Acute hyperglycemia causes microvascular damage, leading to poor functional recovery and remodeling in patients with reperfused ST-segment elevation myocardial infarction.

BACKGROUND: Although acute hyperglycemia (AHG) is associated with poor outcomes in ST-segment elevation myocardial infarction (STEMI) patients, underlying mechanisms have not been fully elucidated. We investigated the influence of AHG on myocardial microcirculation in reperfused STEMI patients. METHODS AND RESULTS: Thirty-four STEMI patients were divided into 2 groups according to the presence (Group H, n 5 11) or the absence (Group L, n 5 23) of AHG. Myocardial blood flow (MBF) and myocardial flow reserve (MFR) in the infarct-related area were compared between 2 groups, using ¹³N-ammonia positron emission tomography. Wall motion abnormality scores (WMASs) and end-diastolic volume indices (EDVI) were also assessed at 1 and 6 months after the onset. Although resting MBF was similar, MFR was lower in Group H than in Group L (1.69 ± 0.37 vs 2.39 ± 0.56, P = .001). WMAS was greater in Group H than in Group L at both 1 month (7.4 ± 3.7 vs 3.7 ± 3.0, P = .011) and 6 months (7.3 ± 3.9 vs 3.1 ± 3.4, P = .015). EDVI tended to be greater in Group H than in Group L at 6 months (103.8 ± 42.9 vs 73.9 ± 16.0 mL/m2, P = .071). Multivariate analysis showed AHG to be independently associated with low MFR. CONCLUSIONS: In STEMI patients, AHG impaired myocardial microcirculation, leading to poor functional recovery and remodeling despite successful reperfusion.

Relationship between impaired microvascular function in the non-infarct-related area and left-ventricular remodeling in patients with myocardial infarction.

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.