Multilayered insights: a machine learning approach for personalized prognostic assessment in hepatocellular carcinoma.

Background: Hepatocellular carcinoma (HCC) is a complex malignancy, and precise prognosis assessment is vital for personalized treatment decisions. Objective: This study aimed to develop a multi-level prognostic risk model for HCC, offering individualized prognosis assessment and treatment guidance. Methods: By utilizing data from The Cancer Genome Atlas (TCGA) and the Surveillance, Epidemiology, and End Results (SEER) database, we performed differential gene expression analysis to identify genes associated with survival in HCC patients. The HCC Differential Gene Prognostic Model (HCC-DGPM) was developed through multivariate Cox regression. Clinical indicators were incorporated into the HCC-DGPM using Cox regression, leading to the creation of the HCC Multilevel Prognostic Model (HCC-MLPM). Immune function was evaluated using single-sample Gene Set Enrichment Analysis (ssGSEA), and immune cell infiltration was assessed. Patient responsiveness to immunotherapy was evaluated using the Immunophenoscore (IPS). Clinical drug responsiveness was investigated using drug-related information from the TCGA database. Cox regression, Kaplan-Meier analysis, and trend association tests were conducted. Results: Seven differentially expressed genes from the TCGA database were used to construct the HCC-DGPM. Additionally, four clinical indicators associated with survival were identified from the SEER database for model adjustment. The adjusted HCC-MLPM showed significantly improved discriminative capacity (AUC=0.819 vs. 0.724). External validation involving 153 HCC patients from the International Cancer Genome Consortium (ICGC) database verified the performance of the HCC-MLPM (AUC=0.776). Significantly, the HCC-MLPM exhibited predictive capacity for patient response to immunotherapy and clinical drug efficacy (P < 0.05). Conclusion: This study offers comprehensive insights into HCC prognosis and develops predictive models to enhance patient outcomes. The evaluation of immune function, immune cell infiltration, and clinical drug responsiveness enhances our comprehension and management of HCC.

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.

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.

Is elevated high-density lipoprotein cholesterol always good for coronary heart disease?

BACKGROUND: High-density lipoprotein (HDL) could enhance inflammation in atherogenesis when inflammatory response is present, and the activity of paraoxonase and antioxidant in HDL in the elderly is significantly decreased. There might be a different role for high-density lipoprotein cholesterol (HDL-C) between different age groups in patients with coronary heart disease (CHD). METHODS: For this study, 225 inpatients with CHD (coronary atherosclerosis stenosis >/= 50% on >/= 1 major coronary arteries by coronary angiography), and 80 without CHD; 120 resting unstable angina patients, and 68 with stable angina were consecutively recruited. Risk factors were analyzed for CHD and resting unstable angina. RESULTS: High-density lipoprotein cholesterol in resting unstable angina was higher than that in stable angina (1.24 +/- 1.05 versus 1.05 +/- 0.29 mmol/L, p = 0.032). After adjustment for age, sex, physical inactivity, hypertension, diabetes, C-reactive protein, triglycerides, total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) the adjusted odds ratio (OR) (95% CI) of resting unstable angina was 10.19 (2.18-47.6, p = 0.003) for HDL-C. Risk factors were further investigated in different age groups. Adjusted OR of CHD associated with HDL-C in < 55-year-old group was 0.09 (0.01-0.66, p = 0.018), in >/= 55-year-old group it was 0.55 (0.08-3.82, p > 0.05). Adjusted OR of resting unstable angina associated with high HDL-C was 19.24 (2.86-129.4, p = 0.002) in patients aged >/= 55 years. CONCLUSIONS: Elevated HDL-C might be an independent risk factor for resting unstable angina, even though HDL-C could play a much more important role in protection against coronary stenosis in younger or middle-aged persons.

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.

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.

Effect of age on progesterone receptor expression, and osteoprogenitor proliferation and differentiation in female rat vertebral cell populations.

In the present investigation, we evaluated whether the capacity for proliferation and differentiation of progesterone (Prog)-dependent osteoprogenitors in the female rat skeleton is related to the level of Prog receptors (PRs) and/or the level of circulating estrogen. We confirmed that in rats, estrogen levels at 18 months of age are higher than those at 3 months, and higher again in rats of 22.5, 25.5, and 26 months of age. Prog levels in rats of ages between 18 and 25.5 months were lower than those at 26 and 3 months of age. PR-A levels were tenfold higher than those of PR-B in cell populations where PR-B was detectable; PR-B receptors were not detectable in all cell populations. In populations derived from 22.5 to 26 months old rats, the basal levels of PR-A were higher than those derived from 3 and 18 months old rats by five- and twofold respectively. Prog treatment enhanced PR-A expression in animals of all ages. Estrogen enhanced the effect of Prog on PR-A expression in cell populations from the 3 and 18 months old rats, but had no effect on PR-A expression in cell populations from 22.5, 25.5, and 26 months old rats. This might be related to the high basal expression of PR in 22.5-26 months old rats (the 'persistent estrous' phase). Our results also confirm our previous observation that in rats, the number of Prog- and dexamethasone (Dex)- dependent osteoprogenitors, and the effect of estrogen on the response to Prog do not decrease with age. In conclusion, we have shown that the basal level of PR-A was increased in old rats, and that this correlated with increased serum estrogen levels, but not with the number of detectable Prog-dependent osteoprogenitors. We also found that Prog upregulates the expression of its own receptors and that estrogen enhances this in young rats but not in rats over 22.5 months of age, in which estrogen levels are elevated.

[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.

Cytomegalovirus infection is associated with elevated interleukin-10 in coronary artery disease.

Previous studies show that cytomegalovirus (CMV) infection could increase the production of inflammatory cytokines in coronary artery disease (CAD). However, little is known about the influence of CMV infection on interleukin-10 (IL-10) levels in CAD. We attempted to investigate the relationships between CMV infection and serum IL-10 levels in patients with CAD. CMV IgG and serum levels of IL-10 were measured with ELISA in patients with CAD (n=463) and smooth coronary artery controls documented by coronary arteriography (n=125). Subjects were dichotomized according to calculated median level of IL-10 (6.84 pg/ml) in different groups or subgroups. The seropositivity of CMV IgG was more frequently found in the high IL-10 group than the low IL-10 group (46.8% versus 30.4%, P<0.001). The prevalence of CMV infection was significantly higher in the high IL-10 group than the low IL-10 group among the patients with CAD (48.1% versus 28.6%, P<0.001), but among the controls (40.4% versus 35.6%, P=0.588). On multiple logistic regression analysis, the adjusted odds ratio (95% confidence intervals) of high IL-10 associated with CMV infection was 2.3 (1.6-3.4, P<0.001) in the patients with CAD, and 1.1 (0.5-2.5, P=0.83) in the controls. We found a significant association of CMV infection with elevated IL-10 in the patients with CAD; therefore, we propose that changes in the immune response to CMV are a compounding factor in CAD.

[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.

Effect of ovariectomy on dexamethasone- and progesterone-dependent osteoprogenitors in vertebral and femoral rat bone cell populations.

We have found previously that the skeleton of adult female rats contains dexamethasone (Dex)- and progesterone (Prog)-dependent osteoprogenitors, and that estrogen treatment in vitro upregulates proliferation and differentiation of the Prog-dependent but not of the Dex-dependent osteoprogenitors (Bone 1997;20:17-25). The purpose of the present study was to determine whether ovariectomy (OVX) would have different effects on these two classes of osteoprogenitors. Six-month-old Sprague-Dawley rats underwent OVX and the lumbar vertebrae and proximal femurs were collected 1.5, 3, and 6 months after OVX. Cells were obtained from outgrowths of explant cultures and grown in alpha-MEM with 10% FBS, 50 microg/ml ascorbic acid, and 5 mM beta-glycerophosphate. Osteoprogenitors were identified by their ability to generate a colony of osteoblastic cells forming bone (bone nodule). We also evaluated the number of colony-forming units-fibroblast (CFU-F) and of alkaline phosphatase (AP)-positive CFU-F. In cell populations obtained from vertebrae of rats ovariectomized for 1.5, 3, and 6 months and their corresponding control rats, both Dex (1-100 nM) and Prog (1-10 microM) dose-dependently stimulated nodule formation. Both Dex- and Prog-induced nodule formation were higher in cell populations from control rats than in those from ovariectomized rats (P < 0.001). Numbers of CFU-F and AP-positive CFU-F were also higher in cell populations from control rats compared with those from ovariectomized rats. Estrogen (10 nM) enhanced Prog-dependent bone nodule formation but decreased Dex-dependent bone nodule formation in populations from both control and ovariectomized rats. In femoral populations, the responses to Dex (10 nM), Prog (3 microM), and estrogen (10 nM) were similar to those of the vertebral populations in both control and ovariectomized rats. Our results demonstrate that ovariectomy in rats results in a dramatic decrease in the number of both Dex- and Prog-dependent osteoprogenitors in cell populations from vertebrae and proximal femurs. In addition, we confirmed our previous observation that estrogen upregulated proliferation and differentiation of Prog-dependent progenitors, but found here that estrogen clearly downregulated proliferation and differentiation of the Dex-dependent progenitors.

Herpes simplex virus type 2 infection is a risk factor for hypertension.

Herpes simplex virus type 2 (HSV-2), which has been recognized as a potential cardiovascular pathogen and implicated in carotid atherosclerosis and coronary artery disease, is independently associated with the future risk of cardiovascular death. Investigations have demonstrated that hypertension may be related to inflammation, and inflammation is one of the symptoms of HSV-2 infection. This cross-sectional study investigated the correlation between HSV-2 infection and essential hypertension. One thousand two hundred and forty four inpatients (488 patients with essential hypertension and 756 normotensives) were investigated serologically for the specific immunoglobulin G (IgG) to HSV-2 by enzyme-linked immunosorbent assay. Patients diagnosed with pheochromocytoma, primary aldosteronism, aorto-arteritis or renal artery stenosis were excluded. The prevalence of HSV-2 IgG seropositivity was significantly higher in the hypertensive group than in the normotensive group (38.3% vs. 29.8%, p =0.002). After adjustment for confounding factors, an association of HSV-2 IgG seropositivity with essential hypertension was found on binary logistic regression analysis. The adjusted odds ratio of essential hypertension was 1.4 (95% confidence intervals, 1.1 to 1.8; p =0.005) for HSV-2 infection; the adjusted covariates included age, male sex, smoking, body mass index, dyslipidemia, diabetes and coronary artery disease. The results of this study indicated that HSV-2 infection might be an independent risk factor for essential hypertension.

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.

[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.

[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.

[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.

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.

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.

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.