2. BIOMATERIAL DELIVERY LEADS TO EPICARDIAL ACTIVATION DELAYS ACUTELY AFTER INJECTION IN VIABLE LV MYOCARDIUM AS ASSESSED BY OPTICAL MAPPING

Department: Bioengineering
Faculty Advisor(s): Karen Christman

Primary Student
Name: Aboli A Rane
Email: arane@ucsd.edu
Phone: 858-822-7863
Grad Year: 2012

Abstract
Background: Recently, injectable biomaterials have been evaluated as potential new therapies for MI and heart failure. While these materials have improved LV geometry and ejection fraction, there remains concerns that biomaterial injection may create a substrate for arrhythmia, but studies of this risk are lacking. Here we utilize optical mapping as a tool to assess the effects of injection on regional epicardial activation patterns. Hypothesis: Injection of a bulk biomaterial in the myocardium can lead to heterogeneous alterations in cardiac action potential propagation. Methods: Rats received an injection of 120 Ál of polyethylene glycol based polymer, acetalated dextran microbeads or saline into the LV free wall, or no injection. Optical mapping studies were performed on the langendorff perfused hearts. Action potentials were optically recorded on the LV epicardium at intrinsic rhythm using a voltage sensitive dye and a high-speed camera. Epicardial activation timing and sequence were assessed using custom software. Statistical analysis was performed using one-way ANOVA followed by Newman-Keuls multiple comparison test. Results: Activation maps demonstrate delayed activation and altered activation sequence with no clear breakthrough site on the LV epicardium in the polymer injected group indicating conduction abnormalities when compared to microbeads, saline and no-injection groups. Injection of polymer led to significant increase in total LV epicardial activation time (mean ▒ SD), 9.9 ▒ 3.1 ms (n = 5) compared to microbeads 5.9 ▒ 3.7 ms (n = 6), saline 4.9 ▒ 1.3 ms (n = 5) and no-injection 5.0 ▒ 2.0 ms (n = 5) (p < 0.05). Conclusion: Injection of a bulk biomaterial in myocardium may create a substrate for arrhythmia by causing activation delays and local heterogeneities in conductivity at the site of injection. While injection into the infarct may not be a concern given the already slowed or perturbed conduction, our results indicate that delivery or spread of a material into viable or border zone myocardium may have deleterious effects.

« Back to Posters or Search Results