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Effect of Thrombolysis on Circulating Microparticles in Patients with ST-Segment Elevation Myocardial Infarction
Zhe Li1, Wei Zhang1, Qun-Rang Wang2
1Department of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, China.
Insights
Microparticles (MPs) are elevated in coronary heart disease. Thrombolysis in ST-segment elevation myocardial infarction (STEMI) did not increase MP levels but altered their function, potentially contributing to ischemia-reperfusion injury.
Area of Science:
- Cardiovascular Biology
- Biochemistry
- Pathophysiology
Background:
- Circulating microparticles (MPs) are elevated in patients with coronary heart disease, including chronic coronary syndrome (CCS) and acute coronary syndrome.
- The impact of thrombolysis on MPs in ST-segment elevation myocardial infarction (STEMI) remains unclear.
Purpose of the Study:
- To investigate the effect of thrombolysis on MP levels and function in STEMI patients.
- To assess the in vitro effects of MPs from STEMI and CCS patients on endothelial function and oxidative stress.
Main Methods:
- Study included STEMI patients undergoing thrombolysis (Group T), CCS patients (Group CCS), and healthy controls.
- MPs were isolated from blood samples collected pre- and post-thrombolysis.
- Effects of MPs on nitric oxide synthase (eNOS, iNOS), nitric oxide (NO), oxygen free radicals (O2•−), and vasodilation were analyzed in vitro.
Main Results:
- MP concentrations were higher in CCS and pre-thrombolysis STEMI patients compared to controls.
- Thrombolysis did not significantly increase MP levels in STEMI patients.
- MPs from CCS and STEMI patients inhibited eNOS and NO production, while stimulating iNOS and O2•− generation, with enhanced effects post-thrombolysis.
Conclusions:
- Thrombolysis in STEMI alters MP function, potentially contributing to ischemia-reperfusion injury.
- MPs may play a role in the pathophysiology of coronary heart disease and its treatment complications.
Objective:
We demonstrated that circulating microparticles (MPs) are increased in patients with coronary heart disease (both chronic coronary syndrome (CCS) and acute coronary syndrome). Whether thrombolysis affects MPs in patients with ST-segment elevation myocardial infarction (STEMI) with or without percutaneous coronary intervention (PCI) is unknown.
Methods:
This study was divided into three groups: STEMI patients with thrombolysis (n = 18) were group T, patients with chronic coronary syndrome (n = 20) were group CCS, and healthy volunteers (n = 20) were the control group. Fasting venous blood was extracted from patients in the CCS and control groups, and venous blood was extracted from patients in the T group before (pre-T) and 2 hours after (post-T) thrombolysis. MPs from each group were obtained by centrifugation. After determining the concentration, the effects of MPs on endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) in rat myocardial tissue in vitro were detected by immunohistochemistry and western blotting. Changes in nitric oxide (NO) and oxygen free radicals (O2•-) were also detected. The effect of MPs on vasodilation in isolated rat thoracic aortae was detected.
Results:
Compared with that in the control group (2.60 ± 0.38 mg/ml), the concentration of MPs was increased in patients with CCS (3.49 ± 0.72 mg/ml) and in STEMI patients before thrombolysis (4.17 ± 0.58 mg/ml). However, thrombolysis did not further increase MP levels (post-T, 4.23 ± 1.01 mg/ml) compared with those in STEMI patients before thrombolysis. Compared with those in the control group, MPs in both CCS and STEMI patients before thrombolysis inhibited the expression of eNOS (both immunohistochemistry and western blot analysis of phosphorylation at Ser1177), NO production in the isolated myocardium and vasodilation in vitro and stimulated the expression of iNOS (immunohistochemistry and western blot analysis of phosphorylation at Thr495), and the generation of O2•- in the isolated myocardium. The effects of MPs were further enhanced by MPs from STEMI patients 2 hours after thrombolysis.
Conclusion:
Changes in MP function after thrombolysis may be one of the mechanisms leading to ischemia-reperfusion after thrombolysis.
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