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Quebec Heart Institute/Laval Hospital, Quebec, Canada
Accepted for publication June 17, 2008.
* Address correspondence to Dr Rodés-Cabau, Quebec Heart Institute/Laval Hospital, 2725 Chemin Ste-Foy, Quebec, G1V 4G5, Canada (Email: josep.rodes{at}crhl.ulaval.ca).
| Drs Rodés-Cabau, Dumont, and Pibarot disclose that they have a financial relationship with Edwards Lifesciences Inc.
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| Abstract |
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Percutaneous aortic valve implantation (PAVI) is emerging as an alternative to surgical aortic valve replacement for patients with symptomatic severe aortic stenosis considered to be at high or prohibitive operative risk [1–3]. We report two life-threatening complications associated with PAVI, and we discuss their potential causes and solutions.
A 79-year-old man diagnosed with symptomatic low-flow, low-gradient aortic stenosis was referred for PAVI. The patient had a history of diabetes, hypertension, coronary artery disease, aortobifemoral bypass grafting, chronic obstructive pulmonary disease, and chronic renal failure. Doppler echocardiographic scan revealed a mean aortic gradient of 20 mm Hg, an aortic valve area of 0.76 cm2, and a left ventricular ejection fraction of 28%. The patient was considered to be too high risk for aortic valve replacement (predicted operative mortality by The Society of Thoracic Surgeons score, 11.5%) and was referred for a PAVI by transapical approach.
The procedure was performed under transesophageal echocardiography (TEE) and fluoroscopy guidance. A left anterior mini-thoracotomy was performed to expose the apex and two large pursestrings with pledgets were placed at the left ventricular apex. After puncturing the apex, a stiff guidewire was positioned in the descending aorta, and a 26-French sheath was inserted into the left ventricle over the wire. On the basis of an aortic annulus measurement of 24 mm by TEE, a 26-mm Edwards SAPIEN valve (Edwards Lifesciences Inc, Irvine, CA) was implanted under rapid pacing. After valve deployment, the TEE showed the presence of a severe central aortic regurgitation (AR) (Fig 1A) that persisted after the guidewire was removed, and a second 26-mm valve was implanted inside the first dysfunctional valve in the same procedure (Fig 2A). This "valve-in-valve" implantation successfully corrected the AR (Fig 1B) and the residual mean transvalvular gradient was 8 mm Hg. The patient's postoperative progress was initially satisfactory, but 2 days after, the procedure suddenly developed a cardiogenic shock refractory to adrenergic support. A transthoracic echocardiography of suboptimal quality due to poor transthoracic acoustic window showed no pericardial effusion, no periprosthetic leak and a left ventricular ejection fraction of 10%. The patient was immediately transferred to the catheterization laboratory where an aortic angiography showed that the two implanted valves had migrated into the left ventricle, causing an obstruction of the left ventricular outflow tract (Fig 2B). Despite the very high operative risk, the two bioprostheses were surgically removed and standard aortic valve replacement was performed. However, the patient developed refractory cardiogenic shock with irreversible metabolic acidosis and disseminated intravascular coagulation, and he subsequently died during weaning from cardiopulmonary bypass. The pathologic study showed that the second implanted valve was correctly positioned and anchored within the first one, with an external diameter of 26 mm. After removing this second valve, a careful examination of the first (dysfunctional) valve showed no evidence of leaflet tear. The explanted native aortic valve was moderately calcified (Fig 3) with a Warren-Young score of 3.
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Procedural embolization of percutaneously implanted valves has been previously reported, with an incidence of 2% to 6% [1, 3]. We believe that the present case is the first report of late migration of a percutaneously implanted aortic valve. The presence of a relatively large and nonseverely calcified annulus may have limited the anchoring of the valve and might have contributed to valve migration in this patient. Moreover, the first valve may have been implanted slightly too ventricular. Maintaining the appropriate positioning of the valve might be more challenging with the transapical approach due to the motion of the sheath in relation to heart contractions. We now systematically check and re-adjust if necessary the position of the valve under rapid pacing just before its deployment with both TEE and angiography. Also, we position half of the valve above and half below the aortic annulus, and not one third above and two thirds below the aortic annulus as previously recommended.
This case demonstrates the feasibility and efficacy of implanting an Edwards Sapien valve (Edwards Lifesciences Inc) within another one during the same procedure to correct severe central AR. It has also shown, for the first time, that late (>24 hrs) valve embolization can occur after PAVI and suggest that this new technology should be used with great caution in patients with relatively large (
24 mm) and mild-to-moderate calcified annulus. Finally, the precise positioning of the valve seems crucial for reducing both the risk of severe AR and valve migration.
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