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To assess the relationship between the levels of HCMV antibodies and the incidence of various types of CHD, we first measured the IgM and IgG levels in the latent CHD, angina pectoris, myocardial infarction, and control groups. The positive rates of HCMV-IgM in the control, latent CHD, angina pectoris, and myocardial infarction groups (Table 1) were 19.0%, 33.8%, 40.6%, and 52.9%, respectively. The positive rates in the latent CHD, angina pectoris, and myocardial infarction groups were higher than in the control group (χ2 = 4.396, P = 0.036; χ2 = 8.094, P = 0.004; χ2 = 16.338, P < 0.001) The positive rates of HCMV-IgG in the control, latent CHD, angina pectoris, and myocardial infarction groups (Table 1) were 44.3%, 62.3%, 67.2%, and 80.3%, respectively. The positive rates in the latent CHD, angina pectoris, and myocardial infarction groups were higher than in the control group (χ2 = 5.094, P = 0.024; χ2 = 7.468, P = 0.006; χ2 = 16.621, P < 0.001) with a gradually increasing trend.
Table 1. Differences in IgM (+) and IgG (+) rates between the disease and control groups
Group (count) IgM (+) IgG (+) Count % P Value Count % P Value Control (79) 15 19.0 / 35 44.3 / LCHD (77) 26* 33.8 0.036 48* 62.3 0.024 AP (64) 26* 40.6 0.004 43* 67.2 0.006 MI (51) 27* 52.9 < 0.001 41* 80.3 < 0.001 Note. The tests were carried out in 4 groups: control, LCHD (latent coronary heart disease), AP (angina pectoris), and MI (myocardial infarction). Data are presented as the mean. Statistical significance of differences between groups was evaluated using the ANOVA test. *P < 0.05 versus control. -
To compare the CD14+CD16+ monocytes in CHD patients versus controls, we assayed the cells using FACS and found that there was an increase in the ratio of mononuclear cells and the expression of CD14+CD16+ mononuclear cells in the latent CHD, angina pectoris, and myocardial infarction groups (Figure 2A). Compared to the control group, the expression of CD14+CD16+ mononuclear cells in the latent CHD, angina pectoris, and myocardial infarction groups were significantly different (t = 4.1776, P < 0.001; t = 8.9747, P < 0.001; t = 16.2291, P < 0.05) (Figure 2A). In addition, there was a significant difference in the IgM (+) and IgM (–) CD14+CD16+ mononuclear cells among the groups (P < 0.05) (Figure 2B). The TG, TC, HDL-C, LDL-C, Lp (a), hs-CRp, and Hcy levels in the myocardial infarction, angina pectoris, and control groups were also significantly different (P < 0.05) (Table 2).
Figure 2. Monocytes and subgroups in latent CHD. LCHD (latent coronary heart disease), AP (angina pectoris), MI (myocardial infarction), and control groups. *P < 0.05 between groups.
Table 2. Blood indexes of atherosclerosis (
${{ \bar {\text{x}}}}$ ± SD)Group TG (mmol/L) TC (mmol/L) HDL-C (mmol/L) LDL-C (mmol/L) Lp (a) (nmol/L) hs-CRp (mg/L) Hcy (µmol/L) Control 1.31 ± 0.47 3.70 ± 0.77 1.25 ± 0.33 1.86 ± 0.78 52.6 ± 9.34 3.78 ± 0.99 12.20 ± 2.60 LCHD 1.42 ± 0.52 3.88 ± 0.77 1.26 ± 0.45 3.11 ± 0.23 70.95 ± 8.45 5.29 ± 1.33 13.40 ± 2.60 AP 2.21 ± 0.21* 5.44 ± 0.54* 1.03 ± 0.25* 3.48 ± 0.35* 81.8 ± 8.44* 8.27 ± 1.39* 16.10 ± 3.60* MI 2.62 ± 0.32* 6.01 ± 0.80* 0.93 ± 0.24* 3.90 ± 0.49* 95.45 ± 8.12* 11.87 ± 2.95* 19.50 ± 4.40* Note. The tests were carried out in 4 groups: control, LCHD (latent coronary heart disease), AP (angina pectoris), and MI (myocardial infarction). Data are expressed as mean ± standard deviation. *P < 0.05 versus control. Triglyceride (TG), Cholesterol (TC), High- and low-density lipoprotein cholesterols (HDL-C, LDL-C), Lipoprotein A [Lp (a)], Hypersensitive C-reactive protein (hs-CRP) and Homocysteine (Hcy). -
To clarify whether HCMV infection is an independent factor leading to CHD, we tested possible predisposing factors in all patients and controls and found that the factors, smoking (P < 0.05), hypertension (P < 0.05), diabetes (P < 0.001), family history (P < 0.001), HCMV-IgM (P < 0.001), and HCMV-IgG (P < 0.001) showed significant association in the single-factor analysis (Figure 3), while age (P = 0.154) and body mass index (P = 0.140) did not (Table 3). Multivariate logistic regression analysis showed that hypertension, diabetes, family history, HCMV-IgM, and HCMV-IgG are independent factors affecting CHD.
Figure 3. Logistic regression analysis of risk factors (smoking, hypertension, diabetes, family history, HCMV-IgM, and HCMV-IgG) in CHD and control groups.
Table 3. Single-factor analysis of general clinical data (risk factors) in CHD and control groups
Risk factors Control group (n = 79) CHD group (n = 192) t P Age 56.6 ± 4.2 57.5 ± 4.9 1.43 0.154 Body mass index (kg/m2) 23.3 ± 4.9 24.2 ± 4.4 1.48 0.140 Note. Data are expressed as mean ± standard deviation. T-tests showed no significance.
doi: 10.3967/bes2020.076
Onset of Coronary Heart Disease is Associated with HCMV Infection and Increased CD14+CD16+ Monocytes in a Population of Weifang, China
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Abstract:
Objective To investigate the relationship between human cytomegalovirus (HCMV) infection and peripheral blood CD14+CD16+ monocytes in the pathogenesis of coronary heart disease (CHD), and to elucidate the mechanism of pathogenesis in CHD by analyzing the correlation between infection, inflammation, and CHD, to provide a basis for the prevention, evaluation, and treatment of the disease. Methods In total, 192 patients with CHD were divided into three groups: latent CHD, angina pectoris, and myocardial infarction. HCMV-IgM and -IgG antibodies were assessed using ELISA; CD14+CD16+ monocytes were counted using a five-type automated hematology analyzer; mononuclear cells were assessed using fluorescence-activated cell sorting; and an automatic biochemical analyzer was used to measure the levels of triglyceride, cholesterol, high- and low-density lipoprotein cholesterols, lipoprotein, hs-CRp and Hcy. Results The positive rates of HCMV-IgM and -IgG were significantly higher in the CHD groups than in the control group. HCMV infection affects lipid metabolism to promote immune and inflammatory responses. Conclusion HCMV infection has a specific correlation with the occurrence and development of CHD. The expression of CD14+CD16+ mononuclear cells in the CHD group was increased accordingly and correlated with acute HCMV infection. Thus, HCMV antibody as well as peripheral blood CD14+CD16+ mononuclear cells can be used to monitor the occurrence and development of CHD. -
Key words:
- Human cytomegalovirus /
- Coronary heart disease /
- Antibody /
- CD14+CD16+ monocytes /
- Weifang
注释: -
Table 1. Differences in IgM (+) and IgG (+) rates between the disease and control groups
Group (count) IgM (+) IgG (+) Count % P Value Count % P Value Control (79) 15 19.0 / 35 44.3 / LCHD (77) 26* 33.8 0.036 48* 62.3 0.024 AP (64) 26* 40.6 0.004 43* 67.2 0.006 MI (51) 27* 52.9 < 0.001 41* 80.3 < 0.001 Note. The tests were carried out in 4 groups: control, LCHD (latent coronary heart disease), AP (angina pectoris), and MI (myocardial infarction). Data are presented as the mean. Statistical significance of differences between groups was evaluated using the ANOVA test. *P < 0.05 versus control. Table 2. Blood indexes of atherosclerosis (
${{ \bar {\text{x}}}}$ ± SD)Group TG (mmol/L) TC (mmol/L) HDL-C (mmol/L) LDL-C (mmol/L) Lp (a) (nmol/L) hs-CRp (mg/L) Hcy (µmol/L) Control 1.31 ± 0.47 3.70 ± 0.77 1.25 ± 0.33 1.86 ± 0.78 52.6 ± 9.34 3.78 ± 0.99 12.20 ± 2.60 LCHD 1.42 ± 0.52 3.88 ± 0.77 1.26 ± 0.45 3.11 ± 0.23 70.95 ± 8.45 5.29 ± 1.33 13.40 ± 2.60 AP 2.21 ± 0.21* 5.44 ± 0.54* 1.03 ± 0.25* 3.48 ± 0.35* 81.8 ± 8.44* 8.27 ± 1.39* 16.10 ± 3.60* MI 2.62 ± 0.32* 6.01 ± 0.80* 0.93 ± 0.24* 3.90 ± 0.49* 95.45 ± 8.12* 11.87 ± 2.95* 19.50 ± 4.40* Note. The tests were carried out in 4 groups: control, LCHD (latent coronary heart disease), AP (angina pectoris), and MI (myocardial infarction). Data are expressed as mean ± standard deviation. *P < 0.05 versus control. Triglyceride (TG), Cholesterol (TC), High- and low-density lipoprotein cholesterols (HDL-C, LDL-C), Lipoprotein A [Lp (a)], Hypersensitive C-reactive protein (hs-CRP) and Homocysteine (Hcy). Table 3. Single-factor analysis of general clinical data (risk factors) in CHD and control groups
Risk factors Control group (n = 79) CHD group (n = 192) t P Age 56.6 ± 4.2 57.5 ± 4.9 1.43 0.154 Body mass index (kg/m2) 23.3 ± 4.9 24.2 ± 4.4 1.48 0.140 Note. Data are expressed as mean ± standard deviation. T-tests showed no significance. -
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