Key result
Intra-coronary administration of tacrolimus after acute myocardial infarction significantly reduced infarct size, suppressed innate immune responses, and preserved left ventricular ejection fraction.
Why the study?
Does intra-coronary tacrolimus reduce infarct size and improve LVEF in a mini-pig model of acute myocardial infarction?
Does intra-coronary tacrolimus reduce infarct size and improve LVEF in a mini-pig model of acute myocardial infarction?
p-value: p=<0.01
In a mini-pig model of acute myocardial infarction, intra-coronary administration of tacrolimus significantly reduced infarct size, preserved left ventricular function, and attenuated the innate immune response.
Should not change AMI practice; leaves open translation of intra-coronary tacrolimus from mini-pig models to humans.
BACKGROUND: This study investigated the association between innate immune reaction and myocardial damage after acute myocardial infarction (AMI) and anti-inflammatory role of tacrolimus in reducing infarct size. Male mini-pigs (n=18) were equally categorized into sham control (SC), untreated AMI (by ligation of left anterior descending coronary artery), and AMI-Tacrolimus (AMI-Tac) (0.5 mg intra-coronary injection 30 minutes post-AMI). Cardiac magnetic resonance imaging (MRI) was performed at post-AMI days 2, 5 and 21 before sacrificing the animals. RESULTS: By post-AMI day 21, left ventricular ejection fraction (LVEF) was lowest in untreated AMI animals, significantly higher in SC than in AMI-Tac group (all p<0.003). Infarct areas at basal, middle, and apical levels, numbers of CD14+ and iNOS+ cells in infarct area (IA) and peri-IA, and protein expression of CD14, CD68, and Ly6g from circulating inflammatory cells showed an opposite pattern compared with that of LVEF in all groups (all p<0.005). Protein expressions of MCP-1, MIP-1, TNF-α, NF-κB, iNOS, and IL-12 in IA and peri-IA exhibited an identical pattern compared to that of CD14, CD68, and Ly6g from circulating inflammatory cells (all p<0.01). Expressions of myocardial damage biomarkers in IA and peri-IA [γ-H2AX, β-myosin heavy chain (MHC), Smad3, TGF-β] were highest in AMI and higher in AMI-Tac than in SC, whereas expressions of myocardial integrity biomarkers (connexin43, mitochondrial cytochrome-C, α-MHC, BMP-2, Smad1/5) were opposite to those of damage biomarkers (all p<0.001). CONCLUSION: Innate immune responses were markedly augmented and LVEF was significantly reduced after AMI but were remarkably improved after tacrolimus treatment.
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Sheu et al. (2013) studied Acute myocardial infarction (n=18). Tacrolimus vs. Untreated AMI (physiological saline) was evaluated on Left ventricular ejection fraction (LVEF) at day 21 (p=<0.01). Intra-coronary administration of tacrolimus after acute myocardial infarction significantly reduced infarct size, suppressed innate immune responses, and preserved left ventricular ejection fraction.
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