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Relevant clinical history and physical exam
An 81 years old gentleman with hypertension, chronic kidney disease (eGFR=16) and severe aortic stenosis with minimal aortic regurgitation (NYHA class II symptom) was referred for transcatheter aortic valve implantation (TAVI).
Angiogram shows short LM 40% stenosis, proximal LAD 80%, LCx and RCA normal and occluded right (Rt) iliac and diseased left (Lt) iliac arteries.
His STS scores are 8.3% for mortality and 35.5% for M&M.
Relevant test results prior to catheterization
Pre-TAVI CT findings are
- Annulus diameter: minimum 22.3 mm, maximum 27.7 mm, mean 25 mm
- Coronary height: Lt 15.8 mm, Rt 18.7 mm
- Aortic valve heavily calcified
Relevant catheterization findings
Contrast limited percutaneous coronary intervention was done 2 weeks ago and direct aortic TAVI was done using #29 Evolut R with pre- (#20 Nucleus) and post-dilatation (#25 Nucleus) resulted in good valve expansion. Yet there was significant paravalvular leak (PVL), which we believe was likely secondary to the oval annulus. As intra-op haemodynamic was stable, we planned for observation. Day 1 post-op, he developed refractory shock. Intensivist used noadrenaline which likely aggravated the PVL.
Emergency percutaneous post-TAVI PVL closure was arranged. The procedure was done under general anaesthesia and transesophagealechocardiogram (TEE) guidance. Left femoral approach (LFA) and a 8Fr Shuttle sheath was used.
First, Confida wire was put into left ventricle (LV) across the PVL. An AVP II 8mm (Amplatzer, St Jude–AGA Medical Corporation, MN, USA) was deployed but kept unreleased. TEE showed the PVL was halfed. We inserted another AVP II 8mm through the same Confida wire but it failed to occlude the residual leak. While planning to upsize the device, the Confida (safety wire) was accidentally lost to aortic root. We rewired the residual PVL defect with terumo wire but the shuttle sheath (8Fr) cannot be crossed due to poor wire support. Hence, we exchanged the terumo wire under Navicross microcatheter (microcatheter used in peripheral intervention) to Confida wire for better support. Yet, 8Fr and 7Fr shuttle sheath still could not be passed hence AVP III could not be used (at least 7Fr compatible). Finally we resorted to the largest AVP II (14 mm), which is 6 Fr compatible. The device was deployed. TEE and angiogram showed significant reduction of PVL and patient was able to wean off all inotropes with stable blood pressure. The two devices were then released. Post-op and 1 month follow-up echocardiogram showed trivial to mild PVL only.
PVL remains a great challenge to TAVI. Some of the current evidence suggested that PVL might improve in self expandable valve with time. However, there is no consensus of when and how to treat PVL. Post-TAVI PVL in patient with minimal pre-operative aortic regurgitation (AR) mimics acute native AR. They can present dramatically as cardiogenic shock as in our patient.
In conclusion, we presented a case of emergency percutaneous closure of severe PVL with cardiogenic shock day 1 post TAVI. The case illustrated the feasibility of PVL closure using amplatzer devices. It also highlighted the importance of international consensus and futher interventional efforts in the management of post-TAVI PVL.