0
Research Papers

Development of a Non-Blood Contacting Cardiac Assist and Support Device: An In Vivo Proof of Concept Study

[+] Author and Article Information
Michael R. Moreno, John C. Criscione

Department of Biomedical Engineering,  Texas A&M University, College Station, TX 77843-3120; CorInnova Incorporated, College Station, TX 77845

Saurabh Biswas

Department of Biomedical Engineering,  Texas A&M University, College Station, TX 77843-3120

Lewis D. Harrison, Guilluame Pernelle

 CorInnova Incorporated, College Station, TX 77845

Matthew W. Miller, Theresa W. Fossum

Texas A&M Institute for Preclinical Studies,  Texas A&M University, College Station, TX 77843; Department of Small Animal Clinical Sciences, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843-4474

David A. Nelson

Texas A&M Institute for Preclinical Studies,  Texas A&M University, College Station, TX 77843

J. Med. Devices 5(4), 041007 (Nov 28, 2011) (9 pages) doi:10.1115/1.4005281 History: Received April 25, 2011; Revised September 12, 2011; Published November 28, 2011; Online November 28, 2011

One of the maladaptive changes following a heart attack is an initial decline in pumping capacity, which leads to activation of compensatory mechanisms, and subsequently, a phenomenon known as cardiac or left ventricular remodeling. Evidence suggests that mechanical cues are critical in the progression of congestive heart failure. In order to mediate two important mechanical parameters, cardiac size and cardiac output, we have developed a direct cardiac contact device capable of two actions: (1) adjustable cardiac support to modulate cardiac size and (2) synchronous active assist to modulate cardiac output. In addition, the device was designed to (1) remain in place about the heart without tethering, (2) allow free normal motion of the heart, and (3) provide assist via direct cardiac compression without abnormally inverting the curvature of the heart. The actions and features described above were mapped to particular design solutions and assessed in an acute implantation in an ovine model of acute heart failure (esmolol overdose). A balloon catheter was inflated in the vena cava to reduce preload and determine the end-diastolic pressure-volume relationship with and without passive support. A Millar PV Loop catheter was inserted in the left ventricle to acquire pressure-volume data throughout the experiments. Fluoroscopic imaging was used to investigate effects on cardiac motion. Implementation of the adjustable passive support function of the device successfully modulated the end-diastolic pressure-volume relationship toward normal. The active assist function successfully restored cardiac output and stroke work to healthy baseline levels in the esmolol induced failure model. The device remained in place throughout the experiment and when de-activated, did not inhibit cardiac motion. In this in vivo proof of concept study, we have demonstrated that a single device can be used to provide both passive constraint/support and active assist. Such a device may allow for controlled, disease specific, flexible intervention. Ultimately, it is hypothesized that the combination of support and assist could be used to facilitate cardiac rehabilitation therapy. The principles guiding this approach involve simply creating the conditions under which natural growth and remodeling processes are guided in a therapeutic manner. For example, the passive support function could be incrementally adjusted to gradually reduce the size of the dilated myocardium, while the active assist function can be implemented as necessary to maintain cardiac output and decompress the heart.

FIGURES IN THIS ARTICLE
<>
Copyright © 2011 by American Society of Mechanical Engineers
Your Session has timed out. Please sign back in to continue.

References

Figures

Grahic Jump Location
Figure 1

Normal, null, and inverted curvature in apex-to-base, radial plane (long axis)

Grahic Jump Location
Figure 2

Contour comparison of device cross-section when fully activated. Note curvature inversion of the Anstadt Cup (left), which is by design as illustrated in Fig. 9 of the Anstadt patent (US 5,119,804) and more recently in Anstadt [22]. Ejection fraction is superb with both devices, but the Criscione device (right) achieves restoration of circulation without inverting the curvature.

Grahic Jump Location
Figure 3

Criscione Device Drawing. The device was constructed with six independent chambers in a spiral orientation. The chambers were sutured to a nitinol scaffold, which was mounted on hub at the base of the device.

Grahic Jump Location
Figure 4

The implanted device. A median sternotomy was performed and the device placed over the cardiac apex. The device drivelines and chest tube were routed caudal to the sternum. The sternum was closed with wire and the fascia was closed tightly with suture to create a pneumatic seal.

Grahic Jump Location
Figure 5

Cross-section of the Criscione device with chambers in the activated and deactivated state. Note that the device is designed to avoid device induced aberrant curvature inversion of the heart when assist is applied.

Grahic Jump Location
Figure 6

(a) PV loops from the left ventricle during vena cava occlusion with a passive constraint of 0 mm Hg. (b) PV loops from the left ventricle during vena cava occlusion with a passive constraint of 7.5 mm Hg. (c) Plot of end-diastolic pressure-volume relationship for vena cava occlusion with a passive constraint of 0 mm Hg (null constraint) versus 7.5 mm Hg. The application of 7.5 mm Hg passive constraint shifts the EDPVR upward and to the left. This could be beneficial as the EDPVR tends to shift in the opposite direction as disease advances. Thus, the left shift is toward the healthy baseline. Note: To better illustrate the EDPVR, the range of the axes on this plot are different than those in Figs.  66, which contain the respective PV loops from which the EDPVR was obtained. Thus, the slopes of the EDPVRs appear steeper but are in fact, the same as those illustrated in the respective figures from which they were taken.

Grahic Jump Location
Figure 7

(a) Comparison of healthy baseline, esmolol induced failure, and 30 mm Hg active assist in the esmolol induced failure model. Here it is evident that assist recovers some of the CO and SW that is lost in failure. (b) Pressure-volume loops of the transition from 30 mm Hg assist to “no assist” in the esmolol induced failure model. Here it is evident that assist significantly improved cardiac metrics, e.g., SW and CO.

Grahic Jump Location
Figure 8

(a) Comparison of CO and SW in the healthy baseline, esmolol induced failure, and 60 mm Hg active assist in the esmolol induced failure model. Here it is evident that assist recovers much of the CO and SW that is lost in failure. (b) Overlay of pressure-volume loops for the healthy baseline and the 60 mm Hg assist in the esmolol failure model. Here it is evident that while assist produces cardiac performance metrics that are similar to the healthy baseline, the PV relationship has unique characteristics. Though SW and SV are similar in magnitude, the PV profile is altered. Note: SV = max LV volume – min LV volume, SW = area of the PV loop.

Grahic Jump Location
Figure 9

Comparison of PV Loops pre- and post-deployment. Note that the deployment of the device had no significant effect on cardiac function and performance as evidenced by the acquired PV data. The PV relationship is unaffected by device placement.

Grahic Jump Location
Figure 10

Application of 30 mm Hg active assist to the healthy heart. Note that though SV, EF, CO, and SW were significantly increased (p = 0.05), assist did not substantially alter the characteristic features of the PV relationship. Compare this result with the esmolol failure model, Fig. 7, where application of 30 mm Hg active assist resulted in a different PV relationship due to the difference in cardiac function.

Grahic Jump Location
Figure 11

Fluoroscopic images of the device at end-diastole (left) and end-systole (right). Here the nitinol scaffold is visible as well as the segmented PV loop catheter. While the image quality is not sufficient for reliable quantitative analysis, visual inspection revealed no evidence of device induced aberrant curvature inversion of the heart when assist was applied.

Tables

Errata

Discussions

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging and repositioning the boxes below.

Related Journal Articles
Related eBook Content
Topic Collections

Sorry! You do not have access to this content. For assistance or to subscribe, please contact us:

  • TELEPHONE: 1-800-843-2763 (Toll-free in the USA)
  • EMAIL: asmedigitalcollection@asme.org
Sign In