore, this scintigraphic technique is ineffective in identifying relatively small thrombi, and it has good specificity and sensitivity only if there is active platelet aggregation on the surface of the LV mural thrombus at the time of imaging. In patients with an elevated left hemidiaphragm, indium-111 activity in the spleen may be confused with that from the LV apex. Finally, in patients with a large LV aneurysm but no LV thrombus, a large amount of relatively static blood within the LV aneurysm may increase indium-111 activity.w16 Echocardiography Two dimensional TTE is the technique used most often for assessing the presence, shape and size of an LV mural thrombus. When the thoracic anatomy of the patient allows sufficient visualisation of the heart, two dimensional echocardiography provides excellent specificity (85–90%) and sensitivity (95%) in detecting LV thrombus.12 w17 w18 LV thrombus on echocardiography is defined as a discrete echodense mass in the left ventricle with defined margins that are distinct from the endocardium and seen throughout systole and diastole. It should be located adjacent to an area of the LV wall which is hypokinetic or akinetic and seen from at least two views (usually apical and short axis). Care must be taken to exclude false tendons and trabeculae and to rule out artefacts (reverberations, side lobe or near field artefacts), which constitute the most common cause for a false diagnosis of a thrombus.13 14 Another source of false-positive studies result from tangentially-cut LV wall. Varying gain settings and depth of field, as well as using transducers with different carrier frequencies in multiple positions and orientations, are helpful to minimise such false-positive studies.w17 In addition, often the LV apex cannot be clearly defined and the presence or absence of a thrombus may be very difficult to establish, leading to an estimated 10–46% of echocardiograms that are inconclusive.w20 w21 Intravenous echo contrast during TTE may improve the diagnostic assessment of LV thrombus.12 w22 However, in Europe the use of most compounds is contraindicated by the European Medicines Agency in cardiac patients with acute coronary syndromes, recent PCI, acute or chronic severe heart failure or severe cardiac arrhythmias. Also non-protruding and small mural LV thrombi may still go undetected.14 Transoesophageal echocardiography (TOE) has little to offer in the detection of LV thrombus. Although it is the technique of choice for detecting atrial masses and thrombi in the left atrial appendage, its value for diagnosing LV thrombus is limited because the apex is most often not well visualised.12 w23 Nevertheless, some data suggest that TOE is superior to TTE in providing optimal visualisation of small LV apical thrombi.w24 Computed tomography CT scanning provides about the same specificity and sensitivity as two dimensional TTE in the identification of LV thrombus.w25 This technique is not used in daily practice since it requires the intravenous injection of radiographic contrast material and exposes the patient to ionising radiation. Magnetic resonance imaging Cardiac magnetic resonance imaging (CMR) with contrast (delayed enhancement (DE)) has significantly better accuracy than TTE and TOE for the diagnosis of LV thrombus7 12 w26 w27 (table 1 and figure 2). A study by Srichai et al compared CMR and late gadolinium enhancement with echocardiography in a cohort of patients undergoing LV reconstruction surgery in whom surgical and/or postmortem verification of thrombus was performed.12 This study reported that the sensitivity of TTE was 40%, compared with 88% for CMR. Another study reported an echo sensitivity and specificity of 33% and 91%, respectively, in a heterogeneous population of patients with LV systolic dysfunction.7 These studies reported lower sensitivity for detection of LV thrombus than previously described, probably due to exclusion of suboptimal echocardiographic examinations in the previously mentioned studies. Also, echocardiographic examinations were often reinterpreted with emphasis on LV thrombus detection and led to different findings when the presence or absence of LV thrombus was based on routine clinical echocardiographic reading as part of the patient’s evaluation. Table 1 Sensitivities and specificities of different diagnostic modalities for the detection of left ventricular thrombus formation Sensitivity Specificity TOE 35% 90% Routine clinical TTE 35–40% 90% TTE (indication suspect LV thrombus) 60% 90% CT Comparable with TTE Cine CMR 60% 90% DE-CMR 88% 99% CMR, cardiac magnetic resonance imaging; CT, computed tomography; DE, delayed enhancement; LV, left ventricular; TOE, transoesophageal echocardiography; TTE, transthoracic echocardiography. Figure 2 Left ventricular (LV) thrombus formation on delayed gadolinium contrast cardiac MRI and transthoracic echocardiography. Transthoracic echocardiographic appearance of a thrombus (asterisk) in the apex of the left ventricle (A); cine cardiovascular magnetic resonance of the same patient also delineates the apical thrombus (B); late gadolinium enhancement imaging clearly confirms the avascular non-enhancing thrombus (asterisk, dark) close to the transmural infarcted myocardium (bright hyperenhanced, black arrowheads) with areas of microvascular obstruction (black, white arrowheads) (C). Courtesy of Dr A C van Rossum, Dr R Nijveldt, Department of Cardiology, VU University Medical Center, Amsterdam, the Netherlands, and Dr B J Bouma, Department of Cardiology, Academic Medical Center, Amsterdam, the Netherlands. DE-CMR allows for a relatively rapid assessment of thrombus presence, size, and location and is nowadays considered the gold standard. The intravenous administration of gadolinium chelates greatly enhances the ability to detect and characterise LV thrombi. Immediately after contrast administration, the homogeneous, strong enhancement of the LV cavity allows easy detection of abnormal intraventricular structures (dark), which frequently occur adjacent to scarred myocardium (bright hyperenhanced). Cine-CMR (without a contrast agent such as gadolinium) seems to be less suitable for LV thrombus detection. Thrombus was missed in 44–50% of the cases as detected by DE-CMR.7 8 The ability of DE-CMR to identify thrombus based on tissue characteristics rather than anatomical appearance alone may explain why it provides improved thrombus imaging compared with cine-CMR. It should be mentioned that the criteria to differentiate no-reflow zones from mural thrombi are not definite, and thus differentiation may not always be straightforward. Also, further research and histopathological correlation is needed to evaluate the role of DE-CMR in differentiating subacute from organised clots. Embolic complications In the prethrombolytic era, embolic complications were reported in approximately 10% of cases,15 w28 w29 whereas in the thrombolytic era, embolic complications occurred in 2–3% of patients. There are poor data regarding embolic complications in LV thrombus patients treated by primary PCI. Also, exact percentages regarding the site of embolisation are not available. Several studies have suggested that LV thrombi that protrude into the ventricular cavity or that exhibit independent mobility are associated with a higher rate of embolisation than thrombi without these features16 17 w30 (figure 3). A thrombus is considered as protruding when it projects predominantly into the LV cavity and as mural when it appears flat and parallel to the endocardial surface. Echocardiographic studies analysing mainly retrospective and non-serial data have indicated a positive relationship between the embolic potential of LV thrombi and their protruding shape and/or intracavitary motion.15 w30 However, spontaneous time-course variation in the morphologic aspects, such as shape and mobility pattern, are common. By performing serial echocardiography on 59 untreated patients, Domenicucci et al found that these morphological features demonstrated pronounced spontaneous variability in the first several months after acute infarction, and therefore suggested that the assessment of these features was not helpful. They noted that 41% of 59 thrombi had significant changes in shape and 29% had changes in mobility.18 Also, it has been reported that up to 40% of embolism episodes occur in patients whose thrombi are neither protuberant nor mobile. Figure 3 Transthoracic echocardiographic appearance of a mobile, protruding left ventricular thrombus. Courtesy of J Vleugels and Rianne H A de Bruin, Department of Cardiology, Department of Cardiology, Academic Medical Center, Amsterdam, the Netherlands. Other thrombus characteristics, such as thrombus size,16 central echolucency17 or hyperkinesia of the myocardial segments adjacent to the thrombus,4 were found in some studies to be associated with an increased risk of embolism, but were not confirmed by others. Other conditions that increase the risk of systemic embolisation are: (1) severe congestive heart failure, (2) diffuse LV dilatation and systolic dysfunction, (3) previous embolisation, (4) atrial fibrillation, and (5) advanced patient age. It has been suggested that the risk of embolisation is lower in patients with LV aneurysm, since the absence of LV contraction near the site of the thrombus makes dislodgement unlikely.w31 Pharmacological management If indeed systemic embolisation is the highest risk of LV thrombus, the central question arises as to how these patients should be treated to prevent embolisation. In the past, if recurrent systemic emboli developed despite anticoagulant therapy, surgical removal of the thrombus was considered necessary.17 w31 w32 Nowadays antithrombotic therapy is thought to prevent embolic complications of LV thrombus. Thrombolysis Vaitkus and Barnathan pooled the data from six studies comprising a total of 390 patients and assessed the incidence of LV thrombus formation in those patients treated with thrombolysis versus those without thrombolytic therapy. They were not able to demonstrate a statistical difference in the incidence of LV thrombus formation, only a trend in favour of thrombolysis.19 These studies were not randomised but often utilised patients seen 3 h after symptom onset as a control group. Data from the GISSI-3 database, including more than 8000 patients, showed no reduced incidence of thrombus formation in patients who received either thrombolytic therapy or heparin.5 Intravenous thrombolysis has also been used for treatment of documented LV thrombus. In a report of 16 patients with LV thrombus on echocardiography, urokinase was infused intravenously at a rate of 60 000 U/h for 2–8 days in combination with intravenous heparin (200 units/kg×12 h). LV thrombi were successfully lysed in 10 of 16 patients. None of the patients suffered from clinical embolism, and therapy had to be discontinued in only one patient due to haematuria.w33 In a later study, four patients with mobile LV thrombus were treated with intravenous urokinase or streptokinase. In the first two cases, lysis of thrombus was achieved without complication. In the latter two cases, however, systemic embolism occurred, with transient diplopia in one and stroke followed by death in the other.1 It was concluded that fibrinolytic agents are capable of lysing ventricular thrombi but that the risks of this therapy are too high. Heparin Data regarding the benefit of heparin treatment in patients with documented LV thrombus on echocardiography during the first 2 weeks are somewhat conflicting, leading us to believe that there may be a benefit, at least in the short term. In a randomised controlled trial, AMI survivors who were treated with high dose heparin (12 500 units subcutaneously every 12 h) showed a lower incidence of LV thrombus formation than those administered a low dose (5000 units subcutaneously every 12 h) (11% vs 32%, p<0.001) during a 10 day period.9 Results from the SCATI study showed a similar reduction in LV thrombus formation for the group that was treated with calcium–heparin compared to the control group in patients undergoing thrombolysis.w34 In the GISSI-2-connected study, however, high dose heparin did not prevent thrombus formation (27% vs 30%, p=NS).10 In a study with 23 consecutive patients with mobile and protruding thrombi, high dose heparin was given intravenously over a period of 14–22 days (mean 14±4). In all 23 patients LV thrombi decreased in size, with disappearance of the high risk features. No embolic events were detected during treatment, and the only complication was an upper gastrointestinal haemorrhage.w35 Dalteparin, a low molecular weight heparin, reduced the incidence of LV mural thrombus formation but had no influence on the risk of systemic embolisation, and its use was associated with an increased risk of haemorrhage.w36 Vitamin K antagonist Observational studies conducted in the pre-thrombolytic and thrombolytic eras have provided support for the hypothesis that anticoagulation reduces the risk of embolisation.1 2 4 w3 w37–w39 A 1993 meta-analysis included 11 studies of 856 patients who had an anterior myocardial infarction; the odds ratio (OR) for an embolic event was 5.5 (95% CI 3.0 to 9.8).19 The meta-analysis included seven studies with 270 patients that included data on the relationship between anticoagulation for 6 months and embolisation. Although all seven studies presented data suggesting that systemic anticoagulation reduces embolic complications, this trend reached significance only in three trials. When pooling the data, anticoagulation compared with no anticoagulation was associated with a reduction in the rate of embolisation (OR 0.14, 95% CI 0.04 to 0.52). Based on these data, both current European Society of Cardiology and American College of Cardiology/American Heart Association guidelines recommend vitamin K antagonist therapy in patients with an LV thrombus after myocardial infarction.w40 w41 However, vitamin K antagonists do not appear to affect the likelihood of resolution of the thrombusw3 and, unfortunately, no large randomised trials have been performed to evaluate the efficacy of long term anticoagulation to prevent embolisation in patients with LV thrombus. Therefore the effects of long term anticoagulants on the risk of embolisation are the subject of debate. Among the many questions left unanswered is when to withdraw anticoagulant medication when thrombus is identified since the risk of embolisation decreases over time, likely as a result of organisation of thrombus which includes thrombus neovascularisation. However, retrospective studies documented ongoing embolic risk in LV thrombus patients.w42 In indium-111 platelet imaging studies most thrombi, regardless of age, have been observed to have externally detectable ongoing platelet accumulation, indicating continued surface activity.20 The European guidelines recommend vitamin K antagonist for at least 3–6 months, while the American guidelines recommend indefinite treatment in patients without increased risk of bleeding. Although there are limited data regarding the appropriate follow-up and timing of cessation of vitamin K antagonists in these patients, the following approach seems appropriate for most patients: Assess LV thrombus within the first month after AMI, preferably with CMR in high risk patients, and start vitamin K antagonist when LV thrombus is present and no contraindication exists Re-evaluate LV thrombus formation after 6 months since data show that LV thrombus resolution in the initial months is very common, also in patients treated with vitamin K antagonistsw43 When LV thrombus is not present and there is no other indication for vitamin K antagonist, assess bleeding risk and consider stopping therapy. Newer anticoagulants are presently being developed and some of them are already registered.w44–w46 It can be envisioned that in the longer term these new anticoagulants will replace vitamin K antagonists. However, at present vitamin K antagonist therapy is still the standard of care for the treatment of LV thrombus. More importantly, the newer anticoagulants also have the risk of fatal and non-fatal bleedings and their role in LV thrombus patients should be further assessed. Antiplatelet therapy and triple therapy in the PCI era Another issue is that nowadays STEMI patients are treated by primary PCI and receive long term dual antiplatelet therapy (including aspirin and a P2Y12 inhibitor). Consequently, patients with LV thrombus or at increased risk of LV thrombus after a myocardial infarction are frequently being treated with vitamin K antagonist in addition to dual antiplatelet therapy (triple antithrombotic therapy) and therefore are subjected to an increased bleeding risk. It is unclear, however, if long term anticoagulation is still necessary in STEMI patients treated by primary PCI and subsequent dual antiplatelet therapy. Large prospective studies show a yearly incidence of bleeding of approximately 3.7% for dual antiplatelet therapy and 12% for triple antithrombotic therapy.w47 The most common site of bleeding is the gastrointestinal tract (30–40%) and cerebrum (9–10%), with 25% of episodes in the latter site proving fatal. Furthermore, non-fatal bleedings are an important predictor of mortality post-PCI at follow-up.w48 Also, in regard to hospitalisation after emergency department visits in the USA for adverse drug events in patients above 65 years, 33.3% of the 99 628 hospitalisations concerned warfarin.w49 Moreover, in the general STEMI population treated with primary PCI and dual antiplatelet therapy but no anticoagulation therapy, symptomatic cerebral infarction is rare, occurring in 0.75–1.2% of all STEMI patients.w50 Thus, the potential benefit of vitamin K antagonist treatment on top of dual antiplatelet therapy may not outweigh the increased bleeding risk. This calls for a randomised trial to be conducted to determine whether anticoagulation treatment prevents embolic complications in AMI patients treated with primary PCI. You can get CPD/CME credits for Education in Heart Education in Heart articles are accredited by both the UK Royal College of Physicians (London) and the European Board for Accreditation in Cardiology—you need to answer the accompanying multiple choice questions (MCQs). To access the questions, click on BMJ Learning: Take this module on BMJ Learning from the content box at the top right and bottom left of the online article. For more information please go to: http://heart.bmj.com/misc/education.dtl RCP credits: Log your activity in your CPD diary online (http://www.rcplondon.ac.uk/members/CPDdiary/index.asp)—pass mark is 80%. EBAC credits: Print out and retain the BMJ Learning certificate once you have completed the MCQs—pass mark is 60%. EBAC/ EACCME Credits can now be converted to AMA PRA Category 1 CME Credits and are recognised by all National Accreditation Authorities in Europe (http://www.ebac-cme.org/newsite/?hit=men02). Please note: The MCQs are hosted on BMJ Learning—the best available learning website for medical professionals from the BMJ Group. If prompted, subscribers must sign into Heart with their journal’s username and password. All users must also complete a one-time registration on BMJ Learning and subsequently log in (with a BMJ Learning username and password) on every visit. Left ventricular thrombus formation after myocardial infarction: key points Left ventricular (LV) regional wall akinesia and dyskinesia resulting in blood stasis, prolonged ischaemia leading to subendocardial tissue injury with inflammatory changes and a hypercoagulable state, are consistent with Virchow's triad, resulting in LV thrombus formation. Risk factors for the development of LV thrombus include: large infarct sizes severe apical asynergy LV aneurysm anterior myocardial infarction There is reported controversy regarding the negative influence of β-blockers and the protective effect of mitral regurgitation. Early data from the prethrombolytic and thrombolytic era suggest that in the setting of acute myocardial infarction, LV thrombus was present in 7–46% of patients. Nowadays the reported incidence is lower, probably due to (1) more aggressive anticoagulation therapies in the acute phase (eg, use of heparin, bivalirudin), (2) smaller infarctions, and (3) improved LV remodelling. Timing of LV thrombus assessment is crucial, as assessment too soon after the onset of myocardial infarction will miss LV thrombus formation. Transthoracic echocardiography is most often used for assessing LV thrombus. However, it is estimated that 10–46% of echocardiograms are inconclusive. Delay enhancement cardiac magnetic resonance imaging (CMR) is nowadays considered the gold standard. Cine-CMR, transoesophageal echocardiography, radionuclide angiography, and CT seem less appropriate for LV thrombus detection. Conditions that increase the risk of systemic embolisation in patients with LV thrombus are: (1) severe congestive heart failure, (2) diffuse LV dilatation and systolic dysfunction, (3) previous embolisation, (4) advanced age, and (5) presence of LV protruding or mobile thrombi. Observational studies conducted in the prethrombolytic and thrombolytic eras have provided support for the hypothesis that warfarin reduces the risk of embolisation.
Author and article information
Contributors
Sagun Dawadi: sagundaw9439@gmail.com
Journal
Journal ID (nlm-ta): Health Sci Rep
Journal ID (iso-abbrev): Health Sci Rep
Journal ID (doi): 10.1002/(ISSN)2398-8835
Journal ID (publisher-id): HSR2
Title:
Health Science Reports
Publisher:
John Wiley and Sons Inc.
(Hoboken
)
ISSN
(Electronic):
2398-8835
Publication date
(Electronic):
24
November
2023
Publication date Collection:
November
2023
Volume: 6
Issue: 11
(
doiID:
10.1002/hsr2.v6.11
)
Electronic Location Identifier: e1736
Affiliations
[
2
]
Department of Internal Medicine
Nepalese Army Institute of Health Sciences
Sanobharyang
Kathmandu
Nepal
Author notes
[*]
[*
]
Correspondence Sagun Dawadi, Department of Internal Medicine, Nepalese Army Institute of Health
Sciences, Sanobharyang, Kathmandu.
Email: sagundaw9439@ 123456gmail.com
Email: sagundaw9439@ 123456gmail.com
Author information
Dhan B. Shrestha
http://orcid.org/0000-0002-8121-083X
Article
Publisher ID: HSR21736DOI: 10.1002/hsr2.1736
PMC ID: 10667961
PubMed ID: 38028683
SO-VID: 13d1c9a8-b79f-4abd-8842-6b471cda72ed
Copyright © © 2023 The Authors.
Health Science Reports published by Wiley Periodicals LLC.
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This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
History
Date
revision received
: 29
October
2023
Date
received
: 15
July
2023
Date
accepted
: 06
November
2023
Page count
Figures: 6,
Tables: 2,
Pages: 15,
Words: 6104
Categories
Subject:
Original Research
Subject:
Original Research
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cover-date November 2023
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