Shiro Nakamori1, Ahmed Fahmy1, Jihye Jang1, Hossam El-Rewaidy1, Ulf Neisius1, Sophie Berg1, Beth Goddu1, Patrick Pierce1, Jennifer Rodriguez1, Thomas Hauser1, Long H Ngo1, Warren J Manning2, Reza Nezafat3. 1. Department of Medicine (Cardiovascular Division), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts. 2. Department of Medicine (Cardiovascular Division), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts; Department of Radiology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts. 3. Department of Medicine (Cardiovascular Division), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts. Electronic address: rnezafat@bidmc.harvard.edu.
Abstract
OBJECTIVES: This study assessed 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. BACKGROUND: With emerging data on the long-term retention of gadolinium in the body and brain, there is a need for an alternative noncontrast cardiovascular magnetic resonance (CMR)-based myocardial ischemia assessment. METHODS: Twenty-eight healthy adult subjects and 14 patients with coronary artery disease (CAD) referred for exercise stress and/or 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 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 W, with exercise duration of 6 to 12 min. After exercise, native T1 was increased in healthy subjects (p < 0.001). T1 reactivity, but not T2 reactivity, correlated with the rate-pressure product as the index of myocardial blood flow during exercise (r = 0.62; p < 0.001). In patients with CAD, T1 reactivity was associated with the severity of myocardial perfusion abnormality on SPECT/MPI (normal: 4.9%; quartiles: 3.7% to 6.3%, mild defect: 1.2%, quartiles: 0.08% to 2.5%; moderate defect: 0.45%, quartiles: -0.35% to 1.4%; severe defect: 0.35%, quartiles: -0.44% to 0.8%) and had similar potential as SPECT/MPI to detect significant CAD (>50% diameter stenosis on coronary angiography). The area under the receiver-operating characteristic curve was 0.80 versus 0.72 (p = 0.40). The optimum cutoff value of T1 reactivity for predicting flow-limiting stenosis was 2.5%, with a sensitivity of 83% and a specificity of 92%, a negative predictive value of 96%, a positive predictive value of 71%, and an area under the curve of 0.86. CONCLUSIONS: Free-breathing stress/rest native T1 mapping, but not T2 mapping, can detect physiological changes in the myocardium during exercise. Our feasibility study in patients shows the potential of this technique as a method for detecting myocardial ischemia in patients with CAD without using a pharmacological stress agent.
OBJECTIVES: This study assessed 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. BACKGROUND: With emerging data on the long-term retention of gadolinium in the body and brain, there is a need for an alternative noncontrast cardiovascular magnetic resonance (CMR)-based myocardial ischemia assessment. METHODS: Twenty-eight healthy adult subjects and 14 patients with coronary artery disease (CAD) referred for exercise stress and/or 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 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 W, with exercise duration of 6 to 12 min. After exercise, native T1 was increased in healthy subjects (p < 0.001). T1 reactivity, but not T2 reactivity, correlated with the rate-pressure product as the index of myocardial blood flow during exercise (r = 0.62; p < 0.001). In patients with CAD, T1 reactivity was associated with the severity of myocardial perfusion abnormality on SPECT/MPI (normal: 4.9%; quartiles: 3.7% to 6.3%, mild defect: 1.2%, quartiles: 0.08% to 2.5%; moderate defect: 0.45%, quartiles: -0.35% to 1.4%; severe defect: 0.35%, quartiles: -0.44% to 0.8%) and had similar potential as SPECT/MPI to detect significant CAD (>50% diameter stenosis on coronary angiography). The area under the receiver-operating characteristic curve was 0.80 versus 0.72 (p = 0.40). The optimum cutoff value of T1 reactivity for predicting flow-limiting stenosis was 2.5%, with a sensitivity of 83% and a specificity of 92%, a negative predictive value of 96%, a positive predictive value of 71%, and an area under the curve of 0.86. CONCLUSIONS: Free-breathing stress/rest native T1 mapping, but not T2 mapping, can detect physiological changes in the myocardium during exercise. Our feasibility study in patients shows the potential of this technique as a method for detecting myocardial ischemia in patients with CAD without using a pharmacological stress agent.
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