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.