Thromboembolic myocardial infarction after transcatheter aortic valve implantation: a spotlight on antithrombotic treatment post-TAVI

The use of dual antiplatelet therapy for the first three–six months after transcatheter aortic valve implantation (TAVI) has been suggested.^[1,2] However, the additional benefit of anticoagulant therapy during the same period has conflicting data and even the guidelines from different cardiology societies are not in line; the American College of Cardiology/American Heart Association Guidelines recommend with an indication class IIb the use of vitamin K anticoagulants with an international normalized ratio (INR) of 2.5 for the first three-months post-TAVI alongside with aspirin to avoid thromboembolic events, while the European Association of Cardiology Guidelines do not.^[1,2] This case report presents a thromboembolic event in the coronary arteries leading to myocardial infarction and death post-TAVI, diagnosed on autopsy by identifying the thrombi on the CoreValve stent.

An 85-year-old man presented to the hospital with deteriorating symptoms of heart failure with New York Heart Association functional class III and peripheral edema, and was diagnosed with severe aortic stenosis. He had a history of permanent atrial fibrillation (AF), arterial hypertension, moderate chronic kidney disease and impaired mobility due to osteoarthritis. Transthoracic echocardiography demonstrated a left ventricular ejection fraction of 45%, a stroke volume index of 34 mL/m², a mean pressure gradient of 48 mmHg and a calculated aortic valve area of 0.45 cm²; the estimated pulmonary artery systolic pressure was 78 mmHg (Figure 1A). The patient’s surgical risk was high based on Logistic EuroSCORE (European System for Cardiac Operative Risk Evaluation) I, at 22%. Accordingly, TAVI was scheduled by the Heart Team consensus. Aortic root and peripheral artery anatomy and dimensions were suitable for TAVI. Preprocedural coronary angiography revealed non-critical coronary artery disease.

Figure  1.  Echocardiography of the implanted CoreValve and cardiac autopsy of the explanted CoreValve.

(A): Continuous-wave Doppler through the calcified aortic valve: the maximum velocity (> 4 m/s) and the mean pressure gradient (> 40 mmHg) are both indicative of severe aortic stenosis; (B): short-axis echocardiographic view of the CoreValve implant, shows a well expanded valve with no evidence of thrombus; (C): continuous-wave Doppler through the CoreValve implant demonstrates significantly improved flow pattern across the aortic prosthesis with decreased the maximum velocity and mean pressure gradient; (D): a photograph of the heart showing the anterior wall of the left ventricle. The arrow indicates the acutely infarcted myocardial territory; (E & F): multiple red thrombi are attached on the CoreValve stent down to the aortic root, close to the coronary ostia (arrow); and (G): explanted CoreValve with multiple thrombi throughout the stent frame (formalin preserved).

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The patient was not receiving anticoagulation therapy and was placed on subcutaneous low-molecular weight heparin, pending the TAVI. He underwent implantation of a 29-mm CoreValve stent (Medtronic, Minneapolis, Minnesota, USA) via the transfemoral access with no procedural complications. Activated clotting time was maintained above 250 s throughout the procedure by intravenous unfractionated heparin. The valve was deployed in a satisfactory position by fluoroscopy guidance after a preparatory balloon dilatation. The patient had an uncomplicated hospital stay and the pre-discharge bioprosthetic valve function was satisfactory on echocardiography (Vmax: 2.6 m/s, mean pressure gradient of 15 mmHg, indexed effective orifice area of 0.75 cm²/m², trivial paravalvular regurgitation) (Figure 1B & 1C). The patient was discharged back to the nursery home on dual antithrombotic therapy: aspirin 100 mg and acenocoumarol.

On the 39^th day after TAVI, the patient was found dead by the caring staff of the nursery home; he had no alerting symptoms prior to the event and the latest INR was 1.7. An autopsy was performed to determine the cause of death. A localized, rounded area of reddish tissue in the anterior wall of the left ventricle was noted (Figure 1D), corresponding to a thrombotic occlusion of the left anterior descending artery. Inspection of the CoreValve stent in situ revealed multiple thrombi attached to the outflow portion of the device and to the aortic surface of the valve cusps (Figure 1E-1G). No thrombi were found in the left atrium on autopsy.

This is one of the few reports of TAVI-associated, delayed coronary obstruction due to thromboembolism,^[3] confirmed by autopsy. Delayed coronary obstruction occurs later than seven days post-TAVI, it has been described in less than 0.3% of patients post-TAVI, and is lethal in 50%.^[3] In the current case, the origin of the thrombus responsible for the myocardial infarct, may have been related to the presence of thrombus attached to the frame of the valve. Considering the absence of thrombus in the left atrium, this case raises the question for anticoagulation in the early post-TAVI period independently of AF presence. Currently, there is evidence for oral anticoagulation therapy only in cases of co-existing AF (33% of TAVI patients) or new-onset AF post-TAVI (36%).^[4] For the rest of TAVI patients, there is not enough evidence to support their use. Although the presence of TAVI leaflet thrombosis has been confirmed in explanted self-expanding valves, the presence of thrombus on the aortic frame of the valve, as seen in our case, has not been emphasized as a possible source of emboli.^[5] Two clinical trials, the GALILEO^[6] and the AUREA^[7], did not demonstrate any advantage of anticoagulation to antiplatelet therapy post-TAVI in patients without indication for oral anticoagulant. However, considering that after TAVI, the subclinical leaflet thrombosis and the early valve dysfunction are present at a lower rate in patients on anticoagulants,^[8] further studies should be conducted regarding the use of anticoagulants post-TAVI.

ACKNOWLEDGMENTS

All authors had no conflicts of interest to disclose.