- Poster presentation
- Open Access
Myocardial T1 responds to adenosine - normal values of stress T1 reactivity at 1.5T and 3T
© Liu et al; licensee BioMed Central Ltd. 2015
- Published: 3 February 2015
- Myocardial Perfusion Imaging
- Late Gadolinium Enhancement
- Adenosine Stress
- Myocardial Perfusion Reserve
- Normal Left Ventricular Function
Myocardial vasodilator reserve is an important surrogate marker of normal and abnormal cardiac physiology. Pharmacological vasodilator agents such as adenosine increase myocardial blood volume, which is expected to prolong the observed T1-relaxation. We explored the novel application of stress T1-mapping by assessing the response of myocardial T1 to the administration of adenosine in healthy volunteers.
Healthy volunteers without history of cardiovascular disease, not on cardiovascular medications with a normal ECG underwent CMR studies at 1.5T (n=10, 33±10 years) and 3T (n=10, 36±11 years). T1-maps were acquired using the shortened Modified Look-Locker Inversion recovery (ShMOLLI, Piechnik, JCMR 2010, 12:69) sequence at rest and under adenosine stress (140 μg/kg/min IV for at least 3 min) in 3 short-axis (basal, mid-ventricular, apical) slices. Mean T1 values were derived for whole-heart, per-slice and segmental analyses (AHA 16-segment model). Stress/rest first-pass myocardial perfusion imaging was performed in matching short-axis slices. Left ventricular function and viability were assessed by CINE and late gadolinium enhancement (LGE), respectively.
Myocardial T1 increases significantly in response to adenosine vasodilator stress in normal controls. The relative T1 change of ~6% is independent of conventional field strengths (1.5/3T) and myocardial slice or segment positioning. This is likely due to the inherent intra-scan compensation of reported known variation sources in T1-mapping. With the presumed vascular origin of the response, the stress T1 holds promise for becoming a novel biomarker for mapping regional ischaemia and for detecting significant coronary artery disease in future studies.
The research was supported by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre based at the Oxford University Hospitals NHS Trust, University of Oxford. AL is a National Institute for Healthy Research (NIHR) funded Academic Clinical Fellow, UK. SN acknowledges support from the British Heart Foundation Centre of Research Excellence, Oxford.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.