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Updated: Mar 28, 2026

In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography
Published on: February 16, 2016
Adenosine Stress and Rest T1 Mapping Can Differentiate Between Ischemic, Infarcted, Remote, and Normal Myocardium
Alexander Liu1, Rohan S Wijesurendra1, Jane M Francis1
1Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom.
Insights
T1 mapping with cardiac magnetic resonance (CMR) can detect myocardial ischemia without gadolinium contrast. This novel technique differentiates normal, infarcted, and ischemic heart tissue using stress/rest T1 profiles.
Area of Science:
- Cardiovascular Imaging
- Medical Physics
Background:
- Accurate ischemia detection is crucial in chronic coronary artery disease (CAD) for effective treatment and improved outcomes.
- Myocardial blood volume (MBV) is a key marker of ischemia, potentially more comprehensive than myocardial blood flow.
- T1 mapping using cardiac magnetic resonance (CMR) is sensitive to changes in myocardial water content, reflecting MBV.
Purpose of the Study:
- To evaluate T1 mapping at rest and during adenosine stress for detecting ischemia without gadolinium contrast.
- To assess if T1 mapping can identify changes in myocardial blood volume in normal and diseased myocardium in CAD patients.
- To compare T1 mapping with conventional CMR methods for ischemia and infarction assessment.
Main Methods:
- Conventional CMR (cine, LGE, first-pass perfusion) and novel pre-contrast stress/rest T1 mapping were performed on 20 controls and 10 CAD patients.
- T1 mapping utilized the heart rate-independent Shortened Modified Look-Locker Inversion recovery technique.
- T1 values were analyzed in normal, infarcted, ischemic, and remote myocardium.
Main Results:
- Normal myocardium showed normal resting T1 and significant positive T1 reactivity during adenosine stress.
- Infarcted myocardium exhibited the highest resting T1 without significant reactivity.
- Ischemic myocardium had elevated resting T1 but no significant reactivity, while remote myocardium showed blunted T1 reactivity.
Conclusions:
- Stress/rest T1 mapping effectively differentiates between normal, infarcted, ischemic, and remote myocardium based on distinct T1 profiles.
- This novel T1 mapping approach shows promise for gadolinium-free ischemia detection in CAD.
- T1 mapping offers a new avenue for assessing myocardial viability and ischemia in cardiovascular magnetic resonance.
Objectives:
The aim of this study was to evaluate the potential of T1 mapping at rest and during adenosine stress as a novel method for ischemia detection without the use of gadolinium contrast.
Background:
In chronic coronary artery disease (CAD), accurate detection of ischemia is important because targeted revascularization improves clinical outcomes. Myocardial blood volume (MBV) may be a more comprehensive marker of ischemia than myocardial blood flow. T1 mapping using cardiac magnetic resonance (CMR) is highly sensitive to changes in myocardial water content, including MBV. We propose that T1 mapping at rest and during adenosine vasodilatory stress can detect MBV changes in normal and diseased myocardium in CAD.
Methods:
Twenty normal controls (10 at 1.5-T; 10 at 3.0-T) and 10 CAD patients (1.5-T) underwent conventional CMR to assess for left ventricular function (cine), infarction (late gadolinium enhancement [LGE]) and ischemia (myocardial perfusion reserve index [MPRI] on first-pass perfusion imaging during adenosine stress). These were compared to novel pre-contrast stress/rest T1 mapping using the Shortened Modified Look-Locker Inversion recovery technique, which is heart rate independent. T1 values were derived for normal myocardium in controls and for infarcted, ischemic, and remote myocardium in CAD patients.
Results:
Normal myocardium in controls (normal wall motion, MPRI, no LGE) showed normal resting T1 (954 ± 19 ms at 1.5-T; 1,189 ± 34 ms at 3.0-T) and significant positive T1 reactivity during adenosine stress compared to baseline (6.2 ± 0.5% at 1.5-T; 6.3 ± 1.1% at 3.0-T; all p < 0.0001). Infarcted myocardium showed the highest resting T1 of all tissue classes (1,442 ± 84 ms), without significant T1 reactivity (0.2 ± 1.5%). Ischemic myocardium showed elevated resting T1 compared to normal (987 ± 17 ms; p < 0.001) without significant T1 reactivity (0.2 ± 0.8%). Remote myocardium, although having comparable resting T1 to normal (955 ± 17 ms; p = 0.92), showed blunted T1 reactivity (3.9 ± 0.6%; p < 0.001).
Conclusions:
T1 mapping at rest and during adenosine stress can differentiate between normal, infarcted, ischemic, and remote myocardium with distinctive T1 profiles. Stress/rest T1 mapping holds promise for ischemia detection without the need for gadolinium contrast.
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