Oral Abstract Session
SCMR 22nd Annual Scientific Sessions
Shiro Nakamori, MD
Research fellow
Beth Israel Deaconess Medical Center
Ahmed Fahmy, PhD, MSc
Research Fellow
Beth Israel Deaconess Medical Center and Harvard Medical School
Jihye Jang, MSc
Research Fellow
Beth Israel Deaconess Medical Center and Harvard Medical School
Hossam El-Rewaidy, MSc, BSc
Research Assistant
Beth Israel Deaconess Medical Center
Ulf Neisius, MD, PhD
Research Fellow
Beth Israel Deaconess Medical Center and Harvard Medical School
Sophie Berg, RN
Nurse
Beth Israel Deaconess Medical Center
Beth Goddu, MRT
CMR Technologist
Beth Israel Deaconess Medical Center
Patrick Pierce, MRT
CMR Technologist
Beth Israel Deaconess Medical Center
Jennifer Rodriguez, BA
Clinical Research Coordinator
Beth Israel Deaconess Medical Center and Harvard Medical School
Thomas Hauser, MD
Assistant professor
Beth Israel Deaconess Medical Center, Harvard Medical School
Long Ngo, PhD
Associate professor
Beth Israel Deaconess Medical Center
Warren Manning, MD
Professor
Beth Israel Deaconess Medical Center
Reza Nezafat, PhD
Associate Professor of Medicine
Department of Medicine (Cardiovascular Division) Beth Israel Deaconess Medical Center
Background: With recent safety concerns regarding gadolinium deposition in the brain and other organs [1], there is a need for an alternative non-contrast cardiovascular magnetic resonance (CMR) based myocardial ischemia assessment. We sought to study changes in myocardial native T1 and T2 values after supine exercise stress in healthy subjects and in patients with suspected ischemia as potential imaging markers of ischemia.
Methods:
Twenty-eight healthy adult subjects and 14 coronary artery disease (CAD) patients referred for exercise stress/rest single photon emission computed tomography/myocardial perfusion imaging (SPECT/MPI) for evaluation of chest pain were prospectively enrolled. Free-breathing myocardial native T1 and T2 mapping [2,3] were performed before and after supine bicycle exercise stress using a CMR-compatible supine ergometer positioned on the MR table. Differences in T1 rest, T2 rest and T1 post-exercise, T2 post-exercise values were calculated as T1 and T2 reactivity, respectively.
Results: The mean exercise intensity was 104 watts with exercise duration of 6 to 12 minutes. After exercise, native T1 was significantly increased in healthy subjects. T1 reactivity, but not T2 reactivity, correlated with rate-pressure product as the index of myocardial blood flow during exercise (r=0.62, p<0.001). In CAD patients, T1 reactivity was associated with the severity of myocardial perfusion abnormality on SPECT/MPI (normal; 5.1 ± 2.1%, mild defect; 1.4 ± 1.3%, moderate defect; 0.70 ± 1.3%, severe defect; 0.35 ± 0.74%) and had comparable ability to SPECT/MPI at detection of significant CAD (>50% diameter stenosis on coronary angiography). The area under the receiver-operating characteristic curve was 0.80 vs. 0.72 (p=0.4). The optimum cut-off value of T1 reactivity for predicting flow-limiting stenosis was 2.5, with an area under the curve of 0.86.
Conclusion:
Free-breathing stress/rest native T1 mapping can detect physiological changes in blood volume/flow in the myocardium during exercise. Our feasibility study in patients shows the potential of this technique to assess myocardial ischemia in CAD patients without the need for gadolinium contrast or a pharmacological stress agent. Larger studies are warranted to confirm the diagnostic accuracy of exercise stress/rest native T1 mapping as an alternative to the currently common methods of non-invasively assessing myocardial perfusion.