Vol.48 - Número 1, Enero/Marzo 2019 Imprimir sólo la columna central

Early transcatheter aortic valve thrombosis


Instituto Cardiovascular de Buenos Aires.
(1428) Buenos Aires, Argentina.
Recibido 17-AGO-2018 – ACEPTADO después de revisión el 24-SETIEMBRE 2018.
There are no conflicts of interest to disclose.



Transcatheter aortic valve implantation (TAVI)-related thrombosis is a serious complication with a very low incidence in registries, which may potentially lead to an increased risk of embolic events, valve obstruction with heart failure or reduction of the long-term durability of the prosthetic valve. The following is a case report of a patient with early prosthetic thrombosis after transaortic TAVI during in-hospital evolution.
Key words: Transcatheter aortic valve thrombosis. Transcatheter aortic valve implantation.


Transcatheter aortic valve implantation (TAVI) is a therapeutic method increasingly widespread in the last decade, to manage patients with severe symptomatic aortic stenosis and intermediate-to-high risk for conventional surgery [1].

Prosthetic thrombosis related to TAVI is a complication with very low incidence in the first published registries, probably underdiagnosed due to its difficult detection by conventional methods [2]. These types of events are of interest, given that the optimal post-implant antithrombotic treatment remains controversial currently, and their appearance is related to more prosthetic dysfunctions, heart failure and embolic events.

The clinical case of a patient with early post-TAVI prosthetic thrombosis during hospitalization, diagnosed by echocardiogram, is described.


Female, 86-year-old patient, who was hypertensive and dyslipidemic, with recent diagnosis of severe aortic stenosis manifest by syncope and dyspnea in functional class II. A multidisciplinary heart team started evaluating her to solve her valvulopathy by catheter, because of conventional surgical risk (Euroscore II 8.2%), so transaortic access was chosen owing to the severe calcification of peripheral arteries.

Transaortic TAVI was scheduled and conducted, with CoreValve nº29. In the postoperative period, she presented cardiac tamponade requiring drainage, severe thrombocytopenia (with a minimum value of 42,000/mm3) and acute renal failure. This situation delayed the onset of dual antiplatelet treatment, usually administered by aspirin (ASA) 100 mg per day, and clopidogrel 75 mg. The treatment was started 12 hours after a better platelet count and bleeding risk on the 5th day after the surgery.

In the transthoracic echocardiogram made immediately after the procedure, aortic valve prosthesis was shown to be in a normal position, with peak velocity of 1.15 m/sec, mean gradient of 2.3 mmHg and absence of paravalvular or aortic valve regurgitation.

Eight days after the procedure, she evolved with signs of heart failure and FC IV (NYHA) dyspnea. Control Doppler echo was made, which showed non-coronary aortic valve thickening with mean aortic transvalvular gradient of 29 mmHg, maximum gradient of 45 mmHg and peak velocity of 2.5 m/sec (Figure 1). It was decided to perform transesophageal cardiac Doppler echo, and possible area of occupation was observed, generating non-coronary valve immobilization with the outcome of significant aortic valve stenosis (Figure 2).

Figure 1. Transesophageal 3D Doppler echo. 135º view. Irregularities appear, adhered to the base of the non-coronary aortic valve.

Figure 2. Transesophageal Doppler echo with X-Plane® imaging processor, with simultaneous visualization at 115º (left) and at 45º (right): motility alteration and irregularities in non-coronary and left coronary valve surface are observed.


Faced with the suspicion of early prosthetic thrombosis, IV anticoagulation was started with low-molecular-weight heparin, with improvement of symptoms and of echocardiographic parameters as well (gradient reduction and transaortic velocity). Because of associated kidney failure (creatinine clearance <30 ml/min), multislice CT was not made at the time. Later, anticoagulation was maintained with vitamin K antagonists (VKA), which she tolerated well. The patient was discharged with no symptoms, and remains stable in the outpatient follow-up.

Figure 3. Continuous Doppler at the level of the aortic valve with transvalvular gradient measurement in transthoracic Doppler echo. A) Presumptive diagnosis of valve thrombosis due to gradient increase; B) After start of anticoagulation treatment.



TAVI-related prosthetic thrombosis has been defined in multiple studies as prosthetic dysfunction manifest in echocardiography by mean gradient >20 mmHg, aortic valve area <1.2 cm2, peak velocity >3 m/sec, Doppler velocity index <0.35, or new moderate or severe aortic valve insufficiency, with suspicion of being a product of additional thrombosis [3,4]. It is suggested to add to this, evidence of mass adhered to the percutaneous valve, ruling out other causes such as infectious endocarditis, prosthesis underexpansion phenomena or native valve prolapse.

The reported incidence of post-TAVI thrombosis ranges from 0.6% to 1.2%, detected in most patients during the first year of implant with progressive dyspnea as the initial symptom. Leetma et al, described greater incidence of prosthetic thrombosis when using multislice CT as an alternative diagnostic method, detecting in 7% of patients, valve thickening and reduced motility in spite of not presenting symptoms.

Recent studies showed an incidence of 13% of subclinical thrombosis when using this method during the follow-up of patients. Larger percutaneous valves and the absence of post-implant anticoagulation treatment were independent predictors of thrombosis [5,6]. Further, in several reports, this phenomenon was related more frequently to balloon expandable prostheses, in comparison to self-expandable prostheses. Blood stasis phenomena have been described in Valsalva sinuses when performing the valve implant, which, added to endothelial damage and microfissures that would lead to an excessive balloon dilatation, stimulate local thrombosis [7].

In regard to the prognosis of these patients, the association of this event to higher mortality or infarctions in clinical follow-up has not been proven; although in recent studies it did represent a three-fold risk of embolic events such as transient ischemic attacks (TIA) unrelated to the immediate procedure [8].

Current clinical practice guidelines recommend to keep a treatment with clopidogrel for 3-6 months depending on the type of valve implanted and ASA for life; although the level of evidence is obtained from studies for coronary stents. On the contrary, anticoagulated patients with VKA and novel oral anticoagulants (NOACs) early, presented significantly less transvalvular gradients and morphological alterations in CT that led to the suspicion of thrombosis in follow-up. Dual antiplatelet therapy (DAPT) did not yield the same outcome [8,9].

Anticoagulation treatment should be established in all patients with suspicion of prosthetic thrombosis with clinical compromise; although at the time there is no strong evidence to start this management in subclinical patients or even preventively when dealing with a population with higher bleeding risk.

There are ongoing randomized studies evaluating the efficacy and safety of vitamin K antagonists and direct oral anticoagulants (DOACs) as a prevention of TAVI-related thromboembolic events that provided evidence for an early use of anticoagulants in this group of patients [10].


Prosthetic thrombosis related to transcatheter aortic valve implantation (TAVI) presents a low incidence, probably because of being underdiagnosed as it presents with no symptoms in a large number of cases.

Causal factors are not completely clear; although it has been observed that variability in regard to post-implant antiplatelet treatment could be related to its presence, as well as the use of large and self-expandable valves.

Anticoagulation proved to improve symptoms, gradients and morphological findings before the suspicion of thrombosis; although there is no substantial evidence to indicate its systematic use as a preventive measure for thromboembolic events.



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Publication: March 2019


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