Acute myocardial infarction represents the most relevant risk factor for LVT development with recent incidence values up to 4-15% of patients.², ³ In this setting, the risk of LVT is greater in anterior wall or large area involvement, in cases of relevant delay to reperfusion-time or pre-angioplasty TIMI flow grade ≤1, and with a reduced left-ventricle ejection fraction. Other risk factors include atrial fibrillation, left-ventricle aneurysm, left-heart valvular disease.¹

LVT may also develop – with lower incidence – in patients with dilated cardiomyopathy, Takotsubo syndrome, left-ventricle non-compaction, peripartum cardiomyopathy, intracardiac devices or anti-cancer treatments, other forms of cardiomyopathy (e.g., hypertrophic cardiomyopathy, cardiac amyloidosis, Chagas disease, eosinophilic myocarditis).¹ The presence of high-risk features (e.g., left-ventricle dysfunction, presence of a scar and of a turbulent intracardiac flow, apical aneurysm) increases the risk of LVT development in these latter cases.¹

The available studies mostly regard patients with acute myocardial infarction and are variable in terms of patients' characteristics, antithrombotics (i.e., low molecular weight heparin, vitamin K antagonists, direct oral anticoagulants), and time of publication. The benefit in incidence of LVT reduction is quite ever counterbalanced by an increased risk of bleedings. ¹ Thus, the identification of patients in whom primary prophylaxis with anticoagulants may have a favourable risk-benefit profile is not well understood. The most recent available randomized trial found lower risk of LVT and doubled risk of bleedings in patients taking low-dose rivaroxaban (2.5 mg q12h) compared to placebo. ⁴ However, methodological issues (e.g., inclusion of patients only from China mostly with a preserved or moderately-reduced left-ventricle ejection fraction, high rate of drop-out) limit the generalisability and robustness of results. ⁴

Anticoagulant treatment needs to be administered with the aim of LVT resolution and embolic stroke prevention. Evidence on the effectiveness and safety of heparins remains limited, is more robust for vitamin K antagonists (VKAs), and is progressively increasing for direct oral anticoagulants (DOACs). Furthermore, most of the studies included patients with ischemic heart disease.¹ In case of VKAs administration, the suggested INR range would be 2.0-3.0 and the highest possible Time in Therapeutic Range (TTR) is advisable.¹ It should be acknowledged that a recent study reported lower incidence of ischemic events and higher rate of thrombus resolution even in patients with a TTR >50%.⁵ The largest and up to date available meta-analysis reported a similar effectiveness and safety profile of DOACs compared to VKAs.⁶ However, DOACs may be considered in patients who are unsuitable for, or refuse, VKAs.¹

LVT recurrence may develop in 10-20% of patients after resolution. ¹⁷ The time (i.e., recent), the type (i.e., protuberant), and the size (i.e., smaller) of LVT appeared to be associated with an earlier resolution. Conversely, a reduced left-ventricle ejection fraction and a left-ventricle apical aneurysm appeared to be associated with a lower odd of resolution.⁸ Longer treatments with anticoagulants may be useful in selected patients. Recent data, indeed, reported higher incidence of LVT resolution in patients receiving 12 than 3 and 6 months of anticoagulation.⁸

Dual antithrombotic therapy may be needed in specific subgroups of patients (e.g., those needing reperfusion therapy), but it is associated with an increased bleeding risk. In these cases, data may be extrapolated from available studies on LVT and from guidelines in other settings (e.g., atrial fibrillation).^{910 11} Briefly, triple therapy with an oral anticoagulant and dual antiplatelets is administered for 7-30 days and is followed by dual therapy with oral anticoagulant and a P2Y12 inhibitor. Oral anticoagulant is replaced by aspirin at LVT resolution and dual antiplatelet is continued. At 12 months from the index event, single P2Y12 inhibitor is continued indefinitely.¹