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CASE SERIES
Year : 2021  |  Volume : 31  |  Issue : 1  |  Page : 51-54

Severe aortic regurgitation of early degenerated mitroflow bioprosthesis: From echocardiographic diagnosis to treatment with valve-in-valve transcatheter aortic valve implantation


1 Department of Cardiology, ‘La Memoria’ Hospital, ASST Garda, Gavardo (Brescia) -, Italy
2 Department of Cardiology, Cath-Lab Unit, ‘Spedali Civili’ Hospital, Brescia, Italy

Date of Submission24-Nov-2020
Date of Acceptance27-Dec-2020
Date of Web Publication20-May-2021

Correspondence Address:
Matteo Pernigo
Cardiology Unit, ‘La Memoria’ Hospital, Via Andrea Gosa 74, 25085 Gavardo, Brescia
Italy
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcecho.jcecho_129_20

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  Abstract 


Valve-in-Valve transcatheter aortic valve implantation (ViV TAVI) is emerging as an effective therapeutic option for bioprosthetic valve failure. Recently, concern has been raised for early valve deterioration of Mitroflow (Sorin) aortic bioprosthesis, with the development of prevalent stenosis. We report cases of pure severe aortic regurgitation (AR) due to early and mid-term prosthesis degeneration. From June 2018 to October 2019, three patients were treated in our division for the new appearance of severe intraprosthetic regurgitation. Patient 1 (man, 85-year-old) and patient 3 (woman, 83-year-old) had a Mitroflow n. 25 and n. 21 implanted, respectively, in 2012 and 2013 for severe aortic stenosis. Patient 2, a 67-year-old woman with Marfan syndrome underwent a Mitroflow n. 25 implant in 2008 for severe AR and presented chronic type-B aortic dissection. Patient 1 was diagnosed with severe AR in the ambulatory setting, while the other patients presented acute heart failure, requiring inotrope support and high doses intravenous diuretics, and in case 3, temporary extracorporeal ultrafiltration. All patients appeared at high surgical risk and were successfully treated with ViV TAVI, through the right axillary artery in patient 2, and through the femoral artery in patients 1 and 3. Results were good at short- and mid-term follow-up. In conclusion, early and midterm bioprosthesis degeneration with the development of severe AR is a possible complication of the Mitroflow aortic valve. ViV TAVI has been confirmed as a safe and effective therapeutic option in our cases.

Keywords: Mitroflow aortic valve, three-dimensional transesophageal echocardiography, Valve-in-Valve transcatheter aortic valve implantation


How to cite this article:
Pernigo M, Triggiani M, Adamo M, Pasini GF. Severe aortic regurgitation of early degenerated mitroflow bioprosthesis: From echocardiographic diagnosis to treatment with valve-in-valve transcatheter aortic valve implantation. J Cardiovasc Echography 2021;31:51-4

How to cite this URL:
Pernigo M, Triggiani M, Adamo M, Pasini GF. Severe aortic regurgitation of early degenerated mitroflow bioprosthesis: From echocardiographic diagnosis to treatment with valve-in-valve transcatheter aortic valve implantation. J Cardiovasc Echography [serial online] 2021 [cited 2021 Jun 25];31:51-4. Available from: https://www.jcecho.org/text.asp?2021/31/1/51/316519




  Introduction Top


The Mitroflow (Sorin Group, Inc., Milan, Italy; now: LivaNova, London, UK) aortic bioprosthetic valve was designed to optimize the effective orifice area (EOA), by mounting a bovine pericardium sheet on the outside of an acetyl homopolymer stent.[1] Although various studies have described satisfactory mid- and long-term results of Mitroflow implants,[2],[3] significant valve stenosis due to early structural valve degeneration (SVD) has recently been reported.[4],[5],[6] The occurrence of pure or prevalent aortic regurgitation (AR) seems uncommon from available data. Valve-in-Valve transcatheter aortic valve implantation (ViV TAVI) is emerging as an effective treatment for aortic bioprosthesis failure, even if it can be complicated by high postoperative gradients and coronary ostia obstruction.[7] We report three consecutive cases of severe intraprosthetic AR due to early- and mid-term degeneration of Mitroflow valves of variable sizes, successfully treated with ViV TAVI. Initial medical management and correct echocardiographic diagnosis were challenging.


  Case Report Top


Patient 1

An 85-year-old male, diagnosed with new intraprosthetic AR during routine follow-up echocardiography in June 2018. His past medical history included aortic valve replacement (AVR) with Mitroflow n. 25 in November 2012 for severe aortic stenosis; percutaneous transluminal coronary angioplasty (PTCA) with drug-eluting stents implantation in mid-LAD for unstable angina (2014); paroxysmal atrial fibrillation (AF); cardioembolic stroke (2015); type 2 diabetes mellitus; and moderate renal impairment. At the first presentation, the patient was asymptomatic for usual efforts. At transthoracic echocardiography (TTE), aortic bioprosthesis appeared degenerated with mild stenosis (mean gradient: 18 mmHg) and Grade 3 (moderate to severe) AR (effective regurgitant orifice area-proximal isovelocity surface area [PISA] method: 0.25 cm2). At 5-month follow-up, the patient appeared dyspneic for moderate efforts (New York Heart Association [NYHA] II). TTE showed severe intraprosthetic regurgitation (reg. fraction-PISA method: 50%), increased left ventricular (LV) volumes (end-diastolic volume: 190 ml– 95 ml/mq body surface area), with normal ejection fraction (EF). A transesophageal echocardiography (TOE) was performed, showing mildly calcified bioprosthetic cusps, marked thickening and hypomobility of one of them, corresponding to the left coronary, with severe regurgitation originating at this level. Surgical re-operation was judged at high risk. The patient underwent TAVI in January 2019, without major complications. A Medtronic Evolut R (26 mm) was successfully implanted through the right femoral artery. Before the procedure, a re-PTCA on LAD was done for documentation of in-stent restenosis. Triple antithrombotic therapy (Dabigatran 110 bid, ASA, Clopidogrel) was performed for 1 month, then switched to ASA + Dabigatran. The patient was asymptomatic at 6-month and 1-year follow-up., the patient was asymptomatic. TTE showed good prosthetic valve function (peak gradient: 15 mmHg; no significant AR), and decrease in LV volumes.

Patient 2

A 67-year-old woman with Marfan syndrome, admitted to our unit for acute heart failure (NYHA class: IV) in June 2019. She had undergone aortic valve repair and ascending aorta replacement in 1999 for type A dissection and AVR with Mitroflow n. 25 in 2008 for severe AR. She presented chronic type-B aortic dissection (from distal aortic arch) and she had an aortobisiliac endoprosthesis implanted in 2010. Two months before admission, she was diagnosed with moderate, apparently peri-prosthetic AR at routine TTE. On admission, blood pressure was 110/80 mmHg, heart rate 80 bpm; pulmonary rales and severe leg swelling were noted. A two-dimensional (2D) and three-dimensional (3D) TOE was performed, revealing severe eccentric intraprosthetic regurgitation due to prolapse of the anterior cusp [Figure 1]. Peak and mean aortic gradients were 43/24 mmHg. There was an anterior mitral leaflet prolapse with moderate regurgitation. LV was severely dilated, with normal EF (68%). The patient was treated with high doses of intravenous diuretics and heart failure therapy successfully. Due to her medical history and two previous cardiac surgery operations, she was a candidate to ViV TAVI. A thoracic and abdominal computed tomography angiogram (CTA) was performed and the procedure was judged feasible through the right axillary artery. TAVI was performed in July 2019 with a Medtronic Evolut R 26 mm. A right axillary hematoma and a left femoral pseudo-aneurysm occurred, but without significant anemia and with good resolution. The patient was asymptomatic at 1-month and 6-month follow-up. Echocardiograms showed good result of the procedure, normalization of LV volumes, and reduction of mitral regurgitation.
Figure 1: Patient 2. Transesophageal echocardiography documentation of anterior cusp prolapse (red arrow) with severe intraprosthetic regurgitation. (a) Two-dimensional color Doppler; mid-esophageal modified long axis (b) three-dimensional-Zoom, aortic short axis: augmented systolic cusp excursion (c) three-dimensional zoom, aortic long axis: diastolic cusp prolapse

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Patient 3

A 83-year-old woman underwent mitral and aortic valve replacement in 2014, for severe mitral regurgitation and concomitant moderate aortic stenosis; She received an Epic(St Jude) n.31 bioprosthesis in mitral position and an aortic Mitroflow n.21. She suffered also from Stage IV chronic kidney disease and paroxysmal AF. Initial Mitroflow degeneration was noted at first during ambulatory TTE in March 2019, showing mild-to-moderate intraprosthetic regurgitation, and normal LV EF. The patient was admitted to our cardiac intensive care unit for acute heart failure in October 2019. Blood pressure was 110/45 mmHg, electrocardiography showed atrial flutter with ventricular heart rate of 110 bpm. She had severe leg swelling, right pleural effusion, and respiratory failure. Blood tests documented worsening of renal impairment and mild anemia. Noninvasive ventilation and extracorporeal ultrafiltration were required. Sinus rhythm was restored through electrical cardioversion. TTE and TOE showed severe aortic intraprosthetic regurgitation due to prolapse of the anterior cusp (aortic peak and mean gradients: 20/10 mmHg; vena contracta: 6 mm; holodiastolic flow reversal in the distal aortic arch); severely dilated LV with severely reduced EF (31%); and normal function of the mitral biological valve. Five days later, clinical conditions were improved, but the patient was still oliguric and dependent on UFH. A new TTE confirmed severe AR and severely reduced LV EF. Surgical re-operation was judged at high risk. CTA showed the feasibility of ViV TAVI through the right femoral artery. The procedure was successfully performed (with a Medtronic Evolut R 23 mm device), without major complications, and no significant peri-prosthetic leaks [Figure 2]. Coronary angiography performed just before valve delivery showed no significant stenoses. The patient had immediate improvement of hemodynamics, and restart of effective diuresis was achieved. At 3-month follow-up, she was in good general conditions; TTE showed no significant aortic stenosis (peak and mean gradients: 21 and 11 mmHg), decrease in LV volumes, and improvement of EF (to 48%).
Figure 2: Patient 3. (a) Left ventricular and aortic pressure curves at catheterization: severe aortic regurgitation. (b) transcatheter aortic valve implantation valve-in-valve: good result, no significant periprosthetic leak

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  Discussion Top


Since 1982, the Mitroflow aortic bioprosthesis has been implanted in >100,000 patients worldwide.[1] Optimization of EOA has made the valve particularly suitable for small aortic annulus diameters. After the first-generation prosthesis (Mitroflow 11), several models have been introduced over time to improve hemodynamic performance and durability (12A in 1991, LXA in 2006, and DL in 2011).[1] Data about the Mitroflow aortic valve are still conflicting. Several studies have presented satisfactory mid- and long-term results.[2],[3] By contrast, recent literature, including mainly large retrospective and registry-based studies,[4],[5],[6] reports increased risk of re-operation or severe SVD, starting as soon as 4 years after implantation, especially if the prosthesis is small (n. 21 and n. 19 mm). Among our patients, only patient 2 was implanted with a Mitroflow LX, while the other three patients had received a Mitroflow DL. Relevant AS, associated in some cases with a mild or moderate degree of AR, is the main mode of valve failure extensively described by the available literature. The peculiar aspect of our cases was the occurrence of pure or prevalent AR, confirmed by invasive hemodynamic findings. Importantly, an accelerated pattern of deterioration was documented since the appearance of moderate AR in all patients, leading patients 2 and 3 to severe acute heart failure before a scheduled follow-up.

According to our experience, echocardiographic evaluation of regurgitation in a Mitroflow degenerated valve was challenging, especially at TTE. The eccentricity of the regurgitant jet aroused the doubt of possible peri-prosthetic regurgitation (as for patient 2) and made it difficult to quantify regurgitation. TOE, with 2D and 3D imaging, allowed the correct diagnosis and leads to the adequate therapeutic option in all cases. Interestingly, in patient 1, TOE showed marked degeneration with possible retraction and hypomotility of a cusp, while in the other patients demonstrated diastolic prolapse in the LV outflow tract of prosthetic material corresponding to one of the cusps. Due to the shadowing effect caused by the stent in the classical three-chamber projection, the cusp prolapse could be evidenced only through an atypical mid-esophageal long axis view [Figure 1]. This finding is in keeping with existing literature: cusps tears appear commonly in Mitroflow degenerated valves, also for relatively recent models.[8] As tears tend to appear on the free edge of cusps, closely and parallel to the stent posts, they can determine cusp prolapse.[8]

ViV TAVI in degenerated surgical aortic bioprostheses is an emergent treatment option for patients at high surgical risk. However, In the Global Valve-in-Valve International Data Registry,[7] patients with a Mitroflow valve had a more than doubled 30-day mortality rate in comparison to those with other types of stented valves. Mitroflow leaflets are mounted on the external side of the valve frame, and Mitroflow is usually implanted in a supra-annular position. These factors increase the risk of coronary obstruction during the procedure and could affect early survival.[7] The risk of coronary obstruction also depends however on the aortic root anatomy. CTA evaluation of aortic root documented feasibility of ViV TAVI in our patients; wiring of the left main was preventively carried on for a faster potential revascularization, but we did not observe myocardial ischemia. Only patient 1 needed preventive coronary angioplasty, which was performed however in mid-LAD. The postprocedural gradients were good in all cases.


  Conclusions Top


Early valve degeneration causing pure or prevalent intraprosthetic regurgitation is a possible complication of the aortic Mitroflow biological valve. The degeneration process can evolve abruptly, leading to acute heart failure and pulmonary edema. Cusp prolapse potentially due to cusp tear appears to be a common mechanism of valve failure; TOE seems crucial for correct evaluation of regurgitation. Once the diagnosis of relevant regurgitation is established, adequate treatment should not be delayed in these patients; ViV TAVI can be a safe and effective therapeutic option.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Balsam LB, DeAnda A Jr. The Mitroflow aortic valve: A past, present, and future illuminated. J Thorac Cardiovasc Surg 2017;153:40-2.  Back to cited text no. 1
    
2.
Yankah CA, Schubel J, Buz S, Siniawski H, Hetzer R. Seventeen-year clinical results of 1,037 Mitroflow pericardial heart valve prostheses in the aortic position. J Heart Valve Dis 2005;14:172-9.  Back to cited text no. 2
    
3.
Mosquera VX, Bouzas-Mosquera A, Velasco-García C, Muñiz J, Estévez-Cid F, Portela-Torron F, et al. Long-term outcomes and durability of the mitroflow aortic bioprosthesis. J Card Surg 2016;31:264-73.  Back to cited text no. 3
    
4.
Sénage T, Le Tourneau T, Foucher Y, Pattier S, Cueff C, Michel M, et al. Early structural valve deterioration of Mitroflow aortic bioprosthesis: mode, incidence, and impact on outcome in a large cohort of patients. Circulation. 2014;130:2012-20. doi: 10.1161/CIRCULATIONAHA.114.010400. Epub 2014 Oct 29.  Back to cited text no. 4
    
5.
Ius F, Schulz J, Roumieh M, Fleissner F, Ismail I, Tudorache I, et al. Long-term results of the Mitroflow aortic pericardial bioprosthesis in over 800 patients: limited durability and mechanisms of dysfunction. Eur J Cardiothorac Surg 2017;52:264-71.  Back to cited text no. 5
    
6.
Issa IF, Poulsen SH, Waziri F, Torp Pedersen C, Nielsen PH, Riber L, et al. Structural valve deterioration in the Mitroflow biological heart valve prosthesis. Eur J Cardiothorac Surg 2018;53:136-42.  Back to cited text no. 6
    
7.
Dvir D, Webb JG, Bleiziffer S, Pasic M, Waksman R, Kodali S, et al. Transcatheter aortic valve implantation in failed bioprosthetic surgical valves. JAMA 2014;312:162-70.  Back to cited text no. 7
    
8.
Luk A, Cusimano RJ, Butany J. Pathologic evaluation of 28 Mitroflow pericardial valves: A 12-year experience. Ann Thorac Surg 2015;99:48-54.  Back to cited text no. 8
    


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