Stage-dependent detection of CD14+ and CD16+ cells in the human heart after myocardial infarction.

Monocytes are critically involved in cardiovascular wound healing processes. Human monocytes can be classified into two subsets based on the expression of CD14 and CD16. Here, we examined the temporal and spatial distribution of CD14⁺ and CD16⁺ cells after myocardial infarction (MI) in human heart and spleen tissue and correlated it with markers of cardiac repair. Heart samples obtained at autopsy were histologically classified into acute (AMI; n = 11), subacute (SAMI; n = 10) and old (OMI; n = 16) MI, or control myocardium (CONTR; n = 8). Histochemical analyses revealed marked fibrosis in OMI (p < 0.001 vs. CONTR). The adhesion molecule CD56 was also strongly expressed in OMI (p < 0.01 vs. CONTR) and found to correlate with fibrosis (p < 0.001). The number of capillaries was reduced in OMI (p < 0.01 vs. CONTR; p < 0.05 vs. AMI), whereas the hypoxia indicator carbonic anhydrase IX was predominantly expressed in AMI (p < 0.01 vs. OMI and CONTR) and SAMI (p < 0.05 vs. OMI and CONTR). The monocyte chemoattractrant osteopontin was also more highly expressed in hearts of SAMI patients (p < 0.01 vs. CONTR). Numbers of CD14⁺ monocytes were found to correlate with CD16⁺ cells (p < 0.05) and inversely with fibrosis (p < 0.05). Regarding a MI-associated release of monocytes from spleen reservoirs, a non-significant reduction of splenic CD14⁺ and CD16⁺ cells was detected in subjects with AMI. In conclusion, disease stage-specific alterations in CD14⁺ and CD16 cells in human heart may contribute to cardiac repair processes following MI.