Increased Formation of Monocyte-Platelet Aggregates in Ischaemic Heart Failure Wrigley et al: Monocyte-Platelet Aggregates

Background—Cross-talk between monocytes and platelets is reflected by the formation of monocyte-platelet aggregates (MPAs). It is not known whether MPAs are affected in heart failure (HF) and we examined differences in patients with acute HF (AHF), stable HF (SHF), stable coronary artery disease (CAD) without HF, and healthy controls (HC). Methods and Results—MPAs were analyzed by flow cytometry for the 3 monocyte subsets [CD14++CD16-CCR2+ (Mon1), CD14++CD16+CCR2+ (Mon2) and CD14+CD16++CCR2(Mon3)] in patients with AHF (n=51), SHF (n=42), stable CAD (n=44) and HC (n=40). Counts of total MPA and MPAs associated with Mon1 and Mon2 were significantly higher in AHF compared to SHF, CAD and HC (p<0.001 for all). The proportion of Mon1 aggregated with platelets was increased in AHF compared to SHF (p=0.033), CAD (p<0.001) and HC (p<0.001). A higher percentage of Mon3 aggregated with platelets was also seen in AHF compared to SHF (p=0.012), and HC (p<0.001) but not compared to CAD (p=0.647). MPAs associated with Mon2 were significantly lower in patients who experienced adverse clinical outcomes of death or re-hospitalization compared to those who remained free of events (p=0.03). Mon2 count remained an independent negative predictor of combined death and rehospitalization after adjustment for age, LVEF, creatinine and BNP [hazard ratio 0.58, 95% CI 0.34-0.98; p=0.043)]. Conclusions—MPA formation in patients with both acute and stable HF is increased and appears to be confined to monocytes from Mon1 and Mon2 subsets. MPAs associated with Mon2 appear to be negatively predictive of a worse prognosis in AHF.