Platelet–leucocyte aggregates (PLA) are a formation of leucocytes and platelets bound by specific receptors. They arise in the condition of sheer stress, thrombosis, immune reaction, vessel injury, and the activation of leukocytes or platelets. PLA participate in cardiovascular diseases (CVD). Increased levels of PLA were revealed in acute and chronic coronary syndromes, carotid stenosis cardiovascular risk factors. Due to accessible, available, replicable, quick, and low-cost quantifying using flow cytometry, PLA constitute an ideal biomarker for clinical practice. PLA are promising in early diagnosing and estimating prognosis in patients with acute or chronic coronary syndromes treated by percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG). PLA were also a reliable marker of platelet activity for monitoring antiplatelet therapy. PLA consist also targets potential therapies in CVD. All of the above potential clinical applications require further studies to validate methods of assay and proof clinical benefits.

(1) Background: Prostacyclin analogues (epoprostenol, treprostinil, and iloprost) induce vasodilation in pulmonary arterial hypertension (PAH) but also inhibit platelet function. (2) Objectives: We assessed platelet function in PAH patients treated with prostacyclin analogues and not receiving prostacyclin analogues. (3) Methods: Venous blood was collected from 42 patients treated with prostacyclin analogues (49.5 ± 15.9 years, 81% female) and 38 patients not receiving prostacyclin analogues (55.5 ± 15.6 years, 74% female). Platelet reactivity was analyzed by impedance aggregometry using arachidonic acid (AA; 0.5 mM), adenosine diphosphate (ADP; 6.5 µM), and thrombin receptor-activating peptide (TRAP; 32 µM) as agonists. In a subset of patients, concentrations of extracellular vesicles (EVs) from all platelets (CD61⁺), activated platelets (CD61⁺/CD62P⁺), leukocytes (CD45⁺), and endothelial cells (CD146⁺) were analyzed by flow cytometry. Platelet-rich thrombus formation was measured using a whole blood perfusion system. (4) Results: Compared to controls, PAH patients treated with prostacyclin analogues had lower platelet reactivity in response to AA and ADP (p = 0.01 for both), lower concentrations of platelet and leukocyte EVs (p ≤ 0.04), delayed thrombus formation (p ≤ 0.003), and decreased thrombus size (p = 0.008). Epoprostenol did not affect platelet reactivity but decreased the concentrations of platelet and leukocyte EVs (p ≤ 0.04). Treprostinil decreased platelet reactivity in response to AA and ADP (p ≤ 0.02) but had no effect on the concentrations of EVs. All prostacyclin analogues delayed thrombus formation and decreased thrombus size (p ≤ 0.04). (5) Conclusions: PAH patients treated with prostacyclin analogues had impaired platelet reactivity, EV release, and thrombus formation, compared to patients not receiving prostacyclin analogues.

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.

The authors would like to make the following correction to the published paper

Acetylsalicylic acid (ASA) is one of the most frequently used medications worldwide. Yet, the main indications for ASA are the atherosclerosis-based cardiovascular diseases, including coronary artery disease (CAD). Despite the increasing number of percutaneous procedures to treat CAD, coronary artery bypass grafting (CABG) remains the treatment of choice in patients with multivessel CAD and intermediate or high anatomical lesion complexity. Taking into account that CABG is a potent activator of inflammation, ASA is an important part in the postoperative therapy, not only due to ASA antiplatelet action, but also as an anti-inflammatory agent. Additional benefits of ASA after CABG include anticancerogenic, hypotensive, antiproliferative, anti-osteoporotic, and neuroprotective effects, which are especially important in patients after CABG, prone to hypertension, graft occlusion, atherosclerosis progression, and cognitive impairment. Here, we discuss the pleiotropic effects of ASA after CABG and provide insights into the mechanisms underlying the benefits of treatment with ASA, beyond platelet inhibition. Since some of ASA pleiotropic effects seem to increase the risk of bleeding, it could be considered a starting point to investigate whether the increase of the intensity of the treatment with ASA after CABG is beneficial for the CABG group of patients.