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Association between hyperglycemia and the no-reflow phenomenon in patients with acute myocardial infarction
Katsuomi Iwakura1, Hiroshi Ito, Masashi Ikushima
1Division of Cardiology, Sakurabashi Watanabe Hospital, Osaka University, Osaka, Japan.
Insights
Hyperglycemia in acute myocardial infarction (AMI) patients is linked to the no-reflow phenomenon, indicating impaired microvascular function. This suggests higher blood glucose levels may worsen infarct size and recovery after AMI.
Area of Science:
- Cardiology
- Metabolic Disorders
Background:
- Hyperglycemia is a known risk factor for adverse outcomes post-acute myocardial infarction (AMI).
- The specific mechanisms linking hyperglycemia to poor outcomes in AMI patients, such as the no-reflow phenomenon, remain unclear.
Purpose of the Study:
- To investigate the association between hyperglycemia and the occurrence of the no-reflow phenomenon in patients experiencing their first AMI.
- To explore the potential impact of hyperglycemia on microvascular function and infarct size following AMI.
Main Methods:
- 146 patients with a first AMI underwent intracoronary myocardial contrast echocardiography (MCE) post-reperfusion.
- Echocardiography was used to assess wall motion score changes (DeltaWMS) at day 1 and 3 months post-infarction.
- Blood glucose levels on admission were analyzed in relation to the presence of the no-reflow phenomenon.
Main Results:
- The no-reflow phenomenon was observed in 33.6% of patients.
- Patients with hyperglycemia (blood glucose ≥160 mg/dl) exhibited a significantly higher incidence of no-reflow (52.0% vs. 14.1%).
- Hyperglycemic patients had higher peak creatine kinase levels and a lower DeltaWMS, suggesting larger infarct size and poorer functional recovery.
Conclusions:
- Hyperglycemia is significantly associated with the no-reflow phenomenon in AMI patients.
- Impaired microvascular function may be a key mechanism linking hyperglycemia to worse outcomes after AMI.
- Blood glucose level is an independent prognostic factor for no-reflow post-AMI.
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 (DeltaWMS; 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 DeltaWMS (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.
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