Abstract

Our aim was to define the distribution of monocyte subsets in a cohort of congestive heart failure (CHF) patients, to verify whether increased severity of CHF is linked to the expansion of specific monocyte subsets, and finally to investigate the relationship between monocyte subset relative frequencies, laboratory parameters of inflammation, and monocyte ACE expression.Thirty consecutive CHF patients and 26 healthy control subjects were evaluated for peripheral blood monocyte expression of CD14, CD16 and CD143 (ACE) by flow-cytometry, and for endothelial-derived soluble CD146 levels by ELISA.CD14++CD16+frequency was significantly higher in CHF patients than in Controls (%, median value and IQ) (12.3, 8.7–14.8 vs 5.9, 4.7–6.9, p++CD16+levels. Frequencies of CD14+CD16+monocytes were significantly lower in CHF patients as compared to Controls, and negatively correlated with levels of soluble CD146 (r= −0.529; p 0.048).In conclusion, monocytic CD14++CD16+frequency and CD143 levels are increased and reflect disease status and progressive cardiac deterioration in CHF patients. The CD14+CD16+subset is depleted in CHF and is linked to endothelial damage in this group of patients.Although the question of whether differences in monocyte CD14CD16 expansion are causal or whether they represent a marker of HF progression which is potentially relevant for risk prediction remains unanswered, we believe that our data represent an important tool for exploring the role of selective inflammatory pathways in CHF progression.

Highlights

  • Congestive heart failure is a malignant condition with sharp upturn in both prevalence and incidence and with high rates of morbidity and mortality [1]

  • We report that the monocyte CD14++CD16+ subset is differently expanded in our congestive heart failure (CHF) population as compared to Control subjects; CD14++CD16+ levels increased depending on CHF disease severity and were associated with renal damage, as well as with monocyte angiotensin converting enzyme (ACE) expression, neutrophil count and with circulating levels of C-reactive protein (CRP) in our CHF patients

  • For the first time we have shown that monocyte CD14++CD16+ levels were raised and had an enhanced ACE expression in CHF patients

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Summary

Introduction

Congestive heart failure is a malignant condition with sharp upturn in both prevalence and incidence and with high rates of morbidity and mortality [1]. CHF patients represent disabled patients with chronic cardiovascular disease who use health care resources [2]. Poor prognosis suggests that important pathogenic mechanisms remain active and unmodified by current treatment regimens. Recent data suggest a role for inflammatory and immunological processes in the pathogenesis and progression of CHF [3]. Increased levels of pro-inflammatory cytokines are related to increased rates of mortality in CHF patients. Monocytes play a key role in a variety of pathophysiological process-

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