TY - JOUR
T1 - TH‐C‐L100J‐06
T2 - Monitoring Myocardial Infarction Induced Calcium Homeostasis Alteration by MRI in a Small Murine Model
AU - hu, T.
AU - Waghorn, B.
AU - Edwards, T.
AU - Yanasak, Nathan Eugene
AU - Allison, Jerry David
PY - 2007/1/1
Y1 - 2007/1/1
N2 - Purpose: Alterations in myocyte calcium regulation for both the mechanical dysfunction and the arrhythmogenesis associated with congestive heart failure. In spite of the established importance calcium regulation in the heart both prior to, and following, myocardial injury, monitoring strategies to assess calcium homeostasis in affected cardiac tissues are extremely limited. We propose to characterize the dynamic and temporal features of calcium responses due to myocardial injury in a small murine model using [formula omitted] as a contrast agent. Method and Materials: There are 3 groups of mice (6–10 weeks) namely control, sham‐operated, and myocardial infarction (MI). In the MI studies, permanent myocardial infarcts were produced by ligating the left anterior descending coronary artery. Images were acquired on a horizontal 7.0 T Bruker BioSpec MRI spectrometer equipped with a micro imaging gradient. A series of short‐axis T1‐weighted cardiac images were acquired as well as pre‐[formula omitted] and post‐[formula omitted] infusion T1 maps using an ECG‐gated, flow‐compensated Lock‐Locker MRI pulse sequence. Results: ECG gated cardiac MRI provided high quality images for left‐ventricle, and the infusion of [formula omitted] clearly showed a large change in T1 values. The left‐ventricular post‐[formula omitted] relaxivity, ΔR1 (=1/ΔT1), thus far for control, sham‐operated, and MI groups are 3.54±0.94, 2.63±1.37, and 1.91 sec−1, respectively. The post‐MI group showed potentially lower ΔR1 values. Increased sample size for each animal group is warranted. Further investigation is necessary to determine if [formula omitted] could provide insights into the temporal myocardial remodeling process where [formula omitted] influx might be altered. Conclusion: One motivation for this study is that myocardial injury causes physiological remodeling leading to potential [formula omitted] handling alteration. This process can be potentially monitored with a cardiac manganese‐enhanced T1 mapping technique. Furthermore, changes in ΔR1 could potentially be calibrated to the absolute manganese content for left‐ventricular myocardium.
AB - Purpose: Alterations in myocyte calcium regulation for both the mechanical dysfunction and the arrhythmogenesis associated with congestive heart failure. In spite of the established importance calcium regulation in the heart both prior to, and following, myocardial injury, monitoring strategies to assess calcium homeostasis in affected cardiac tissues are extremely limited. We propose to characterize the dynamic and temporal features of calcium responses due to myocardial injury in a small murine model using [formula omitted] as a contrast agent. Method and Materials: There are 3 groups of mice (6–10 weeks) namely control, sham‐operated, and myocardial infarction (MI). In the MI studies, permanent myocardial infarcts were produced by ligating the left anterior descending coronary artery. Images were acquired on a horizontal 7.0 T Bruker BioSpec MRI spectrometer equipped with a micro imaging gradient. A series of short‐axis T1‐weighted cardiac images were acquired as well as pre‐[formula omitted] and post‐[formula omitted] infusion T1 maps using an ECG‐gated, flow‐compensated Lock‐Locker MRI pulse sequence. Results: ECG gated cardiac MRI provided high quality images for left‐ventricle, and the infusion of [formula omitted] clearly showed a large change in T1 values. The left‐ventricular post‐[formula omitted] relaxivity, ΔR1 (=1/ΔT1), thus far for control, sham‐operated, and MI groups are 3.54±0.94, 2.63±1.37, and 1.91 sec−1, respectively. The post‐MI group showed potentially lower ΔR1 values. Increased sample size for each animal group is warranted. Further investigation is necessary to determine if [formula omitted] could provide insights into the temporal myocardial remodeling process where [formula omitted] influx might be altered. Conclusion: One motivation for this study is that myocardial injury causes physiological remodeling leading to potential [formula omitted] handling alteration. This process can be potentially monitored with a cardiac manganese‐enhanced T1 mapping technique. Furthermore, changes in ΔR1 could potentially be calibrated to the absolute manganese content for left‐ventricular myocardium.
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U2 - 10.1118/1.2761644
DO - 10.1118/1.2761644
M3 - Article
AN - SCOPUS:85024811055
SN - 0094-2405
VL - 34
JO - Medical Physics
JF - Medical Physics
IS - 6
ER -