Circulating microparticles are associated with clinical severity of persistent ST-segment elevation myocardial infarction complicated with cardiogenic shock. (1st May 2018)

• Record Type: Journal Article
• Authors: Sionis, A.; Suades, R.; Sans-Roselló, J.; Sánchez-Martínez, M.; Crespo, J.; Padró, T.; Cubedo, J.; Ferrero-Gregori, A.; Vila-Perales, M.; Duran-Cambra, A.; Badimon, L.
• Is Part Of: International journal of cardiology. Volume 258(2018)
• Page Start: 249
• Page End: 256
• Publication Date: 2018-05-01
• Subjects: Biomarkers -- Cardiogenic shock -- Circulating microparticles -- Myocardial infarction -- Prognosis; Cardiology -- Periodicals; Electronic journals; 616.12
• DOI: 10.1016/j.ijcard.2017.10.044
• Languages: English
• ISSNs: 0167-5273

Abstract

Abstract: Background: Cardiogenic shock (CS) is the leading cause of death in patients admitted for acute myocardial infarction (MI). Despite the recent advances in reperfusion and medical treatment mortality remains unacceptably high. Whether cells of the blood compartment in CS-patients are activated and release microparticles (cMPs) that may be both messengers and biomarkers of cell damage is not known. We aimed to investigate the cMP subtypes and parental activated cells of ST-elevation MI (STEMI)-patients complicated by CS and that of non-CS STEMI-patients (non-CS) in order to identify a cMP signature that could aid CS patient's risk stratification. Methods: Clinically-characterized STEMI-patients with and without CS (36/group) were included. Treatment was delivered according to guidelines and included primary percutaneous coronary intervention. cMPs were characterized by triple-labeling flow cytometry using Annexin V and cell surface-specific monoclonal antibodies. Results: Increased levels of leukocyte-derived (neutrophil and granulocyte origin) and platelet-derived cMPs were detected in CS compared to non-CS patients. A signature of cMPs derived from platelets, leukocytes, and endothelium discriminated CS-patients (AUC of 0.743 ± 0.059 [95% CI: 0.628–0.859], P < 0.0001) and predicted mortality in CS (AUC of 0.869 ± 0.06 [95% CI: 0.750–0.988], P < 0.0001). In CS-patients, a higher number of platelet- and monocyte-cMPs and of tissue factor-rich cMPs associated to worse myocardial blush grade and thrombolysis in myocardial infarction flow. Conclusions: cMPs derived from proinflammatory and prothrombotic cells were found to be elevated in CS-patients. In treated as per guidelines CS patients, granulocytes and neutrophils remained activated and actively shed cMPs. These cMPs were biomarkers of adverse prognosis in CS. Translational aspect: Increased levels of leukocyte and platelet-derived circulating microparticles (cMPs) are found in cardiogenic shock (CS) patients as compared to non-CS patients. In CS-patients, a higher number of platelet- and monocyte-cMPs and a higher number of tissue factor-rich cMPs were associated to worse myocardial reperfusion. A specific prothrombotic and proinflammatory cMPs signature in cardiogenic shock (CS) patients is a potential discriminator and survival prognostic biomarker for CS, which could aid management and improve clinical outcomes. Graphical abstract: Schematic illustration of main changes of shed MPs from activated cells in CS. Increased levels of leukocyte-derived (of neutrophil and granulocyte origin) and platelet-derived cMPs are detected in CS compared to non-CS patients while neither monocyte- and lymphocyte-derived MPs nor erythrocyte-derived MPs show significant changes. Highlights: Cardiogenic shock (CS) patients show changes in microparticle (MP) signature. Leukocyte and platelet-derived MPs increase in CS as compared to non-CS patients. A MP signature discriminates CS from non-CS and predicts mortality in CS patients. The CS-MP profile associates to worse myocardial reperfusion index in CS patients.