Our aim was to develop an easy-to-induce, reproducible, and low mortality clinically relevant closed-chest model of chronic myocardial infarction in swine using intracoronary ethanol
and characterize its evolution using MRI and pathology. We injected 3-4 mL of 100% ethanol into the mid-LAD of anesthetized swine. Heart function and infarct size were assessed serially using MRI.
Pigs were euthanized on days 7, 30, and 90 (n=5 at each timepoint). Postoperative MRI revealed compromised contractility and decreased ejection fraction, from 53.8% ± 6.32% to 43.79% ±
7.72%
(P=0.001). These values remained lower than baseline thorough the followup (46.54% ± 11.12%, 44.48% ± 7.77%, and 40.48% ± 6.40%, resp., P<0.05). Progressive remodeling was seen in all animals.
Infarcted myocardium decreased on the first 30 days (from 18.09% ± 7.26% to 9.9% ± 5.68%) and then stabilized (10.2% ± 4.21%). Pathology revealed increasing collagen content and fibrous organization
over time, with a rim of preserved endocardial cells. In conclusion, intracoronary ethanol administration in swine consistently results in infarction. The sustained compromise in heart function and myocardial
thinning over time indicate that the model may be useful for the preclinical evaluation of and training in therapeutic approaches to heart failure.
Heart function and molecular biological parameters are comparable in young adult and aged rats after chronic myocardial infarction