Iliac fixation inhibits migration of both suprarenal and infrarenal aortic endografts

ObjectiveTo evaluate the role of iliac fixation in preventing migration of suprarenal and infrarenal aortic endografts.MethodsQuantitative image analysis was performed in 92 patients with infrarenal aortic aneurysms (76 men and 16 women) treated with suprarenal (n = 36) or infrarenal (n = 56) aortic endografts from 2000 to 2004. The longitudinal centerline distance from the superior mesenteric artery to the top of the stent graft was measured on preoperative, postimplantation, and 1-year three-dimensional computed tomographic scans, with movement more than 5 mm considered to be significant. Aortic diameters were measured perpendicular to the centerline axis. Proximal and distal fixation lengths were defined as the lengths of stent-graft apposition to the aortic neck and the common iliac arteries, respectively.ResultsThere were no significant differences in age, comorbidities, or preoperative aneurysm size (suprarenal, 6.0 cm; infrarenal, 5.7 cm) between the suprarenal and infrarenal groups. However, the suprarenal group had less favorable aortic necks with a shorter length (13 vs 25 mm; P < .0001), a larger diameter (27 vs 24 mm; P < .0001), and greater angulation (19° vs 11°; P = .007) compared with the infrarenal group. The proximal aortic fixation length was greater in the suprarenal than in the infrarenal group (22 vs 16 mm; P < .0001), with the top of the device closer to the superior mesenteric artery (8 vs 21 mm; P < .0001) as a result of the 15-mm uncovered suprarenal stent. There was no difference in iliac fixation length between the suprarenal and infrarenal groups (26 vs 25 mm; P = .8). Longitudinal centerline stent graft movement at 1 year was similar in the suprarenal and infrarenal groups (4.3 ± 4.4 mm vs 4.8 ± 4.3 mm; P = .6). Patients with longitudinal centerline movement of more than 5 mm at 1 year or clinical evidence of migration at any time during the follow-up period comprised the respective migrator groups. Suprarenal migrators had a shorter iliac fixation length (17 vs 29 mm; P = .006) and a similar aortic fixation length (23 vs 22 mm; P > .999) compared with suprarenal nonmigrators. Infrarenal migrators had a shorter iliac fixation length (18 vs 30 mm; P < .0001) and a similar aortic fixation length (14 vs 17 mm; P = .1) compared with infrarenal nonmigrators. Nonmigrators had closer device proximity to the hypogastric arteries in both the suprarenal (7 vs 17 mm; P = .009) and infrarenal (8 vs 24 mm; P < .0001) groups. No migration occurred in either group in patients with good iliac fixation. Multivariate logistic regression analysis revealed that iliac fixation, as evidenced by iliac fixation length (P = .004) and the device to hypogastric artery distance (P = .002), was a significant independent predictor of migration, whereas suprarenal or infrarenal treatment was not a significant predictor of migration. During a clinical follow-up period of 45 ± 22 months (range, 12-70 months), there have been no aneurysm ruptures, abdominal aortic aneurysm–related deaths, or surgical conversions in either group.ConclusionsDistal iliac fixation is important in preventing migration of both suprarenal and infrarenal aortic endografts that have longitudinal columnar support. Secure iliac fixation minimizes the risk of migration despite suboptimal proximal aortic neck anatomy. Extension of both iliac limbs to cover the entire common iliac artery to the iliac bifurcation seems to prevent endograft migration

Big bottlenecks in cardiovascular tissue engineering.

Although tissue engineering using human-induced pluripotent stem cells is a promising approach for treatment of cardiovascular diseases, some limiting factors include the survival, electrical integration, maturity, scalability, and immune response of three-dimensional (3D) engineered tissues. Here we discuss these important roadblocks facing the tissue engineering field and suggest potential approaches to overcome these challenges

Stretching skeletal muscle: chronic muscle lengthening through sarcomerogenesis.

Skeletal muscle responds to passive overstretch through sarcomerogenesis, the creation and serial deposition of new sarcomere units. Sarcomerogenesis is critical to muscle function: It gradually re-positions the muscle back into its optimal operating regime. Animal models of immobilization, limb lengthening, and tendon transfer have provided significant insight into muscle adaptation in vivo. Yet, to date, there is no mathematical model that allows us to predict how skeletal muscle adapts to mechanical stretch in silico. Here we propose a novel mechanistic model for chronic longitudinal muscle growth in response to passive mechanical stretch. We characterize growth through a single scalar-valued internal variable, the serial sarcomere number. Sarcomerogenesis, the evolution of this variable, is driven by the elastic mechanical stretch. To analyze realistic three-dimensional muscle geometries, we embed our model into a nonlinear finite element framework. In a chronic limb lengthening study with a muscle stretch of 1.14, the model predicts an acute sarcomere lengthening from 3.09[Formula: see text]m to 3.51[Formula: see text]m, and a chronic gradual return to the initial sarcomere length within two weeks. Compared to the experiment, the acute model error was 0.00% by design of the model; the chronic model error was 2.13%, which lies within the rage of the experimental standard deviation. Our model explains, from a mechanistic point of view, why gradual multi-step muscle lengthening is less invasive than single-step lengthening. It also explains regional variations in sarcomere length, shorter close to and longer away from the muscle-tendon interface. Once calibrated with a richer data set, our model may help surgeons to prevent muscle overstretch and make informed decisions about optimal stretch increments, stretch timing, and stretch amplitudes. We anticipate our study to open new avenues in orthopedic and reconstructive surgery and enhance treatment for patients with ill proportioned limbs, tendon lengthening, tendon transfer, tendon tear, and chronically retracted muscles

Temporal evolution of serial sarcomere number in chronically stretched skeletal muscle.

<p>Upon stretching the biceps brachii muscle by 1.14, the sarcomere number increases gradually from to within two weeks, bringing the individual sarcomere lengths back to their initial values. Sarcomere numbers at discrete time points (white circles) correspond to the volume averaged inelastic stretches , averaged over the muscle tissue region in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0045661#pone-0045661-g009" target="_blank">Figure 9</a>.</p

Sarcomere units in striated muscle.

<p>Sarcomeres consist of a parallel arrangement of thick filaments of myosin (gray) sliding along thin filaments of actin (green). They are embedded between Z-lines (red), which appear as dark lines under the transmission electron microscope. In healthy muscle, through the dynamic assembly and disassembly, individual sarcomere units maintain an optimal operating length. Adopted with permission from <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0045661#pone.0045661-Gktepe1" target="_blank">[16]</a>.</p

Biceps brachii muscle.

<p>The finite element model reconstructed from magnetic resonance images consists of 2,705 nodes and a total of 11,816 linear tetrahedral elements. The muscle tissue, discretized by 9,393 elements (red), is attached to the elbow (left) and to the shoulder (right) through tendon tissue, discretized by 2,423 elements (gray). The biceps brachii is a classical fusiform muscle with fibers arranged in parallel bundles along its long axis <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0045661#pone.0045661-Bl1" target="_blank">[38]</a>.</p

Stretching skeletal muscle.

<p>In a controlled limb lengthening model in rabbits, the radius and the ulna of the left forearm are lengthened by 4% inducing a stretch of 1.14 in the extensor digitorum lateralis muscle. Chronic eccentric muscle growth through sarcomerogenesis is characterized in situ using light diffraction imaging. Adopted with permission from <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0045661#pone.0045661-Matano1" target="_blank">[8]</a>.</p