Mechanolytic management of transcatheter aortic valve thrombosis.

Data on the incidence, characteristics, and treatment of thrombosis of a transcatheter aortic valve implantation (TAVI) implant are scarce. We report a challenging case of a TAVI thrombosis occurring 6 months after the procedure. Initial anticoagulation using low-molecular-weight heparin followed by thrombolytic therapy failed to both relieve symptoms and alleviate thrombosis. However, the condition of the patient deteriorated rapidly, necessitating the use of balloon valvuloplasty followed by low-dose thrombolysis. The uniqueness of the case can be summarized as follows: (1) first report of balloon valvuloplasty to manage a case of TAVI thrombosis; (2) thrombolytic therapy after balloon valvuloplasty was successful to further reduce gradient from valve thrombosis.

Introduction

Transcatheter aortic valve implantation (TAVI) has emerged as a therapeutic option for patients with severe aortic valve stenosis who are inoperable or deemed high risk for conventional surgical aortic valve replacement [1]. Recently, there has been a substantial increase in the use of TAVI, attributed to favorable clinical outcomes and minimally invasive nature [2]. A rare but serious complication following TAVI is valve thrombosis, which has yet to be fully evaluated because data on the incidence, characteristics, and treatment are still scarce [3].

Case report

We report a case of an 84-year-old male patient who presented to our hospital with severe shortness of breath. Review of his medical history revealed multiple medical comorbidities, including coronary artery disease, heart failure (New York Heart Association Class 3), stroke with residual facial hemiparesis, diabetes, hypertension, and chronic renal failure. His symptoms had progressed over an 8-day period, culminating in severe dyspnea at rest. The patient had undergone a TAVI 6 months before this presentation; at that time a 25-mm Lotus valve (Boston Scientific; Marlborough, MA, USA) was implanted. Postinterventional transthoracic echocardiography follow-up after the index transcatheter aortic valve replacement implantation showed a good functioning and well-seated Lotus valve with a peak gradient of 16 mmHg and a mean gradient of 12 mmHg. The patient was discharged home and was followed-up at an outpatient cardiology service near his hometown. Review of the antiplatelet regimen revealed that the patient was on dual antiplatelet therapy (aspirin and clopidogrel) at the time of presentation. A transesophageal echocardiography (TEE) at presentation showed thickened leaflets with an opening area of 0.6 cm2, a mean gradient of 45 mmHg, no evidence of paravalvular leakage, and an ejection fraction (EF) of 20%. Initial intravenous low-molecular-weight heparin therapy failed to both relieve symptoms and alleviate thrombosis, and the patient’s condition rapidly deteriorated into cardiogenic shock, necessitating the administration of 100-mg tissue plasminogen activator infusion; however, his condition still did not improve. At that stage, a repeat TEE showed barely opening leaflets, an EF of 10%, and a mean aortic valve pressure gradient (mAVPG) of 45 mmHg (Figure 1A). With a EuroSCORE II of 41, open surgery was deemed too risky. In addition, a Lotus valve-in-valve implantation was not an option as it is considered too risky due to subsequent increase in coronary artery obstruction; the architecture of the Lotus valve is critical in this regard and the Lotus valve system is not suitable for a valve-in-valve procedure. Therefore, a decision was made to perform a TEE-guided, transfemoral aortic valvuloplasty using a Tyshak 18-mm balloon. Unfortunately, carotid filters as an option to protect from cerebral embolization were not available at the time of the valvuloplasty, and therefore as an alternative method we applied, during balloon inflation and until retraction into the descending aorta, instant bilateral manual compression to the carotid artery over 6 seconds to minimize chances of embolization and cerebral embolic accident. Immediately postintervention, TEE showed improved leaflet motion and a drop in the mAVPG to 35 mmHg without evidence of valve damage or insufficiency. The stable patient was transferred to the intensive care unit and received further thrombolytic therapy (4 mg/h over 6 hours) to reduce residual thrombus formation at the TAVI valve. TEE on the 5th postinterventional day revealed a further decrease of the mAVPG down to 18 mmHg, no signs of valve incompetence, and an EF of 20% (Fig. 1B). Throughout the postballoon aortic valvuloplasty hospitalization period (8 days), no signs or symptoms of distal embolization to other organ systems or extremities were observed. Subsequently, the patient was discharged home, free of symptoms, on the 8th postintervention day with 3-mg warfarin once daily and 75-mg clopidogrel once daily as anticoagulation regimen.

Figure 1

(A) Transesophageal echocardiography (TEE) before valvuloplasty showing severe aortic stenosis and barely moving leaflets. (B) TEE before discharge showing decrease in mean aortic valve pressure gradient and good leaflet opening.

Discussion

Despite the lack of histological confirmation, our patient suffered most likely from a TAVI cusp thrombosis. The timing (6 months) and the absence of valve calcification and valve insufficiency on echocardiography are certainly unusual for early bioprosthesis degeneration, while the formation of pannus should take a longer time.

The literature on the incidence and characteristics of a TAVI thrombosis remains scarce and limited mostly to case reports or small case series [3], [4]. Anticoagulation therapy using heparin and/or a vitamin K antagonist forms the cornerstone of management of this complication, with most patients showing resolution of thrombosis within 2 months [3]. The few reported cases that were not managed with anticoagulation underwent a percutaneous valve-in-valve or surgical aortic valve replacement for an initially unsuspected thrombosis [5], [6]. The literature is lacking any further therapeutic options for inoperable patients who fail to respond to therapeutic anticoagulation or thrombolytics. Thus, this is the first report of the successful use of a balloon valvuloplasty in combination with thrombolytic therapy to deal with such a challenging case of TAVI thrombosis. Further studies addressing this clinical problem are needed, first to validate the safety and efficacy of our approach; and second, to be able to early identify the group of patients who would not benefit from therapeutic anticoagulation after TAVI rather than antithrombotic treatment, for example, requiring an early more aggressive therapy. While we used instant manual compression of the carotid arteries as a pragmatic way to deflect any thrombotic debris and avoid cerebroembolic accident, we opted not to perform brain imaging after the procedure to confirm absence of a cerebral embolic accident due to absence of clinical symptoms.

Conflicts of interest

The authors have no conflicts of interest to declare.