David B. Melvin

CardioClasp: a new passive device to reshape cardiac enlargement.

In dilated heart failure, geometric distortions place an extra load on the myocardial cells. If this extra burden can be eliminated, the myocardial wall stress would decrease leading to improved systolic ventricular performance. In a dilated heart failure model, we wanted to see whether the CardioClasp™ (which uses two indenting bars to reshape the left ventricle [LV] as two widely communicating “lobes” of reduced radius) could improve systolic performance by passively reshaping the LV and reducing the wall stress.In mongrel dogs (n = 7; 25–27 kg), rapid ventricular pacing (210 ppm 1st week to 240 ppm 4th week) induced dilated heart failure. After 4 weeks, LV performance was evaluated at baseline and with the CardioClasp™ by measuring LV end-diastolic and peak LV systolic pressure, LV +dP/dt, LV −dP/dt, and cardiac output. With the Clasp on, LV wall stress was reduced to 58.6 ± 3.5 from 108.3 ± 8.2 g/cm2. The fractional area of contraction (FAC) with the Clasp on (28.4 ± 4.4) was significantly increased (p < 0.05) from baseline (20.8 ± 4.6) and consistent with improved systolic performance. Cardiac output, LV peak systolic and end-diastolic pressures, and regional myocardial blood flow were unaltered.The Clasp was able to acutely reshape the left ventricle, while preserving the contractile mass, and reduced the tension on the myocardial cells and increased the fractional area of contraction without decreasing the systolic blood pressure.

Reduced cardiac myofibrillar Mg-ATPase activity without changes in myosin isozymes in patients with end-stage heart failure.

In this study we tested the hypothesis that reduced myofibrillar ATPase activities in end-stage heart failure are associated with a redistribution of myosin isozymes. Cardiac myofibrils were isolated from left ventricular free wall from normal human hearts and hearts at end-stage heart failure caused by coronary artery diseases, cardiomyopathy or immunological rejection. The hearts had been excised in preparation for a heart transplant. Myofibrillar Ca2−-dependent Mg-ATPase and myosin Ca−- and K−EDTA-ATPase activities were compared. Possible changes in myosin isozyme distribution in the diseased heart were investigated using polyacrylamide gel electrophoresis of native myosin in the presence of pyrophosphate. Significant reduction in myofibrillar Ca2+-dependent Mg-ATPase with no changes in the sensitivity of the myofibrils to Ca+ was observed in heart with coronary artery diseases (25.2 to 27.1% at pCa 5.83 to pCa 5.05), cardiomyopathy (21.1 to 25.5% at pCa 5.41 to pCa 5.05), and in the immunologically rejected heart (18.4 to 22.8% at pCa 5.41 to pCa 5.05). Significantly lower myosin Ca2+-ATPase was observed with coronary artery diseases only and myosin K-EDTA activities did not differ in diseased and normal hearts. Polyacrylamide gel electrophoresis of native myosin from the normal and three models of end-stage heart failure revealed two distinct bands in the human left ventricle and one diffuse band in the human right atria. No apparent differences in myosin isoenzyme pattern were observed between the normal and diseased hearts. Further evaluation is needed to clarify the ATPase nature of the two bands.

Method for anchoring biomechanical implants to muscle tendon and chest wall.

Reliable tissue fixation is of fundamental importance to the successful development of muscle powered motor prostheses. This report describes a series of canine implant trials used to develop stable tissue-device interface mechanisms. Muscle pumps were fitted with prototype tendon and chest wall anchoring schemes and secured to the ribs and humeral insertion of latissimus dorsi (LD) muscles. LD stimulation was initiated 1 week postimplantation and continued throughout the implant period to stress these fixation sites. Design modification and implant testing were continued until both muscle and chest wall attachment points were found to be stable. Chest wall fixation was best achieved using perforated metallic plates wired to the ribs, as opposed to bone screws or wire mesh, which were subject to degradation. Direct attachment of the native tendon by means of spiked clamping plates proved ineffective. Stable muscle attachment was ultimately achieved by replacing the humeral tendon with an artificial substitute formed from fine polyester fibers gathered into 6–8 bundles and sewn into the LD insertion. Braided into a single cord, these fibers were fixed to the device by means of spiked clamping plates. Based on these findings, we conclude that perforated anchor plates and multifibrous artificial tendons can function as effective tissue-device interface mechanisms.

Coupling of Skeletal Muscle to a Prosthesis for Circulatory Support

A durable bond between the end of skeletal muscles and prosthetic structures could, with appropriate linkage, allow circulatory support power by synchronous and/or sequential contraction of several in situ conditioned muscles. Potential advantages relative to a myoplasty wrap involve 1) less traumatic dissection, 2) efficient linear force development, 3) selectable contraction rate, 4) greater stroke work, 5) independent control of muscle pre-load and end diastolic pressure, and 6) independent control of duration of muscle tension and ejection time. However, no existing means of tissue-prosthetic bonding appears adequate. Practicality would demand that full tension bearing capacity by the bond take no longer than muscle conditioning. A prosthesis was developed to achieve those goals. As scaled for this study, it is made of 7,200–7,800 unspun, unplaited, 22 to 26 μ diameter polyester fibers swaged into four taper needles for weaving through distal muscle. The other end is formed into a polyurethane sheathed kernmantel cord for distal fixation. Devices were implanted in six 3 to 4 kg rabbits (unilateral posterior tibial tendon replacement, random side selection with contralateral dissection/closure controls), and their tensile strength was tested at 30 days. All healed well; leg movements were normal after 1 week. Limbs were frozen at −70°C between death and testing. Control failure occurred at 243 ± 94 N and experimental at 163 ± 44 N (p = 0.065, t-test); highest estimated requirement was 17.2 N. Interface strength was adequate by 30 days. Continued investigations, addressing other questions, are warranted.

Early and late results of left ventricular reshaping by passive cardiac-support device in canine heart failure.

BACKGROUND We tested whether the CardioClasp, a passive non-blood-contacting device could decrease excessive geometric burden in dilated cardiomyopathy and improve left ventricular systolic function and contractility by reshaping the left ventricle (LV) and by decreasing LV wall stress (LVWS) without decreasing arterial blood pressure. METHODS In mongrel dogs (n = 6, the early group; n = 6, the chronic group; 25-27 kg), 4 weeks of rapid right ventricular pacing (210 to 240 bpm) induced dilated cardiomyopathy with heart failure. In the early group, we used hemodynamic data and echocardiography to evaluate LV systolic function immediately after placing the CardioClasp device. In the chronic group, we also evaluated LV systolic function immediately after placing the device on dilated hearts and then left the device in place for 30 days. At the end of 30 days, before explantation of the device, we again assessed LV systolic function. We measured fractional area of contraction (FAC), LVWS, and hemodynamic data in both groups. RESULTS In the early group, use of the CardioClasp device decreased the LV end-diastolic anterior-to-posterior dimension by 27.8% +/- 2.6% at implantation (p < 0.05). In the chronic group, use of the CardioClasp decreased the LV end-diastolic anterior-to-posterior dimension by 19.4% +/- 2.0% at implantation (p < 0.05) and by 22.0% +/- 3.10% at explantation (p < 0.05). Use of the CardioClasp did not alter LV end-diastolic and peak pressure, LV dP/dts, or cardiac output at implantation or at explantation. In the early group, use of the CardioClasp decreased the LVWS by 43.4% +/- 3.1% at implantation (p < 0.05). In the chronic group, LVWS decreased by 28.8% +/- 2.1% at implantation (p < 0.05) and by 43.3% +/- 5.2% at explantation (p < 0.05). In the early group, FAC increased significantly, by 28.9% +/- 7.8% at implantation (p < 0.05). In the chronic group, FAC increased significantly, by 18% +/- 12% at implantation (p < 0.05) and by 19% +/- 12% at explantation (p < 0.05). CONCLUSIONS As expected, use of the CardioClasp device increased FAC and decreased LVWS by reshaping the LV. Use of the CardioClasp device maintained cardiac output and arterial pressure. In 30-day experiments, the increased FAC and decreased LVWS were maintained at explantation.

Fiber technology for reliable repair of skeletal muscle

Conventional soft-tissue reclosure methods-sutures and staples-require substantial organized-collagen content. Some tissues lack extensive intrinsic collagenous content. Wound disruption consequences range from newly closed abdominal wounds bursting open, to post-cesarean wombs splitting at delivery, to heart valves loosening. Although sutures do approach the theoretical limit of normal force transfer-cross-sectional area times compressive strength, a different paradigm-shear force transfer across the far greater surface attainable by fine fibers parallel to the potential disruptive force could exceed that theoretical limit. Capacity is now the product of frictional coefficient, existing tissue pressure, and contact area. Using a device comprising bundles of poly(ethylene terephthalate) fibers through tissue, we previously coupled muscles to devices and bones. Here we tested an analogous device for reclosing fascia-stripped abdominal wall muscles. In 28 rabbits, fascia-deprived rectus abdominus muscles were reclosed, using the experimental device or conventional sutures. Testing muscles from the 21 three-week survivors, (with closure devices retained-the usual clinical practice) demonstrated experimental failure strength which exceeded that of controls by 58%. Histologically, solid tissue elements did in-grow between fibers for an extensive tissue-prosthetic interface. Both histology and mechanical performance suggest the fiber technology presented herein surpasses conventional sutures in closure of collagen-deficient tissues.

In vivo performance of a muscle-powered drive system for implantable blood pumps.

A unique biomechanical implant has been developed to convert muscle power into hydraulic energy for the purpose of driving an implanted blood pump. This device, called a muscle energy converter (MEC), is designed to attach to the humeral insertion of the latissimus dorsi (LD) muscle, so that stimulated contractions cause a rotary cam to compress a fluid-filled bellows. Here we report results from the latest in a series of canine implant trials where the MEC was connected to an adjustable pressure load to measure power output and assess long-term function. Full-length (2 cm) actuator strokes were maintained for a period of 1 month with no discernable discomfort to the animal. Load conditions were cycled periodically to measure stroke work capacity and pressure production. The peak driveline pressure recorded in this experiment was 1743 mm Hg. Steady state power generation was measured to 478 ± 21 mJ/stroke (mean ± SD) with stroke work levels reaching 785 mJ in one test. Normal left and right ventricular stroke work levels in dogs this size (35 kg) are 700 and 150 mJ, respectively. These data confirm that MEC/LD power levels—maintained in tandem with an appropriate cardiac assist device—are sufficient to provide significant long-term circulatory support. Further testing, however, is still needed to demonstrate the long-term stability of this drive system.

An artificial tendon with durable muscle interface

A coupling mechanism that can permanently fix a forcefully contracting muscle to a bone anchor or any totally inert prosthesis would meet a serious need in orthopaedics. Our group developed the OrthoCoupler™ device to satisfy these demands. The objective of this study was to test OrthoCouplers performance in vitro and in vivo in the goat semitendinosus tendon model. For in vitro evaluation, 40 samples were fatigue‐tested, cycling at 10 load levels, n = 4 each. For in vivo evaluation, the semitendinosus tendon was removed bilaterally in eight goats. Left sides were reattached with an OrthoCoupler, and right sides were reattached using the Krackow stitch with #5 braided polyester sutures. Specimens were harvested 60 days postsurgery and assigned for biomechanics and histology. Fatigue strength of the devices in vitro was several times the contractile force of the semitendinosus muscle. The in vivo devices were built equivalent to two of the in vitro devices, providing an additional safety factor. In strength testing at necropsy, suture controls pulled out at 120.5 ± 68.3 N, whereas each OrthoCoupler was still holding after the muscle tore, remotely, at 298 ± 111.3 N (mean ± SD) (p < 0.0003). Muscle tear strength was reached with the fiber–muscle composite produced in healing still soundly intact. This technology may be of value for orthopaedic challenges in oncology, revision arthroplasty, tendon transfer, and sports‐injury reconstruction.

CardioClasp Changes Left Ventricular Shape Acutely in Enlarged Canine Heart

Abstract Background: In dilated cardiomyopathy (DCM), eliminating or reducing extra‐geometric burden to the myocardial cells would directly reduce myocardial wall stress leading to improved LV systolic performance. In acute experiments, we tested whether a passive non‐blood contacting CardioClasp™ device, which employs two indenting bars to reshape the left ventricle (LV), could reduce extra‐geometric burden, LV wall stress (LVWS) and improve LV systolic function and contractility without decreasing arterial blood pressure. Methods: In mongrel dogs (n = 5), 4 weeks of right ventricular pacing (210–220–230–240 ppm) induced DCM with severe heart failure. After placing the CardioClasp™ device, LV performance was evaluated immediately by measuring hemodynamics, echocardiography, and Sonometrics® crystal data. Eleven sonometric crystals were placed into endocardial positions (8 in anterior, posterior, mid‐anterior, mid‐posterior, apex, base, free and septal wall) and in myocardial (2 as regional) and epicardial (1) positions to assess the LV end‐systolic pressure‐segment length relationships (ESPSR) and cross‐sectional area (ESPAR) relationship. Results: CardioClasp™ decreased the LV end‐diastolic anterior‐posterior (A‐P) dimensions at two levels (15% and 25%). With CardioClasp™, LVWS decreased from 93.1 ± 7.2 to 59.1 ± 3.2  g/cm2 (P < 0.05) and fractional area of contraction (FAC) increased from 27.6 ± 3.8 to 33.1 ± 3.7% (P < 0.01). Peak LV and arterial pressures, LV +dP/dt, LV −dP/dt, and cardiac output were unaltered with CardioClasp™. CardioClasp™ placement significantly increased the slopes of LV pressure versus anterior‐posterior segment relationship from 7.3 ± 0.6 to 15.8 ± 1.8 mmHg/mm and septal‐free wall segment relationship from 6.3 ± 0.9 to 9.8 ± 0.5 mmHg/mm. At both 15% and 25% LV A‐P dimension reductions, the slopes of ESPAR showed significant steepening and increased from 10.1 ± 0.7 (baseline) to 15.5 ± 1.7 (15% reduction) and 19.0 ± 1.4 mmHg/cm2 (25% reduction). The larger the reduction, the greater was the steepening of the slopes of ESPSR and ESPAR. Conclusions: CardioClasp™ reduced LV diameter and thereby decreased LVWS and increased FAC. CardioClasp™ was able to reshape the left ventricle, while preserving the contractile mass, which increased the slopes of ESPSR and ESPAR. This reshaping was associated with maintained systolic pressures, cardiac output, and increased contractility. (J Card Surg 2003;18(Suppl 2):S49‐S60)

An Artificial Tendon to Connect the Quadriceps Muscle to the Tibia

No permanent, reliable artificial tendon exists clinically. Our group developed the OrthoCoupler™ device as a versatile connector, fixed at one end to a muscle, and adaptable at the other end to inert implants such as prosthetic bones or to bone anchors. The objective of this study was to evaluate four configurations of the device to replace the extensor mechanism of the knee in goats. Within muscle, the four groups had: (A) needle‐drawn uncoated bundles, (B) needle‐drawn coated bundles, (C) barbed uncoated bundles, and (D) barbed coated bundles. The quadriceps tendon, patella, and patellar tendon were removed from the right hind limb in 24 goats. The four groups (n = 6 for each) were randomly assigned to connect the quadriceps muscle to the tibia (with a bone plate). Specimens were collected from each operated leg and contralateral unoperated controls both for mechanical testing and histology at 90 days post‐surgery. In strength testing, maximum forces in the operated leg (vs. unoperated control) were 1,288 ± 123 N (vs. 1,387 ± 118 N) for group A, 1,323 ± 144 N (vs. 1,396 ± 779 N) for group B, 930 ± 125 N (vs. 1,337 ± 126 N) for group C, and 968 ± 109 N (vs. 1,528 ± 146 N) for group D (mean ± SEM). The strengths of the OrthoCoupler™ legs in the needled device groups were equivalent to unoperated controls (p = 0.6), while both barbed device groups had maximum forces significantly lower than their controls (p = 0.001). We believe this technology will yield improved procedures for clinical challenges in orthopaedic oncology, revision arthroplasty, tendon transfer, and tendon injury reconstruction. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 29:1775–1782, 2011