We identified two important clinical issues from this case. Postoperative prosthetic mitral valve occlusion due to left atrial thrombus and bioprosthetic valve thrombosis could occur during VA-ECMO despite appropriate systemic anticoagulation and loading of antiplatelet agents. Exploratory TEE in the ICU was useful for the detection of unexpected intracardiac thrombus formation and surgical decision-making.
While bioprosthetic valve thrombosis, including in the chronic phase, was reported to have occurred in 11.6% of patients who underwent bioprosthetic valve replacement, early thrombosis around the bioprosthetic mitral valve is a rare phenomenon [2]. Although bleeding has been emphasized as a complication during MCS after cardiac surgery, a retrospective single-center study reported that 10% of patients with prosthetic valves developed prosthetic valve thrombosis during VA-ECMO for post-cardiotomy shock [3, 4]. The risk factors for bioprosthetic valve thrombosis include extremely low cardiac output, low transvalvular flow, left atrial dilatation, atrial fibrillation, and hypercoagulability [5]. On the other hand, there are several factors related to intracardiac thrombus formation with VA-ECMO, including altered circulatory flow, vascular injury, and altered blood coagulability [6]. In particular, low cardiac output and low transvalvular flow as a consequence of VA-ECMO can lead to thrombus formation in the left heart chambers [7, 8]. The LV afterload increases due to retrograde blood flow from peripheral VA-ECMO with femoral artery cannulation and femoral vein drainage; thus, in cases with low cardiac output, intracardiac blood stasis is likely to occur, promoting thrombus formation [9]. In the present case, the patient’s cardiac output was extremely low because of frequent potentially fatal arrhythmias and prolonged cardiogenic shock. Spontaneous echo contrast distal to the aortic valve in intraoperative TEE in the initial MVR indicated the presence of blood stasis in the sinus of Valsalva. Additionally, the patient’s cardiac function deteriorated further after surgery, resulting in additional stasis in the left atrium and ventricle, as well as in the ascending aorta, which probably led to the development of a thrombus that occluded the prosthetic mitral valve.
The fundamental approach to preventing thrombus formation during MCS is reportedly anticoagulant therapy and ventricular unloading for the prevention of LV distention [10]. Since thrombus formation can occur in patients with extremely low cardiac function despite appropriate systemic anticoagulation, early LV unloading for the prevention of blood stasis is critical to preventing thrombus formation [10]. In the present case, the extreme LV dysfunction contributed to blood stasis and thrombus formation, because LV failed to resist retrograde blood flow from the femoral artery cannula and could not generate an adequate cardiac output after the initial MVR. By contrast, thrombus formation did not occur after the re-MVR. Improved cardiac function and antegrade blood flow of the central ECMO from the ascending aorta cannula might have led to unloading of LV and reduction of blood stasis after the re-MVR [3, 6, 9]. These differences from the first surgery might have contributed to the prevention of thrombus formation. LV unloading techniques such as Impella or LV venting cannula were not used, given the risk of vascular complications and bleeding and our institution's limited experience with their use in the perioperative period [11].
Monitoring of anticoagulation therapy for VA-ECMO differs from facilities. ACT, aPTT, and the anti-factor Xa assay can be used for monitoring anticoagulation with heparin. In the present case, ACT and aPTT were measured. The target ACT of 180 to 220 s is recommended for anticoagulation of VA-ECMO [12]. However, because of concerns about the risk of bleeding, the target ACT was set at 140 to 180 in the present case. There is little evidence regarding anticoagulation during ECMO in such complicated situations as in the present case. A systematic review of ECMO cases managed without anticoagulation reported that the incidence of thrombosis was comparable with or without anticoagulation and severe bleeding occurred even in 28% of ECMO patients without anticoagulation [13]. In addition, there are some reports that the management with low ACT or without anticoagulation was beneficial in patients with a high risk of bleeding [14, 15]. Given these results, the anticoagulation strategy at a lower ACT value than recommended in the ELSO guidelines would be acceptable in patients at high risk of bleeding.
Exploratory TEE for hemodynamic instability in the ICU played a pivotal role in the detection of intracardiac thrombus formation and surgical decision-making. Vigilant monitoring with echocardiography is important in diagnosing thrombus formation in the prosthetic valve or cardiac chambers and in determining treatment strategy [8, 16]. In most previously reported cases, intracardiac thrombus during VA-ECMO was diagnosed using TEE [6]. TEE has certain advantages in the diagnosis of intracardiac thrombus after cardiac surgery, because obtaining images of sufficient quality for the diagnosis of thrombus formation is sometimes difficult with transthoracic echocardiography due to the narrow acoustic windows and artifacts [17]. In post-cardiac surgery patients with severe cardiac dysfunction requiring MCS and at risk for thrombus formation, such as the present case, early and vigilant monitoring with TEE might facilitate the diagnosis of thrombus formation and early therapeutic intervention [18, 19].
In conclusion, thrombus formation could occur during VA-ECMO after cardiac surgery despite appropriate anticoagulation and loading of antiplatelet agents. Exploratory TEE in the ICU was helpful for the detection of thrombus formation and surgical decision-making in such cases. In post-cardiac surgery patients with severe cardiac dysfunction requiring VA-ECMO, TEE in the ICU might improve patient outcomes by facilitating therapeutic intervention.
