Chronic pretreatment of metformin is associated with the reduction of the no-reflow phenomenon in patients with diabetes mellitus after primary angioplasty for acute myocardial infarction.

INTRODUCTION: Metformin is one of the most commonly prescribed antihyperglycemic agents for the treatment of type 2 diabetes. However, little is known about the effect of metformin on no-reflow in diabetic patients. AIM: In this study, we investigated retrospectively whether chronic pretreatment with metformin was associated with no-reflow in diabetic patients who underwent primary coronary intervention for acute myocardial infarction (AMI). RESULTS: A total of 154 consecutive diabetic patients who underwent primary angioplasty for a first ST-segment elevation myocardial infarction were studied. No-reflow was defined as a final TIMI flow of ≤2 or final TIMI flow of 3 with a myocardial blush grade of <2. The no-reflow phenomenon was found in 53 of 154 patients. There were no significant differences in clinical characteristics between the patients with and without metformin pretreatment. However, the 65 patients receiving chronic metformin treatment before admission had lower incidence of the no-reflow than those without it (4.2 and 14.6%, P < 0.05). Multivariable logistic regression analysis revealed that absence of metformin pretreatment was a significant predictor of the no-reflow along with high-burden thrombus, ejection fraction on admission and anterior AMI. CONCLUSION: These results suggested that chronic pretreatment with metformin may be associated with the reduction of the no-reflow phenomenon in patients with diabetes mellitus after primary angioplasty for AMI.

The effect of statins on the no-reflow phenomenon: an observational study in patients with hyperglycemia before primary angioplasty.

BACKGROUND: An association between admission plasma glucose levels and an increased risk of no-reflow has been well documented. Although HMG-CoA reductase inhibitor (statin) therapy can reduce no-reflow, little is known about its effect on no-reflow in patients with hyperglycemia. In the present study, we investigated whether pretreatment with a statin could reduce no-reflow in patients with hyperglycemia, who underwent primary coronary intervention for acute myocardial infarction (AMI). METHODS: A total of 259 consecutive patients who underwent primary angioplasty for a first AMI were studied. Blood glucose and creatinine kinase levels were measured on admission. All patients underwent 2-dimensional echocardiography and electrocardiographic analysis just after admission. No-reflow was defined as a Thrombolysis in Myocardial Infarction (TIMI) flow grade <3. Hyperglycemia was defined as a blood glucose level >or=10 mmol/L. Statin administration prior to admission was determined by detailed interview or information in the medical records. RESULTS: Hyperglycemia was diagnosed in 154 patients on admission. The no-reflow phenomenon was found in 31 of the 154 patients with hyperglycemia. The incidence of no-reflow was significantly greater in patients with hyperglycemia compared with no hyperglycemia. A multivariable logistic regression analysis showed that hyperglycemia on admission was an independent predictor of no-reflow. Among the 154 patients with hyperglycemia, there were no significant differences in baseline clinical characteristics between patients who received statin pretreatment and those who did not; however, hyperlipidemia occurred in a greater number of the patients who did not receive statin pretreatment. The 40 patients with hyperglycemia who received statins before admission had a lower incidence of no-reflow than those who did not receive statin pretreatment (5% and 25.4%; p < 0.05). Multivariable logistic regression analysis revealed that absence of statin pretreatment was a significant predictor of no-reflow in patients with hyperglycemia, along with ejection fraction on admission, initial TIMI 0 flow, number of Q waves, and anterior AMI. CONCLUSION: The results of our study show that pretreatment with statins could attenuate no-reflow after AMI in patients with acute hyperglycemia.

Remote periconditioning reduces myocardial no-reflow by the activation of K ATP channel via inhibition of Rho-kinase.

UNLABELLED: Remote periconditioning is induced by brief cycles of ischemia and reperfusion of a remote organ applied during sustained myocardial ischemia. It remains unknown whether the remote periconditioning reduces myocardial no-reflow. The adenosine triphosphate-sensitive potassium (K(ATP)) channel opening and inhibition of Rho-kinase may be the important mechanism of protection against myocardial no-reflow. Therefore, this study was sought to assess the effect of remote periconditioning on myocardial no-reflow and explore the possible mechanism. METHODS: Coronary ligation area and area of no-reflow were determined with pathological means in 58 mini-swines randomized into 7 study groups: 9 controls, 8 in remote periconditioning, 8 in hydroxyfasudil (a specific inhibitor of Rho-kinase)-treated, 9 in glibenclamide (K(ATP) channel blocker)-treated, 8 in remote periconditioning and glibenclamide, 8 in hydroxyfasudil and glibenclamide and 8 sham-operated. The ischemia and reperfusion model was created with 3 h of left anterior descending artery occlusion followed by 2 h of reperfusion. RESULTS: Compared with the control group, remote periconditioning decreased Rho-kinase activity (P<0.01), increased coronary blood volume (P<0.05), decreased area of no-reflow (from 82.3+/-3.9% to 45.5+/-5.7% of ligation area, P<0.01) and reduced necrosis size (from 98.5+/-1.3% to 74.7+/-6.3% of ligation area, P<0.05). Hydroxyfasudil had the same effect on the above parameters as remote periconditioning. Glibenclamide abrogated the effect of remote periconditioning or hydroxyfasudil on area of no-reflow and necrosis area, but not Rho-kinase activity. CONCLUSION: Remote periconditioning can reduce myocardial no-reflow after ischemia and reperfusion. This beneficial effect could be due to its activation of K(ATP) channel via inhibition of Rho-kinase.

Intravenous adenosine reduces myocardial no-reflow by decreasing endothelin-1 via activation of the ATP-sensitive K+ channel.

UNLABELLED: It has been verified that adenosine can attenuate myocardial no-reflow. However, the effects of adenosine on adenosine triphosphate-sensitive K+ (KATP) channel and endothelin-1 (ET-1) are unknown. METHODS: Forty mini-swines were randomized into 5 study groups: 8 in the control group, 8 in the adenosine pretreatment group, 8 in the glibenclamide (K(ATP) channel blocker)-treated group, 8 in the adenosine and glibenclamide-pretreated group and 8 in the sham-operated group. An acute myocardial infarction and reperfusion model was created with three-hour occlusion of the left anterior descending coronary artery followed by a one-hour reperfusion. RESULTS: Compared with the control group, adenosine significantly decreased the area of no-reflow (myocardial contrast echocardiography: from 78.5 +/- 4.5% to 20.7 +/- 4.1%, pathological means: from 82.3 +/- 1.9% to 21.5 +/- 4.3% of ligation area, respectively; all P < 0.01), reduced necrosis size from 98.5 +/- 1.3% to 75 +/- 4.7% of ligation area, P < 0.05). It also decreased plasma ET-1 and myocardial tissue ET-1. However, glibenclamide abrogated the protective effect of adenosine. CONCLUSION: The beneficial effect of adenosine on myocardial no-reflow could be due to its effect on ET-1 via the activation of K(ATP) channel.

Effect of statin therapy on reperfusion arrhythmia in patients who underwent successful primary angioplasty.

BACKGROUND: In animal models, pretreatment with statin can prevent reperfusion arrhythmia. In the observational study, we investigated whether pretreatment with statin may prevent reperfusion arrhythmia in patients who underwent primary coronary intervention for acute myocardial infarction (AMI). METHOD AND RESULTS: A total of 226 consecutive patients who underwent successful primary angioplasty for a first AMI were studied. Reperfusion arrhythmias were defined as all arrhythmias that occurred within 2 h after successful primary angioplasty. The reperfusion arrhythmia was found in 130 of 226 patients. There were no significant differences in clinical characteristics between the patients with and without statin pretreatment. However, the 41 patients receiving statin treatment before admission had lower incidence of the reperfusion arrhythmia than those without it (19.5% and 65.9%, P < 0.01). Multivariable logistic regression analysis revealed that absence of statin pre-treatment was a significant predictor of the reperfusion arrhythmia along with absence of pre-infarction angina and inferior AMI. CONCLUSION: Pre-treatment with statin could reduce the reperfusion arrhythmias after acute myocardial infarction in human.

Comparison of in-hospital and long-term outcomes between a Cypher stent and a Taxus stent in Chinese diabetic patients with coronary artery disease.

BACKGROUND: The sirolimus and paclitaxel distribution patterns and tissue residence time may be modified in atherosclerotic lesions for patients with diabetes, and the biological mechanisms of action for these agents differ significantly. Previous clinical trials have yielded discrepant results of major adverse cardiac events and restenosis between a sirolimus-eluting stent and a paclitaxel-eluting stent in coronary artery disease. Therefore, this study was conducted to compare in-hospital and long-term clinical outcomes between patients receiving sirolimus-eluting stent (Cypher or Cypher Select stent) and paclitaxel-eluting stent (Taxus Express stent) after percutaneous intervention (PCI) in Chinese patients with diabetes. METHODS: One hundred and sixty-four consecutive diabetic patients underwent PCI in Fuwai Hospital from April 2004 to December 2004. Of them, 101 patients received Cypher or Cypher Select stents (Cypher group, 145 stents) and 63 patients received Taxus Express stents (Taxus group, 129 stents). Repeat coronary angiography was performed at 6-month and clinical outcomes were evaluated at 1- and 3-year follow-up. Stent thrombosis was classified according to Academic Research Consortium (ARC). RESULTS: The two groups did not differ significantly with respect to cardiac death, recurrent myocardial infarction (re-MI), target vessel revascularization (TVR) and occurrence of major adverse cardiac events (MACE). And the MACE-free cumulative survival at 1- and 3-year follow-up and early, late and very late thrombosis rates were also similar in the two groups (all P > 0.05). There was a trend favoring PES over SES with regard to reducing cardiac death (0 vs 2.0%, P = 0.524), re-MI (0 vs 2.0%, P = 0.524), the composite of the cardiac death and re-MI (0 vs 4.0%, P = 0.299) and very late thrombosis (0 vs 3.0%, P = 0.295) between 1-year and 3-year follow-up. CONCLUSION: The study indicates that PCI with either Cypher or Taxus stents is associated with similar efficacy and safety in the small population of Chinese diabetic patients during long-term follow-up.

Chronic pretreatment of ACEI reduces no-reflow in patients with acute myocardial infarction treated with primary angioplasty.

BACKGROUND: In animal models, pretreatment with angiotensin-converting enzyme inhibitor (ACEI) can reduce no-reflow. In the present study, we investigated whether pretreatment with ACEI may prevent no-reflow in patients who underwent primary coronary intervention for AMI. METHOD AND RESULTS: A total of 259 consecutive patients who underwent primary angioplasty for a first AMI were studied. No-reflow was defined as a TIMI flow grade < 3. The no-reflow phenomenon was found in 33 of 259 patients. There were no significant differences in clinical characteristics between the patients with and without ACEI pretreatment. However, the 47 patients receiving chronic ACEI treatment before admission had lower incidence of the no-reflow than those without it (4.2 and 14.6%, p<0.05). Multivariable logistic regression analysis revealed that absence of ACEI pretreatment was a significant predictor of the no-reflow along with absence of preinfarction angina, complete occlusion of the culprit lesion, high-burden thrombus, ejection fraction on admission, number of Q-waves, absence of statin pretreatment, and anterior AMI. CONCLUSION: Pretreatment with ACEI could preserve the microvascular integrity after acute myocardial infarction in humans.

Associations of apolipoprotein B with pulse pressure and glucose in Chinese families with familial combined hyperlipidemia.

Familial combined hyperlipidemia (FCHL), with a marked elevation of apolipoprotein B (apoB), is estimated to cause 10-20% of premature coronary artery disease. However, little data are available to demonstrate the associations of apoB with pulse pressure and glucose levels in FCHL families in China. This study was to investigate the potential influence factors for blood pressure and glucose phenotypes in FCHL families by multiple linear regression analysis. We recruited 147 FCHL relatives and 90 spouses, aged 30 to 60 years, from 42 Chinese families with FCHL. Our results showed that triglyceride and low density lipoprotein cholesterol were associated with fasting glucose levels (all P<0.05). Body mass index and glucose significantly correlated to systolic blood pressure, diastolic blood pressure, and mean arterial pressure, respectively (all P<0.05). Furthermore, apoB was significantly related to pulse pressure and glucose in FCHL families (all P<0.05). Thus, this study demonstrates that apoB is significantly associated with pulse pressure and glucose levels in FCHL families. Accordingly, our data suggest that apoB may be a candidate risk marker for pulse pressure and glucose in FCHL populations.

Apolipoprotein B is associated with metabolic syndrome in Chinese families with familial combined hyperlipidemia, familial hypertriglyceridemia and familial hypercholesterolemia.

There is a paucity of data concerning the metabolic syndrome (MetS) in families with familial combined hyperlipidemia (FCHL), familial hypertriglyceridemia (FHTG), familial hypercholesterolemia (FH) and normolipidemic families in China. This study investigated the prevalence of MetS in these families and explored potential factors relevant to MetS. We recruited 70 families with 560 individuals > or = 20 years of age, including 43 FCHL families with 379 individuals, 3 FHTG families with 30 individuals, 16 FH families with 102 individuals and 8 normolipidemic families with 49 individuals. The definition of MetS is determined using modified criteria of National Cholesterol Education Program substituting body mass index for waist circumference. MetS is identified in 60.7% of FCHL patients and 71.4% of FHTG patients. The prevalence of MetS in family members is 36.7% for FCHL, 33.3% for FHTG, 17.6% for FH and 16.3% for normolipidemic families, with an odds ratio (OR) of 2.97 (95% CI 1.29-7.07, P=0.007) in FCHL families compared with normolipidemic families. Apolipoprotein B (apoB) is associated with MetS by multiple logistic analysis with an OR of 1.05 (1.03-1.07, P<0.001) in FCHL families, OR of 1.26 (1.03-1.55, P=0.026) in FHTG and OR of 1.07 (1.01-1.12, P=0.014) in FH families, independent of variables including age, gender, apolipoprotein A1, and low density lipoprotein cholesterol. Apolipoprotein A1 provided an OR of 0.95 (0.94-0.97, P<0.001) in FCHL families and OR of 0.94 (0.90-0.97, P=0.011) in FH families, but neither in FHTG nor in normolipidemic families (both P>0.05). Thus, apoB may be regarded as a relevant factor in the assessment of MetS in FCHL, FHTG and FH families. However, this finding needs to be verified by prospective studies in diverse ethnicities and warrants additional studies to elucidate possible mechanisms linking apoB to MetS.

Patients with low high-density lipoprotein-cholesterol or smoking are more likely to develop myocardial infarction among subjects with a visible lesion or stenosis in coronary artery.

BACKGROUND: Traditional contrast coronary arteriography affords only an indirect view of aspects of atheromata related to their propensity to trigger thromboses, so it is urgent to recognize the vulnerable person who is more likely to develop myocardial infarction (MI) among patients with visible lesion or stenosis in coronary artery. METHODS AND RESULTS: Two hundred and eighty-eight patients (144 MI patients, 144 controls) who had either a visible lesion or differing extent of stenosis in 1 or more major coronary arteries were consecutively enrolled. Lipid profile, C-reactive protein (CRP), smoking, hypertension, dyslipidemia and diabetes were analyzed for their association with MI. No differences in the prevalence of dyslipidemia, hypertension or diabetes was found between the patients with MI and those without, and CRP, triglycerides, total cholesterol and low-density lipoprotein-cholesterol levels did not differ between the 2 groups (all p>0.05). However, high-density lipoprotein-cholesterol (HDL-C) was significantly lower in the patients with MI than in those without (1.06+/-0.30 vs 1.14+/-0.32 mmol/L, p=0.024). On multivariate analysis after adjustment for age and gender, adjusted odds ratio (95% confidence interval) of MI was 0.44 (0.20-0.96) for HDL-C, p=0.038; 2.6 (1.48-4.56, p=0.001) for smoking, which indicated that high HDL-C was protective for MI, and smoking was associated with an increased risk of MI. CONCLUSIONS: The present findings indicate that among subjects with a visible lesion or stenosis in coronary arteries, those with low HDL-C or smokers are more likely to develop MI.

Apolipoprotein E polymorphism influences lipid phenotypes in Chinese families with familial combined hyperlipidemia.

BACKGROUND: Apolipoprotein E (apoE) polymorphism is associated with changes in the lipoprotein profile of individuals with familial combined hyperlipidemia (FCHL), but its effects on the lipoprotein profiles of members of Chinese families with FCHL remain uncertain. METHODS AND RESULTS: 43 FCHL families (n=449) and 9 normolipidemic families (n=73) were recruited to assess the influence of apoE polymorphism on plasma lipids. The relative frequency of the epsilon4 allele in affected and unaffected FCHL relatives, spouses and normolipidemic members was 13.8%, 5.3%, 9.1% and 6.8%, respectively, with a significantly higher frequency in affected FCHL relatives, compared with unaffected FCHL relatives or normolipidemic members (p=0.0002 or p=0.029). In FCHL relatives, the apoE4 subset (E4/4 and E4/3) exhibited significantly higher levels of apoB, total cholesterol and low-density lipoprotein-cholesterol (LDL-C) than did the apoE3 (E3/3) subset, especially in women (all p<0.05), and there was significant elevation of LDL-C concentrations in men only (p<0.05). In men, the apoE2 (E3/2) subset indicated a decreased level of apoB and increased apoA1 compared with those in the apoE3 subset (p<0.05). CONCLUSIONS: ApoE polymorphism appears to be associated with variance of the lipoprotein phenotype in Chinese families with FCHL.

[Glycolytic and fatty acid metabolic enzyme changes early after acute myocardial ischemia].

OBJECTIVE: To explore the changes of mRNA and protein expressions of glycolytic and fatty acid metabolic enzymes early after acute myocardial ischemia. METHODS: Twelve dogs were randomly divided into 3 groups (sham, 20 min ischemia and 40 min ischemia, n = 4 each). Myocardial samples from ischemic and nonischemic zone were obtained for histology examination, and the mRNA expressions for Phosphofructokinase (PFK), Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), GLUT1, GLUT4, Medium-chain acyl-CoA dehydrogenase (MCAD) and Heart-fatty acid binding protein (H-FABP) were determined by Real Time PCR-SYBR Green RT-PCR. GLUT1 protein expression was determined by immunohistochemistry. The apoptotic cardiomyocytes was evaluated by TUNEL. RESULTS: Compared to sham hearts, H-FABP mRNA was decreased in nonischemic and ischemic zone (P < 0.05) while GLUT1 mRNA expression was significantly increased in nonischemic and ischemic zone (P < 0.05) in dogs underwent 20 and 40 min ischemia. PFK mRNA tended to be higher in ischemic myocardium (P = 0.065) and GAPDH, MCAD as well as GLUT4 remained unchanged post ischemia (all P > 0.05). Positive GLUT1 protein staining was visualized in ischemic myocardium of hearts underwent 20 and 40 min ischemia. The myocardial apoptosis cells was 6.4% +/- 0.9% in sham hearts, 28.0% +/- 3.7% in hearts underwent 20 min ischemia (P < 0.05 vs. sham) and 38.4% +/- 1.9% in hearts underwent 40 min ischemia (P < 0.05 vs. sham). CONCLUSIONS: Significant down and up-regulated glycolytic and fatty acid metabolic enzymes early after myocardial ischemia suggested that these enzymes might play an important role in acute myocardial ischemia.

[Apolipoprotein B is associated with metabolic syndrome in Chinese pedigrees with familial hyperlipidemia].

OBJECTIVE: To investigate the prevalence of metabolic syndrome (MS) as well as the potential predictors in families with familial combined hyperlipidemia (FCHL), familial hypertriglyceridemia (FHTG), familial hypercholesterolemia (FH) and normolipidemic families in China. METHODS: The prevalence of MS was identified among 70 different families with 560 individuals aged > or = 20, including 43 FCHL families with 379 individuals, 3 FHTG families with 30 individuals, 16 FH families with 102 individuals and 8 normolipidemic families with 49 individuals. Diagnosis of MS was based on the modified criteria of National Cholesterol Education Program, US, substituting body mass index for waist circumference. Multivariate logistic regression was used to analyze the association between MS and different pedigrees. RESULTS: MS was identified in 60.7% of the FCHL patients and 71.4% of the FHTG patients. The prevalence of MS in the family members was 36.7% for the FCHL families, 33.3% for the FHTG families, 17.6% for the FH families, and 16.3% for the normolipidemic families, with an odds ratio (OR) of 2.97 (95% CI 1.29 to 7.07) in the FCHL families compared with in the normolipidemic families. Multivariate logistic regression showed an association between apolipoprotein (apo) B and MS with an OR of 1.05 (1.03 to 1.07) in the FCHL families, an OR of 1.26 (1.03 to 1.55) in the FHTG families, and an OR of 1.07 (1.01 to 1.12) in the FH families, independent of variables such as age, gender, apoA1, and LDL cholesterol, but showed no association in the normolipidemic families (P >0.05). Similarly, apo A1 provided an OR of 0.95 (0.94 to 0.97) in the FCHL families and an OR of 0.94 (0.90 to 0.99) in the FH families, but neither in the FHTG families nor in the normolipidemic families (both P >0.05). CONCLUSION: Apo B may be regarded as a relevant factor in the assessment of MS in FCHL, FHTG and FH families in Chinese. However, this finding needs to be verified by prospective studies in diverse ethnicities and warrants additional studies to elucidate the possible mechanisms linking apoB to MS.

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.

[An association of apolipoprotein B with pulse pressure in Chinese pedigrees with familial combined hyperlipidemia].

OBJECTIVE: To investigate the influencing factors of blood pressure phenotypes and the distribution of FDH in FCHL families. METHODS: Forty-two FCHL families with 435 members, 147 consanguine members and 90 members without consanguinity from Beijing area were studied. Eleven of the 42 FCHL families (26.2%) were identified as families with FDH syndrome. Stepwise regression analysis was used to analyze the association between the target variables and blood pressure phenotypes, such as systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and pulse pressure (PP), of the 237 FCHL members aged 30 to 60 years. RESULTS: The prevalence of dyslipidemic hypertension in the FCHL relatives was significantly higher than that in the spouses (29.9% versus 8.9%, P < 0.01), with an odds ratio of 3.37 (95% CI 1.44 to 8.14). In the FCHL families body mass index (BMI), age and blood sugar were independent contributors to SBP, DBP, and MAP, respectively (all P < 0.05). Age and apolipoprotein B (apoB) were important contributors to pulse pressure (both P < 0.05). CONCLUSIONS: BMI and glucose are significant contributors to different phenotypes of blood pressure. Moreover, apoB is a significant contributor to pulse pressure in FCHL families.

[Chlamydia pneumoniae infection increases the risk of coronary artery disease in the patients with dyslipidemia].

OBJECTIVE: To investigates the role of chlamydia pneumoniae (CP) infection in the development of coronary artery disease (CAD) in the patients with dyslipidemia, and to examine the gender related differences in this role. METHODS: 523 inpatients with dyslipidemia and 1196 inpatients without dyslipidemia tested for specific CP IgG by enzyme-linked immunoassay. Multivariate analyses were performed in the patients with and without dyslipidemia, and in the subgroups of male and female dyslipidemic patients to get the adjusted odds ratio (OR) (95% confidence intervals) of CAD for a given risk factor. RESULTS: After adjusting for age over 55 years, male sex, smoking, hypertension and diabetes, the OR of CAD associated with CP infection was 2.5 (1.4 to 4.6, P = 0.002) in the patients with dyslipidemia, and was 0.967 (0.7 - 1.4, P = 0.851) in those without dyslipidemia. In comparison with the male patients with dyslipidemia, the adjusted OR of CAD was 2.1 (1.1 to 4.1) for CP infection and 3.3 (1.9 - 5.9) for smoking; only CP infection was significantly contributed to CAD in female dylipidemic patients, with an adjusted OR of 4.4 (1.4 to 14.6). CONCLUSION: CP infection increases the risk of CAD only in patients with dyslipidemia, and this increase was greater in women than in men.

[Association of herpes simplex virus type2 infection with dyslipidemia in Chinese].

OBJECTIVE: To investigate the relationship between herpes simplex virus type 2 (HSV-2) infection and dyslipidemia. METHODS: ELISA was used to detect the specific IgG to HSV-2 in the samples of peripheral blood collected in succession from 1 244 inpatients, 408 with dyslipidemia and 836 controls without dyslipidemia. Univariate and multivariate analyses were preformed. RESULTS: No significant differences were found in sex and smoking status between the patients with and without dyslipidemia (both P > 0.05). However, the body mass index was significantly higher in the patients with dyslipidemia than in those without dyslipidemia (24.9 +/- 6.6 vs 23.9 +/- 7.6, P = 0.001). Diabetes and hypertension were more frequently found in patients with dyslipidemia in comparison with those without dyslipidemia (both P < 0.05). The prevalence of HSV-2 IgG seropositivity was significantly higher in the patients with dyslipidemia than those without dyslipidemia (38.2% vs 30.6%, P = 0.007). Binary Logistic regression analysis showed an association of HSV-2 IgG seropositivity with dyslipidemia, after adjustment for confoundings, the odds ratio for dyslipidemia was 1.34 (95% confidence interval, 1.04 to 1.72; P = 0.025) for HSV-2 IgG seropositivity. Other traditional risk factors, body mass index [adjusted OR 1.03 (1.01 - 1.05), P = 0.002], hypertension [adjusted OR 1.39 (1.09 - 1.79), P = 0.008] and diabetes [adjusted OR 1.50 (1.05 - 2.15), P = 0.028]. CONCLUSION: HSV-2 infection is an independent risk factor for dyslipidemia, and HSV-2 infection may increase the risk of dyslipidemia.