Monocyte subpopulation counts and functional characteristics predict adverse clinical events post ST elevation myocardial infarction

A.A. Ghattas, G.Y.H. Lip, H. Griffiths, E. Shantsila

Research output: Contribution to journalMeeting abstract

Abstract

Background: Monocytes are implicated in the initiation of the atherosclerotic plaque through to plaque instability and rupture during presentation with an acute coronary syndrome (ACS). Little is known about the predictive role of monocytes on clinical outcome. We studied the role of the three phenotypically and functionally discrete monocyte subpopulations in predicting major adverse cardiac events (MACE)—defined as recurrent ACS, heart failure and death- following ST elevation myocardial infarction (STEMI).
Method: STEMI patients treated with percutaneous revascularisation, were recruited in the first 24 h post-infarction. Peripheral blood monocyte subpopulations were enumerated and characterised using flow cytometry after staining for CD14, CD16 and CCR2. Phenotypically, monocyte subpopulations are defined as: CD14++CD16−CCR2+ (Mon1), CD14++CD16+CCR+ (Mon2) and CD14+CD16++CCR2− (Mon3) cells. Functionally, monocyte subpopulation activation of nuclear factor κ B (NFκB) was analysed. Activation of NFκB was determined by flow cytometry as the mean fluorescent intensity (MFI) of intracellular κ-B kinase β (IKKβ), as a downstream activation product of the NFkB pathway. MACE events were recorded at follow-up.
Results: We recruited 96 patients (average age 61.5 years±13.3; 64.6% male). Patients were followed-up for a median of 187 days (112–222 days). MACE events occurred in 14 patients (14.6%). Using logistic regression analysis, increased total monocyte count (p<0.032), Mon2 counts (p<0.047) and Mon3 IKKβ (p<0.013) were significantly predictive of MACE at follow-up (Abstract 125 table 1). Mon2 counts were an independent predictor of MACE after adjusting for age and sex
Original languageEnglish
Article number125
Pages (from-to)A70-A71
Number of pages2
JournalHeart
Volume98
Issue numberSuppl.1
DOIs
Publication statusPublished - May 2012
EventBritish Cardiovascular Society Annual Conference - Manchester Central, Manchester, United Kingdom
Duration: 28 May 201230 May 2012

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Monocytes
Acute Coronary Syndrome
Flow Cytometry
Atherosclerotic Plaques
ST Elevation Myocardial Infarction
Infarction
Rupture
Phosphotransferases
Heart Failure
Logistic Models
Regression Analysis
Staining and Labeling

Cite this

Ghattas, A.A. ; Lip, G.Y.H. ; Griffiths, H. ; Shantsila, E. / Monocyte subpopulation counts and functional characteristics predict adverse clinical events post ST elevation myocardial infarction. In: Heart. 2012 ; Vol. 98, No. Suppl.1. pp. A70-A71.
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abstract = "Background: Monocytes are implicated in the initiation of the atherosclerotic plaque through to plaque instability and rupture during presentation with an acute coronary syndrome (ACS). Little is known about the predictive role of monocytes on clinical outcome. We studied the role of the three phenotypically and functionally discrete monocyte subpopulations in predicting major adverse cardiac events (MACE)—defined as recurrent ACS, heart failure and death- following ST elevation myocardial infarction (STEMI).Method: STEMI patients treated with percutaneous revascularisation, were recruited in the first 24 h post-infarction. Peripheral blood monocyte subpopulations were enumerated and characterised using flow cytometry after staining for CD14, CD16 and CCR2. Phenotypically, monocyte subpopulations are defined as: CD14++CD16−CCR2+ (Mon1), CD14++CD16+CCR+ (Mon2) and CD14+CD16++CCR2− (Mon3) cells. Functionally, monocyte subpopulation activation of nuclear factor κ B (NFκB) was analysed. Activation of NFκB was determined by flow cytometry as the mean fluorescent intensity (MFI) of intracellular κ-B kinase β (IKKβ), as a downstream activation product of the NFkB pathway. MACE events were recorded at follow-up.Results: We recruited 96 patients (average age 61.5 years±13.3; 64.6{\%} male). Patients were followed-up for a median of 187 days (112–222 days). MACE events occurred in 14 patients (14.6{\%}). Using logistic regression analysis, increased total monocyte count (p<0.032), Mon2 counts (p<0.047) and Mon3 IKKβ (p<0.013) were significantly predictive of MACE at follow-up (Abstract 125 table 1). Mon2 counts were an independent predictor of MACE after adjusting for age and sex",
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Monocyte subpopulation counts and functional characteristics predict adverse clinical events post ST elevation myocardial infarction. / Ghattas, A.A.; Lip, G.Y.H.; Griffiths, H.; Shantsila, E.

In: Heart, Vol. 98, No. Suppl.1, 125, 05.2012, p. A70-A71.

Research output: Contribution to journalMeeting abstract

TY - JOUR

T1 - Monocyte subpopulation counts and functional characteristics predict adverse clinical events post ST elevation myocardial infarction

AU - Ghattas, A.A.

AU - Lip, G.Y.H.

AU - Griffiths, H.

AU - Shantsila, E.

PY - 2012/5

Y1 - 2012/5

N2 - Background: Monocytes are implicated in the initiation of the atherosclerotic plaque through to plaque instability and rupture during presentation with an acute coronary syndrome (ACS). Little is known about the predictive role of monocytes on clinical outcome. We studied the role of the three phenotypically and functionally discrete monocyte subpopulations in predicting major adverse cardiac events (MACE)—defined as recurrent ACS, heart failure and death- following ST elevation myocardial infarction (STEMI).Method: STEMI patients treated with percutaneous revascularisation, were recruited in the first 24 h post-infarction. Peripheral blood monocyte subpopulations were enumerated and characterised using flow cytometry after staining for CD14, CD16 and CCR2. Phenotypically, monocyte subpopulations are defined as: CD14++CD16−CCR2+ (Mon1), CD14++CD16+CCR+ (Mon2) and CD14+CD16++CCR2− (Mon3) cells. Functionally, monocyte subpopulation activation of nuclear factor κ B (NFκB) was analysed. Activation of NFκB was determined by flow cytometry as the mean fluorescent intensity (MFI) of intracellular κ-B kinase β (IKKβ), as a downstream activation product of the NFkB pathway. MACE events were recorded at follow-up.Results: We recruited 96 patients (average age 61.5 years±13.3; 64.6% male). Patients were followed-up for a median of 187 days (112–222 days). MACE events occurred in 14 patients (14.6%). Using logistic regression analysis, increased total monocyte count (p<0.032), Mon2 counts (p<0.047) and Mon3 IKKβ (p<0.013) were significantly predictive of MACE at follow-up (Abstract 125 table 1). Mon2 counts were an independent predictor of MACE after adjusting for age and sex

AB - Background: Monocytes are implicated in the initiation of the atherosclerotic plaque through to plaque instability and rupture during presentation with an acute coronary syndrome (ACS). Little is known about the predictive role of monocytes on clinical outcome. We studied the role of the three phenotypically and functionally discrete monocyte subpopulations in predicting major adverse cardiac events (MACE)—defined as recurrent ACS, heart failure and death- following ST elevation myocardial infarction (STEMI).Method: STEMI patients treated with percutaneous revascularisation, were recruited in the first 24 h post-infarction. Peripheral blood monocyte subpopulations were enumerated and characterised using flow cytometry after staining for CD14, CD16 and CCR2. Phenotypically, monocyte subpopulations are defined as: CD14++CD16−CCR2+ (Mon1), CD14++CD16+CCR+ (Mon2) and CD14+CD16++CCR2− (Mon3) cells. Functionally, monocyte subpopulation activation of nuclear factor κ B (NFκB) was analysed. Activation of NFκB was determined by flow cytometry as the mean fluorescent intensity (MFI) of intracellular κ-B kinase β (IKKβ), as a downstream activation product of the NFkB pathway. MACE events were recorded at follow-up.Results: We recruited 96 patients (average age 61.5 years±13.3; 64.6% male). Patients were followed-up for a median of 187 days (112–222 days). MACE events occurred in 14 patients (14.6%). Using logistic regression analysis, increased total monocyte count (p<0.032), Mon2 counts (p<0.047) and Mon3 IKKβ (p<0.013) were significantly predictive of MACE at follow-up (Abstract 125 table 1). Mon2 counts were an independent predictor of MACE after adjusting for age and sex

UR - http://heart.bmj.com/content/98/Suppl_1/A70.2

U2 - 10.1136/heartjnl-2012-301877b.125

DO - 10.1136/heartjnl-2012-301877b.125

M3 - Meeting abstract

VL - 98

SP - A70-A71

JO - Heart

JF - Heart

SN - 1355-6037

IS - Suppl.1

M1 - 125

ER -