Transcatheter Mitral Valve Replacement: A Novel Anchor Technology.

BACKGROUND: Mitral valved stents tend to migrate or to develop paravalvular leakage due to high-left ventricular pressure in this cavity. Thus, this study describes a newly developed mitral valved stent anchoring technology. METHODS: Based on an existing mitral valved stent, four anchoring units with curved surgical needles were designed and fabricated using three-dimensional (3D) software and print technology. Mitral nitinol stents assembled with four anchoring units were successively fixed on 10 porcine annuli. Mechanical tests were performed with a tensile force test system and recorded the tension forces of the 10 nitinol stents on the annulus. RESULTS: The average maximum force was 28.3 ± 5.21 N, the lowest was 21.7 N, and the highest was 38.6 N until the stent lost contact with the annulus; for the break force (zero movement of stent from annulus), the average value was 18.5 ± 6.7 N with a maximum value of 26.9 N and a minimum value of 6.07 N. It was additionally observed that the puncture needles of the anchoring units passed into the mitral annulus in all 10 hearts and further penetrated the myocardium in only one additional heart. The anchoring units enhanced the tightness of the mitral valved stent and did not destroy the circumflex coronary artery, coronary sinus, right atrium, aortic root, or the left ventricular outflow tract. CONCLUSION: The new anchoring units for mitral nitinol stents were produced with 3D software and printing technology; with this new type of anchoring technology, the mitral valved stent can be tightly fixed toward the mitral annulus.

Biodegradable Poly-ε-Caprolactone Scaffolds with ECFCs and iMSCs for Tissue-Engineered Heart Valves.

Clinically used heart valve prostheses, despite their progress, are still associated with limitations. Biodegradable poly-ε-caprolactone (PCL) nanofiber scaffolds, as a matrix, were seeded with human endothelial colony-forming cells (ECFCs) and human induced-pluripotent stem cells-derived MSCs (iMSCs) for the generation of tissue-engineered heart valves. Cell adhesion, proliferation, and distribution, as well as the effects of coating PCL nanofibers, were analyzed by fluorescence microscopy and SEM. Mechanical properties of seeded PCL scaffolds were investigated under uniaxial loading. iPSCs were used to differentiate into iMSCs via mesoderm. The obtained iMSCs exhibited a comparable phenotype and surface marker expression to adult human MSCs and were capable of multilineage differentiation. EFCFs and MSCs showed good adhesion and distribution on PCL fibers, forming a closed cell cover. Coating of the fibers resulted in an increased cell number only at an early time point; from day 7 of colonization, there was no difference between cell numbers on coated and uncoated PCL fibers. The mechanical properties of PCL scaffolds under uniaxial loading were compared with native porcine pulmonary valve leaflets. The Young's modulus and mean elongation at Fmax of unseeded PCL scaffolds were comparable to those of native leaflets (p = ns.). Colonization of PCL scaffolds with human ECFCs or iMSCs did not alter these properties (p = ns.). However, the native heart valves exhibited a maximum tensile stress at a force of 1.2 ± 0.5 N, whereas it was lower in the unseeded PCL scaffolds (0.6 ± 0.0 N, p < 0.05). A closed cell layer on PCL tissues did not change the values of Fmax (ECFCs: 0.6 ± 0.1 N; iMSCs: 0.7 ± 0.1 N). Here, a successful two-phase protocol, based on the timed use of differentiation factors for efficient differentiation of human iPSCs into iMSCs, was developed. Furthermore, we demonstrated the successful colonization of a biodegradable PCL nanofiber matrix with human ECFCs and iMSCs suitable for the generation of tissue-engineered heart valves. A closed cell cover was already evident after 14 days for ECFCs and 21 days for MSCs. The PCL tissue did not show major mechanical differences compared to native heart valves, which was not altered by short-term surface colonization with human cells in the absence of an extracellular matrix.