Hyperglycemia in STEMI patients was associated with larger coronary thrombi, increased miR33, and lower SIRT1 expression, which negatively correlated with 1-year clinical outcomes.
Observational
Does the miR33/SIRT1 pathway influence the pro-inflammatory and pro-coagulable state of coronary thrombi and 1-year outcomes in hyperglycemic STEMI patients?
The miR33/SIRT1 pathway contributes to the increased pro-inflammatory and pro-coagulable state of coronary thrombi in hyperglycemic STEMI patients, correlating with worse 1-year outcomes.
Primary percutaneous coronary intervention (PPCI) is a pivotal treatment in ST-segment elevation myocardial infarction (STEMI) patients. However, in hyperglycemic-STEMI patients, the incidence of death is still significant. Here, the involvement of sirtuin 1 (SIRT1) and miR33 on the pro-inflammatory/pro-coagulable state of the coronary thrombus was investigated. Moreover, 1-year outcomes in hyperglycemic STEMI in patients subjected to thrombus aspiration before PPCI were evaluated. Results showed that hyperglycemic thrombi displayed higher size and increased miR33, reactive oxygen species, and pro-inflammatory/pro-coagulable markers. Conversely, the hyperglycemic thrombi showed a lower endothelial SIRT1 expression. Moreover, in vitro experiments on endothelial cells showed a causal effect of SIRT1 modulation on the pro-inflammatory/pro-coagulative state via hyperglycemia-induced miR33 expression. Finally, SIRT1 expression negatively correlated with STEMI outcomes. These observations demonstrate the involvement of the miR33/SIRT1 pathway in the increased pro-inflammatory and pro-coagulable state of coronary thrombi in hyperglycemic STEMI patients.
D’Onofrio et al. (2019) conducted an observational in Hyperglycemic ST-segment elevation myocardial infarction (STEMI). Hyperglycemia was evaluated on Pro-inflammatory/pro-coagulable state of the coronary thrombus and 1-year outcomes. Hyperglycemia in STEMI patients was associated with larger coronary thrombi, increased miR33, and lower SIRT1 expression, which negatively correlated with 1-year clinical outcomes.