This single-center study confirmed the feasibility of transfemoral TAVR with the Venus A-Valve in patients with PNAR. The procedure was successful in 97.8%. No patient died intraoperatively. No second valve was implanted in any case. Echocardiographic measurements showed adequate hemodynamic function without PVL > moderate degree, significant improvement in LVEF and decreased mean pressure gradient during one-year follow-up.
The Venus A-Valve system has some unique advantages [16–17]. First, it can be fully retrievable if there is significant residual PVL or the prosthesis position is not proper; second, it has the repositionability to fine tune the final deployment; third, it can check the stability of the prosthesis by a push-and-pull test using the positioning wires. Despite these advantages, in our early procedures, one patient was converted to SAVR due to valve embolism into the aortic arch. Of note, prosthetic valve dimension was not the only factor implied in this valve embolization event. The increased stroke volume caused by significant AR and the low implantation height due to the absence of fluoroscopic calcific landmarks may also be the important factors [18]. To prevent this complication, we updated our protocol in subsequent cases, such as a prolonged observation time without removing the wires to avoid valve inversion in case of embolization and to allow subsequent balloon recapture maneuvers. Since then, valve embolization never happened again.
The diameter of aortic annulus for sizing the prosthesis was calculated by the perimeter and area of the native aortic annulus [19]. Of note, it was necessary to have 10–20% oversizing of the native aortic annulus to minimize the risk of insufficient prosthesis anchoring and PVL [20]. Oversizing beyond 20% was not recommended due to the risk of annular rupture and conduction system abnormality [21]. Published data suggested that PNAR relied on AA, LVOT, STJ, and thickening leaflet to provide the anchoring force for the prosthetic valve [22]. AA and LVOT played a major anchoring role. STJ may provide an anchoring for the “crown” of the prosthetic valve and avoid it slipping down. Moreover, the thickening leaflets provides the much greater friction between the native valve and prosthetic valve frame. In our study, no patient had balloon post-dilation, prosthesis malposition, annulus rupture or second valve implantation. Only one patient (1/41, 2.4%) had new permanent pacemaker who developed a third-degree atrioventricular block 10 months after the procedure. Overall, the complications are less frequent than other studies using self-expanding valves [23–24].
A proportion of PNAR is caused by annular dilation due to aortic aneurysm, Marfan syndrome, bicuspid aortic valve, etc [25]. It is important that TAVR may be ineffective in altering the prognosis of these patients. Some studies suggested [26] that patients with ascending aorta aneurysm responded poorly to treatment of TAVR (75% of the patients died 6 months after valve implantation). It may be due to that the aortic diameter is still increasing after TAVR. Additionally, bicuspid aortic valve, especially Type-0 (2 aortic sinuses and 2 valve leaflets with no raphe), was regarded as a contradiction to TAVR because of no inadequate anchoring position [27]. In our study, one patient with bicuspid aortic valve (type 1) had moderate PVL after the treatment, as the positioning of the prosthesis was affected by the raphe of the native valve. So, careful selection and morphology assessment was needed for bicuspid aortic valve patients.
Notley, 13 of 16 patients had amelioration of concomitant mitral regurgitation from moderate or greater to mild or trace in our study. The progression of mitral regurgitation is secondary to the increase of the left ventricle-to-atrium pressure gradient and progressive left ventricle adverse remodeling which involves the mitral valve structure [28]. After TAVR implantation, two mechanisms act together contributing to the regression of mitral regurgitation [29]: (1) the reduction of left ventricle diastolic volume and the change of left ventricle geometry; and (2) the reduction of left ventricle cavity pressure leading to the reduction of the ventricle-to-atrium pressure gradient. Thereafter, left ventricle adverse remodeling is gradually reversed, including mitral valve morphology.
In our experience, several technical points should be noted. First, it is critical to determine the size of the prosthetic valve accurately before implantation. Second, high valve implantation (not lower than 4–5 mm in the left ventricular) assures a more proper valve oversizing, reducing PVL, and minimizing the risk of damaging the atrioventricular conduction system. Third, two pigtail catheters should be positioned in the aortic sinuses and transesophageal echocardiography is essential to guide the valve implantation. Moreover, rapid ventricular pacing is necessary to reduce stroke volume, stabilize the annulus, and limit prosthesis motion. Last but not least, cardiopulmonary bypass should be prepared in some special cases.
Study Limitations
This study included a relatively small number of patients. The longest follow-up period was limited to one year. Further research with a larger patient population and longer follow-up duration are scheduled.