Risk Of Coronary Artery Disease In Subjects Research Articles

Genetic Predisposition to Coronary Artery Disease in Type 2 Diabetes Mellitus.

Coronary artery disease (CAD) is accelerated in subjects with type 2 diabetes mellitus (T2D). To test whether this reflects differential genetic influences on CAD risk in subjects with T2D, we performed a systematic assessment of genetic overlap between CAD and T2D in 66 643 subjects (27 708 with CAD and 24 259 with T2D). Variants showing apparent association with CAD in stratified analyses or evidence of interaction were evaluated in a further 117 787 subjects (16 694 with CAD and 11 537 with T2D). None of the previously characterized CAD loci was found to have specific effects on CAD in T2D individuals, and a genome-wide interaction analysis found no new variants for CAD that could be considered T2D specific. When we considered the overall genetic correlations between CAD and its risk factors, we found no substantial differences in these relationships by T2D background. This study found no evidence that the genetic architecture of CAD differs in those with T2D compared with those without T2D.

Positive Correlation between Circulating Fetuin-A and Severity of Coronary Artery Disease in Men.

Fetuin-A serves a dual function; its high levels are associated with metabolic syndrome, type 2 diabetes, obesity, insulin resistance, and nonalcoholic fatty liver disease, and on the other hand, it serves as a potent inhibitor of ectopic vascular calcification. Due to the opposing findings, the aim of the current study was to investigate serum fetuin-A levels in men with coronary artery disease (CAD). In the case-control study, anthropometric and biochemical parameters were determined in 83 men (43 CAD patients and 40 control subjects). At last, the serum fetuin-A levels were measured using the fetuin-A human enzyme-linked immunosorbent assay (ELISA) kit. A significant difference was detected among the two groups for triglyceride and cholesterol levels (P=0.003 and P=0.002, respectively). The mean fetuin-A levels were determined 230.57 ± 63.76 and 286.35 ± 64.07 μg/ml for the control group and the CAD patients, respectively (P<0.001). Fetuin- A was significantly correlated to the severity of CAD (r 0.393, P<0.001) and associated with the risk of CAD in subjects (OR [CI] = 1. 144 [1.060-1. 235]; p = 0.001). A cut-off value of 237.4 μg/ml had good sensitivity (76.7%) and specificity (65.0%) for differentiating between two groups [area under curve (AUC) = 0.732 (CI=0.621-0.842); p < 0.001]. Our results indicated that fetuin-A levels were positively correlated to the severity of CAD. The findings suggest that there is a possible link between pathogenic mechanisms of atherosclerosis and fetuin-A; however, more investigations are needed in this regard.

The LOX1 Gene Polymorphisms and Coronary Artery Disease in North Indian Population

Background: The lectin-like oxidized-LDL receptor 1 (LOX1) is considered as a key receptor for internalizing oxidized LDL (oxLDL) and hence influencing manifestation of coronary artery disease (CAD). Aim: The study aimed to explore the association of LOX1 rs11053646 G/C and rs1050283 C/T polymorphisms and the risk of CAD in North Indian population. Methods: Angiographically confirmed 500 CAD patients and 500 healthy controls were recruited and genotyped by PCRRFLP. Results: Multiple logistic regression revealed mutant genotype of both the polymorphisms viz. CC of rs11053646 and TT of rs1050283 to confer CAD risk after adjustment for confounders (p<0.001, OR=3.072, 95% CI (1.765-5.347) and p<0.001, OR=3.487, 95% CI (1.945-6.254) respectively). Risk association was reported in recessive model for both the polymorphisms indicating that two copies of the allele are required for disease manifestation. Stratified analysis on the basis of gender showed risk association in males for both the polymorphisms with the mutant genotype exhibiting highly significant p values. However, only the LOX1 rs11053646 G/C showed the risk association in females in the mutant genotype with OR=3.179, 95% CI (1.071-9.438) and p=0.037. Stratified analysis for age reported that the mutant genotypes for both the polymorphisms significantly contributed to CAD risk in subjects above 40 years of age with OR=3.702, 95% CI (1.962-6.983) and a highly significant p<0.001 for rs11053646 G/C and OR=4.308, 95% CI (2.198-8.445) and p<0.001 for rs1050283 C/T.Conclusion: The study reveals that LOX1 rs11053646 G/C and rs1050283 C/T polymorphisms increase CAD risk in the North Indian population.

Genetic risk analysis of coronary artery disease in Pakistani subjects using a genetic risk score of 21 variants

Background and aimsConventional coronary artery disease (CAD) risk factors like age, gender, blood lipids, hypertension and smoking have been the basis of CAD risk prediction algorithms, but provide only modest discrimination. Genetic risk score (GRS) may provide improved discrimination over and above conventional risk factors. Here we analyzed the genetic risk of CAD in subjects from Pakistan, using a GRS of 21 variants in 18 genes and examined whether the GRS is associated with blood lipid levels. Methods625 (405 cases and 220 controls) subjects were genotyped for variants, NOS3 rs1799983, SMAD3 rs17228212, APOB rs1042031, LPA rs3798220, LPA rs10455872, SORT1 rs646776, APOE rs429358, GLUL rs10911021, FTO rs9939609, MIA3 rs17465637, CDKN2Ars10757274, DAB2IP rs7025486, CXCL12 rs1746048, ACE rs4341, APOA5 rs662799, CETP rs708272, MRAS rs9818870, LPL rs328, LPL rs1801177, PCSK9 rs11591147 and APOE rs7412 by TaqMan and KASPar allele discrimination techniques. ResultsIndividually, the single SNPs were not associated with CAD except APOB rs1042031 and FTO rs993969 (p = 0.01 and 0.009 respectively). However, the combined GRS of 21 SNPs was significantly higher in cases than controls (19.37 ± 2.56 vs. 18.47 ± 2.45, p = 2.9 × 10−5), and compared to the bottom quintile, CAD risk in the top quintile of the GRS was 2.96 (95% CI 1.71–5.13). Atherogenic blood lipids showed significant positive association with GRS. ConclusionsThe GRS was quantitatively associated with CAD risk and showed association with blood lipid levels, suggesting that the mechanism of these variants is likely to be, in part at least, through creating an atherogenic lipid profile in subjects carrying high numbers of risk alleles.

Association of two Common Single Nucleotide Polymorphisms (+45T/G and +276G/T) of ADIPOQ Gene with Coronary Artery Disease in Type 2 Diabetic Patients.

Background:Adiponectin, an adipocyte-secreted hormone, is known to have anti-atherogenic, anti-inflammatory, and anti-diabetic properties. In the present study, the association between two common single nucleotide polymorphisms (SNPs) (+45T/G and +276G/T) of ADIOPQ gene and coronary artery disease (CAD) was assessed in the subjects with type 2 diabetes (T2DM). Methods:Genotypes of two SNPs were determined by polymerase chain reaction-restriction fragment length polymorphism in 200 subjects with T2DM (100 subjects with CAD and 100 without CAD). Results:The frequency of TT genotype of +276G/T was significantly elevated in CAD compared to controls (χ2=7.967, P=0.019). A similar difference was found in the allele frequency of +276G/T between two groups (χ2=3.895, P=0.048). The increased risk of CAD was associated with +276 TT genotype when compared to reference GG genotype (OR=5.158; 95% CI=1.016-26.182, P=0.048). However, no similar difference was found in genotype and allele frequencies of SNP +45T/G between two groups. There was a CAD protective haplotype combination of +276 wild-type and +45 mutant-type allele (276G-45G) (OR=0.37, 95% CI=0.16-0.86, P=0.022) in the subject population. Conclusion:Our findings indicated that T allele of SNP +276G/T is more associated with the increased risk of CAD in subjects with T2DM. Also, a haplotype combination of +45G/+276G of these two SNPs has a protective effect on the risk of CAD.

Association of branched-chain amino acids with coronary artery disease: A matched-pair case–control study

Background and aimSeveral recent studies have found an independent relationship between levels of plasma branched-chain amino acids (BCAAs) and risk factors for coronary artery disease (CAD); however, few studies have investigated the associations of BCAAs with CAD and the risk of cardiovascular events. Therefore, the aim of this study was to investigate the relationship between BCAAs and CAD. Methods and resultsWe studied 143 patients with CAD diagnosed by coronary angiography at Beijing Hospital (Beijing, China) during 2008–2011. Apparently healthy control individuals (n = 286) and the patients with CAD were matched (2:1 ratio) by age and gender. The healthy control individuals were selected at random from a set of subjects who attended an annual physical examination at the same hospital in 2011. Conditional logistic regression models were used to evaluate the associations between measured variables and CAD. After multivariate adjustment for traditional CAD risk factors, each one-standard-deviation increase in BCAA concentration was associated with an approximately twofold increase in the risk of CAD (odds ratio = 1.63, 95% confidence interval (CI): 1.21–2.20, P = 0.001). As compared with subjects in the lowest quartile of BCAA levels, the odds ratios (95% CIs) for CAD risk in subjects belonging to quartiles 2, 3, and 4 were 1.65 (0.75–3.61), 2.04 (0.92–4.53), and 3.86 (1.71–8.69), respectively (P trend = 0.01). ConclusionOur results demonstrate that BCAAs are significantly related to CAD development. This relationship is independent of diabetes, hypertension, dyslipidemia, and body mass index.

Effect of Low Serum Total Bilirubin Levels (≤0.32 mg/dl) on Risk of Coronary Artery Disease in Patients With Metabolic Syndrome

The objective of this study was to investigate the effects of low serum bilirubin levels on the risk for future coronary artery disease (CAD) in a prospective cohort. CAD events were examined according to baseline serum bilirubin levels in a prospective large-scale, community-based Korean cohort in 2 subsequent prospective biennial surveys. A total of 8,593 subjects were included, 0.9% of whom reported newly developed CAD events during the 4 years of follow-up. Cox regression analyses showed that the lowest serum total bilirubin level category (bilirubin ≤0.32 mg/dl) was an independent risk factor for future CAD events (adjusted hazard ratio [HR] 1.890, 95% confidence interval [CI] 1.088 to 3.284; p = 0.024). Subjects with metabolic syndrome had a higher risk for future CAD events than those without metabolic syndrome (HR 3.366, 95% CI 2.079 to 5.448, p <0.001). Low bilirubin levels increased the CAD risk in subjects with metabolic syndrome further (HR 2.016, 95% CI 1.069 to 3.800; p = 0.030), with these subjects showing a >6 times higher risk for CAD than subjects with bilirubin levels >0.32 mg/dl and no metabolic syndrome (HR 6.228, 95% CI 3.118 to 12.437; p <0.001). In conclusion, the addition of low serum bilirubin levels to the traditional risk factors for CAD, such as metabolic syndrome, may yield an improvement of risk prediction.

Role of thrombomodulin gene in Indian population with coronary artery disease

Context: Thrombomodulin (TM), a natural anticoagulant have been implicated in the pathogenesis of coronary artery disease (CAD) thus emphasizing its potential role as a biomarker.Objectives: To investigate the role of the TM genetic variants and soluble TM (sTM) plasma levels in Indian population with CAD.Materials and methods: This case–control study involved genotyping of the entire TM gene and sTM levels estimation in 266 subjects.Results: None of the four TM genetic variants identified significantly increased CAD risk in the study population. However, further subgroup analysis revealed that in subjects ≤49 years, C1418T variant (Ala455Val substitution) was significantly associated with CAD.Conclusion: The increased CAD risk in subjects ≤49 years due to TM Ala455Val substitution is a promising finding. Further validation on large Indian cohorts is required in order to screen asymptomatic young subjects for CAD risk and to establish the clinical utility of Ala455Val substitution.

Coexistence of Visceral Fat and Multiple Risk Factor Accumulations is Strongly Associated with Coronary Artery Disease in Japanese (The VACATION-J Study)

Multiple risk factor syndrome is a target for the prevention of coronary artery disease (CAD). A cluster of multiple risk factors, such as hypertension, glucose intolerance, and/or dyslipidemia, is encountered in Japanese without and with excess visceral fat. The present study investigated the relationship between multiple risk factor accumulation and CAD in Japanese without and with visceral fat accumulation. The study subjects comprised 257 Japanese with suspected CAD (males/females= 153/ 104), who underwent 64-row multislice computed tomography (CT) coronary angiography and visceral fat area (VFA) measurement by CT. Based on the Japanese criteria for visceral fat accumulation, they were divided into those with VFA <100 and ≥10 cm(2). In subjects with VFA <100 cm(2), the age- and sex-adjusted odds ratios (ORs) for 2 and 3 risk factors were 5.33 (95% confidence intervals; 1.04-27.38, p=0.0449) and 4.07 (0.72-23.15, p=0.1138), respectively, compared with VFA <100 cm(2) and 0 risk factor set at 1.0 (p=0.0569 for trend). In contrast, the respective ORs for subjects with VFA ≥100 cm(2) were much higher [6.46 (1.25-33.44, p=0.0261) and 20.42 (3.60-115.73, p=0.0007)] (p<0.0001 for trend). The multivariate adjusted model demonstrated a significant relative excess CAD risk of 1.08 (p=0.0484) and 5.01 (p<0.0001) for the interactions of 2 risk factors and VFA ≥100 cm(2), and 3 risk factors and VFA ≥100 cm(2), whereas multiple risk factor accumulation was not related with the increase of CAD risk in subjects with VFA <100 cm(2). Coexistence of visceral fat and risk factor accumulations is strongly associated with CAD in Japanese.

Study of the association between growth differentiation factor 15 gene polymorphism and coronary artery disease in a Chinese population

Growth differentiation factor (GDF)-15 belongs to a member of the transforming growth factor-β cytokine superfamily, and elevated GDF-15 concentrations are linked to increased risk of cardiovascular diseases and future adverse cardiac events in apparently healthy elderly women, acute coronary syndrome, and chronic heart failure. However, its genetic mechanisms are still unknown. We investigated whether GDF-15 -3148C>G variant (SNP, rs4808793) is associated with a predisposition to coronary artery disease (CAD) and its severity in a Chinese population. We studied 418 consecutive patients, including 192 with coronary stenosis ≥50% or previous myocardial infarction and 226 controls without documented CAD. Coronary artery disease cases and controls were genotyped for SNP rs4808793 by using the ligase detection reaction method. The three genotypes CC, CG, and GG were present in rs4808793. No differences were found in genotype distribution and allele frequencies of rs4808793 between subjects with and without CAD, or when grouped according to sex. Logistic regression did not reveal any increased risk of CAD in subjects carrying the CG, GG genotype, or G allele at rs4808793 compared with individuals carrying the CC genotype or C allele; this finding was the same when subjects were grouped by sex (all P>0.05). Rs4808793 does not affect main anthropometric and metabolic characteristics, nor did there exists any association between rs4808793 and the severity of coronary lesions (all P>0.05). Our data do not support an association of rs4808793 with CAD or its severity in a Chinese population.

Two single nucleotide polymorphisms in ALOX15 are associated with risk of coronary artery disease in a Chinese Han population

Arachidonate 12/15-lipoxygenase (12/15-LOX) has been implicated in the pathogenesis of atherosclerosis, but with contradicting results. The aim of this study was to investigate the association of two polymorphisms in ALOX15 and the risk of coronary artery disease (CAD) in a Chinese Han population. A total of 519 unrelated CAD patients and 608 unrelated control subjects of the Chinese Han population were recruited in the case-control study. Two tagSNPs, rs7217186:T>C and rs2619112:G>A, were selected and genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The carriers of the C allele (the CC homozygote and the CT heterozygote) of rs7217186:T>C and the carriers of the A allele (the AA homozygote and the GA heterozygote) of rs2619112:G>A displayed elevated odds ratios (ORs) for CAD compared with the TT homozygotes and GG homozygotes, respectively, after adjusting for other potential confounders including age, sex, body mass index, systolic blood pressure, diastolic blood pressure, glucose, triglyceride, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and smoking status (adjusted odds ratio [OR] = 3.2, 95% confidence interval [CI]: 1.335-7.665, P = 0.009 and adjusted OR = 3.5, 95% CI: 1.343-9.330, P = 0.011). In stratified analyses, after adjusting those aforementioned confounders, the CC and CT genotypes of rs7217186:T>C were associated with a greater risk of CAD in subjects <60 years (adjusted OR = 5.7, 95% CI: 1.557-21.097, P = 0.009) and in females (adjusted OR = 9.3, 95% CI: 1.048-82.213, P = 0.045). For rs2619112:G>A, subjects (<60 years) carrying the A allele had a greater risk of CAD than the GG homozygotes (adjusted OR = 4.9, 95% CI: 1.215-19.547, P = 0.025); the male carriers of A allele also had a greater risk (adjusted OR = 3.5, 95% CI: 1.136-11.006, P = 0.029). In summary, the present study shows that after adjustment for other confounding CAD factors, rs7217186:T>C and rs2619112:G>A of ALOX15 are associated with increased risk of CAD in this Chinese Han population.

Functional polymorphisms of matrix metallopeptidase-9 and risk of coronary artery disease in a Chinese population

Matrix metallopeptidase-9 (MMP-9) plays a pivotal role in vascular remodeling and development of atherosclerotic lesion. The potentially functional MMP-9 polymorphisms may contribute to the susceptibility of coronary artery disease (CAD). A case-control study composed of 762 CAD cases and 555 CAD-free controls was conducted in a Chinese population to investigate the association between the MMP-9 -1562 C>T, R279Q, P574R and R668Q polymorphisms and CAD risk. It was found that the variant genotypes of R279Q, P574R and R668Q were associated with a non-significant decreased risk of CAD when compared with their wild-type genotypes, respectively, Furthermore, compared with those without any variant genotypes for these four nonsynonymouse loci, individuals carrying all four variant genotypes (-1562 CT/TT, 279 RQ/QQ, 574 PR/RR and 668 RQ/QQ) had a 51% decreased risk of CAD (adjusted OR = 0.49; 95% CI = 0.26-0.95, P = 0.033). Although no significant main effects were observed for MMP-9 -1562 C>T locus on CAD risk, variant genotypes of -1562 C>T were associated with a 2.53 increased risk of CAD in subjects with diabetes mellitus (DM) (95% CI = 1.18-5.45, P = 0.018). In CAD cases, variant genotypes of -1562 C>T were associated with a significantly increased risk of MI (adjusted OR, 1.48, 95% CI, 1.01-2.20, P = 0.048). These findings suggest that MMP-9 R279Q, P574R and R668Q may have combined effect in the occurrence of CAD and -1562 CT/TT genotypes may contribute to CAD in diabetics and MI in CAD patients.

Myeloperoxidase gene-463G &gt; a polymorphism and premature coronary artery disease

We investigated the association between myeloperoxidase gene -463G > A polymorphism and premature coronary artery disease (CAD) in two Chinese population samples: 229 patients and 230 controls. Genotypes were determined by ligase detection reaction-polymerase chain reaction sequencing and the grouping technique. We found lower frequencies of both the A/A genotype and the A allele in patients (p < 0.05). Multivariate logistic regression showed that the risk of premature CAD in subjects carrying the AA genotype was reduced by 83% in relation to individuals carrying the G/G genotype (OR = 0.172, 95% CI: 0.057-0.526, p = 0.002). Our results indicate that -463G > A polymorphism of the myeloperoxidase gene is associated with premature CAD in Chinese individuals, suggesting that the AA genotype is a protective factor against premature CAD.

Genetic variant in glutathione peroxidase 1 gene is associated with an increased risk of coronary artery disease in a Chinese population

Background Glutathione peroxidase 1 (GPX1), the key antioxidant enzyme in vascular endothelial cells, has been shown to exert a protective effect against the presence of coronary artery disease (CAD). The 198Pro/leu variant , located at codon 198 of GPX1 gene, has recently been linked to cardiovascular disease, but data were inconsistent. We investigated the association between the occurrence of CAD and the 198Pro/leu variant in a Chinese population. Methods A total of 265 unrelated CAD patients and 265 age- and sex-matched control subjects were recruited in this study. The GPX1 198Pro/leu genotype was determined using polymerase chain reaction–restriction fragment length polymorphism. Results Compared to the 198Pro/Pro carriers, subjects with the variant genotypes (198Pro/leu and 198Leu/leu) had a significantly higher risk of CAD (adjusted OR = 2.02, 95%CI = 1.27–3.22). In stratified analyses, the variant genotypes were significantly associated with increased CAD risk in subjects < 64 y (adjusted OR = 2.41, 95%CI = 1.16–4.98), males (adjusted OR = 1.86, 95%CI = 1.09–3.18) and non-smokers (adjusted OR = 2.40, 95%CI = 1.15–5.01). However, no significant association was observed between this variant and the severity of CAD. Conclusion These data provide evidence that GPX1 198Pro/leu variant genotypes are significantly associated with CAD risk in this Chinese population.

Relationship between Arterial Stiffness and the Risk of Coronary Artery Disease in Subjects with and without Metabolic Syndrome

We examined the influence of metabolic syndrome (MetS) on the relationship between arterial stiffness and the risk of coronary artery disease (CAD). In 396 subjects (age, 63+/-11 years) who underwent coronary angiography, multiple linear regression analysis demonstrated that the brachial-ankle pulse wave velocity (PWV), but not the presence of MetS, was a significant determinant of the number of diseased coronary arteries (beta=0.10, p<0.05), even though both the brachial-ankle PWV and the number of diseased coronary arteries were higher in subjects with MetS (n=100) than in those without MetS (n=296). However, in subjects with MetS, multiple linear regression analysis demonstrated that the brachial-ankle PWV was not a significant determinant of the number of diseased coronary arteries. The brachial-ankle PWV values were classified into tertile ranges in subjects with and without MetS. The number of diseased coronary arteries increased significantly with an increase in the tertile number of the brachial-ankle PWV in the subjects without MetS (tertile 1=1.00+/-0.86, tertile 2=1.29+/-1.01, and tertile 3=1.45+/-1.05), but not in those with MetS. In conclusion, the results of this study suggest that arterial stiffness is a marker of the risk of CAD in subjects without MetS, whereas in subjects with MetS, the syndrome may directly produce clinically significant atherosclerotic stenosis of the coronary arteries independent of its significant promotion of the development of coronary atherosclerosis via an increase of arterial stiffness.

Enhanced linkage of a locus on chromosome 2 to premature coronary artery disease in the absence of hypercholesterolemia

Linkage studies of complex diseases have so far had limited success in producing significant and replicable results, in part owing to genetic heterogeneity. We recently reported the results of a large genome-wide linkage scan for coronary artery disease (CAD) based on 1933 families. The greatest evidence for linkage was to a region of chromosome 2, with a logarithm of odds (LOD) score of 1.86, based on the non-parametric S(ALL) statistic, which did not reach genome-wide significance (P>0.3). Inclusion of a covariate in linkage analysis can be a powerful method of accounting for disease heterogeneity. As CAD is a heterogeneous disease, we carried out a linkage analysis of chromosome 2 incorporating covariates. Increased evidence for linkage was found when hypercholesterolemia was considered (LOD score including covariate of 4.4) reaching genome-wide significance as assessed by simulation (P=0.04). Results showed that the original evidence for linkage was largely attributable to the subset of 108 non-hypercholesterolemic affected sibling pairs. In separate linkage analyses of subsets of hypercholesterolemic and non-hypercholesterolemic sibling pairs, the maximum LOD scores were 1.09 in the former group and 3.74 in the latter. This result illustrates the potential to increase the power of linkage analysis in the presence of heterogeneity by inclusion of covariates. This linked locus on chromosome 2 should now be investigated further to identify the gene(s) influencing risk of CAD in subjects with a normal level of total cholesterol. Candidate genes include the interleukin 1 cluster and two potential regulators of high-density lipoprotein cholesterol level, PLA2R1 and OSBPL6.

Smoking increases the risk of coronary artery disease in Chinese with Chlamydia pneumoniae infection

Background: The infection with Chlamydia pneumoniae (Cp) has been claimed to associate with coronary artery disease (CAD). However, the seroepidemiological study of association between Cp infection and CAD still remains a source of controversy. The aim of the present study is to investigate the possible association of Cp infection with CAD in Chinese mainland population and the potential role of Cp infection combined with the traditional risk factors in CAD. Methods: 1422 hospitalized patients with angiographically demonstrated CAD and 297 controls were recruited and tested for specific Cp IgG with enzyme-linked immunoassay (ELISA). Results: The prevalence of Cp IgG seropositivity in patients with CAD was significantly higher than that in controls (31.1% vs. 24.9%, P=0.035). Unadjusted odds ratios (OR) and 95% confidence intervals (CI) for CAD with the presence of seropositivity of IgG to Cp was 1.4 (1.0–1.8). After full adjustment for possible confounders on multiple logistic regression analysis, only a weak association of Cp infection with CAD was found. The adjusted OR (95% CI) for CAD associated with Cp infection was 1.3 (0.95–1.71, P=0.1). To further delineate the potential role of Cp infection in CAD, we divided subjects into seropositive ( n=516) and seronegative ( n=1203) groups according to their Cp IgG status. Notably, the adjusted OR (95% CI) for CAD associated with smoking was 4.0 (1.8–8.6) in the seropositive group, 0.9 (0.5–1.4) in the seronegative group, indicating that smoking can significantly increase the risk of CAD in subjects with Cp infection. Conclusions: Cp infection is not strongly associated with CAD in Chinese mainland population; however, smoking increases the risk of CAD in those with Cp infection.