University of Edinburgh



Progressive breathlessness following transcatheter aortic valve replacementDr Jack PM AndrewsDr Nicholas L CrudenDr Alastair J MossCorresponding Author: Dr. Jack PM Andrews, Centre for Cardiovascular Science, University of Edinburgh, Chancellor’s Building, Royal Infirmary of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB, UK. e-mail: Jack.Andrews@ed.ac.ukCo-author: Dr. Nicholas L Cruden, Edinburgh Heart Centre, Royal Infirmary of Edinburgh, 51 Little France Crescent, Edinburgh EH16 4SB, UK. E-mail: Nick.Cruden@ed.ac.ukCo-author: Dr. Alastair J Moss, Centre for Cardiovascular Science, University of Edinburgh, Chancellor’s Building, Royal Infirmary of Edinburgh, 49 Little France Crescent, Edinburgh EH16 4SB, UK. e-mail: alastairmoss@Word count 430References 5An 84-year-old man presented urgently to the cardiology clinic with rapid onset exertional dyspnea whilst walking on the flat. Five months previously, he underwent implantation of a balloon-expandable 26-mm transcatheter heart valve (SAPIEN 3, Edwards Lifesciences) for severe aortic stenosis. On clinical examination, the jugular venous pressure was elevated and a mid-late ejection systolic murmur was audible in the aortic region. Electrocardiography demonstrated sinus rhythm with a left ventricular strain pattern. Transthoracic echocardiography and cardiac computed tomography (CT) were performed. (Figure 1)QuestionWhich aetiology best explains this presentation?A. Pannus formationB. Transcatheter bioprosthetic valve endocarditisC. Patient-prosthesis mismatchD. Transcatheter bioprosthetic valve leaflet thrombosisE. Structural valve degenerationAnswer – D The correct answer is transcatheter bioprosthetic valve leaflet thrombosis. The aortic flow profile obtained with echocardiography demonstrates severe prosthetic valve obstruction (Figure 1A). Left ventricular function is preserved with an acceleration time and acceleration time/LV ejection time ratio indicative of the delayed ejection flow profile observed in prosthetic valve obstruction. These parameters can be measured independent of the angulation of the Doppler beam. [1] The cardiac CT demonstrates hypoattenuation leaflet thickening and restricted excursion of the leaflets during systole (Figure 1B & inset). Evidence of subclinical leaflet thrombosis on cardiac CT has been reported in 13 - 40% of patients treated with transcatheter bioprosthetic aortic valves. [2-4]Pannus formation typically occurs twelve months after bioprosthesis implantation, encroaching from below the prosthetic annulus and associated calcium deposition may be visible on cardiac CT. Large vegetations due to prosthesis endocarditis can obstruct leaflet motion, however the absence of an irregular mass or symptoms and signs suggestive of an infective component effectively exclude this diagnosis. Severe calcification of the native aortic valve leaflets or annulus can restrict full expansion of the transcatheter valve generating patient-prosthesis mismatch (PPM). At the time of deployment, the effective orifice area indexed to body surface area (EOAI) was 1.15cm2/m2. PPM is defined by an EOAI <0.85cm2/m2 and is more prevalent in females with a small annulus. [5] The long-term outcomes associated with transcatheter aortic valves remain unclear. Although rare, structural failure of transcatheter aortic bioprosthetic valves usually involves leaflet calcification and/or cusp rupture, and both these can be assessed using echocardiography and cardiac CT.Bioprosthesis thrombosis without neurological sequelae occurred whilst on aspirin monotherapy. Anticoagulation with intravenous heparin was administered with an improvement in leaflet motion and a reduction in the transprosthesis gradient after only five days. Oral anticoagulation with warfarin restored bioprosthesis function, as evidenced on echocardiography. (Figure 2) Leaflet thrombosis is an important reversible cause to consider in patients presenting with bioprosthetic valve obstruction.ACKNOWLEDGEMENTSThe authors wish to thank Dr. Timothy Cartlidge, Edinburgh Heart Centre at the Royal Infirmary of Edinburgh, for his assistance in providing the computed tomography images.REFERENCES1. Zekry SB, Saad RM, Ozkan M, Al Shahid MS, Pepi M et al. Flow acceleration time and ratio of acceleration time to ejection time for prosthetic aortic valve function. J Am Coll Cardiol Img. 2011;4:1161-1170.2. Makkar RR, Fontana G, Jilaihawi H, Chakravarty T, Kofoed KF et al. Possible subclinical leaflet thrombosis in bioprsothetic aortic valves. N Engl J Med. 2015;373:2015-2024.3. ADDIN PAPERS2_CITATIONS <papers2_bibliography/>Holmes DR, Mack, MJ. Aortic Valve Bioprostheses: Leaflet Immobility and Valve Thrombosis. Circulation. 2017;135:1749–1756. 4. Jilaihawi H, Asch FM, Manasse E, Ruiz CE, Jelnin V, et al. Systematic CT Methodology for the Evaluation of Subclinical Leaflet?Thrombosis. JACC Cardiovascular Imaging. 2017;10:461–470.5. Daneshvar SA, Rahimtoola SH. Valve prosthesis-patient mismatch (VP-PM): a long-term perspective. J Am Coll Cardiol. 2012;60:1123-1135.FIGURE LEGENDSFigure 1. Transthoracic continuous wave Doppler through the transcatheter aortic valve (A). ECG-gated cardiac CT oblique reconstruction of the left ventricular outflow tract and aortic root in mid-diastole (B) with axial reconstruction of the transcatheter aortic valve in end-systole (inset).Figure 2. Transthoracic continuous wave Doppler through the transcather aortic valve at 10-months post-anticoagulation (A). 2 dimension parasternal long axis echocardiograph showing full excursion of the prosthesis cusps (B). ................
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