Ashley E Morgan1, Yue Zhang2, Mehrzad Tartibi2, Samantha Goldburg3, Jiwon J Kim3, Thanh D Nguyen4, Julius Guccione5, Liang Ge5, Jonathan W Weinsaft3, Mark B Ratcliffe6. 1. East Bay Surgical Residency, University of California, San Francisco, California. 2. Surgical Service, Veterans Affairs Medical Center, San Francisco, California. 3. Department of Medicine (Cardiology), Weill Cornell Medical College, New York, New York. 4. Department of Radiology, Weill Cornell Medical College, New York, New York. 5. Department of Bioengineering, University of California, San Francisco, California; Surgical Service, Veterans Affairs Medical Center, San Francisco, California; Department of Surgery, University of California, San Francisco, California. 6. Department of Bioengineering, University of California, San Francisco, California; Surgical Service, Veterans Affairs Medical Center, San Francisco, California; Department of Surgery, University of California, San Francisco, California. Electronic address: mark.ratcliffe@va.gov.
Abstract
BACKGROUND: Therapy for moderate ischemic mitral regurgitation remains unclear. Determination of myocardial viability, a necessary prerequisite for an improvement in regional contractility, is a likely key factor in determining response to revascularization alone. Myocardial strain has been proposed as a viability measure but has not been compared with late gadolinium enhancement (LGE) cardiac magnetic resonance imaging. We hypothesized that abnormal strain overestimates nonviable left ventricular (LV) segments measured with LGE and that ischemia and mechanical tethering by adjacent transmural myocardial infarction (TMI) also decreases strain in viable segments. METHODS: Sixteen patients with mild or greater ischemic mitral regurgitation and 7 healthy volunteers underwent cardiac magnetic resonance imaging with noninvasive tags (complementary spatial modulation of magnetization [CSPAMM]), LGE, and stress perfusion. CSPAMM images were post-processed with harmonic phase and circumferential and longitudinal strains were calculated. Viability was defined as the absence of TMI on LGE (hyperenhancement >50% of wall thickness). The borderzone was defined as any segment bordering TMI. Abnormal strain thresholds (±1 to 2.5 SDs from normal mean) were compared with TMI, ischemia, and borderzone. RESULTS: 7.4% of LV segments had TMI on LGE, and more than 14.5% of LV segments were nonviable by strain thresholds (p < 0.005). In viable segments, ischemia impaired longitudinal strain (least perfused one-third of LV segments: -0.18 ± 0.08 versus most perfused: -0.22 ± 0.1, p = 0.01) and circumferential strain (-0.12 ± 0.1 versus -0.16 ± 0.08, p < 0.05). In addition, infarct proximity impaired longitudinal strain (-0.16 ± 0.11 borderzone versus -0.18 ± 0.09 remote, p = 0.05). CONCLUSIONS: Impaired LV strain overestimates nonviable myocardium compared with TMI on LGE. Ischemia and infarct proximity also decrease strain in viable segments.
BACKGROUND: Therapy for moderate ischemic mitral regurgitation remains unclear. Determination of myocardial viability, a necessary prerequisite for an improvement in regional contractility, is a likely key factor in determining response to revascularization alone. Myocardial strain has been proposed as a viability measure but has not been compared with late gadolinium enhancement (LGE) cardiac magnetic resonance imaging. We hypothesized that abnormal strain overestimates nonviable left ventricular (LV) segments measured with LGE and that ischemia and mechanical tethering by adjacent transmural myocardial infarction (TMI) also decreases strain in viable segments. METHODS: Sixteen patients with mild or greater ischemic mitral regurgitation and 7 healthy volunteers underwent cardiac magnetic resonance imaging with noninvasive tags (complementary spatial modulation of magnetization [CSPAMM]), LGE, and stress perfusion. CSPAMM images were post-processed with harmonic phase and circumferential and longitudinal strains were calculated. Viability was defined as the absence of TMI on LGE (hyperenhancement >50% of wall thickness). The borderzone was defined as any segment bordering TMI. Abnormal strain thresholds (±1 to 2.5 SDs from normal mean) were compared with TMI, ischemia, and borderzone. RESULTS: 7.4% of LV segments had TMI on LGE, and more than 14.5% of LV segments were nonviable by strain thresholds (p < 0.005). In viable segments, ischemia impaired longitudinal strain (least perfused one-third of LV segments: -0.18 ± 0.08 versus most perfused: -0.22 ± 0.1, p = 0.01) and circumferential strain (-0.12 ± 0.1 versus -0.16 ± 0.08, p < 0.05). In addition, infarct proximity impaired longitudinal strain (-0.16 ± 0.11 borderzone versus -0.18 ± 0.09 remote, p = 0.05). CONCLUSIONS: Impaired LV strain overestimates nonviable myocardium compared with TMI on LGE. Ischemia and infarct proximity also decrease strain in viable segments.
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