Paper 2 – An Intrapericardial Injectable Hydrogel Patch for Mechanical-Electrical Coupling with Infarcted Myocardium
Overview:
Due to the poor clinical outcomes associated with myocardial infarction (MI), the development of novel therapeutic technologies in this domain is imperative. Hydrogels have shown promise as therapeutic interventions, however, hydrogels need further structural and electrical optimization to have clinical significance. In 2022, Yu et al. performed a study aimed at developing an injectable mechanical-electrical coupled hydrogel patch (MEHP) for cardiac repair after MI. Further, a rat model was used to assess pericardial injection and treatment with MEHP in vivo.
Figure 1. Components of MEHP Visualized. Figure adapted from Yu et al., 2022 and created with BioRender.com
Structural notes:
MEHP is composed of a polyaniline gelatin-polyvinyl alcohol complex (bPANi:Gel) held together by covalent borate ester bonds as well as non-covalent bonds. The side chain modification introduced to aniline monomers gives bPANi:Gel hydrophilic and self-assembling capabilities. These properties allowed strong attachment of bPANi:Gel to infarcted myocardial tissue, which enabled the complex to accomplish its electrical and mechanical functions. As compared to hydrogels composed of just conducting polymers (CP) such as polyethylene glycol (see Hydrogels), bPANi:Gel showed improved homogeneity, hydrophilicity, electroactivity, and biocompatibility.
Preparation and assembly of MEHP:
Hydrogen bonds and electrostatic interactions between bPANi and the gel improved its stability, allowing for rapid preparation and injection times. The gelation time (time to assemble) of the complex was 3-7 minutes and was found to decrease as cross-linkage was increased.
Mechanical and electrical properties of MEHP:
MEHP was applied to porcine myocardium and the authors observed that increased bPANi and gel content allowed the complex to mimic the viscoelastic properties of biological tissues. Higher water content also allowed the complex to stretch and compress like cardiac tissue to resist mechanical deformation. Further, the spontaneous reassembly of bPANi:gel complex after injury (being cut) suggests that the structure is durable and has longitudinal potential; that said, this was not a robust finding, more-so an extrapolation.
CPs carry electrical signals through a delocalized pi system; charge transfer resistance (ease of electron flow) by way of this mechanism was lower in MEHP compared to polyvinyl alcohol (PVA) hydrogels. The use of a gel dispersant further improved the conductivity of MEHP by inducing a more heterogeneous structure. The energetic stability of the MEHP network allowed for reconfiguration of conductive paths upon fusion of separate segments. MEHP also improved blocked electrical conduction in scar tissue, suggesting potential for electrical activation of infarcted areas.
Therapeutic efficacy of MEHP in animal model:
MEHP proved to be suited for cell encapsulation and proliferation in vitro (specifically, good cell retention and viability was observed). In vivo, adipose derived stem cells (ADSCs) introduced along with MEHP were retained to some degree; by 14 days post-injection a negligible amount of injected ADSCs were retained by fluorescence imaging. MEHP was then assessed in a rat model where the left anterior descending artery was ligated to induce MI. A four week-assessment of MEHP treatment with this model revealed decreased infarcted area in the MEHP treatment group, with the MEHP/ADSC group showing the most repair as compared to the control (see Figure 2). Further, MEHP treatment promoted blood vessel growth of the infarcted area; increased alpha-SMA and CD34 expression – markers indicating the growth of cardiac cells – was observed in both MEHP and MEHP/ADSC treatment groups. Vessel growth within MEHP complex could suggest the promotion of endothelial proliferation, adhesion, and migration to enhance vascular regeneration by the treatment. Since this was most prominent in the MEHP/ADSC group, it is possible that the driving mechanism involves the expression of angiogenic growth factors by ADSCs.
Role of MEHP in restoration of electrophysiological cardiac function:
The impact of MEHP was assessed using the rat model described above. As compared to the control group, the MEHP treatment group saw reduced activation time of action potential (AP) in the left ventricle (the main pumping chamber of the heart) upon stimulation, suggesting restored electrophysiological function of cardiomyocytes. Further, MEHP had the power to modulate rhythm of electrical signal conduction and thus prevent arrhythmia. Though not well described, the mechanism for this result, as proposed by the authors, was that the conduction of electrical signals through the MEHP network carries signals to healthy peripheral cardiomyocytes which complete the contractions. Such a mechanism could have detrimental effects in the longterm as it suggests that neighboring cardiomyocytes must be overworked. Also, using electrocardiogram analysis, the MEHP-treatment groups showed shorter Q and S wave intervals, improved heart beat volume, and improved cardiac input as compared to the PVA/gel hydrogel treatment group, indicating less pathological AP activity – see Figure 3. Finally, MEHP treatment groups limited anatomical change in the left ventricle associated with pathological conditions.
Conclusions:
This study highlights a promising application of hydrogel technology for myocardial infarction. The authors thoroughly discussed the many relevant properties of their technology and offered mechanistic rationale for many of their findings. Although the invasive nature of this technology would make performing randomized clinical trials difficult (part of our discussion with Dr. Shakur in The Interview), the validation of MEHP in an animal model is exciting and suggests that hydrogels are a clinically relevant technology.
December 8, 2023 at 4:49 pm
This therapy really interesting. I feel like you could do an entire project unpacking just this! All that aside, it;s interesting that the cells managed to assimilate enough to at least participate in restoring the electrophysiological function of surrounding cardiomyocytes. I am curious, though what are factors are preventing the new cells from directly participating, given that the transplanted cardiomyocytes should have all the “parts” to participate. I wished that the conception of this model was a bit better described to better understand the connection between the “knowledge” that led to this “innovation.”
December 8, 2023 at 7:58 pm
Can you expand on the risks of the invasive nature of hydrogels?
December 8, 2023 at 8:00 pm
I really like that you decided to explore a specific type of hydropatch in this section – it connects perfectly with your section introducing hydrogels! I especially found interest in the mechanistic understanding of how MEHP impacts electrophysiological cardiac function. You mention reduced activation time of action potential, modulation of electrical signal conduction, and prevention of arrhythmia, but state that the underlying mechanisms behind these effects are not deeply explored. Having spent a semester exploring this topic, do you guys have any ideas or theories about the unexplored parts of the mechanisms at play? I would be interested in reading more on your own takes on this area!
December 8, 2023 at 10:16 pm
Good discussion, I like how you tied in the composition of the patch with their effects, especially with the visualization of repair over time! I also appreciate the mention of some potential drawbacks with the therapies explored. With the rat model, was MI induced prior to testing the therapy or was it done on healthy hearts? Moreover, do you see the limitations from your previous exploration of rat models as affecting this experiment as well? My other question would be to maybe include how the patches are finding their way to damaged heart tissue? I might’ve missed this but I wasn’t sure if they were being inserted there or somehow bound and self-aggregated there themselves.
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