PREVENTION OF LEFT VENTRICULAR THROMBUS FORMATION AND SYSTEMIC EMBOLISM AFTER ANTERIOR MYOCARDIAL INFARCTION: A SYSTEMATIC LITERATURE REVIEW

PREVENTION OF LEFT VENTRICULAR THROMBUS FORMATION AND SYSTEMIC EMBOLISM AFTER ANTERIOR MYOCARDIAL INFARCTION: A SYSTEMATIC LITERATURE REVIEW

S112 antiplatelet monotherapy, may deserve consideration and a randomized controlled trial on this subject would appear warranted. Canadian Journal ...

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S112

antiplatelet monotherapy, may deserve consideration and a randomized controlled trial on this subject would appear warranted.

Canadian Journal of Cardiology Volume 33 2017

181 PREVENTION OF LEFT VENTRICULAR THROMBUS FORMATION AND SYSTEMIC EMBOLISM AFTER ANTERIOR MYOCARDIAL INFARCTION: A SYSTEMATIC LITERATURE REVIEW A Bastiany, M Grenier, A Matteau, S Mansour, B Daneault, B Potter Laval, Québec BACKGROUND:

BMS/Pfizer Alliance

Anterior myocardial infarction (MI) with apical dysfunction is associated with left ventricular thrombus (LVT) formation and an increased risk of systemic embolism (SE). However, the role for prophylactic anticoagulation in current practice is a matter of debate. We therefore propsed a systematic review of peer-reviewed data regarding the efficacy and safety of adding anticoagulation to standard therapy following anterior myocardial infarction for the prevention LVT/SE. METHODS AND RESULTS: We conducted a systematic review of full peer-reviewed original articles involving human clinical subjects in either English or French by searching PubMed, Ovid/MEDLINE/Embase, the Cochrane Library, and Google Scholar. An initial search returned 7,380 records. However, only 14 were ultimately retained for quantitative analysis according to our selection criteria. Nine articles addressed anticoagulation for patients not treated with percutaneous coronary intervention (PCI). Another five included at least some patients treated with PCI. Only one study specifically addressed prophylaxis in an exclusively primary PCI population. Some studies showed a benefit for adding anticoagulation to standard therapy in patients not treated with PCI, but results were inconsistent. No evidence of benefit was found when PCI patients were included and one study found a signal for net harm. No studies included a significant number of patients treated with the newer P2Y12-inhibitors. Also, there was no data on the use of non-vitamin K antagonist oral anticoagulants for the sole purpose of LVT/SE prevention in the setting of LV apical dysfunction. There was important inter-study heterogeneity in terms of the therapies studied, Background therapy, revascularization therapy, and study design that precluded formal meta-analysis. All studies were likely individually underpowered. CONCLUSION: Studies of LVT/SE prevention following MI to date have generally lacked statistical power and there is significant heterogeneity in terms of the treatments evaluated, revascularization METHODS, Background optimal medical therapy, and study design. We conclude that there is no compelling evidence thus far either for or against adding anticoagulation to standard therapy following MI for patients with apical dysfunction.