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Updated: Jan 30, 2026

A Magnetic Resonance Imaging Protocol for Stroke Onset Time Estimation in Permanent Cerebral Ischemia
Published on: September 16, 2017
Stress T1-mapping cardiovascular magnetic resonance imaging and inducible myocardial ischemia
Sebastian Bohnen1, Lennard Prüßner2, E Vettorazzi3
1General and Interventional Cardiology, University Heart Center, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, Hamburg, 20246, Germany. s.bohnen@uke.de.
Background:
Alterations in native myocardial T1 under vasodilation stress ("T1 reactivity") were recently proposed as a non-contrast cardiovascular magnetic resonance (CMR) method to detect myocardial ischemia. This study evaluated the performance of a segmental, truly non-contrast stress T1 mapping CMR approach to detect inducible ischemia.
Methods And Results:
One-hundred patients with suspected/known coronary artery disease underwent CMR at 3.0 or 1.5 T. T1 mapping was performed using the 5s(3s)3s-modified look-locker inversion-recovery (MOLLI) sequence at rest and under regadenoson stress. We defined T1 reactivity as the change in native T1 from rest to stress (1) in the 16-segment AHA model independent from perfusion images and (2) in focal regions of interest that were copied from perfusion images to T1 maps. We compared T1 reactivity between segments/regions with inducible ischemia, scar, and remote myocardium for both approaches. Segmental T1 reactivity was significantly lower in segments including inducible ischemia [- 1.15 (95% CI, - 2.16 to - 0.14)%] compared to remote segments [2.49 (95% CI, 1.87 to 3.11)%; p < 0.001]. Focal T1 reactivity was also significantly lower [- 2.65 (95% CI, - 3.84 to - 1.46)%] in regions with stress-perfusion defects compared to remote regions [4.72 (95% CI, 3.90 to 5.54)%; p < 0.001]. However, the performance of segmental T1 reactivity to depict inducible ischemia was significantly inferior compared to the focal approach (AUCs 0.68 versus 0.85; p < 0.0001).
Conclusions:
Myocardium with inducible ischemia is characterized by the absence of significant T1 reactivity, but a clinically applicable approach for truly non-contrast stress T1 mapping remains to be determined.
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