BACKGROUND: Myocardial flow reserve (MFR) in the non-infarct-related area (NIRA) has been reported to be impaired after the onset of myocardial infarction (MI). The aim of this study was to determine whether microvascular dysfunction in the NIRA is related to left-ventricular remodeling after MI. METHODS: We prospectively studied 17 patients who suffered their first single-vessel MI, and who underwent successful revascularization. The MFR in the NIRA was assessed quantitatively using (13)N-ammonia positron emission tomography within 2 weeks after the onset. Peak creatinine kinase and the defect score on (99m)Tc-tetrofosmin myocardial perfusion imaging were used as an index of the severity of MI. The left-ventricular end-diastolic volume index (LVEDVI) was calculated using left ventriculography at 1 month and 6 months after the onset. RESULT: Patients with severely impaired MFR (<2.09) had higher peak creatinine kinase values (6000+/-5485 IU/L vs. 2250+/-1950 IU/L, p=0.0081), defect scores (16.3+/-5.9 vs. 7.9+/-6.5, p=0.0404), and LVEDVI at 1 month (125.6+/-34.4 mL/m2 vs. 82.8+/-17.7 mL/m2, p=0.0036) than those with mildly impaired MFR (> or =2.09). Moreover, the differences of LVEDVI between 2 groups persisted over 6 months (133.3+/-43.6 mL/m2 vs. 89.5+/-17.3 mL/m2, p=0.0078). The MFR in the NIRA correlated inversely with the LVEDVI at 1 month and 6 months (r=-0.590, p=0.0127 and r=-0.729, p=0.0031, respectively). CONCLUSIONS: These data indicate that microvascular impairment in the NIRA might have contributed to left-ventricular remodeling after MI.
BACKGROUND: Myocardial flow reserve (MFR) in the non-infarct-related area (NIRA) has been reported to be impaired after the onset of myocardial infarction (MI). The aim of this study was to determine whether microvascular dysfunction in the NIRA is related to left-ventricular remodeling after MI. METHODS: We prospectively studied 17 patients who suffered their first single-vessel MI, and who underwent successful revascularization. The MFR in the NIRA was assessed quantitatively using (13)N-ammonia positron emission tomography within 2 weeks after the onset. Peak creatinine kinase and the defect score on (99m)Tc-tetrofosmin myocardial perfusion imaging were used as an index of the severity of MI. The left-ventricular end-diastolic volume index (LVEDVI) was calculated using left ventriculography at 1 month and 6 months after the onset. RESULT: Patients with severely impaired MFR (<2.09) had higher peak creatinine kinase values (6000+/-5485 IU/L vs. 2250+/-1950 IU/L, p=0.0081), defect scores (16.3+/-5.9 vs. 7.9+/-6.5, p=0.0404), and LVEDVI at 1 month (125.6+/-34.4 mL/m2 vs. 82.8+/-17.7 mL/m2, p=0.0036) than those with mildly impaired MFR (> or =2.09). Moreover, the differences of LVEDVI between 2 groups persisted over 6 months (133.3+/-43.6 mL/m2 vs. 89.5+/-17.3 mL/m2, p=0.0078). The MFR in the NIRA correlated inversely with the LVEDVI at 1 month and 6 months (r=-0.590, p=0.0127 and r=-0.729, p=0.0031, respectively). CONCLUSIONS: These data indicate that microvascular impairment in the NIRA might have contributed to left-ventricular remodeling after MI.
Authors: Anne Bethke; Limalanathan Shanmuganathan; Christian Shetelig; David Swanson; Geir Øystein Andersen; Jan Eritsland; Nils Einar Kløw; Pavel Hoffmann Journal: PLoS One Date: 2018-11-09 Impact factor: 3.240