Small-size Microparticles as Indicators of Acute Decompensated State in Ischemic Heart Failure.

INTRODUCTION AND OBJECTIVES Microparticles are markers for cell activation and apoptosis and could provide valuable information that is not available from clinical data. This study assesses the clinical and biological relationship of small-sized microparticles in different forms of ischemic systolic heart failure and their relation to markers of inflammation and repair. METHODS We compared 49 patients with acute heart failure, 39 with stable heart failure and 25 patients with stable coronary artery disease. Small-size microparticles counts were determined by high-resolution flow cytometry. Moreover, 3 different monocyte subpopulations and their expression of inflammatory and adhesive scavenger receptors were analyzed using a conventional flow cytometer. RESULTS Endothelial CD144+ microparticle counts were decreased in heart failure groups (P=.008). Annexin V-binding microparticle counts were found increased in heart failure (P=.024) and in patients with lower functional class (P=.013). Platelet CD42b+ microparticle counts positively correlated with left ventricular ejection fraction (P=.006), and annexin V-binding microparticle counts with interleukin-6 levels in stable heart failure (P=.034). Annexin V-binding microparticle counts in the acute status strongly correlated with toll-like receptor-4 expression on all monocyte subsets (all P<.01). Three months after admission with acute heart failure, annexin V-binding microparticle counts were positively correlated with receptors for interleukin-6, CD163 and CD204 (all P<.05). CONCLUSIONS Annexin V-binding microparticle counts constitute valuable hallmarks of acute decompensated state in systolic heart failure. The observed relationship between small-size annexin V-binding microparticles and scavenger receptors supports their involvement in the progression of the acute response to injury, and thus their contribution to the pathogenesis of acute decompensated heart failure.