Abstract Body (Do not enter title and authors here): Background and Hypothesis: Early detection of acute ischemia in non-ST-elevation MI (NSTEMI+) patients is crucial for timely treatment. Traditional biomarkers like high sensitivity cardiac troponin-I level [hs-cTnI] can take hours after myocardial injury to rise in NSTEMI+ patients and potentially delay diagnosis and treatment. We hypothesized that hyper-acute native T1 mapping with cardiac MRI (CMR) can rapidly identify ongoing ischemia. We studied this in canine models of ischemia and then in patients suspected of NSTEMI+.

Methods: We performed LAD coronary artery ligation inside a CMR system to induce no-flow ischemia in a canine model (n=18) and performed repeat T1 and T2 mapping every 5 min. We also biopsied myocardial tissue at baseline and at defined time points from ischemic and remote areas. We used transmission electron microscopy (TEM) to analyze cardiac ultrastructure. Patients suspected of NSTEMI+ (n=16) underwent native cine, T1, and T2 CMR 3T.

Results: T1 values increased significantly from 1182±51ms (baseline) to 1265±56ms (5 to 10 min after onset of ischemia), p<0.05; and continue to rise through 90 min (1327±56ms), while T2 values showed no significant changes over the first 90 min. TEM showed that the mitochondrial cristae density in ischemic zones was significantly decreased: 100±9.8%(baseline) vs 54±4.4% (5 min of ischemia), p<0.01, and decline to 40.6±9.8% by 90 min. After 5 min of ischemia, both mitochondrial width and circuity index showed no difference compared to baseline, but both paraments increased significantly: (a) mitochondrial width: 990.4±118.6nm (15 min of ischemia) vs 577±61nm (baseline), p<0.01; (b) circuity index: 0.87±0.04 (15 min of ischemia) vs 0.8±0.04 (baseline), p<0.01, and continued to rise and persist at high levels at 90 min: 1091±148 nm (mitochondrial width) and 0.94±0.01 (circuity index), respectively. Cristae number was significantly reduced 13.8±2.7 (baseline) vs 24.4±2.9 (5 min of ischemia), p<0.01, and remained low and reduced to 7.6±1.8 by 90 min. ΔT1 value in patients were significantly higher in NSTEMI+ than in NSTEMI- (11.51±3.7% vs 2.06±1.7%, p<0.0001), while [hs-cTnI] levels from NSTEMI+ gradually increased over time and were only significantly higher than NSTEMI-, several hours after CMR and peaked at 24 h (12.6±7.3% (24 h) vs 0.03±0.02% (baseline), p<0.05).

Conclusions: Hyper-acute native T1 mapping has the potential to rapidly identify ongoing ischemia even in the absence of troponin-I rise.