TH‐C‐L100J‐06

Monitoring Myocardial Infarction Induced Calcium Homeostasis Alteration by MRI in a Small Murine Model

T. hu, B. Waghorn, T. Edwards, Nathan Eugene Yanasak, Jerry David Allison

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Number of pages1
JournalMedical Physics
Volume34
Issue number6
DOIs
StatePublished - Jan 1 2007

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Homeostasis
Myocardial Infarction
Calcium
Wounds and Injuries
Manganese
Sample Size
Muscle Cells
Contrast Media
Coronary Vessels
Myocardium
Electrocardiography
Heart Failure

ASJC Scopus subject areas

  • Biophysics
  • Radiology Nuclear Medicine and imaging

Cite this

@article{482425076b354090b4e593b5072c9868,
title = "TH‐C‐L100J‐06: Monitoring Myocardial Infarction Induced Calcium Homeostasis Alteration by MRI in a Small Murine Model",
abstract = "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.",
author = "T. hu and B. Waghorn and T. Edwards and Yanasak, {Nathan Eugene} and Allison, {Jerry David}",
year = "2007",
month = "1",
day = "1",
doi = "10.1118/1.2761644",
language = "English (US)",
volume = "34",
journal = "Medical Physics",
issn = "0094-2405",
publisher = "AAPM - American Association of Physicists in Medicine",
number = "6",

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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

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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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