The effects of selenium supplementation on antibody titres in patients with Hashimoto's thyroiditis.

INTRODUCTION: The objective of this study was to evaluate the effect of selenium supplementation on autoantibody titres, thyroid ultrasonography, and thyroid function in patients with Hashimoto's thyroiditis (autoimmune thyroiditis) and normal thyroid reference range. MATERIAL AND METHODS: A total of 100 patients were given 200 ug/d selenium yeast orally, their thyroid function, levels of serum selenium, thyroid peroxidase antibodies (TPOAb), thyroglobulin antibodies (TGAb), and urine iodine were measured, and thyroid ultrasonography was performed before administration and three and six months afterwards, and the data were statistically analysed. RESULTS: The subjects exhibited a selenium deficiency before the administration of selenium, and the serum levels increased to moderate levels three and six months after the selenium supplementation (p < 0.05). The titres of TGAb decreased significantly in patients after six months of selenium supplementation (p < 0.05). In the high antibody group, TgAb decreased after 6 months compared with baseline (p = p < 0.05), and TPOAb decreased after 3 and 6 months of selenium supplementation compared with baseline (p < 0.05). CONCLUSION: In patients with autoimmune thyroiditis and normal thyroid reference range, there was a general selenium deficiency, but after six months of treatment it was shown that selenium supplementation may be effective in reducing the titres of TGAb and TPOAb.

miRNA-21 Expression in the Serum of Elderly Patients with Acute Myocardial Infarction.

BACKGROUND The aims of this study were to examine the expression of miRNA-21 in the serum of elderly patients (>65 years) with acute myocardial infarction (AMI) and to investigate the potential role of serum miRNA-21 as a marker of early cardiac myocyte damage. MATERIAL AND METHODS Thirty-eight elderly patients with recent AMI, 27 elderly patients with unstable angina pectoris, and 25 healthy elderly individuals were included in the study. Serum miRNA-21 expression was determined following total RNA extraction and reverse-transcribed into cDNA, followed by reverse transcription-polymerase chain reaction (RT-PCR). Serum creatine kinase MB isoenzyme (CK-MB) and cardiac troponin I (cTnI) levels were analyzed by electrochemiluminescence. Apoptosis of human cardiac myocytes (HCM) was analyzed using fluorescence-activated cell sorting (FACS), and protein expression of caspase-3 was detected using Western blot. RESULTS Expression levels of miRNA-21 in the serum of elderly patients with AMI were positively correlated with serum levels of CK-MB (r=0.3683, P=0.0229) and cTnI (r=0.5128, P=0.009). Following tumor necrosis factor (TNF)-α induction, the apoptosis rates of HCM transfected with the miRNA-21 mimic short hairpin RNA (shRNA) were downregulated by 39.1% compared with control HCM cells, and protein expression of c-Jun N-terminal kinases (JNK) and p38 were unchanged (P>0.05); protein expression of p-JNK, p-p38 and caspase-3 were downregulated by 37.1%, 35.8%, and 36.0%, respectively. CONCLUSIONS Expression of miRNA-21 was upregulated in the serum of elderly patients with AMI, which inhibited TNF-a induced apoptosis in HCM by activating the JNK/p38/caspase-3 signaling pathway.

Recent advances in understanding the biochemical and molecular mechanism of diabetic nephropathy.

Diabetic nephropathy (DN) is a chronic disease characterized by proteinuria, glomerular hypertrophy, decreased glomerular filtration and renal fibrosis with loss of renal function. DN is the leading cause of end-stage renal disease, accounting for millions of deaths worldwide. Hyperglycemia is the driving force for the development of diabetic nephropathy. The exact cause of diabetic nephropathy is unknown, but various postulated mechanisms are: hyperglycemia (causing hyperfiltration and renal injury), advanced glycosylation products, activation of cytokines. In this review article, we have discussed a number of diabetes-induced metabolites such as glucose, advanced glycation end products, protein kinase C and oxidative stress and other related factors that are implicated in the pathophysiology of the DN. An understanding of the biochemical and molecular changes especially early in the DN may lead to new and effective therapies towards prevention and amelioration of DN.

Effect of spironolactone on cardiac remodeling after acute myocardial infarction.

BACKGROUND: Few studies have reported the effect of aldosterone receptor antagonist (ARA) on myocardial remodeling after acute myocardial infarction (AMI). This study was undertaken to investigate the preventive effect of ARA on myocardial remodeling after AMI. METHODS: A total of 616 patients who had been admitted into the CCU of the First Affiliated Hospital of Harbin Medical University from January 2008 to January 2010 were studied prospectively. Only 528 patients were observed completely, including 266 of the control group and 262 of the treatment group. There was no statistical difference in age, gender, medical history, admission situation, and treatment between the two groups (P>0.05). The preventive effects of spironolactone on cardiac remodeling, left ventricular function, renal function and blood levels of potassium were evaluated by echocardiography, serum potassium and serum creatinine at one-month and one-year follow-up. RESULTS: The echocardiography indicators such as LVESD, LVEDD, LVEF, LAD-ML and LAD-SI were significantly improved in the treatment group compared with the control group at one year (P<0.05). In the treatment group, LVESD, LVEDD, LVPWT, LVEF, LAD-ML and LAD-SI were more significantly improved at one year than one month (P<0.05, P=0.007 to LVEF), and in the control group LVEF was more significantly improved at one year than one month (P=0.0277). There were no significant differences in serum potassium and serum creatinine levels between the two groups. CONCLUSION: On the basis of conventional treatment, the early combination of low-dose spironolactone (20 mg/d) could inhibit cardiac remodeling at late stage and prevent heart failure.

Role of the Na(+)/H(+) exchanger on the development of diabetes mellitus and its chronic complications.

Micro- and macrovascular complications are the main cause of morbidity and mortality in diabetes mellitus. The Na(+)/H(+) exchanger (NHE) is a family of proteins which exchange Na(+) for H(+) according to their concentration gradients in an electroneutral manner. The exchanger also plays a key role in several other cellular functions including proliferation, differentiation, apoptosis, migration, and cytoskeletal organization. Since not much is known on the relationship between NHE and diabetes mellitus, this review outlines the contribution of NHE to chronic complications of diabetes mellitus, such as diabetic nephropathy; diabetic cardiomyopathy.

Impact of emergency percutaneous coronary intervention on outcomes of ST-segment elevation myocardial infarction patients complicated by out-of-hospital cardiac arrest.

BACKGROUND: Cardiac arrest is one of the most serious complications of acute myocardial infarction (AMI), especially in the out-of-hospital patients. There is no general consensus as to whether percutaneous coronary intervention (PCI) is effective in treating ST-segment elevation myocardial infarction (STEMI) patients complicated by out-of-hospital cardiac arrest (OHCA). In our study, we evaluated the efficacy of PCI in treating STEMI patients complicated by OHCA through observing their clinical conditions in hospital; including total mortality, adverse cardiac events, stroke, acute renal failure, and gastrointestinal bleeding events. METHODS: A total of 1827 STEMI patients were enrolled in this study, where 81 were STEMI with OHCA. Between the patients with and without OHCA, and the OHCA patients with and without PCI, we compared the clinical characteristics during hospitalization, including total mortality and incidences of adverse cardiac events, and stroke. RESULTS: Compared to the patients without OHCA, the OHCA patients had significantly lower systolic blood pressure (P < 0.05) and a faster heart rate (P < 0.05), and a higher percentage of Killip class IV or Glasgow coma scale (GCS) ≤ 7 on admission (P < 0.001). And the in-hospital mortality was higher in the OHCA patients (55.6% vs. 2.4%, P < 0.001). Comparing the OHCA patients without PCI to the patients with PCI, there was no obvious difference of heart rate, blood pressure or the percentage of Killip class IV and GCS ≤ 7 on admission, but the incidences of cardiogenic shock, stroke were significantly lower in the with-PCI group during hospitalization (P < 0.001, P < 0.05). And the in-hospital mortality of the OHCA patients receiving PCI was significantly lower (36.7% vs. 84.3%, P < 0.001). CONCLUSIONS: During hospitalization, the incidence of adverse events and mortality are higher in the STEMI with OHCA patients, comparing with the STEMI without OHCA. Emergency PCI reduces the incidence of adverse events and decreases mortality during hospitalization, which is effective for treating STEMI with OHCA patients.

[Outcome of patients with ST-elevation myocardial infarction complicated by pre-hospital cardiac arrest underwent emergency percutaneous coronary intervention].

OBJECTIVE: To evaluate the outcome of ST-elevation acute myocardial infarction (STEMI) patients complicated pre-hospital cardiac arrest underwent percutaneous coronary intervention (PCI). METHODS: From September 2004 to November 2008, 1446 consecutive patients with acute STEMI underwent PCI in our department. 49 out of 1446 patients complicated by pre-hospital cardiac arrest. Clinical outcome including total mortality, adverse cardiac events, stroke and bleeding events during the hospitalization period and within 1 year after discharge was compared between patients with or without pre-hospital cardiac arrest. RESULTS: PCI success rate was similar (85.7% vs. 88.8%, P = 0.497) while the incidence of in-hospital cardiogenic shock 22.4% vs. 3.0%, P < 0.001 and cardiac arrest (44.9% vs. 5.9%, P < 0.001) and in-hospital mortality (36.7% vs. 2.0%, P < 0.001) were significantly higher in patients with pre-hospital cardiac arrest than patients without pre-hospital cardiac arrest. Time from symptom onset to emergency treatment, asystole as initial rhythm, Glasgow coma scale (GCS ≤ 7) and cardiogenic shock on admission were independent risk factors of in-hospital death in patients with pre-hospital cardiac arrest. During follow up, incidences of overall mortality, re-infarction, revascularization and stroke were similar between the two groups. CONCLUSIONS: STEMI patients with pre-hospital cardiac arrest undergoing emergency PCI are facing higher risk of cardiogenic shock and cardiac arrest and higher in-hospital mortality compared to those without pre-hospital cardiac arrest. However, the post-hospital discharge outcome was similar between the two groups.

[A prospective randomized trial of poly-DL-lactic acid absorbable and metallic screws for treatment of syndesmotic disruptions].

OBJECTIVE: To compare the clinical effect of poly-DL-lactic acid (PDLLA) absorbable screws and titanium metallic screws in the treatment of syndesmotic disruptions in ankle fractures. METHODS: In this prospective, randomized clinical trial, 58 patients with or suspected of syndesmotic disruption associated with ankle fractures were randomly allocated to receive either bioabsorbable PDLLA or metallic titanium screwing fixation. Using preoperative radiography and intraoperative hook test, syndesmotic disruption was confirmed in 47 cases (25 with metallic screwing and 22 with PLLA screwing). Statistical analyses were performed at 6 months postoperatively to compare the AOFAS score, range of motion of the joint, TFCS width and TFO width on anteroposterior view radiographs, and inflammatory reactions between the two groups. RESULTS: The PDLLA screws showed good therapeutic effect similar to that of titanium metallic screws in syndesmosis fixation in these patients. No significant differences were found in the AOFAS score, range of motion of the joint, or TFCS width or TFO width between two groups (P>0.05). One patient in PDLLA screw group showed inflammatory reactions to the implants. CONCLUSION: PDLLA screws allow effective and reliable stabilization of syndesmotic disruptions without a second operation for screw removal.

Respiratory syncytial virus infection and risk of acute myocardial infarction.

INTRODUCTION: Increasing evidences have shown that pathogens may promote atherosclerosis and trigger acute myocardial infarction (AMI). There is no report on the association between respiratory syncytial virus (RSV) infection and AMI. The case-control study was used to assess the association of previous RSV infection and acute myocardial infarction. METHODS: AMI cases and non-AMI controls were recruited from patients at a large teaching hospital in Harbin, China, during October 1, 2005, to March 31, 2006, and October 1, 2006, to March 31, 2007. Questionnaire survey was conducted to collect information on demographic characteristics and heart disease risk factors. Fasting blood sample was obtained to measure immunoglobulin G antibodies to RSV, Cytomegalovirus, herpes simplex virus type-1 and type-2, adenovirus, Rubella virus, Chlamydia pneumoniae and Helicobacter pylori and to measure the level of cholesterol, fasting serum glucose, triglycerides and high-sensitivity C-reactive protein. RESULTS: AMI group had more smokers than controls (56.9% versus 18.0%) and were more likely to have positive immunoglobulin G antibodies to RSV (OR, 6.2; 95% CI, 3.5-10.7; P < 0.001). After adjustment for potential confounding variables, the association between RSV and AMI remained (adjusted odds ratio, 11.1; 95% confidence interval, 3.3-29.5). CONCLUSIONS: Our study supported the hypothesis that the previous RSV infection was associated with AMI. This indicates that prevention and proper treatment of RSV infection are of great clinical importance for the reduction of AMI risk.

Comparison of effects of simvastatin versus atorvastatin on oxidative stress in patients with coronary heart disease.

BACKGROUND: HMG-CoA reductase inhibitors (statins) have antiatherogenic effects beyond their cholesterol-lowing effect. Whether atorvastatin has a stronger antioxidant effect than other statins is uncertain. HYPOTHESIS: To determine the effects of simvastatin and atorvastatin on markers of oxidative stress in patients with coronary heart disease (CHD). METHODS: This study was comprised of 164 patients with CHD and a control population of 122 healthy subjects. The patients with CHD were divided into 2 groups and treated with either simvastatin 20 mg/day or atorvastatin 10 mg/day. The markers of oxidative stress were measured before and after 12 weeks of treatment. RESULTS: The effects of atorvastatin on reducing oxidative stress were significantly greater compared with those of simvastatin (P < 0.05). The changes in the markers of oxidative stress did not correlate with the changes in the plasma lipid profile (P > 0.05). CONCLUSIONS: This study suggests that atorvastatin reduces oxidative stress more effectively than simvastatin.

Effect of statin therapy on leptin levels in patients with coronary heart disease.

The goal of this study was to investigate the effects of simvastatin on the levels of plasma leptin and nitric oxide (NO) in patients with coronary heart disease (CHD). The study population consisted of 65 patients with CHD and 48 control individuals without signs or symptoms of CHD. The patients with CHD were treated with simvastatin 20mg/day. Fasting serum lipids, leptin and NO were determined before and after 12 weeks of treatment. Leptin levels were higher in patients with CHD than control (P<0.05). Statin treatment significantly decreased plasma lipids and leptin levels and increased NO concentration in all CHD patients (P<0.05). Serum leptin levels after treatment correlated negatively with the NO concentration (P<0.05). Simvastatin may provide beneficial effects of reducing leptin levels, independent of its lipid-lowering action, which may play an important role in patients with CHD.

Effect of percutaneous thrombectomy on echocardiographic measures of myocardial microcirculation in elderly patients with acute myocardial infarction.

OBJECTIVES: To study the efficacy of percutaneous thrombectomy (PT) in improving myocardial microcirculation in elderly acute myocardial infarction (AMI) patients. METHODS: A total of 104 patients (> or = 65 years) with AMI and coronary thrombus shown by angiography were randomly divided into a group of percutaneous coronary intervention (PCI) (n=52) and a group of PCI plus PT (n=52). At 24 h and 1 week after PCI, real-time myocardial contrast echocardiography was performed by contrast pulse sequencing technology. Contrast score index, contrast defect length/left ventricle length [CDL/LVL (%)], wall motion score index and wall motion abnormal length/LVL (%) were calculated. RESULTS: At each time point, in patients treated with PCI plus PT, contrast score index, CDL/LVL (%), wall motion score index and wall motion abnormal length/LVL (%) were significantly lower than that in the PCI group. CONCLUSION: Thrombectomy reduces the noreflow and the extent of microvascular obstruction, thus it was a feasible therapy in elderly patients with AMI.

KB-R7943 inhibits high glucose-induced endothelial ICAM-1 expression and monocyte-endothelial adhesion.

Hyperglycemia is the major cause of diabetic angiopathy. The aim of our study was to evaluate the impact of KB-R7943, an inhibitor of Na+/Ca2+ exchanger (NCX) on cell growth and function of human "diabetic" endothelial cells (EC). Intercellular adhesion molecule-1 (ICAM-1) expression and NCX activity were determined after EC were exposed to high glucose in the absence and presence of KB-R7943. Coincubation of EC with high glucose for 24 h resulted in a significant increase of monocyte-endothelial cell adhesion and the expression of ICAM-1. These effects were abolished by KB-R7943 and KB-R7943 significantly decreased the activation of NCX induced by high glucose. These findings suggested that KB-R7943 may play a role in inhibiting expression of adhesion molecules by inhibiting the reverse activation of NCX.

Intracoronary nitroprusside in the prevention of the no-reflow phenomenon in acute myocardial infarction.

BACKGROUND: No-reflow phenomenon during percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) is a predictive factor of continuous myocardial ischemia, ventricular remodeling and cardiac dysfunction, which is closely associated with a worse prognosis. This study aimed to evaluate intracoronary nitroprusside in the prevention of the no-reflow phenomenon in AMI. METHODS: Ninety-two consecutive patients with AMI, who underwent primary PCI within 12 hours of onset, were randomly assigned to 2 groups: intracoronary administration of nitroprusside (group A, n = 46), intracoronary administration of nitroglycerin (group B, n = 46). The angiographic results were observed. The real-time myocardial contrast echocardiography (RT-MCE), including contrast score index (CSI), wall motion score index (WMSI), transmural contrast defect length (CDL) and serious WM abnormal length (WML) were recorded at 24 hours and 1 week post-PCI. High sensitivity C-reactive protein (Hs-CRP) was examined by immune rate nephelometry. N-terminal prohormone brain natriuretic peptide (NT-proBNP) was tested with enzyme-linked immunosorbent assay. Patients were followed up for six months. Major adverse cardiac events (MACE) were recorded. RESULTS: The incidence of final TIMI-3 flow in group A was much higher than that in Group B (P < 0.05), final corrected TIMI frame count (cTFC) in group A decreased significantly than that in group B (P < 0.01). The CSI, CDL/LV length, WMSI and WL/LV length in group A were significantly lower than that in group B (P < 0.01). Levels of Hs-CRP and NT-proBNP at 1 week post-PCI decreased significantly in group A than that in group B (P < 0.01). Patients were followed up for 6 months and the incidence of MACE in group A was significantly lower than that in group B (P < 0.05). CONCLUSION: Intracoronary nitroprusside can improve myocardial microcirculation, leading to the decrease of the incidence of no-reflow phenomenon and better prognosis.

Effect of R219K polymorphism of the ABCA1 gene on the lipid-lowering effect of pravastatin in Chinese patients with coronary heart disease.

1. In the present study, we investigated the effects of the R219K polymorphism of the ATP-binding cassette transporter A1 (ABCA1) gene on serum lipid levels and the response to statin therapy in Chinese patients with coronary heart disease (CHD). 2. The study population consisted of 365 patients with CHD and 246 control subjects without signs or symptoms of CHD. Patients with CHD were treated with 20 mg/day pravastatin. Fasting serum lipids were determined before and after 12 weeks of treatment. Genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). 3. The R219K polymorphism of the ABCA1 gene was not significantly associated with CHD (P > 0.05). Compared with controls, patients with the RR genotype had significantly higher serum triglyceride levels and lower high-density lipoprotein-cholesterol (HDL-C) levels than those with the KK genotype (P < 0.05). In addition, the effects of pravastatin in increasing HDL-C levels were significantly greater in patients with the KK genotype compared with those with the RR genotype (P < 0.05). 4. In conclusion, the R219K polymorphism of ABCA1 was associated with altered lipoprotein levels and the R219K variant significantly modulated the HDL-C response to pravastatin in Chinese patients with CHD.

Effect of atorvastatin on expression of IL-10 and TNF-alpha mRNA in myocardial ischemia-reperfusion injury in rats.

Myocardial ischemia and reperfusion (MI/R) is associated with an intense inflammatory reaction, which may lead to myocyte injury. Because statins protect the myocardium against ischemia-reperfusion injury via a mechanism unrelated to cholesterol lowering, we hypothesized that the protective effect of statins was related to the expression of TNF-alpha (TNF-alpha) and interleukin-10 (IL-10) mRNA. Seventy-two rats were randomly divided into three groups as follows: sham, I/R and I/R+atorvastatin. Atorvastatin (20 mg kg(-1)day(-1)) treatment was administered daily via oral gavage to rats for 2, 7 or 14 days. Ischemia was induced via a 30-min coronary occlusion. Reperfusion was allowed until 2, 7 or 14 days while atorvastatin treatment continued. We measured infarct size, hemodynamics and the plasma levels and the mRNA expression of TNF-alpha and IL-10 in the three groups. We demonstrated that the up-regulation of expression of both TNF-alpha mRNA and IL-10 mRNA was associated the increased plasma levels of TNF-alpha and IL-10 in the ischemic and reperfused myocardium compared with that in the sham group (P<0.01). Atorvastatin treatment prevented ischemia-reperfusion-induced up-regulation of both TNF-alpha and IL-10 mRNA, and improved left ventricular function (P<0.01). Our findings suggested that atorvastatin may attenuate MI/R and better recovery of left ventricle function following ischemia and reperfusion and IL-10 was not directly likely involved in this protective mechanism.

Early use of omeprazole benefits patients with acute myocardial infarction.

BACKGROUND: Bleeding complications are not uncommon in patients with acute myocardial infarction (AMI) during treatments. How to prevent the occurrence of upper gastrointestinal bleeding in AMI patients has become one of the most intractable problems. And there are conflicting data on the efficacy and complication rate of omeprazole treatment. We conducted an intervention study to determine whether using omeprazole could benefit AMI patients. METHODS: A total of 237 patients with AMI were divided into two groups at random: omeprazole group including 114 patients and control group including 123 patients. Omeprazole 40 mg by intravenous drip was given to the patients in omeprazole group when they were admitted to the hospitals. From the second day they were given omeprazole 20 mg per day by oral administration for 7 days. In contrast, no gastric acid inhibitor was given to the patients in control group. The incidence of upper gastrointestinal bleeding, the recanalization rate and overall mortality in both groups were observed. RESULTS: The incidence of upper gastrointestinal bleeding in omeprazole group was 5.3% (6/114) which was much lower than 14.6% (18/123) in control group (P = 0.017), but the recanalization rate had no significant difference between the two groups (P = 0.681). The overall mortality in omeprazole group was lower than that of control group (3.5% vs. 10.6%, P = 0.035). CONCLUSIONS: Our findings suggest that early use of omeprazole in AMI patients could decrease the incidence of upper gastrointestinal bleeding and the overall mortality, without influencing the recanalization rate. Early use of omeprazole might benefit AMI patients.

The 223A>G polymorphism of the leptin receptor gene and lipid-lowering efficacy of simvastatin in Chinese patients with coronary heart disease.

OBJECTIVE: To investigate whether leptin receptor (LEPR) 223A>G polymorphism influences serum lipid levels and whether this polymorphism affects the effectiveness of simvastatin in Chinese patients with coronary heart disease (CHD). METHODS: A total of 312 patients with CHD were treated with simvastatin 20 mg/day. Fasting serum lipids were determined before and after 12 weeks of treatment. RESULTS: Patients with AA genotype had significantly higher total cholesterol (TC) levels and lower high-density lipoprotein cholesterol (HDL-C) levels than those with GG genotype (P < 0.05) before simvastatin treatment. In addition, the ability of simvastatin to increase HDL-C levels was significantly lower in patients with AA genotype than those with GG genotype (P < 0.05). CONCLUSIONS: The 223A>G polymorphism of LEPR significantly modulates the HDL-C response to simvastatin in Chinese patients with CHD.

[Intensive atorvastatin therapy in patients with acute myocardial infarction].

OBJECTIVE: To assess the safety and efficacy of 40 mg daily atorvastatin in patients with acute myocardial infarction. METHODS: A total of 1102 patients with AMI admitted to our hospital from 2003 to 2007 were assigned to atorvastatin 40 mg daily within 24 hours of hospitalization and continued till 3 months post discharge. Patients with LDL-C < 2.0 mmol/L or increased liver enzyme level (3 times higher than normal) at discharge received atorvastatin 20 mg daily. Lipid profiles, high-sensitivity C-reactive protein, liver enzyme level were measured at admission, hospital discharge and 3 months after discharge. RESULTS: (1)The mean hospitalization duration was (10.17 +/- 1.83) days. LDL-C was continuously decreased [(3.24 +/- 1.04) mmol/L at admission, (2.27 +/- 2.00) mmol/L at discharge and (1.48 +/- 0.78) mmol/L at 3 months after discharge, all P < 0.05]. HDL-C decreased from (1.45 +/- 0.38) mmol/L to (1.20 +/- 0.30) mmol/L at hospital discharge, then increased to (1.65 +/- 1.79) mmol/L at 3 months after hospital discharge (all P < 0.05). TC and apoB were also significantly decreased from admission to discharge (all P < 0.05). (2) high-sensitivity C-reactive protein level significantly decreased from admission to hospital discharge and at 1 months after hospital discharge [(49.71 +/- 50.46) mg/L vs. (8.80 +/- 17.66) mg/L vs. (2.61 +/- 2.30) mg/L, all P < 0.05]. (3) Increased ALT > 120 U/L (3 times higher than normal) were found in 127(11.25%), AST > 120 U/L were found in 26(2.40%) patients at discharge. There were still 4 patients with increased ALT (> 120 U/L) at 1 months after discharge and all returned to normal at 3 months after discharge. CONCLUSION: Intensive atorvastatin therapy with a dose of 40 mg daily is safe and effective for patients with AMI.

Influenza virus infection and risk of acute myocardial infarction.

Increasing evidences have shown that pathogens might promote atherosclerosis and trigger acute myocardial infarction (AMI). But the conclusions from various studies on the correlation between previous influenza virus (IV) infection and AMI were inconsistent. We conducted a case-control study to assess the association of previous IV infection and AMI. Questionnaire survey was conducted to collect information about demographic characteristics and heart disease risk factors. Fasting blood sample was obtained to measure IgG antibodies to influenza virus A(IV-A), influenza virus B(IV-B), cytomegalovirus (CMV), herpes simplex virus type-1 (HSV-1) and type-2 (HSV-2), adenovirus (ADV), rubella virus (RV) and Chlamydia pneumoniae (CP) and measure the level of some biochemistry markers. Compared to controls, cases were more likely to have positive IgG antibodies to IV-A and IV-B (IV-A: OR, 3.3; 95%CI, 1.5 to 7.4; IV-B: OR, 17.2; 95%CI, 7.7 to 38.0). After adjustment for potential confounding variables, the risk of AMI was still associated with the presence of IgG antibodies to IV-A (adjusted OR, 7.5; 95%CI, 1.3 to 43.0) and IV-B (adjusted OR, 27.3; 95%CI, 6.6 to 113.8). The study supported the hypothesis that previous IV infection took part in the development of atherosclerosis and trigger the occurrence of AMI.