Impact of Selective Posterior Cruciate Ligament Fiber Release on Femoral Rollback in Cruciate-Retaining Total Knee Arthroplasty: A Computational Study.

BACKGROUND: Partial or total release of the posterior cruciate ligament (PCL) is often performed intraoperatively in cruciate-retaining total knee arthroplasty (CR-TKA) to alleviate excessive femoral rollback. However, the effect of the release of selected fibers of the PCL on femoral rollback in CR-TKA is not well understood. Therefore, we used a computational model to quantify the effect of selective PCL fiber releases on femoral rollback in CR-TKA. METHODS: Computational models of 9 cadaveric knees (age: 63 years, range 47 to 79) were virtually implanted with a CR-TKA. Passive flexion was simulated with the PCL retained and after serially releasing each individual fiber of the PCL, starting with the one located most anteriorly and laterally on the femoral notch and finishing with the one located most posteriorly on the medial femoral condyle. The experiment was repeated after releasing only the central PCL fiber. The femoral rollback of each condyle was defined as the anterior-posterior distance between tibiofemoral contact points at 0° and 90° of flexion. RESULTS: Release of the central PCL fiber in combination with the anterolateral (AL) fibers, reduced femoral rollback a median of 1.5 [0.8, 2.1] mm (P = .01) medially and by 2.0 [1.2, 2.5] mm (P = .04) laterally. Releasing the central fiber alone reduced the rollback by 0.7 [0.4, 1.1] mm (P < .01) medially and by 1.0 [0.5, 1.1] mm (P < .01) laterally, accounting for 47 and 50% of the reduction when released in combination with the AL fibers. CONCLUSIONS: Releasing the central fibers of the PCL had the largest impact on reducing femoral rollback, either alone or in combination with the release of the entire AL bundle. Thus, our findings provide clinical guidance regarding the regions of the PCL that surgeons should target to reduce femoral rollback in CR-TKA.

Computational modelling of multi-temporal ventricular-vascular interactions during the progression of pulmonary arterial hypertension.

A computational framework is developed to consider the concurrent growth and remodelling (G&R) processes occurring in the large pulmonary artery (PA) and right ventricle (RV), as well as ventricular-vascular interactions during the progression of pulmonary arterial hypertension (PAH). This computational framework couples the RV and the proximal PA in a closed-loop circulatory system that operates in a short timescale of a cardiac cycle, and evolves over a long timescale due to G&R processes in the PA and RV. The framework predicts changes in haemodynamics (e.g. 68.2% increase in mean PA pressure), RV geometry (e.g. 38% increase in RV end-diastolic volume) and PA tissue microstructure (e.g. 90% increase in collagen mass) that are consistent with clinical and experimental measurements of PAH. The framework also predicts that a reduction in RV contractility is associated with long-term RV chamber dilation, a common biomarker observed in the late-stage PAH. Sensitivity analyses on the G&R rate constants show that large PA stiffening (both short and long term) is affected by RV remodelling more than the reverse. This framework can serve as a foundation for the future development of a more predictive and comprehensive cardiovascular G&R model with realistic heart and vascular geometries.

Inverse modeling framework for characterizing patient-specific microstructural changes in the pulmonary arteries.

Microstructural changes in the pulmonary arteries associated with pulmonary arterial hypertension (PAH) is not well understood and characterized in humans. To address this issue, we developed and applied a patient-specific inverse finite element (FE) modeling framework to characterize mechanical and structural changes of the micro-constituents in the proximal pulmonary arteries using in-vivo pressure measurements and magnetic resonance images. The framework was applied using data acquired from a pediatric PAH patient and a heart transplant patient with normal pulmonary arterial pressure, which serves as control. Parameters of a constrained mixture model that are associated with the structure and mechanical properties of elastin, collagen fibers and smooth muscle cells were optimized to fit the patient-specific pressure-diameter responses of the main pulmonary artery. Based on the optimized parameters, individual stress and linearized stiffness resultants of the three tissue constituents, as well as their aggregated values, were estimated in the pulmonary artery. Aggregated stress resultant and stiffness are, respectively, 4.6 and 3.4 times higher in the PAH patient than the control subject. Stress and stiffness resultants of each tissue constituent are also higher in the PAH patient. Specifically, the mean stress resultant is highest in elastin (PAH: 69.96, control: 14.42 kPa-mm), followed by those in smooth muscle cell (PAH: 13.95, control: 4.016 kPa-mm) and collagen fibers (PAH: 13.19, control: 2.908 kPa-mm) in both the PAH patient and the control subject. This result implies that elastin may be the key load-bearing constituent in the pulmonary arteries of the PAH patient and the control subject.