Background: Patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS) have varying degrees\r\nof salvageable myocardium at risk of irreversible injury. We hypothesized that a novel model of NSTE-ACS produces\r\nacute myocardial injury, measured by increased T2 cardiovascular magnetic resonance (CMR), without significant\r\nnecrosis by late gadolinium enhancement (LGE).\r\nMethods: In a canine model, partial coronary stenosis was created and electrodes placed on the epicardium.\r\nMyocardial T2, an indicator of at-risk myocardium, was measured pre- and post-tachycardic pacing.\r\nResults: Serum troponin-I (TnI) was not detectable in unoperated sham animals but averaged 1.97 �± 0.72 ng/mL\r\nin model animals. Coronary stenosis and pacing produced significantly higher T2 in the affected vs. the remote\r\nmyocardium (53.2 �± 4.9 vs. 43.6 �± 2.8 ms, p < 0.01) with no evident injury by LGE. Microscopy revealed no significant\r\nirreversible cellular injury. Relative respiration rate (RRR) of affected vs. remote myocardial tissue was significantly\r\nlower in model vs. sham animals (0.72 �± 0.07 vs. 1.04 �± 0.07, p < 0.001). Lower RRR corresponded to higher final\r\nTnI levels (R2 = 0.83, p = 0.004) and changes in CaMKIID and mitochondrial gene expression.\r\nConclusions: A large animal NSTE-ACS model with mild TnI elevation and without ST elevation, similar to the\r\nhuman syndrome, demonstrates signs of acute myocardial injury by T2-CMR without significant irreversible damage.\r\nReduced tissue respiration and associated adaptations of critical metabolic pathways correspond to increased\r\nmyocardial injury by serum biomarkers in this model. T2-CMR as a biomarker of at-risk but salvageable myocardium\r\nwarrants further consideration in preclinical and clinical studies of NSTE-ACS
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