Circulating Platelet–Progenitor Cell Coaggregate Formation Is Increased in Patients With Acute Coronary Syndromes and Augments Recruitment of CD34+ Cells in the Ischaemic Microcirculation
What is the effect of acute coronary syndromes (ACS) on circulating platelet-progenitor cell aggregates?
Platelet-progenitor cell aggregates, defined by the presence of the platelet-specific marker CD42b on the surface of CD34+ cells using flow cytometry, were measured in patients with stable angina (SAP) or ACS. Correlations were made with cardiac function 3 months later. Adhesive characteristics of coaggregates were also measured.
CD34+/CD42b+ cell coaggregates were increased in patients with ACS (n = 162), and especially in patients with ST-segment elevation myocardial infarction (STEMI) (n = 44), compared with patients with SAP (n = 116; p < 0.001). Platelet/CD34+ cell coaggregate formation correlated with platelet activation (p = 0.001). In patients with AMI (n = 40), patients with increased baseline platelet/CD34+ cell coaggregates presented with reduced MI size and better left ventricular function at a 3-month follow-up compared to patients with lower coaggregates (p < 0.05 for all measures). In vitro studies revealed that adhesion of platelet/CD34+ cell coaggregates onto the extracellular matrix and to endothelial monolayers was enhanced compared with CD34+ cells under high shear rates (p < 0.05) and within the microcirculation in mice after ischaemia/reperfusion injury, as assessed by intravital microscopy (p < 0.05).
These findings imply that circulating platelet/CD34+ cell coaggregate levels are increased in ACS, especially in STEMI, which may be a novel mechanism of recruiting CD34+ progenitor cells to the injured microvasculature after AMI.
Recruitment of endogenous circulating progenitor cells to myocardial injury may facilitate cardiac recovery, although the causal relationship between the increased circulating platelet/CD34+ cell coaggregates following AMI and preserved LV function still needs to be proven. If mechanisms responsible for recruitment of these cells can be elucidated and then enhanced, this may serve as a more practical approach to cell-based therapy following MI.
Keywords: Myocardial Infarction, Acute Coronary Syndrome, Extracellular Matrix, Reperfusion Injury, Biological Markers, Angina, Stable, Ventricular Function, Left, Microcirculation, Blood Platelets, Platelet Activation
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