Circulating endothelial and platelet derived microparticles reflect the size of myocardium at risk in patients with ST-elevation myocardial infarction
Highlights
► Microparticles are small membrane vesicles, released from activated, damaged and apoptotic cells. ► Endothelial (EMP) and platelet (PMP) microparticles were quantified in patients with first time ST-elevation myocardial infarction (STEMI). ► The numbers of EMP and PMP correlated to the myocardium at risk, but not to infarct size assessed by cardiac magnetic resonance.
Section snippets
Study subjects
Following written informed consent 36 consecutive patients with STEMI planned for primary percutaneous coronary intervention (PCI) were enrolled. The study complies with the Declaration of Helsinki. All patients were admitted for primary PCI due to a first time STEMI. Inclusion criteria were: chest pain ≥30 min and ≤6 h duration, ST-elevation in at least two contiguous ECG leads or left bundle branch block and a complete coronary occlusion (TIMI flow grade 0) of the infarct-related artery at the
Results
The baseline characteristics are summarized in Table 1. All patient characteristics related to the PCI procedure are presented in Table 2. Plasma levels of CD31+/CD42− EMP were 251.0 ± 178.8/μl and CD144+ 106.3 ± 33.7/μl. Platelet CD31+/CD42+ MP were 579.2 ± 631.8/μl. MaR was 31.0 ± 11.2% and IS was 11.1 ± 7.6% of the left ventricle, respectively. Details regarding the number of EMP and PMP as well as CMR data are presented in Table 3.
CD31+CD42−, CD144+ EMP and CD31+CD42+ PMP counts did not correlate to
Discussion
The present study demonstrates that circulating CD31+/CD42− EMP and CD31+/CD42+ PMP correlate to the size of MaR in patients with STEMI. This observation suggests that the number of CD31+/CD42− EMP reflect the coronary endothelial region affected by ischemia. Furthermore, it supports the view that PMP are a marker of ongoing thrombosis adding to the body of knowledge that circulating levels correlate to the extent of the ischemic and thrombotic burden.
It is well established that apoptotic or
Disclosure
None.
Acknowledgements
We thank Marita Wallin and Kerstin Höglund for their excellent technical assistance. Supported by the Swedish Heart and Lung Foundation, the Swedish Research Council (10857), Karolinska Institutet/Stockholm County Council Strategic Cardiovascular Programme, Gustav V and Queen Victoria Foundation, and the Novo Nordisk Foundation.
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