Reversal of Total Artificial Heart Mechanical Valve Thrombosis Using Catheter-Directed Thrombolysis : ASAIO Journal

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Reversal of Total Artificial Heart Mechanical Valve Thrombosis Using Catheter-Directed Thrombolysis

Yemul Golhar, Shweta R.*; Trinh, Muoi A.*; Anyanwu, Anelechi C.; Williams, Elbert; Chen, Martin*

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ASAIO Journal 69(1):p e38-e41, January 2023. | DOI: 10.1097/MAT.0000000000001665
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The Syncardia total artificial heart (TAH) (Syncardia Systems Inc., Tucson, AZ) is the only implantable biventricular circulatory support device approved for use as a bridge to heart transplantation, but its use remains restricted by limited indications, limited surgical, and center expertise and high complication rate postimplant. Because of its four mechanical valves, anticoagulation is critical for patients supported with the Syncardia TAH. Thrombosis of the valves can occur and because of the single disc nature of the valves, this can lead to acute valve dysfunction with catastrophic device failure as the valve can remain fixed in a closed, semiclosed, or open position. Treatment for such catastrophic device failure conventionally involves immediate reoperation for device exchange, but this can be challenging, and it may not be possible to do this in a timely fashion. Because of positive experience with off-label use of systemic thrombolysis (tPA) for mechanical valve thrombosis in patients after conventional valve replacement,1–3 we considered this option for patients with TAH valve thrombosis. We report on two Syncardia TAH patients with acute atrioventricular valve thrombosis who were successfully treated with intravenous thrombolysis.

Case 1

A 57 years old male with restrictive cardiomyopathy, paroxysmal atrial fibrillation, hypothyroidism, cardiac cirrhosis, and multiple episodes of decompensated cardiac failure underwent TAH implantation as a bridge to transplant. His postoperative course was complicated by respiratory failure requiring tracheostomy, ischemic stroke, acute kidney injury, depression, and gastrointestinal bleeding requiring multiple blood transfusions. Continuous veno-venous hemofiltration was being administered through a right internal jugular vein tunneled dialysis catheter.

On day 42, the patient became acutely hypotensive. The right-sided device output dropped precipitously to 1.1 L/min, while left-sided output was 3.7 L/min and right fill dropped to 9 ml. The central venous pressure (CVP) increased to high 30s. The clinical diagnosis was acute malfunction of the right-sided device. There had been no recent central venous catheterization and chest x-ray confirmed that the tip of the dialysis catheter was distant from the right atrioventricular valve. A transesophageal echocardiogram (TEE) revealed a thrombus on the tricuspid positioned valve with immobilized leaflet (Figure 1).

Figure 1.:
(A) shows the thrombus seen in the right AV valve. (B) Highlights the high velocity of 2.5 m/s across the right AV valve due to the thrombus causing the leaflet to remain fixed in semiclosed position. AV, atrioventricular.

Surgery was deemed not an option, as he was debilitated with multiorgan dysfunction. We therefore decided to attempt thrombolysis of the valve using protocols developed for thrombolysis for thrombosed mechanical valves. Because the patient already had a catheter in the right atrium, we were able to use a catheter-directed approach as opposed to systemic administration through a peripheral vein. A 10 mg bolus of alteplase followed by 90 mg infusion over 120 minutes was administered directly on the right side of the TAH through the perma-cath. Over the course of the next two hours, the CVP gradually reduced to 18 mm Hg and the blood pressure normalized. Right fill improved to 57 ml and output to 7 L/min (Table 1). Repeat TEE after 2 hours showed resolution of the thrombus and improved valve opening (Figure 2). Within an hour, the patient was awake and neurologically intact with no neurologic deficits. The patient went on to survive for another 183 days without recurrence of valve thrombosis. There were no neurologic or pulmonary sequelae of thrombolysis. The patient died on day 247 post TAH implant from sepsis postpneumonia.

Table 1. - Total Artificial Heart Parameters
Parameters Case 1 Case 2
Before Event During Event After tPa* Before Event During Event After tPa
Left CO 8.1 3.7 7.0 5.8 3.7 8.2
Right CO 8 1.1 7.1 4.9 1.9 7.3
Left fill 67 31 56 48 41 63
Right fill 65 9 57 41 21 56
Rate 125 120 125 120 90 130
Left pressure 190 200 200 200 200 200
Right pressure 95 95 95 100 100 100
Left vacuum –5 –5 –5 –12 –10 –14
Right vacuum –10 –10 –10 –12 –10 –14
*Tissue plasminogen activator.
Cardiac output.

Figure 2.:
Improved velocities across right AV valve after thrombolysis. AV, atrioventricular.

Case 2

A 43 years old male with obesity, obstructive sleep apnea, orthotopic heart transplant in 1998 followed by severe cardiac failure due to posttransplant vasculopathy was listed for retransplantation. His prior history included an intraabdominal first generation left ventricular assist device before the previous transplant which led to multiple bowel complications leading to a series of abdominal operations in the years after his transplant for management of bowel obstruction and multiple fistulae. He underwent a difficult Syncardia TAH implantation as a bridge to transplantation due to a frozen mediastinum and abdomen. His postoperative course was complicated by acute kidney injury followed by continuous veno-venous hemofiltration through the right internal jugular vein tunneled dialysis catheter.

On postoperative day 11, the patient became acutely hypotensive with reduced right-sided device filling and output and CVP in 40s. The differential diagnosis included pneumothorax, hemorrhage, cardiac tamponade, or malfunction of the TAH. He was immediately intubated and resuscitated with pressors and transfusion. A bedside TEE revealed an occlusive thrombus on the atrial side of the tricuspid valve of the TAH with flow acceleration across the valve (Figure 3). Immediately, 10 mg tPA was given as a bolus and 90 mg infusion was given through the perma-cath. The clot disappeared within the hour, confirmed with TEE, with normalization of device parameters, blood pressures, and CVP (Figure 4, Table 1). Post tPA, chest tube drainage increased to 200 ml/h but resolved with protamine and blood transfusion. The patient woke up and moved all extremities with no evidence of a stroke. His gastrointestinal leak, however, did not resolve with conservative measures. He underwent surgical repair but then continued to have anastomotic breakdowns requiring multiple laparotomies. He ultimately had untreatable gastrointestinal fistulae, sepsis, and died 81 days postimplant. There was no recurrence of the atrioventricular valve thrombosis during the support period.

Figure 3.:
A: Visible thrombus at the right AV valve. B: High velocity across right AV valve indication partial stenosis/obstruction. AV, atrioventricular.
Figure 4.:
After thrombolysis the thrombus has disappeared, and valve leaflet motion improved.


Between 2006 and 2017, there were 315 documented TAH implantations (1.3% of circulatory support devices). SynCardia showed a 79% success rate as a bridge to transplantation.4 Early postimplant multisystem organ failure and stroke pose the greatest risks for mortality and after the first 6 months, stroke remains the major cause of death. These patients suffer from substantial thromboembolic phenomenon despite apparently adequate anticoagulation and dual antiplatelet therapy.5,6 A 4.5% incidence of acute pulmonary embolism and an incidence of 19% of other thromboembolic episodes have been reported.4,7

Right-sided atrioventricular valve dysfunction is a rare complication after TAH implantation. It is more typically caused by entrapment of the valve by a catheter or atrial tissue but can also be caused by valve thrombosis or embolism. Small right arial or thoracic cage size can make it more likely for central venous catheters/atrial tissue to impinge on the valve causing malfunction. Cather entrapment is more commonly seen immediately after insertion or if the catheter is displaced from previous location.8

Neither of our patients had small atrium or thoracic cavity size or other factors that may make them more prone to right-sided atrioventricular valve obstruction. Atrioventricular valve dysfunction is a surgical emergency that results in sudden severe hypotension and hemodynamic collapse. The treatment is immediate return to an operating room for device exchange. The reality, however, is that immediate surgery is rarely possible, and as there are no means of temporizing when the device has failed (such as chest compressions and pharmacologic interventions) by the time patients are placed on cardiopulmonary bypass, there has already been irreversible brain injury. TAH failures are, therefore, typically fatal if not immediately reversed. In this study, we have demonstrated successful and rapid reversal of two TAH failures caused by right atrioventricular valve thrombosis using thrombolysis.

Our findings have two main implications (1) Prompt TEE should be undertaken in cases of TAH dysfunction to exclude this potentially reversible cause of dysfunction. (2) TAH valve thrombosis can be successfully reversed by thrombolysis. Of note, thrombosis should always be regarded as a possibility regardless of the anticoagulation status of the patient. In both cases, the patients were therapeutically anticoagulated. In the first case, the patient was receiving aspirin and unfractionated heparin with an activated partial thromboplastin time (aPTT) of 85, while the second patient was on warfarin with an international normalized ratio of 3.6. Despite adequate anticoagulation based on laboratory data, both patients in the report developed thrombus on their TAH.

TAH poses unique diagnostic challenges, most imaging modalities like transthoracic echocardiogram are not particularly fruitful due to extensive acoustic shadowing by the TAH components. The gold standard for diagnosis is computed tomography with contrast but in unstable patients this is rarely possible. TEE however is relatively devoid of these acoustic shadowing and artifacts and an echocardiographer with experience in TAH imaging can readily identify the right atrioventricular valve and confirm or exclude valve thrombosis, so this should be one of the earliest steps in the management of suspected TAH malfunction. Hence, TEE can provide valuable diagnostic information and rule out potentially fatal conditions very early during hemodynamic collapse. Our experience with early TEE has yielded positive results.

Understanding that TEE is limited to the availability of trained skilled echocardiographer with experience in TAH, situations may present where TEE may not be available. In such cases, some information can be obtained by evaluating the TAH parameters and the graph. This however is limited to pointing toward the side of malfunction of the TAH and is certainly not specific enough to warrant initiation of a risky treatment like thrombolysis without any confirmatory imaging. While other causes of severe hypotension in TAH patients do occur like bleeding and sepsis, we strongly urge early TEE exam in the course of emergent workup alongside other blood tests and imaging to rule out right- or left-sided malfunction due to potentially reversible causes like thrombus.

Our patients were critically ill with multiple comorbidities and the risk of surgery for device replacement was unacceptably high. Although both patients ultimately died of their comorbidities, there was no recurrence of the valve dysfunction, and we do not think the valve thrombosis or its treatment contributed to their deaths. While emergent extracorporeal membrane oxygenation could have been an option, it would not address the primary problem and the patients would still require definitive surgery. This could also paradoxically lead to worsening thrombosis due to the low flow through the TAH.

There are potential limitations and caveats with our approach. Thrombolysis is not without risk. While we did not encounter any adverse event, we were cognizant of the possibility for bleeding complications and would not have undertaken this option if there had been an active history of surgical bleeding, hemorrhagic stroke, or gastrointestinal bleeding. In particular, the urgency to resolve the valve thrombosis must be balanced against the potential for a catastrophic intracranial bleed, especially considering that patients already have a baseline predisposition to ischemic and hemorrhagic neurologic complications. We were partly able to mitigate this risk by using a catheter-directed approach, administering the thrombolytic via an existing dialysis catheter in the right atrium. We do not know if our experience would be replicated if the thrombolytic is administered through a peripheral vein, both in terms of effectiveness and safety. We also do not know whether this technique would be effective in patients with thrombosis of the left-sided valves. For these reasons, surgical treatment should still be the default and be undertaken if possible. Our experience, however, does demonstrate that thrombolysis can effectively reverse TAH valve thrombosis, and may be worth considering in patients who are not candidates for reoperation, or if reoperation cannot be performed in a timely fashion.


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thrombus; total artificial heart; thrombolysis; Syncardia; prosthetic valves

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