Key result
STEMI patients and those developing acute heart failure during myocardial infarction had significantly higher levels of platelet- and monocyte-derived circulating microparticles compared to NSTEMI patients and those without heart failure.
Cross-Sectional (n=200)
No
Platelet- and monocyte-derived circulating microparticles carrying tissue factor remain elevated in AMI patients and correlate with infarct severity and the development of heart failure.
Answers are grounded in this paper and cite their sources.
TF+ platelet- and monocyte-derived cMPs associate with STEMI and post-AMI HF; hypothesis-generating for thrombotic burden, needs prospective validation.
OBJECTIVE: Circulating microparticles (cMPs) are phospholipid-rich vesicles released from cells when activated or injured, and contribute to the formation of intracoronary thrombi. Tissue factor (TF, CD142) is the main trigger of fibrin formation and TF-carrying cMPs are considered one of the most procoagulant cMPs. Similar types of atherosclerotic lesions may lead to different types of AMI, although the mechanisms behind are unresolved. Therefore, we aimed to investigate the phenotype of cMPs found in plasma of ACS patients and its relation to AMI severity and thrombotic burden. METHODS: In a cross-sectional study, two hundred patients aged 75±4 years were included in the study 2-8 weeks after suffering an AMI. Annexin V positive (AV+)-cMPs derived from blood and vascular cells were measured by flow cytometry. Plasma procoagulant activity (TF-PCA) was measured through a chromogenic assay. RESULTS: STEMI patients (n = 75) showed higher levels of platelet-derived cMPs [CD61+/AV+, CD31+/AV+, CD42b+/AV+ and CD31+/CD42b+/AV+, P = 0.048, 0.038, 0.009 and 0.006, respectively], compared to NSTEMI patients (n = 125). Patients who suffered a heart failure during AMI (n = 17) had increased levels of platelet (CD61+)-and monocyte (CD14+)-derived cMPs carrying TF (CD142+) (P<0.0001 and 0.004, respectively). Additionally, NYHA class III (n = 23) patients showed higher levels of CD142+/AV+, CD14+/AV+ and CD14+/CD142+/AV+ cMPs than those in class I/II (P = 0.001, 0.015 and 0.014, respectively). The levels of these cMPs positively correlated with TF-PCA (r≥0.166, P≤0.027, all). CONCLUSIONS: Platelets and monocytes remain activated in AMI patients treated as per guidelines and release cMPs that discriminate AMI severity. Therefore, TF-MPs, and platelet- and monocyte-MPs may reflect thrombotic burden in AMI patients.
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Chiva‐Blanch et al. (2017) conducted a cross-sectional in Acute myocardial infarction (AMI) (n=200). ST-elevation myocardial infarction (STEMI) and acute heart failure vs. Non-ST-elevation myocardial infarction (NSTEMI) and no acute heart failure was evaluated on Levels of platelet-derived circulating microparticles (CD31+/CD42b+/AV+) (p=0.006). STEMI patients and those developing acute heart failure during myocardial infarction had significantly higher levels of platelet- and monocyte-derived circulating microparticles compared to NSTEMI patients and those without heart failure.
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