Why the study?
The mechanisms underlying left ventricular remodelling after AMI remain obscure, and it was hypothesized that post-AMI changes in extracellular vesicle concentrations may underlie it.
Do baseline plasma concentrations of extracellular vesicles predict left ventricular remodelling at 6 months in patients with a first acute myocardial infarction?
Do baseline plasma concentrations of extracellular vesicles predict left ventricular remodelling at 6 months in patients with a first acute myocardial infarction?
Decreased baseline plasma concentrations of extracellular vesicles from endothelial cells, erythrocytes, and platelets can predict left ventricular remodelling 6 months after a first acute myocardial infarction.
EV changes post-AMI may aid LVR risk stratification; leaves open causal mechanisms and therapeutic targeting.
Background, the mechanisms underlying left ventricular remodelling (LVR) after acute myocardial infarction (AMI) remain obscure. In the course of AMI, blood cells and endothelial cells release extracellular vesicles (EVs). We hypothesized that changes in EV concentrations after AMI may underlie LVR. Methods, plasma concentrations of EVs from endothelial cells (CD146+), erythrocytes (CD235a+), leukocytes (CD45+), platelets (CD61+), activated platelets (P-selectin+), and EVs exposing phosphatidylserine after AMI were determined by flow cytometry in 55 patients with the first AMI. LVR was defined as an increase in left ventricular end-diastolic volume by 20% at 6 months after AMI, compared to baseline. Results, baseline concentrations of EVs from endothelial cells, erythrocytes and platelets were lower in patients who developed LVR (p ≤ 0.02 for all). Concentrations of EVs from endothelial cells and erythrocytes were independent LVR predictors (OR 8.2, CI 1.3–54.2 and OR 17.8, CI 2.3–138.6, respectively) in multivariate analysis. Combining the three EV subtypes allowed to predict LVR with 83% sensitivity and 87% specificity. Conclusions, decreased plasma concentrations of EVs from endothelial cells, erythrocytes and platelets predict LVR after AMI. Since EV release EVs contributes to cellular homeostasis by waste removal, decreased concentrations of EVs may indicate dysfunctional cardiac homeostasis after AMI, thus promoting LVR.
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Gąsecka et al. (2021) studied this question.
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