[Abstract ] Objective Modern pharmacological studies confirmed Zhigancao Decoction total extract, single active ingredients and their combinations could obviously inhibit arrhythmia.This study was to investigate the effects of Zhigancao Decoction medicated serum combined with myocardial tissue/silicon substrate microelectrode arrays (MEA) on rapid atrial pacing(RAP). Methods New Zealand white rabbits were randomly divided into normal control group, normal serum control group, Zhigancao Decoction medica-ted serum group and water decoction group, 8 in each group.After the establishment of an atrial fibrillation rabbit model, the field ac-tion potential duration ( fAPD) of the right atrial appendage ( RAA ) tissue was measured and the effections of Zhigancao Decoction medicated serum and water decoction on the fAPD of RAA were observed. Results The successful modeling of rapid atrial pacing induced atrial fibrillation in rabbits contributed to the significant shortening of fAPD 12 h after pacing compared to that before pacing ([174.30 ±1.36]ms vs[162.48 ±0.88]ms, P<0.05).After giving 10%~25% Zhigancao Decoction medicated serum and water decoction, the fAPDs of RAA tissue in rabbits with atrial fibrillation were prolonged, which represented positive dose-response relation-ship.The fAPDs of the rabbits given serum containing 10%, 15%, 20%and 25%Zhigancao Decoction were respectively (170.81 ± 0.61)ms, (171.00 ±0.46)ms, (179.08 ±0.67)ms, (179.76 ±2.26)ms, which were longer than those of water decoction group ([163.82 ±0.780]ms, [163.66 ±0.95]ms, [174.06 ±1.32]ms, [176.84 ±1.19]ms), and the difference was statistically sig-nificant (P<0.05). Conclusion The fAPD can be taken as one index of cardiac electrophysiological change, and 10%~25%Zh-igancao Decoction medicated serum can lead to fAPD extension in rabbit model of atrial fibrillation, which might be the electrophysio-logical mechanism of anti-atrial fibrillation.

Cytochrome P-450 CYP1A1 ; genetics ; Genetic Predisposition to Disease ; Humans ; Logistic Models ; Pulmonary Disease, Chronic Obstructive ; complications ; Risk Factors ; Smoking ; adverse effects ; Venous Thromboembolism ; etiology ; genetics

OBJECTIVETo observe the outcome and assess related factors affecting left atrial remodeling after percutaneous balloon mitral valvuloplasty (PBMV) in patients with mitral valve stenosis.

METHODSFrom March 1998 to June 2002, there were 96 mitral valve stenosis patients who underwent PBMV in our hospital. Echocardiographic, 12 leads united electrocardiogram and other clinical datas were collected at preoperation, 1 week after operation, and 4 - 6 years after operation to retrospective analysis. Multiple stepwise regression analysis was used to assess controllable factors of left atrial remodeling.

RESULTSLeft atrial diameter reduced from (44.6 +/- 6.6) cm before PBMV to (42.8 +/- 6.5) cm (P > 0.05) 1 week after PBMV and enlarged to (47.2 +/- 5.7)cm (all P < 0.05) at the end of 4 - 6 years follow up post operation. The mitral valve area (MVA) increased from (1.06 +/- 0.32) cm2 before PBMV to (2.02 +/- 0.43) cm2 1 week after PBMV and (1.98 +/- 0.36) cm2 4 - 6 years post operation (all P < 0.05). Heart function assessed by NYHA classification improved significantly at 1 week and 4 - 6 years after surgery compared with pre-operation (P < 0.01). Multiple stepwise regression analysis showed that systolic blood pressure at 4 - 6 years after operation, MVA at 1 week after operation, preoperative atrial fibrillation, Wilkins score < or = 8, preoperative left atrial diameter were the independent predictive factors of left atrial remodeling at 4 - 6 years after PBMV.

CONCLUSIONSPBMV was an effective therapy option for patients with mitral valve stenosis. Systolic blood pressure at 4 - 6 years after operation, MVA at 1 week after operation, preoperative atrial fibrillation, Wilkins < or = 8, preoperative left atrial diameter are the predictive factors of left atrial remodeling after PBMV.

Adult ; Catheterization ; Female ; Heart Atria ; Humans ; Male ; Middle Aged ; Mitral Valve Stenosis ; therapy ; Prognosis ; Retrospective Studies ; Treatment Outcome

OBJECTIVETo investigate methylenetetrahydrofolate reductase (MTHFR) gene C677T mutation and plasma homocysteine (Hcy) levels in Uygur patients with venous thromboembolism (VTE) in Xinjiang.

METHODSA total of 222 VTE patients including 74 Uygur and 148 Han ethnic patients were examined, and 86 Uygur ethnic and Han 134 ethnic healthy people were included as controls. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was applied to detect MTHFR gene C677T polymorphism and plasma Hcy levels were measured by fluorescence polarization immunoassay.

RESULTSThe MTHFR gene C677T genotypes distribution in Uygur VTE patients and control groups were: TT [28.38% (35/86) vs. 12.79% (11/86), P < 0.05], CT [41.89% (31/74) vs. 52.33% (45/86), P > 0.05]and CC [29.73% (22/74) vs. 34.88% (30/86), P > 0.05], respectively; and in Han VTE patients and control groups were: TT[27.03% (40/148) vs. 14.92% (20/134), P < 0.05], CT [44.59% (66/148) vs. 52.99% (71/134), P > 0.05] and CC [28.38% (42/148) vs. 32.09% (43/134), P > 0.05], respectively. SNP genotyping distribution frequency in Uygur and Han ethnic population was similar between controls and between VTE patients (P > 0.05). Plasma levels of Hcy in MTHFR gene TT genotype were statistically higher than CT and CC genotype (P < 0.05). After adjusting for age, gender, smoking history, hyperlipidemia, hypertension, diabetes, and MTHFR genotype, multifactor logistic regression analysis showed that plasma Hcy level (OR = 1.025, 95%CI 1.003 - 1.046, P = 0.024) and obesity (OR = 4.660, 95%CI 1.417 - 15.324, P = 0.011) were independent risk factors for Uygur ethnic patients with VTE while plasma Hcy level (OR = 1.020, 95%CI 1.006 - 1.034, P = 0.004) and smoking (OR = 2.867, 95%CI 1.062 - 6.586, P = 0.024) were independent risk factors for Han ethnic patients with VTE.

CONCLUSIONMTHFR C677T polymorphism (TT genotype carrier) and increased plasma levels of Hcy are risk factors for Uygur and Han ethnic patients with VTE in Xinjiang.

Adult ; Aged ; Asian Continental Ancestry Group ; genetics ; Ethnic Groups ; genetics ; Female ; Gene Frequency ; Genotype ; Homocysteine ; blood ; Humans ; Male ; Methylenetetrahydrofolate Reductase (NADPH2) ; genetics ; Middle Aged ; Oxidoreductases Acting on CH-NH Group Donors ; genetics ; Polymorphism, Single Nucleotide ; Risk Factors ; Venous Thromboembolism ; blood ; genetics

BACKGROUNDIncreased levels of interleukin-6 (IL-6) and C-reactive protein (CRP) have been reported in patients with venous thromboembolisms (VTE). However, prospective studies did not confirm an association between IL-6, CRP and their polymorphism with the risk of VTE.

METHODSOne hundred and forty patients (including 66 males and 74 females, mean age (55.55 ± 17.11) years) and one hundred and sixty controls (including 74 males and 86 females, mean age (56.58 ± 12.24) years) were involved. An enzyme linked immunosorbent assay (ELISA) method was used for detecting the serum levels of inflammatory factors IL-6 and CRP in both groups. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used for analyzing the distribution of polymorphisms at the -572C/G and -597G/A sites of the promoter of the IL-6 gene and at 1059G/C of the CRP gene.

RESULTSSerum levels of IL-6 and CRP were significantly higher in the VTE group than in the control group (P < 0.05). The frequencies of -572C/G promoter polymorphisms CC, CG, and GG in the IL-6 gene were found to be 34%, 48%, and 18%, respectively, and the derived allele frequencies for the C and G alleles were 58% and 42%. There was a significant difference in the -572C/G promoter polymorphisms between the VTE group and control group (P < 0.05). For the -597G/A polymorphism, individuals all carried the GG and GA type; AA genotypes were not detected. The frequency of the GG, GC, and CC genotypes at the CRP1059G/C promoter was 87.57%, 7.86% and 3.57% in VTE group, while 86.25%, 10%, and 3.75% in control group, respectively. The frequency of G and C alleles at CRP 1059G/C was 91.43% and 8.57% in VTE group and 91.56% and 8.44% in the control group. The results showed that there was no statistically significant difference of 1059G/C genotype and mutation frequency of the allele between the VTE group and control group (P > 0.05). Multiple Logistic regression analysis showed CC homozygotes of the IL-6 -572G/C, body mass index (BMI), and CRP, IL-6, and high-density lipoprotein cholesterol (HDL-C) were independent risk factors for VTE (P < 0.05).

CONCLUSIONSWe found that VTE was associated with IL-6 and CRP levels, and there was an association of IL-6 and its promoter polymorphism at -572G/C with the risk of VTE. Thus far, a causal relationship between inflammation and VTE remains to be clarified and more prospective data are required.

Adult ; Aged ; C-Reactive Protein ; genetics ; Female ; Genetic Predisposition to Disease ; genetics ; Humans ; Interleukin-6 ; genetics ; Male ; Middle Aged ; Polymorphism, Genetic ; genetics ; Venous Thromboembolism ; genetics

BACKGROUNDEarly local platelet activation after coronary intervention identifies patients at increased risk of acute stent thrombosis (AST). However, early changes in platelet activation in coronary circulation following drug-eluting stent (DES) implantation have never been reported.

METHODSIn a prospective study of 26 consecutive elective stable angina patients, platelet activation was analyzed by measuring soluble glycoprotein V (sGPV) and P-selectin (CD62P) before and after implantation of either DES or bare metal stent (BMS). All patients were pretreated with clopidogrel (300 mg loading dose) and aspirin (75 mg orally) the day before the procedure. Blood samples were drawn from the coronary ostium and 10 - 20 mm distal to the lesion site.

RESULTSConsistent with the lower baseline clinical risk, the levels of CD62P and sGPV were within normal reference range, both in the coronary ostium and distal to the lesion before percutaneous coronary intervention (PCI) procedure. The levels of CD62P and sGPV did not change significantly (CD62P: (31.1 +/- 9.86) ng/ml vs (29.5 +/- 9.02) ng/ml, P = 0.319 and sGPV: (52.4 +/- 13.5) ng/ml vs (51.8 +/- 11.7) ng/ml, P = 0.674, respectively) after stent implantation when compared with baseline. Changes in these platelet activation markers did not differ between stent types.

CONCLUSIONSIntracoronary local platelet activation does not occur in stable angina patients before and immediately following DES implantation when dual anti-platelet is administered.

Adult ; Aged ; Angina Pectoris ; blood ; surgery ; Biomarkers ; Drug-Eluting Stents ; Female ; Humans ; Male ; Middle Aged ; P-Selectin ; blood ; Platelet Activation ; Platelet Membrane Glycoproteins ; analysis ; Prospective Studies

BACKGROUNDSmall noncoding microRNAs regulate gene expression in cardiac development and disease and have been implicated in the aging process and in the regulation of extracellular matrix proteins. However, their role in age-related cardiac remodeling and atrial fibrillation (AF) was not well understood. The present study was designed to decipher molecular mechanisms underlying age-related atrial structural remodeling and AF.

METHODSThree groups of dogs were studied: adult and aged dogs in sinus rhythm and with persistent AF induced by rapid atrial pacing. The expressions of microRNAs were measured by quantitative real-time polymerase chain reaction. Pathohistological and ultrastructural changes were tested by light and electron microscopy. Apoptosis index of myocytes was detected by TUNEL.

RESULTSSamples of atrial tissue showed the abnormal pathohistological and ultrastructural changes, the accelerated fibrosis, and apoptosis with aging and/or in AF dogs. Compared to the adult group, the expressions of microRNAs-21 and -29 were significantly increased, whereas the expressions of microRNAs-1 and -133 showed obvious downregulation tendency in the aged group. Compared to the aged group, the expressions of microRNAs-1, -21, and -29 was significantly increased in the old group in AF; contrastingly, the expressions of microRNA-133 showed obvious downregulation tendency.

CONCLUSIONThese multiple aberrantly expressed microRNAs may be responsible for modulating the transition from adaptation to pathological atrial remodeling with aging and/or in AF.

Age Factors ; Animals ; Apoptosis ; Atrial Fibrillation ; etiology ; Atrial Remodeling ; Connective Tissue Growth Factor ; physiology ; Dogs ; Electrocardiography ; Fibrosis ; In Situ Nick-End Labeling ; MicroRNAs ; analysis ; physiology ; Myocardium ; pathology ; ultrastructure