Table 3.
Included studies examining the association between the distribution of monocyte subsets and cardiovascular diseases.
| Reference | Study designa | Subjects | Outcomes | ||||||
|---|---|---|---|---|---|---|---|---|---|
| Clinical conditions | N (Male %) | Ageb | Distribution of monocyte subsetsc | Other outcomes related to monocytesd | |||||
| Unit | CM | IM | NCM | ||||||
| Atherosclerosis (AS) | |||||||||
| Chelombitko et al. (46) | CSS | Healthy AS |
15 (ND) 25 (ND) |
25 55 |
% | ↑ | ↑ | ~ | – The expression of CX3CR1 on IM and NCM was higher in patients with AS compared to healthy controls, suggesting a pre-activated state of monocytes in atherosclerosis. |
| Williams et al. (27) | CSS | Healthy AS |
33 (52) 31 (65) |
50 68 |
% | ~ | ↑ | ~ | – Patients with AS had a higher CD86/CD163 ratio, indicating a more inflammatory monocyte phenotype in atherosclerosis. – In CM, CD163 expression was positively associated with ApoA1, and CD86/CD163 ratio was negatively associated with ApoA1 and HDL cholesterol. |
| Xiang et al. (47) | CSS | Healthy Coronary AS |
112 (53) 110 (49) |
58 57 |
% | ↓ | ↑ | ~ | – The number of monocytes was higher in patients with coronary AS compared to healthy controls. |
| Coronary artery/heart disease (CAD/CHD) | |||||||||
| Czepluch et al. (48) | CSS | Healthy CAD |
18 (78) 52 (77) |
58 70 |
% | ~ | ~ | ~ | – The expression of KLF4, which involves in lowering vascular inflammation, was reduced on all monocyte subsets in patients with CAD compared to healthy controls. – KLF4 expressing monocytes were negatively correlated with plasma TNF-α. |
| Czepluch et al. (49) | CSS | Healthy CAD |
64 (72) 60 (77) |
54 70 |
% Number |
↑ ~ |
~ ~ |
↓ ↓ |
– Patients with CAD had a higher MPA proportion on all three monocyte subsets and a lower expression of CCR5 on all three monocyte subsets compared to healthy controls. |
| Jaipersad et al. (41) | CSS | Healthy CAD w/ carotid stenosis |
40 (43) 40 (60) |
67 70 |
Number | ↑ | ~ | ~ | – Patients with CAD and carotid stenosis had a higher IL6R and CXCR4 expression on CM and IM, a higher VEGF expression on IM and NCM, and a higher Tie2 expression on all three monocyte subsets compared to healthy controls, suggesting a higher surface expression of receptors implicating angiogenesis and tissue remodeling. – The number of CM significantly predicts carotid stenosis, intima-medial thickness, and grade 2 neovascularization. |
| Jaipersad et al. (41) | CSS | Healthy CAD w/o carotid stenosis |
40 (43) 40 (68) |
67 69 |
Number | ↑ | ~ | ↑ | – Patients with CAD had a higher IL6R expression on CM and IM, a higher CD49d and Tie2 expression on all three monocyte subsets compared to healthy controls. – The number of CM significantly predicts carotid stenosis, intima-medial thickness, and grade 2 neovascularization. |
| Shantsilaet al. (50) | CSS | Healthy CAD |
50 (66) 53 (72) |
61 64 |
Number | ~ | ~ | ~ | – Patients with CAD had a higher IL6R expression on CM and IM compared to healthy controls, suggesting CM and IM may be responsible for IL6R-mediated atherogenesis. – Patients with CAD had a higher expression CXCR4 on CM and NCM compared to healthy controls, suggesting CM and NCM may be mobilized to the tissues in a CXCR4-dependent manner. – Patients with CAD had a higher expression of CD34 on all three monocytes compared to healthy controls, suggesting an enhancement of the angiogenic process in response to the low-grade ischemia present in stable CAD. |
| Tallone et al. (51) | CSS | Healthy CAD |
13 (38) 14 (64) |
59 60 |
% | ↓ | ~ | ↑ | – Patients with CAD had a higher CCR2 and CX3CR1 expression on CM, suggesting an elevated adhesion and accumulation of CM to vascular endothelium. |
| Tapp et al. (52) | CSS | Healthy | 40 (80) | 60 | % | ~ | ~ | ~ | - |
| CAD | 40 (83) | 60 | Number | ~ | ~ | ~ | |||
| Zhou et al. (53) | CSS | Healthy | 35 (69) | 59 | Number | ~ | ~ | ~ | - |
| CHD | 60 (68) | 61 | |||||||
| Chronic/acute heart failure (CHF/AHF) | |||||||||
| Amir et al. (54) | CSS | Healthy CHF |
29 (52) 59 (76) |
60 58 |
% | ↓ | ~ | ↑ | – Patients with CHF had a higher intracellular IL-13 concentration in IM compared to healthy controls and the percentage of IM was positively correlated with serum IL-13, suggesting that IL-13 and IM may play a role in the process in heart failure. |
| Van Craenenbroeck et al. (55) | CSS | Healthy CHF |
15 (60) 20 (65) |
44 51 |
% Number |
~ ↑ |
~ ~ |
~ ↑ |
- |
| Goonewardena et al. (56) | CSS | Healthy AHF at admission |
11 (73) 19 (79) |
60 56 |
% Number |
↓ ↑ |
↑ ↑ |
↑ ↑ |
– The number of monocytes was higher in patients with AHF compared to healthy controls. |
| Acute myocardial infarction (AMI)/Acute coronary syndrome (ACS) | |||||||||
| Kazimierczyk et al. (57) | CSS | Healthy | 18 (78) | 57 | % | ↓ | ~ | ~ | - |
| AMI at admission (before pPCI, median time of 4 h after onset) | 18 (78) | 65 | |||||||
| Tapp et al. (52) | CSS | Healthy | 40 (80) | 60 | % | ~ | ↑ | ↑ | - |
| AMI at admission (after pPCI, first 24 h) | 50 (86) | 58 | Number | ↑ | ↑ | ~ | |||
| Zhou et al. (53) | CSS | Healthy AMI at admission (after pPCI, first 24 h) |
35 (69) 100 (78) |
59 60 |
Number | ↑ | ↑ | ~ | – Patients with AMI had a higher MPA proportion in CM and IM compared to healthy controls. |
| Zhu et al. (58) | CSS | Healthy ACS (unstable angina + AMI) |
27 (81) 68 (79) |
63 66 |
% Number |
↑ ↑ |
↓ ~ |
~ ↑ |
– Patients with ACS had a higher percentage and number of monocytes compared to healthy controls. – The number of CM was positively correlated with serum concentrations of lactate dehydrogenase, creatine kinase, myoglobin, suggesting that CM may play a proinflammatory role in the acute onset of ACS. – The percentage of IM was negatively correlated with serum myoglobin levels, which is a myocardial injury marker. – The number of NCM was positively correlated with the serum levels of lactate dehydrogenase, creatine kinase, myoglobin. |
a
Study design: CSS; cross-sectional study.
b
Age: is presented as in the original article (mean or median).
c
Distribution of monocyte subsets: Unit number, the absolute counts of monocyte subsets (cells/μl); Unit %, the percent distribution of monocyte subsets; ↑/↓ monocyte subsets in subjects with cardiovascular disease are significantly higher/lower compared to healthy control.
d
Other outcomes related to monocytes: Outcomes with significant difference are presented.
ApoA1, apolipoprotein A1; CCR, C-C Motif Chemokine Receptor; CM, classical monocytes; CXCR4, C-X-C chemokine receptor type 4; CX3CR1, CX3C chemokine receptor 1; HDL, high-density lipoprotein; IL, interleukin; IL6R, interleukin 6 receptor; IM, intermediate monocytes; KLF, Krüppel-like factor 4; MPA, monocyte-platelet aggregate; NCM, non-classical monocytes; ND, No data; pPCI, primary percutaneous coronary intervention; Tie, TEK receptor tyrosine kinase; TLR, Toll-like receptor; TNF, Tumor Necrosis Factor; VEGF, Vascular endothelial growth factor.