Author + information
- Rui Xia, PhD,
- Xi Lu, MSc,
- Bing Zhang, MSc,
- Yuqing Wang, PhD,
- Jichun Liao, PhD,
- Jie Zheng, PhD and
- Fabao Gao, MD∗ ()
- ↵∗Department of Radiology, West China Hospital, Sichuan University, No. 37 Guoxuexiang, 610041 Chengdu, China
The goal of this study was to determine the effects of early reperfusion on the sizes of salvaged myocardium using cardiac magnetic resonance (CMR) imaging on a 7.0-T system (BioSpec 70/30, Bruker, Karlsruhe, Germany) in acute myocardial infarction in rats.
Two groups (nonreperfusion n = 15; reperfusion n = 12) were investigated. For reperfusion, the left anterior descending coronary artery was occluded for 30 min and released. CMR was performed for all of the rats 24 h after occlusion, and 6 of the reperfusion rats were followed at different reperfusion times (3, 6, 12, and 24 h; late gadolinium enhancement [LGE] 6 and 24 h). After the 24-h CMR scans, 14 (7 from each group) of the rats were sacrificed and the hearts were excised and incubated with 2,3,5-triphenyltetrazolium chloride (TTC, Sigma-Aldrich, St. Louis, Missouri) for identification of the infarcted areas.
For CMR scans, LGE (repetition time [TR]/echo time [TE] 5.2 ms/1.8 ms; flip angle 25°; matrix 256 × 256; field of view [FOV] 50 × 50 mm; slice thickness 1.5 mm) and simplified T2 mapping (TR/TE 1,500 ms/10, 20, 30 ms; matrix 192 × 192; FOV 50 × 50 mm; slice thickness 1.5 mm) images were acquired to measure infarcted and salvaged areas, respectively. The former was determined by the signal intensity >5 SD above the mean of remote myocardium signal intensity on LGE image, and the latter was defined as the difference in area between edema (T2 value >2 SD above the mean of remote myocardium T2 on T2 map) and infarction (Figure 1). The T2 values for the edematous areas were normalized to the T2 values of the remote tissue regions. All areas were expressed as percentages of the total left ventricle myocardial tissue.
No significant difference was observed in the infarcted areas defined by LGE and TTC staining for both reperfusion (17.7 ± 2% vs. 15.1 ± 4%; p = NS) and nonreperfusion rats (23.2 ± 3.9% vs. 22.9 ± 3.2%; p = NS). Both infarcted and edematous areas at 24 h were significantly larger in the nonreperfusion group than those in the reperfusion group (23 ± 3.7% vs. 16.3 ± 4.6%; p < 0.01 for infarction; 28 ± 5.4% vs. 21.6 ± 6.8%; p < 0.05 for edema). However, there was no significant difference in the salvaged myocardial areas between the groups (reperfusion 5.3 ± 3.2%; nonreperfusion 5.1 ± 3.1%; p = NS). The normalized T2 values were significantly higher in the nonreperfusion group than the reperfusion group (1.76 ± 0.11 vs. 1.57 ± 0.08; p < 0.001).
For the reperfusion rats monitored by multiple CMR scans, the normalized T2 values in the myocardial edematous areas were the same before 12 h (3 h 1.68 ± 0.16; 6 h 1.71 ± 0.21; 12 h 1.71 ± 0.3; p = NS) and then decreased at 24 h (1.5 ± 0.14; p < 0.05). The areas of myocardial edema decreased from 3 h (25.8 ± 7.4%) to 6 h (21.5 ± 8.9%; p < 0.05) and then stayed the same after 6 h (6 h 21.5 ± 8.9%; 12 h 21.7 ± 7.7%; 24 h 22.3 ± 8.4%; p = NS). Infarction areas at 24 h were significantly reduced, compared with those at 6 h (18.1 ± 6.1% vs. 20 ± 3.9%; p < 0.05), whereas salvaged myocardial areas increased from 6 h to 24 h (1.5 ± 1.2% vs. 4.3 ± 1.1%; p < 0.05).
Ischemia with reperfusion will induce reperfusion injuries that consequently provoke fluid overload and swelling, which result in an abrupt increase in T2 that then progressively returns to baseline within days. Without reperfusion, T2 will increase further (1). This can explain our findings that nonreperfusion was associated with higher T2 values and T2 values of early post-reperfusion (3, 6, and 12 h) have been much higher than those at 24 h.
The infarcted areas were larger in the nonreperfusion group than the reperfusion group, and infarcted areas of reperfusion heart decreased from 6 to 24 h, from which we may conclude that early reperfusion during the evolution of myocardial infarction is essential for myocardial salvage. However, there was no difference in salvaged myocardial areas between the reperfusion and nonreperfusion group in our study. This may be explained by reperfusion injuries and short delay between occlusion and reopening of the infarct-related artery (2).
In conclusion, compared with nonreperfusion ischemia, early reperfusion may not change salvaged myocardial areas, which should be used cautiously as an endpoint in clinical trials investigating the success of reperfusion strategies.
Please note: This study was supported by the Major Program of National Natural Science Foundation of China (81130027), Key Projects in the National Science & Technology Pillar Program during the Twelfth Five-year Plan Period (2012BAI23B08) and the Major State Basic Research Development of China (2011CB935800). All authors have reported that they have no relationships relevant to the contents of this paper to disclose. Drs. Xia and Zheng contributed equally to this paper.
- 2015 American College of Cardiology Foundation