TY - JOUR
T1 - Association between hyperglycemia and the no-reflow phenomenon in patients with acute myocardial infarction
AU - Iwakura, Katsuomi
AU - Ito, Hiroshi
AU - Ikushima, Masashi
AU - Kawano, Shigeo
AU - Okamura, Atsushi
AU - Asano, Katsuaki
AU - Kuroda, Tadashi
AU - Tanaka, Koji
AU - Masuyama, Tohru
AU - Hori, Masatsugu
AU - Fujii, Kenshi
PY - 2003/1/1
Y1 - 2003/1/1
N2 - OBJECTIVES: We investigated the association between hyperglycemia and the no-reflow phenomenon in patients with acute myocardial infarction (AMI). BACKGROUND: Hyperglycemia is associated with increased risks of heart failure, cardiogenic shock, and death after AMI, but its underlying mechanism remains unknown. METHODS: A total of 146 consecutive patients with a first AMI were studied by intracoronary myocardial contrast echocardiography (MCE) after successful reperfusion within 24 h after symptom onset. Two-dimensional echocardiography was recorded on day 1 and three months later to determine the change in the wall motion score (δWMS; sum of 16 segmental scores; dyskinesia = 4 to normokinesia = 0). RESULTS: The no-reflow phenomenon was found on MCE in 49 (33.6%) of 146 patients; their glucose level on hospital admission was significantly higher than that of patients who did not exhibit this phenomenon (209 ± 79 vs. 159 ± 56 mg/dl; p < 0.0001). There was no difference in glycosylated hemoglobin or in the incidence of diabetes mellitus between the two subsets. The no-reflow phenomenon was more often observed in the 75 patients with hyperglycemia (≥160 mg/dl) than in those without hyperglycemia (52.0% vs. 14.1%; p < 0.0001). Patients with hyperglycemia had a higher peak creatine kinase level (2,497 ± 1,603 vs. 1,804 ± 1,300 IU/l; p = 0.005) and a lower δWMS (3.7 ± 4.8 vs. 5.7 ± 4.3; p = 0.01) than did those without hyperglycemia. The blood glucose level was an independent prognostic factor for no reflow, along with age, gender, absence of pre-infarction angina, complete occlusion of the culprit lesion, and anterior AMI. CONCLUSIONS: Hyperglycemia might be associated with impaired microvascular function after AMI, resulting in a larger infarct size and worse functional recovery.
AB - OBJECTIVES: We investigated the association between hyperglycemia and the no-reflow phenomenon in patients with acute myocardial infarction (AMI). BACKGROUND: Hyperglycemia is associated with increased risks of heart failure, cardiogenic shock, and death after AMI, but its underlying mechanism remains unknown. METHODS: A total of 146 consecutive patients with a first AMI were studied by intracoronary myocardial contrast echocardiography (MCE) after successful reperfusion within 24 h after symptom onset. Two-dimensional echocardiography was recorded on day 1 and three months later to determine the change in the wall motion score (δWMS; sum of 16 segmental scores; dyskinesia = 4 to normokinesia = 0). RESULTS: The no-reflow phenomenon was found on MCE in 49 (33.6%) of 146 patients; their glucose level on hospital admission was significantly higher than that of patients who did not exhibit this phenomenon (209 ± 79 vs. 159 ± 56 mg/dl; p < 0.0001). There was no difference in glycosylated hemoglobin or in the incidence of diabetes mellitus between the two subsets. The no-reflow phenomenon was more often observed in the 75 patients with hyperglycemia (≥160 mg/dl) than in those without hyperglycemia (52.0% vs. 14.1%; p < 0.0001). Patients with hyperglycemia had a higher peak creatine kinase level (2,497 ± 1,603 vs. 1,804 ± 1,300 IU/l; p = 0.005) and a lower δWMS (3.7 ± 4.8 vs. 5.7 ± 4.3; p = 0.01) than did those without hyperglycemia. The blood glucose level was an independent prognostic factor for no reflow, along with age, gender, absence of pre-infarction angina, complete occlusion of the culprit lesion, and anterior AMI. CONCLUSIONS: Hyperglycemia might be associated with impaired microvascular function after AMI, resulting in a larger infarct size and worse functional recovery.
UR - http://www.scopus.com/inward/record.url?scp=0037221899&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0037221899&partnerID=8YFLogxK
U2 - 10.1016/S0735-1097(02)02626-8
DO - 10.1016/S0735-1097(02)02626-8
M3 - Article
C2 - 12570936
AN - SCOPUS:0037221899
VL - 41
SP - 1
EP - 7
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
SN - 0735-1097
IS - 1
ER -