The results of the present study revealed that patients with CHD have a higher CP infection rate, and the CP infection rate and serum levels of CP-IgA, hs-CRP and IL-6 also increased with the exacerbation of the severity of CHD. This suggests that CP infection and inflammation play important roles in promoting the pathogenesis and progression of CHD. Recently, the investigation on new risk factors for the occurrence and development of CHD has become a hot academic topic. The study on the role of pathogenic microorganism infection in CHD has attracted much attention on this background. CP can be propagated through peripheral blood mononuclear cells and replicated in vascular cells after entering the vascular tissue, and can promote the occurrence and persistence of inflammation through a variety of intracellular signaling pathways, such as the nuclear factor-κB signaling pathway. This affects the physiological functions of vascular endothelial cells, mononuclear-macrophages, smooth muscle cells and platelets, and induces oxidative stress, eventually causing damage to endothelial cells, the formation of foam cells and the proliferation of smooth muscle cells, and leading to the formation of coronary atherosclerosis. This is the basic mechanism of CP in the pathogenesis of CHD. The results of recent studies have revealed that [
12,
13] CP infection is correlated to carotid intima-media thickness (IMT) in patients with CHD. Furthermore, the level of IMT is significantly higher in CHD patients with CP infection than in CHD patients without CP infection, and unstable plaques mostly manifest as common in carotid plaques. The results of the study conducted by Oh J et al. revealed that [
14,
15] CP infection was also correlated to the severity of CHD, and that the positive rate of serum CP-IgG was significantly higher in patients with acute myocardial infarction and unstable angina pectoris, when compared to patients with stable angina pectoris or healthy people. In the study conducted by Yuguang Sun et al. [
16‐
19], the researchers analyzed the correlation between CP infection and levels of inflammatory factors and blood lipids in patients with CHD. The results revealed that high CP infection rate, dyslipidemia and the overexpression of inflammatory factors, such as IL-6, hs-CRP and tumor necrosis factor-ɑ (TNF-α), can be commonly found in patients with CHD. Moreover, these pathological changes were highly correlated. Through clinical observation, all the above-mentioned study results confirmed that CP infection, dyslipidemia and inflammatory response may jointly play an important role in the pathogenesis of CHD and atherosclerosis, and as an important pathological mechanism in pathogenesis of CHD.
The present study revealed that the CP-IgA level was higher in patients with poor prognosis. This suggests that the prognosis of patients with CHD who underwent PCI has a certain correlation with the severity of CP infection. This may be because the formation of CP infection can continue to promote coronary arteriosclerosis plaque after PCI, and that this was also correlated to the damage to vascular endothelial function caused by CP infection-induced persistent inflammatory response. Sygitowicz G et al. revealed that [
20,
21] CP infection and hyperlipidemia have a superposition effect on atherosclerosis, when compared to simple hyperlipidemia, and hyperlipidemia combined with CP infection can not only increase the expression of IL-1β and TNF-a, but also increase the area of atherosclerotic plaques. It was found that the plaque area of a CP-infected animal model increased by 25%, when compared with the control group, and that the plaque area of a hyperlipidemia animal model with CP infection was 23% larger than that of a simple hyperlipidemia animal model. This mechanism may be correlated to the ability of CP infection to decrease the protein expression of extracellular signal-regulating kinase (p-ERK1/2) and p-P38 by affecting the MAPK signaling pathway. A study also revealed that [
22] CP infection could increase the levels of total cholesterol, free cholesterol and cholesteryl ester in THP-1 macrophage-derived foam cells, and decrease the level of cholesterol outflow. This reflects that CP can increase cholesterol levels in atherosclerotic plaques by promoting macrophage lipid accumulation and producing cholesterol outflow obstacles. Its mechanism may be correlated to the regulation of CP on the LXRα-ABCA1 signaling pathway. A study conducted by Min Zhou et al. revealed that [
23] the levels of serum endothelin-1 (ET-1), fibrinogen (Fg), soluble vascular cell adhesion factor-1 (sVCAM-1), creatine kinase (CK), creatine kinase isoenzyme (CK-MB) and troponin I (CTn I) were higher in elderly CHD patients with CP infection, when compared to elderly CHD patients without CP infection. This shows that CP infection can not only increase the levels of inflammatory factors in patients with CHD, but also increase the damage to vascular endothelial function and myocardial function. This increases the risk of cardiovascular events in patients, and azithromycin treatment can effectively stabilize the patient’s condition. Wen Xiao et al. confirmed that [
24] the CP-IgG positive rate was higher in patients with unstable angina pectoris, while the activities of tissue plasminogen activator (tPA) and plasma plasminogen activator inhibitor-1 (PAT-1) were higher in CP-IgG positive patients. This also shows that CP infection is closely correlated to relatively serious unstable angina pectoris. The above-mentioned studies suggest that CP infection can cause persistent arterial endothelial damage, such damage that may lead to the recurrence of cardiovascular events in CHD patients after PCI. This may be a mechanism underlying the correlation between CP infection and poor prognosis in patients with CHD. It is particularly noteworthy that the results of recent studies revealed that in addition to CP, the infections of other pathogenic microorganisms are also correlated to high levels of serum inflammatory factors in patients with CHD. Sfyroeras GS et al. revealed that [
25] patients with CHD had a co-infection of CP with pathogenic microorganisms, such as
Helicobacter pylori (Hp) and human cytomegalovirus (HCMV), and the long-term, repeated and chronic mixed infections of various pathogenic microorganisms could induce synergies between inflammatory markers, which jointly promote the occurrence and development of CHD. Therefore, CP infection may be one of the infectious factors that lead to poor prognosis in patients with CHD. The roles of various microbial infections, including CP infection, in the occurrence and outcome of CHD should be comprehensively evaluated, and should be the focus of further research. However, the prognosis of patients with CHD remains unknown and need further research.