An 83-year old female with severe aortic stenosis (peak gradient 45 mm Hg; mean gradient 25 mm Hg; effective orifice area [EOA] 0.8 cm2) and reduced left ventricular function (LVEF 15 – 20%) underwent transfemoral transcatheter aortic valve implantation (TAVI). The patient had a history of prior myocardial infarction, percutaneous coronary intervention (PCI), moderate renal insufficiency and abdominal aortic aneurysm, indicating high surgical risk (Society of Thoracic Surgeons score of 9.5%). The patient's treatment with aspirin (75 mg/d) and clopidogrel (75 mg/d) due to recent PCI was not discontinued prior to the procedure.
A 26-mm Edwards Sapien XT transcatheter heart valve (THV) was implanted corresponding to a nominal oversizing of 15% relative to MDCT annular area. Re-dilatation of the THV was not performed. During the procedure the patient was stabilized using extracorporeal cardiopulmonary support (CPS) and inotropic therapy. The CPS circuit was heparin-coated and additionally 5000 IE of unfractionated heparin was administered during the procedure.
On pre-discharge transthoracic echocardiography (TTE) the THV was well functioning (peak gradient 9 mm Hg; mean gradient 5 mm Hg; EOA 1.6 cm2, trivial paravalvular leakage) and the low LVEF persisted. The remaining hospitalization was uneventful, and the patient was discharged on standard post-TAVI dual antiplatelet therapy with aspirin (75 mg/d lifelong) and clopidogrel (75 mg/d for 12 months).
At routine 3 months follow-up the patient's symptoms had improved from New York Heart Association functional class IV to II. Transesophageal echocardiography and TTE showed normal transvalvular gradient (peak gradient 13 mm Hg; mean gradient 8 mm Hg; EOA 1.5 cm2) but restricted motion of the posterior THV cusp (Movies IA–IC in the online-only Data Supplement). No paravalvular or central leakage was detected and LVEF was unaltered. Echocardiographic image quality did not allow for adequate assessment with regard to the mechanism of THV dysfunction. Contrast-enhanced multidetector computed tomography (MDCT) was performed. The THV was well-positioned and circular both at the ventricular and aortic rim. The posterior THV cusp was thickened by a low-attenuation mass consistent with thrombus (Fig. 1). Oral anticoagulation therapy with warfarin was initiated in combination with ongoing clopidogrel treatment while aspirin was discontinued. Three months later, MDCT demonstrated normal THV cusps with dissolution of the thrombus (Fig. 2), and correspondingly echocardiography showed normalized cusp mobility with normal transvalvular gradient (peak gradient 13 mm Hg; mean gradient 6 mm Hg; EOA 1.2 cm2) (Movies IIA–IIC in the online-only Data Supplement).
Fig. 1.
Multidetector computed tomography 3 months after transcatheter aortic valve implantation. Short-axis (A) and long-axis (B) views of the transcatheter heart valve demonstrating low-attenuation mass on the posterior cusp consistent with thrombus (black arrows).
Fig. 2.
Multidetector computed tomography after 3 months of oral anticoagulation therapy. Short-axis (A) and long-axis (B) views of the transcatheter heart valve demonstrating successful dissolution of the thrombus.
Even though THV thrombosis is rare with an estimated incidence of 1%, several case reports have described THV stenosis caused by thrombosis 1, 2, 3, 4. In these cases the diagnosis was mainly based on a high transvalvular gradient on echocardiography, most often without direct visualization of the thrombus. As demonstrated in the present case visualization of thrombus by echocardiography may be limited due to acoustic shadows and reverberations from the prosthetic valve. In contrast, MDCT offers superior spatial resolution and produces isotropic data allowing 3-dimensional imaging assessment. It should be noted that although echocardiography demonstrated restrictive cusp motion there was no evident THV stenosis. However, THV thrombosis could potentially cause cerebrovascular embolization or affect long-term THV durability, thus underlining that even subtle signs of THV dysfunction should warrant further imaging. If only echocardiography was performed, the restrictive cusp motion could falsely have been interpreted as primary structural failure of the THV.
This patient developed early THV thrombosis despite receiving unfractionated heparin during the procedure followed by dual antiplatelet therapy as most commonly used [5]. The severely reduced LVEF is likely to have contributed to induce a prothrombotic state.
The optimal antithrombotic/anticoagulation treatment after THV still remains uncertain, and further studies are warranted. Moreover, it is important to identify individual patient and procedural characteristics that are likely to increase the risk of thrombosis after TAVI, and to test whether such modifiers should result in individual modification of the antithrombotic/anticoagulation treatment.
In conclusion, this case emphasizes the role of MDCT in evaluating the mechanism underlying THV dysfunction when not apparent from echocardiography.
The following are the supplementary data related to this article
Two-dimensional transesophageal echocardiographic short-axis view demonstrates restricted motion of the posterior transcatheter heart valve cusp.
Two-dimensional transesophageal echocardiographic long-axis view demonstrates restricted motion of the posterior transcatheter heart valve cusp.
Three-dimensional transesophageal echocardiographic imaging demonstrates restricted motion of the posterior transcatheter heart valve cusp.
Two-dimensional transesophageal echocardiographic short-axis view demonstrates normalized mobility of the posterior transcatheter heart valve cusp.
Two-dimensional transesophageal echocardiographic long-axis view demonstrates normalized mobility of the posterior transcatheter heart valve cusp.
Three-dimensional transesophageal echocardiographic imaging demonstrates normalized mobility of the posterior transcatheter heart valve cusp.
Supplementary data to this article can be found online at http://dx.doi.org/10.1016/j.ijchv.2013.11.006.
Funding sources
NCH and BLN have received grant support from Edwards Lifesciences.
Disclosures
None
Footnotes
Available online 27 November 2013
References
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Two-dimensional transesophageal echocardiographic short-axis view demonstrates restricted motion of the posterior transcatheter heart valve cusp.
Two-dimensional transesophageal echocardiographic long-axis view demonstrates restricted motion of the posterior transcatheter heart valve cusp.
Three-dimensional transesophageal echocardiographic imaging demonstrates restricted motion of the posterior transcatheter heart valve cusp.
Two-dimensional transesophageal echocardiographic short-axis view demonstrates normalized mobility of the posterior transcatheter heart valve cusp.
Two-dimensional transesophageal echocardiographic long-axis view demonstrates normalized mobility of the posterior transcatheter heart valve cusp.
Three-dimensional transesophageal echocardiographic imaging demonstrates normalized mobility of the posterior transcatheter heart valve cusp.