Jaime L Shaw1, Michael D Nelson2, Janet Wei2, Manish Motwani3, Sofy Landes4, Puja K Mehta4, Louise E J Thomson5, Daniel S Berman6, Debiao Li7, C Noel Bairey Merz8, Behzad Sharif9. 1. Biomedical Imaging Research Institute, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, United States; Department of Bioengineering, University of California Los Angeles, CA, United States. 2. Biomedical Imaging Research Institute, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, United States; Women's Heart Center, Cedars-Sinai Heart Institute, Los Angeles, CA, United States. 3. Department of Imaging, Cedars-Sinai Medical Center, Los Angeles, CA, United States. 4. Women's Heart Center, Cedars-Sinai Heart Institute, Los Angeles, CA, United States. 5. Women's Heart Center, Cedars-Sinai Heart Institute, Los Angeles, CA, United States; Department of Imaging, Cedars-Sinai Medical Center, Los Angeles, CA, United States. 6. Biomedical Imaging Research Institute, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, United States; Department of Imaging, Cedars-Sinai Medical Center, Los Angeles, CA, United States; David Geffen School of Medicine, University of California Los Angeles, CA, United States. 7. Biomedical Imaging Research Institute, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, United States; Department of Bioengineering, University of California Los Angeles, CA, United States; David Geffen School of Medicine, University of California Los Angeles, CA, United States. 8. Women's Heart Center, Cedars-Sinai Heart Institute, Los Angeles, CA, United States; David Geffen School of Medicine, University of California Los Angeles, CA, United States. 9. Biomedical Imaging Research Institute, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, United States; Department of Bioengineering, University of California Los Angeles, CA, United States; David Geffen School of Medicine, University of California Los Angeles, CA, United States. Electronic address: behzad.sharif@cshs.org.
Abstract
BACKGROUND: It has recently been shown that magnetic resonance (MR) "native T1" mapping is capable of characterizing abnormal microcirculation in patients with obstructive coronary artery disease (CAD). In studies involving women with signs and symptoms of ischemia and no obstructive CAD (INOCA), however, the potential role of native T1 as an imaging marker and its association with indices of diastolic function or vasodilator-induced myocardial ischemia have not been explored. We investigated whether native T1 in INOCA is associated with reduced myocardial perfusion reserve index (MPRI) or with diastolic dysfunction. METHODS: Twenty-two female patients with INOCA and twelve female reference controls with matching age and body-mass index were studied. The patients had evidence of vasodilator-induced ischemia without obstructive CAD or any prior infarction. All 34 subjects underwent stress/rest MR including native T1 mapping (MOLLI 5(3)3) at 1.5-Tesla. RESULTS: Compared with controls, patients had similar morphology/function. As expected, MPRI was significantly reduced in patients compared to controls (1.78 ± 0.39 vs. 2.49 ± 0.41, p < 0.0001). Native T1 was significantly elevated in patients (1040.1 ± 29.3 ms vs. 1003.8 ± 18.5 ms, p < 0.001) and the increased T1 showed a significant inverse correlation with MPRI (r = -0.481, p = 0.004), but was not correlated with reduced diastolic strain rate. CONCLUSIONS: Symptomatic women with INOCA have elevated native T1 compared to matched reference controls and there is a significant association between elevated native T1 and impaired MPRI, considered a surrogate measure of ischemia severity in this cohort. Future studies in a larger cohort are needed to elucidate the mechanism underlying this inverse relationship.
BACKGROUND: It has recently been shown that magnetic resonance (MR) "native T1" mapping is capable of characterizing abnormal microcirculation in patients with obstructive coronary artery disease (CAD). In studies involving women with signs and symptoms of ischemia and no obstructive CAD (INOCA), however, the potential role of native T1 as an imaging marker and its association with indices of diastolic function or vasodilator-induced myocardial ischemia have not been explored. We investigated whether native T1 in INOCA is associated with reduced myocardial perfusion reserve index (MPRI) or with diastolic dysfunction. METHODS: Twenty-two female patients with INOCA and twelve female reference controls with matching age and body-mass index were studied. The patients had evidence of vasodilator-induced ischemia without obstructive CAD or any prior infarction. All 34 subjects underwent stress/rest MR including native T1 mapping (MOLLI 5(3)3) at 1.5-Tesla. RESULTS: Compared with controls, patients had similar morphology/function. As expected, MPRI was significantly reduced in patients compared to controls (1.78 ± 0.39 vs. 2.49 ± 0.41, p < 0.0001). Native T1 was significantly elevated in patients (1040.1 ± 29.3 ms vs. 1003.8 ± 18.5 ms, p < 0.001) and the increased T1 showed a significant inverse correlation with MPRI (r = -0.481, p = 0.004), but was not correlated with reduced diastolic strain rate. CONCLUSIONS: Symptomatic women with INOCA have elevated native T1 compared to matched reference controls and there is a significant association between elevated native T1 and impaired MPRI, considered a surrogate measure of ischemia severity in this cohort. Future studies in a larger cohort are needed to elucidate the mechanism underlying this inverse relationship.
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