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Division of Cardiovascular Surgery, Toronto General Hospital, 4N-470, 200 Elizabeth St, Toronto, Ontario, M5G 2C4 Canada
(Email: andrewsycheng88{at}gmail.com; terry.yau{at}uhn.on.ca).
Cell transplantation has undergone intense investigation as a novel therapy for congestive heart failure. There has been concurrent interest in tissue-engineering approaches, largely with the application of cell-seeded biodegradable patches on the epicardial surface of the dilating heart. These constructs have often been associated with enhanced donor cell retention, significant angiogenesis, and reduced infarct expansion, although the relative importance of the donor cells versus the passive mechanical properties of the scaffold has yet to be completely elucidated. Although this approach is promising, surgical implantation of such a cell-seeded patch is a nontrivial undertaking in patients with advanced heart failure.
In this study, Mukherjee and colleagues [1] evaluated an alternative approach, the implantation of a novel fibrin-alginate composite, which was injected directly into the infarcted myocardium of adult pigs rather than being applied to the epicardium. They concluded that their fibrin-alginate biocomposite reduced infarct expansion, as evaluated by radiopaque markers and preserved posterior wall thickness. Paradoxically, they did not find any effect on infarct size as assessed by morphologic examination. Relative collagen volume, soluble collagen content, and matrix metalloproteinase-2 activity in the infarct were reduced by injection of the composite material, suggesting an effect on local matrix and collagen remodeling.
Of concern was their observation of refractory ventricular fibrillation in 2 of 11 pigs during injection of the composite material, and of refractory ventricular tachycardia in another pig in the same group 14 days later. Only one pig in the saline injection group developed ventricular tachycardia on day 28, and it was successfully cardioverted. Although the infarct itself is certainly arrythmogenic, these findings raise some concern about the safety of this approach in humans. Injection of such a material directly into the myocardium could exacerbate repolarization heterogeneity in the infarct and peri-infarct zone and provide further substrate for arrhythmias.
It is still unclear what inflammatory response (both early and late) is induced by this biomaterial. The interval to which it degrades, and whether or not it spreads, migrates, or can be embolized are unknown. Still, this novel approach bears further study. Whether this composite is safe, works best with or without cells, slow-release chemokines, or in conjunction with another therapy are questions the answers to which may shed further light on tissue-engineering based approaches to myocardial repair.
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