Monocytes play important roles in inflammation, angiogenesis and tissue repair and may contribute to the pathophysiology of heart failure (HF).

We examined differences in monocyte subset numbers and expression of cell surface markers of activation (CD14) and chemotaxis (CCR2) in patients with acute HF (AHF), stable HF (SHF), and controls and evaluated their impact on clinical outcomes.

Three monocyte subsets [CD14++CD16−CCR2+ (Mon1), CD14++CD16+CCR2+ (Mon2) and CD14+CD16++CCR2− (Mon3)] were analysed by flow cytometry in 51 patients with AHF, 42 patients with SHF, 44 patients with stable coronary artery disease and without HF (CAD) and 40 healthy controls (HC). The prognostic impact of monocyte subsets was examined in AHF.

Patients with AHF had significantly higher Mon1 counts compared to the three control groups (P < 0·001 for all). Similarly, Mon2 levels were increased in AHF compared to SHF (P = 0·004) and CAD (P < 0·001) and increased in SHF vs. CAD (P = 0·009). There were no differences in Mon3 counts between the groups. Twenty patients (39·2%) with AHF reached the primary end‐point of death or re‐hospitalisation, and after adjustment for confounders, Mon2 count remained negatively associated with a combined end‐point of death and re‐hospitalisation [hazard ratio (per 10 cells/μL): 0·79; confidence interval: 0·66–0·94; P = 0·009].

Mon2 counts are increased in patients with both acute and stable HF, with enhanced expression of surface markers of activation (CD14) and chemotaxis (CCR2). This subset was also associated with an adverse prognosis in patients with AHF.