Discussion
Left atrial appendage occlusion is an alternative to oral anticoagulants for prevention of stroke in patients with atrial fibrillation who are not optimal candidates for long-term anticoagulation1. Device related thrombus (DRT) is considered an important issue and associated with increased risk of ischemic events after LAAO2-4. Current published report suggests that DRT occurs about 3.7% of patients between 3 and 6 months post-procedure of LAAO3. The mechanism underlying DRT is incompletely understood. Some known factors such as hypercoagulability disorder, pericardial effusion, renal insufficiency, implantation depth >10 mm and non-paroxysmal atrial fibrillation are risk predictors of DRT following LAAO5.
Intraprocedural thrombosis during LAAO has been rarely reported. A case report firstly described the acute thrombus formation on the surface of the occlusion device immediately after release6. The patient’s recent COVID-19 infection may contribute to acute thrombus formation. Thrombus formation on the delivery sheath during LAAO has been reported7,8. To prevent thrombus migration, thrombus were retrieved and sucked by sheath without cerebral embolic protection device. However, suction of thrombus within the left atrial by sheath may have high risk of embolism. Prevention of periprocedural complications especially stroke is a major issue during LAAO.
In our case-series, we followed the standard LAAO procedure and heparin was used at a dosage 100 U/kg. We found that: 1) floating thrombus formed on the tip of the delivery sheath during LAAO; 2) ACT value was <200s when acute clotting formed and which only achieved acceptable low limit value after repeatedly giving heparin even thrombolytic therapy; 3) we try to suck the thrombus but failed for both cases; 4) it is feasible and safe to place cerebral embolic protection devices to prevent neurological events; 5) in the follow-up, there are no DRT and new-onset stroke.
Periprocedural stroke during LAAO which is a preventive therapy for stroke in patients with atrial fibrillation, is extremely unacceptable. Although heparin was generally administered to prevent thrombosis in the procedure, heparin-induced anticoagulation has a high interindividual variability either in terms of dosage or time duration requiring a frequent ACT monitoring. However, optimal ACT cut-off value is currently unknown during LAAO. Previous mentioned reports showed ACT >250s when thrombus formed on the deliver sheath during LAAO procedure. Preoperative coagulation tests were within normal reference values although our two patients take rivaroxaban. And persistent low ACT value in the procedure indicated that heparin resistance and stasis of left atrial dilation predispose to coagulopathy and consequently to thrombus formation. Unfortunately, antithrombin III in blood samples were not tested. A study demonstrate that lower ACT level was significantly associated with the development of procedure-related silent cerebral embolism9. Underlying genetic susceptibility of heparin resistance induced lower ACT level and impaired left atrial endothelial function both would be more likely to activate coagulopathy. Further studies should be conducted to determine the optimal ACT level for LAAO procedure. The use of cerebral embolic protection devices during percutaneous LAAO was a feasible and safe therapeutic option for patients with LAA thrombus10. It is hard to suck when acute floating thrombus formed on the sheath after occlusion device released. Placement of cerebral embolic protection devices could be a rational option for neurological protection. Indeed, our two cases showed no neurological function impairment after the procedure. In addition, continuous drip of heparin saline to the delivery and guide system may be ensure the local heparin concentration around the instruments in the left atrium.