PMID- 26890234
OWN - NLM
STAT- MEDLINE
DCOM- 20170216
LR  - 20181202
IS  - 1875-8622 (Electronic)
IS  - 1386-0291 (Linking)
VI  - 64
IP  - 1
DP  - 2016 Nov 4
TI  - Intracoronary platelet and monocyte activation status within platelet-monocyte 
      complexes are determinants of inflammation in ST elevation myocardial 
      infarction1.
PG  - 35-46
AB  - INTRODUCTION: Platelet Monocyte Complexes (PMCs) are commonly expressed in 
      coronary artery disease but their pathologic significance in ST elevation 
      myocardial infarction (STEMI) is unclear. This study evaluates the relationship 
      between locally activated PMCs and intracoronary inflammation in stable and 
      unstable coronary disease. MATERIAL AND METHODS: Micro catheter aspirated blood 
      samples of 15 STEMI and 7 stable angina patients are collected from the coronary 
      artery (CA), aorta (AO) and right atrium (RA). Samples are labelled with 
      monoclonal antibodies and prepared for flow cytometry. CD 14 and CD 61 double 
      positive cells are identified as PMC. P-selectin expression is identified by 
      additional CD62P positivity and TF expression by additional CD142 positivity. 
      Plasma TNF-alpha and IL-6 are measured using ELISA and CRP is measured in plasma 
      using a high sensitivity automated microparticle enhanced latex turbidimetric 
      immunoassay. RESULTS: No site-specific difference is seen in overall PMC 
      expression in STEMI or stable angina. Surface P-selectin expression in STEMI 
      [median (IQR)] is significantly higher in CA [35.01 (23.15-56.99)] compared with 
      AO [15.99 (10.3-18.85)] or RA [14.02 (10.42-26.08)] (p = 0.003). Intracoronary 
      PMC correlates significantly with intracoronary TNF-alpha (r = 0.87, p = 0.001) 
      and intracoronary IL-6 (r = 0.76, p = 0.03). Bound monocytes within P-selectin 
      positive and tissue factor positive complexes correlate positively with 
      intracoronary TNF-alpha (r = 0.81, p = 0.008 & r = 0.80, p = 0.009 respectively) 
      and IL-6 (r = 0.54, p = 0.16 & r = 0.71, p = 0.05 respectively). No such 
      correlation is observed in the peripheral circulation of STEMI and stable angina 
      patients. CONCLUSION: Inflammation is not attributable to PMC formation per se. 
      However, increased intracoronary P-selectin expression by activated platelets and 
      tissue factor expression by activated monocytes within the complexes are 
      determinants of local intracoronary inflammatory burden in STEMI.
FAU - Majumder, B
AU  - Majumder B
AD  - Department of Cardiology, Royal Free Hospital, London, UK.
FAU - Koganti, S
AU  - Koganti S
AD  - Department of Cardiology, Royal Free Hospital, London, UK.
FAU - Lowdell, M W
AU  - Lowdell MW
AD  - Department of Haematology, Royal Free Hospital, London, UK.
FAU - Rakhit, R D
AU  - Rakhit RD
AD  - Department of Cardiology, Royal Free Hospital, London, UK.
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - Clin Hemorheol Microcirc
JT  - Clinical hemorheology and microcirculation
JID - 9709206
SB  - IM
MH  - Aged
MH  - Blood Platelets/*metabolism
MH  - Female
MH  - Humans
MH  - Inflammation/*blood
MH  - Male
MH  - Middle Aged
MH  - Monocytes/*metabolism
MH  - Myocardial Infarction/*blood
MH  - Myocardium/pathology
OTO - NOTNLM
OT  - Platelet monocyte complex
OT  - ST elevation myocardial infarction
OT  - intracoronary inflammation
OT  - platelet and monocyte activation status
EDAT- 2016/02/19 06:00
MHDA- 2017/02/17 06:00
CRDT- 2016/02/19 06:00
PHST- 2016/02/19 06:00 [pubmed]
PHST- 2017/02/17 06:00 [medline]
PHST- 2016/02/19 06:00 [entrez]
AID - CH2040 [pii]
AID - 10.3233/CH-162040 [doi]
PST - ppublish
SO  - Clin Hemorheol Microcirc. 2016 Nov 4;64(1):35-46. doi: 10.3233/CH-162040.