Genetic susceptibility of five tagSNPs in the endothelin-1 (EDN1) gene to coronary artery disease in a Chinese Han population.

Endothelin-1 (ET-1) plays important roles in endothelial dysfunction, vascular physiology, inflammation, and atherosclerosis. Nonetheless, the role of ET-1 (EDN1) gene variants on coronary artery disease (CAD) risk remains poorly understood. The aim of the present study was to evaluate the role of EDN1 gene polymorphisms on individual susceptibility to CAD. We genotyped five tagSNPs (single-nucleotide polymorphisms) (rs6458155, rs4145451, rs9369217, rs3087459, and rs2070699) within EDN1 gene in 525 CAD patients and 675 control subjects. In a multivariate logistic regression analysis, we detected an association of rs6458155 in EDN1 gene with the CAD risk; compared with the TT homozygotes, the CT heterozygotes (odds ratio (OR) = 1.53, 95% confidence interval (CI) = 1.02-2.29, P=0.040) and the CC homozygotes (OR = 1.55, 95% CI = 1.01-2.36, P=0.043) were statistically significantly associated with the increased risk for CAD. A similar trend of the association was found in dominant model (OR = 1.53, 95% CI = 1.05-2.25, P=0.029). Consistently, the haplotype rs6458155C-rs4145451C containing rs6458155 C allele exhibited the increased CAD risk (OR = 1.22, 95% CI = 1.03-1.43, and P=0.018). In addition, CT genotype of rs6458155 conferred the increased plasma ET-1 levels compared with TT genotype (P<0.05). No association of the other four tagSNPs in EDN1 gene with CAD risk was observed. In conclusion, our study provides the first evidence that EDN1 tagSNP rs6458155 is associated with CAD risk in the Chinese Han population, which is probably due to the influence of the circulating ET-1 levels.

The Impact of tagSNPs in CXCL16 Gene on the Risk of Myocardial Infarction in a Chinese Han Population.

CXCL16 has been demonstrated to be involved in the development of atherosclerosis and myocardial infarction (MI). Nonetheless, the role of the CXCL16 polymorphisms on MI pathogenesis is far to be elucidated. We herein genotyped four tagSNPs in CXCL16 gene (rs2304973, rs1050998, rs3744700, and rs8123) in 275 MI patients and 670 control subjects, aimed at probing into the impact of CXCL16 polymorphisms on individual susceptibility to MI. Multivariate logistic regression analysis showed that C allele (OR = 1.31, 95% CI = 1.03-1.66, and P = 0.029) and CC genotype (OR = 1.84, 95% CI = 1.11-3.06, and P = 0.018) of rs1050998 were associated with increased MI risk; and C allele (OR = 0.77, 95% CI = 0.60-0.98, and P = 0.036) of rs8123 exhibited decreased MI risk, while the other two tagSNPs had no significant effect. Consistently, the haplotype rs2304973T-rs1050998C-rs3744700G-rs8123A containing the C allele of rs1050998 and A allele of rs8123 exhibited elevated MI risk (OR = 1.41, 95% CI = 1.02-1.96, and P = 0.037). Further stratified analysis unveiled a more apparent association with MI risk among younger subjects (≤60 years old). Taken together, our results provided the first evidence that CXCL16 polymorphisms significantly impacted MI risk in Chinese subjects.

Variants in ANRIL gene correlated with its expression contribute to myocardial infarction risk.

ANRIL (antisense non-coding RNA in the INK4 locus), located at the 9p21.3 locus, has been known to be closely associated with the risk of coronary artery disease (CAD). To date, studies of the 9p21.3 variants on CAD risk mainly focus on the non-coding region of ANRIL. However, the biological significance of the variants on ANRIL promoter and exons is still unknown. Here we investigate whether the variants on ANRIL promoter and exons have an effect on myocardial infarction (MI) risk, and further analyze the association of these variants with the expression of ANRIL transcript. We did not find any common variants with minor allele frequencies (MAF) larger than 5% in ANRIL promoter by sequencing 1.6kb upstream of the start codon. Unconditional logistic regression analysis revealed that two SNPs in ANRIL exons, rs10965215 and rs10738605, were significantly associated with MI risk. Further studies revealed that ANRIL transcript EU741058.1 expression levels of rs10965215 and rs10738605 risk genotypes were borderline lower than those of protective genotypes. Our data provide the evidence that the variants rs10965215 and rs10738605 in ANRIL exons contribute to MI risk in the Chinese Han population which might be correlated with the expression of its transcript EU741058.1.

Association of lincRNA-p21 Haplotype with Coronary Artery Disease in a Chinese Han Population.

lincRNA-p21 plays an important role in the pathogenesis and progression of coronary artery disease (CAD). To date, the biological significance of polymorphisms in lincRNA-p21 on CAD risk remains unknown. Here we aimed to evaluate the influence of lincRNA-p21 polymorphisms on individual susceptibility to CAD. Genotyping of four tagSNPs (rs9380586, rs4713998, rs6930083, and rs6931097) within lincRNA-p21 gene was performed in 615 CAD and 655 controls. The haplotype analysis showed that the haplotype G-A-A-G (rs9380586-rs4713998-rs6930083-rs6931097) was statistically significantly associated with the reduced risk for CAD (OR = 0.78, P = 0.023). Stratified analysis revealed that G-A-A-G haplotype was at a significantly lower risk for myocardial infarction (MI) (OR = 0.68, P = 0.010). We also found that haplotype G-A-A-G had a more pronounced decreased risk for premature CAD or MI subjects (OR = 0.67, P = 0.017 for premature CAD, and OR = 0.65, P = 0.041 for premature MI, resp.). Our data provide the first evidence that the G-A-A-G haplotype of lincRNA-p21 is associated with decreased risk of CAD and MI, particularly among premature CAD/MI in the Chinese Han population. Further studies with more subjects and in diverse ethnic populations are warranted to clarify the general validity of our findings.

Two tagSNPs rs352493 and rs3760908 within SIRT6 Gene Are Associated with the Severity of Coronary Artery Disease in a Chinese Han Population.

SIRT6 has been demonstrated to exert protective effects on endothelial cells and is closely associated with lipid metabolism, glucose metabolism, and obesity, indicating an important role in the pathogenesis and progression of coronary artery disease (CAD). Nonetheless, the biological significance of SIRT6 variants on CAD is far to be elucidated. Here we aimed to investigate the influence of SIRT6 polymorphisms on individual susceptibility and severity of CAD. Multivariate logistic regression analysis exhibited no significant association between these five polymorphisms and CAD risk in the genotype and allele frequencies. However, we found that the rs352493 polymorphism in SIRT6 exhibited a significant effect on the severity of CAD; C allele (χ(2) = 7.793, adjusted P = 0.013) and the combined CC/CT genotypes (χ(2) = 5.609, adjusted P = 0.031) presented the greater CAD severity. In addition, A allele (χ(2) = 5.208, adjusted P = 0.046) and AA (χ(2) = 4.842, adjusted P = 0.054) of rs3760908 were also associated with greater CAD severity in Chinese subjects. Our data provided the first evidence that SIRT6 tagSNPs rs352493 and rs3760908 play significant roles in the severity of CAD in Chinese Han subjects, which might be useful predictors of the severity of CAD.

Study of the features of coronary artery atheromatous plaque using intravascular ultrasound in patients with impaired glucose tolerance.

OBJECTIVE: We used intravascular ultrasound (IVUS) to analyze the features of coronary artery atheromatous plaque in patients with impaired glucose tolerance and mild-to-moderate angiographic coronary stenosis. The aim was to determine the clinical significance of plaque characteristics as well as the relationship between hemoglobin A1c (HbA1c) levels and coronary artery lesions. METHODS: HbA1c levels were evaluated in 85 patients (96 lesions), of whom 46 had impaired glucose tolerance (IGT Group) and 39 had normal blood glucose (NBG Group). IVUS was used to analyze the lesion vessel of both groups qualitatively and quantitatively. The external elastic membrane area (EEMA), minimal lumen area (MLA), plaque area (PA), and plaque burden (PB) were measured for both the target lesion and the reference segments (reference external elastic membrane area (REEMA), reference minimal lumen area (RMLA), reference plaque area (RPA), and reference plaque burden (RPB), respectively). RESULTS: HbA1c levels were significantly higher in the IGT Group than in the NBG Group (P < 0.05). In the IGT Group there was more soft plaque, eccentric plaque, and positive remodeling, and less calcification, while in the NBG Group there was much harder plaque and calcification, no reconstruction, and negative remodeling (P < 0.05). MLA was smaller in the IGT Group than in the NBG Group, while EEMA, PA, and PB were clearly greater (P < 0.05). In the meantime, RMLA was clearly smaller in the IGT Group than in the NBG Group, while RPA and RPB were greater (P < 0.05). HbA1c levels were positively correlated with PA and PB, and negatively correlated with MLA. CONCLUSION: IVUS is very valuable for the evaluation of mild-to-moderate coronary lesions. The coronary artery lesions in patients with IGT are more serious and widespread than those in patients with NBG. HbA1c levels might be of some value in assessing the severity of coronary artery lesions.

The association of APOC4 polymorphisms with premature coronary artery disease in a Chinese Han population.

BACKGROUND: Hypercholesterolemia arising from abnormal lipid metabolism is one of the critical risk factors for coronary artery disease (CAD), however the roles of genetic variants in lipid metabolism-related genes on premature CAD (≤ 60 years old) development still require further investigation. We herein genotyped four single nucleotide polymorphisms (SNPs) in lipid metabolism-related genes (rs1132899 and rs5167 in APOC4, rs1801693 and rs7765781 in LPA), aimed to shed light on the influence of these SNPs on individual susceptibility to early-onset CAD. METHODS: Genotyping of the four SNPs (rs1132899, rs5167, rs1801693 and rs7765781) was performed in 224 premature CAD cases and 297 control subjects (≤ 60 years old) using polymerase chain reaction-ligation detection reaction (PCR-LDR) method. The association of these SNPs with premature CAD was performed with SPSS software. RESULTS: Multivariate logistic regression analysis showed that C allele (OR = 1.50, P = 0.027) and CC genotype (OR = 2.84, P = 0.022) of APOC4 rs1132899 were associated with increased premature CAD risk, while the other three SNPs had no significant effect. Further stratified analysis uncovered a more evident association with the risk of premature CAD among male subjects (C allele, OR = 1.65, and CC genotype, OR = 3.33). CONCLUSIONS: Our data provides the first evidence that APOC4 rs1132899 polymorphism was associated with an increased risk of premature CAD in Chinese subjects, and the association was more significant among male subjects.

A TagSNP in SIRT1 gene confers susceptibility to myocardial infarction in a Chinese Han population.

SIRT1 exerts protective effects against endothelial cells dysfunction, inflammation and atherosclerosis, indicating an important role on myocardial infarction (MI) pathogenesis. Nonetheless, the effects of SIRT1 variants on MI risk remain poorly understood. Here we aimed to investigate the influence of SIRT1 polymorphisms on individual susceptibility to MI. Genotyping of three tagSNPs (rs7069102, rs3818292 and rs4746720) in SIRT1 gene was performed in a Chinese Han population, consisting of 287 MI cases and 654 control subjects. In a logistic regression analysis, we found that G allele of rs7069102 had increased MI risk with odds ratio (OR) of 1.57 [95% confidence interval (CI) = 1.15-2.16, Bonferroni corrected P (Pc) = 0.015] after adjustment for conventional risk factors compared to C allele. Similarly, the combined CG/GG genotypes was associated with the increased MI risk (OR = 1.64, 95% CI = 1.14-2.35, Pc = 0.021) compared to the CC genotype. Further stratified analysis revealed a more significant association with MI risk among younger subjects (≤ 55 years old). Consistent with these results, the haplotype rs7069102G-rs3818292A-rs4746720T containing the rs7069102 G allele was also associated with the increased MI risk (OR = 1.41, 95% CI = 1.09-1.84, Pc = 0.040). However, we did not detect any association of rs3818292 and rs4746720 with MI risk. Our study provides the first evidence that the tagSNP rs7069102 and haplotype rs7069102G-rs3818292A-rs4746720T in SIRT1 gene confer susceptibility to MI in the Chinese Han population.

Study on the correlation between the concentration of plasma lipoprotein-associated phospholipase A2 and coronary heart disease.

OBJECTIVE: This study explores the correlation between plasma lipoprotein-associated phospholipase A2 (Lp-PLA2) and coronary heart disease (CHD) by comparing the level of plasma Lp-PLA2 in the plasma of patients with different types of CHD. METHODS: Blood samples were collected from 56 patients diagnosed with CHD by the Department of Cardiology of the First People's Hospital of Foshan and 34 healthy subjects from February 2013 to January 2014. We measured the concentration of plasma Lp-PLA2 and determined the levels of total cholesterol (Tch), triglyceride (TG), apolipoprotein A1 (Apo-A1), apolipoprotein B (Apo-B), high density lipoprotein-cholesterol (HDL-c), low density lipoprotein-cholesterol (LDL-c), lipoprotein a (Lp(a)), glucose (Glu), and high-sensitivity C-reactive protein (hs-CRP). The concentration of plasma Lp-PLA2 in the healthy control group and each subgroup of CHD patients were compared and analyzed for correlations of plasma Lp-PLA2 between the patients in different CHD subgroups and several laboratory indicators. RESULTS: The concentration of plasma Lp-PLA2 in each subgroup of CHD was significantly higher than in the control group (P < 0.05). The concentration of Lp-PLA2 in the unstable angina pectoris (UAP) group and acute myocardial infarction (AMI) group were significantly higher than in the stable angina pectoris (SAP) group (P < 0.05), and the concentration of plasma Lp-PLA2 in the AMI group was significantly higher than in the UAP group (P < 0.05). The concentration of plasma Lp-PLA2 in the CHD group merely showed a positive correlation (r = 0.493, P < 0.05) with the hs-CRP group, but the levels of Tch, TG, Apo-A1, Apo-B, HDL-c, LDL-c, Lp(a) and Glu did not. CONCLUSIONS: The concentration of plasma Lp-PLA2 in patients with CHD was higher than that in the control group. The concentration of plasma Lp-PLA2 in the subgroups of CHD patients varied greatly from each other. The inflammatory response of atherosclerosis might be resulted from the synergy of plasma Lp-PLA2 and hs-CRP.

The LRP6 rs2302685 polymorphism is associated with increased risk of myocardial infarction.

BACKGROUND: Abnormal lipids is one of the critical risk factors for myocardial infarction (MI), however the role of genetic variants in lipid metabolism-related genes on MI pathogenesis still requires further investigation. We herein genotyped three SNPs (LRP6 rs2302685, LDLRAP1 rs6687605, SOAT1 rs13306731) in lipid metabolism-related genes, aimed to shed light on the influence of these SNPs on individual susceptibility to MI. METHODS: Genotyping of the three SNPs (rs2302685, rs6687605 and rs13306731) was performed in 285 MI cases and 650 control subjects using polymerase chain reaction-ligation detection reaction (PCR-LDR) method. The association of these SNPs with MI and lipid profiles was performed with SPSS software. RESULTS: Multivariate logistic regression analysis showed that C allele (OR = 1.62, P = 0.039) and the combined CT/CC genotype (OR = 1.67, P = 0.035) of LRP6 rs2302685 were associated with increased MI risk, while the other two SNPs had no significant effect. Further stratified analysis uncovered a more evident association with MI risk among younger subjects (≤60 years old). Fascinatingly, CT/CC genotype of rs2302685 conferred increased LDL-C levels compared to TT genotype (3.0 mmol/L vs 2.72 mmol/L) in younger subjects. CONCLUSIONS: Our data provides the first evidence that LRP6 rs2302685 polymorphism is associated with an increased risk of MI in Chinese subjects, and the association is more evident among younger individuals, which probably due to the elevated LDL-C levels.

A common variant in pre-miR-146 is associated with coronary artery disease risk and its mature miRNA expression.

miRNAs are small non-coding RNAs that play an important role in numerous physiological processes. Common single nucleotide polymorphisms (SNPs) in pre-miRNAs may change their property through altering miRNAs expression and/or maturation, resulting in diverse functional consequences. To date, the role of genetic variants in pre-miRNAs on coronary artery disease (CAD) risk remains poorly understood. Here we aimed to evaluate the influence of three common SNPs in pre-miRNAs (miR-146a rs2910164 G>C, miR-196a2 rs11614913 C>T, miR-499 rs3746444 T>C) on individual susceptibility to CAD in a Chinese population of 295 CAD patients and 283 controls. Genotyping was performed using polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP) method. In a logistic regression analysis, we detected an association of rs2910164 in pre-miR-146a with the CAD risk; compared with the GG homozygotes, the GC heterozygotes [odds ratio (OR)=1.89, 95% confidence interval (CI)=1.06-3.36, P=0.029] and the CC homozygotes (OR=1.83, 95% CI=1.01-3.32, P=0.046) genotype were statistically significantly associated with the increased risk for CADs. As we used further genotype association models, we found a similar trend of the association in recessive model (OR=1.86, 95% CI=1.09-3.19, P=0.023). We also found that the genotypes of miR-146a rs2910164 were associated with its mature miRNA expression by analyzing 23 PBMC samples from CAD patients. Individuals carrying rs11614913 GC or CC genotypes showed 3.2-fold higher expression compared to GG genotype carriers (P<0.05). We observed no association of the other two SNPs in miR-196a2 (rs11614913) and miR-499 (rs3746444) with the CAD incidence. Our data provide the first evidence that the miR-146a rs2910164 polymorphism is associated with increased risk of CAD in Chinese Han population, which may be through influencing the expression levels of the miRNA.

Effect of matrix metalloproteinase and their inhibitors on atrial myocardial structural remodeling.

AIMS: To explore the expression of matrix metalloproteinase and tissue inhibitor of metalloproteinase of atrial myocardial structure of rheumatic and coronary heart disease. METHODS: Fifty patients with rheumatic heart disease (RHD) undergoing artificial mitral valve replacement surgery were selected: 20 with sinus rhythm and 30 with atrial fibrillation. Another 40 patients with coronary artery disease (CAD) undergoing coronary artery bypass surgery were selected: 22 with myocardial infarction (MI) and 18 with unstable angina. During thoractomy, samples of the right auricle were taken and immunohistochemical staining and fluorescence quantitative PCR were performed to test matrix metalloproteinase (MMP) 1, MMP-3, MMP-7, MMP-9, tissue inhibitor of metalloproteinase (TIMP) 1, TIMP-2, TIMP-3 and TIMP-4 expression of the samples. RESULTS: In RHD, the left and right atrial diameters of the atrial fibrillation group were significantly larger than those of the sinus rhythm group (P < 0.01), but there was no significant difference between the left ventricular diastolic diameter and the left ventricular ejection. The immunohistochemical staining and real-time (RT)-PCR show that the expression of MMP-3, MMP-7, MMP-9, TIMP-1, TIMP-2, TIMP-3 and TIMP-4 were significantly increased in the atrial fibrillation group compared with the sinus rhythm group (all P < 0.01). The difference in MMP-1 of the two groups was not statistically significant. In CAD patients, the left and right atrial diameters and left ventricular diameter of the MI group were significantly larger than those of the unstable angina group (P < 0.01), but the left ventricular ejection fraction was obviously lower than that of the unstable angina group (P < 0.05). Immunohistochemical staining and RT-PCR show that the expression of MMP-3, MMP-9, TIMP-1 TIMP-2, TIMP-3, TIMP-4 were significantly increased in MI group compared with the unstable angina (P < 0.01, P < 0.01, P < 0.05, P < 0.05, P < 0.01 and P < 0.01, respectively). CONCLUSION: The expression of MMPs and TIMPs increased in RHD patients and MI patients. Regulating the expression and activity of MMPs and TIMPs may be an important clinical treatment and method to prevent, and even reverse, atrial remodeling.

[Relationship between Tpeak-Tend interval and coronary artery stenosis and effects of percutaneous transluminal coronary angioplasty on Tpeak-Tend].

OBJECTIVE: To explore the relationship between Tpeak-Tend interval (Tpe) and the extent and severity of coronary artery stenosis, and evaluate the effect of percutaneous transluminal coronary angioplasty and stent implantation (PCI) on Tpe in the patients with coronary heart disease (CHD). METHODS: The ECG data were collected from 187 CHD patients undergoing coronary angiography and PCI to evaluate the extend and severity of coronary artery stenosis before and after the interventions. RESULTS: The Tpe of patients with severe stenosis increased significantly as compared with that in patients with moderate stenosis (138.9-/+16.2 ms vs 116.5-/+13.7 ms, P<0.05), and a significant difference was also noted between the moderate stenosis and mild stenosis (86.4-/+12.9 ms) groups (P<0.05). The Tpe decreased significantly in the patients in the order of multi-vessel involvement (140.7-/+17.8 ms), double vessel involvement (118.6-/+14.9 ms), singly vessel involvement (100.5-/+13.2 ms), and stenosis-free (84.3-/+12.4 ms) groups (P<0.05). Tpe was correlated to the extent and severity of coronary artery stenosis (r>0.4). In patients with severe stenosis, the Tpe was significantly reduced at 1 h, 24 h, and 1 week after PCI (115.8-/+14.5, 92.7-/+12.9, and 88.2-/+11.3 ms, respectively, P<0.05). CONCLUSION: The Tpe can reflect the severity and range of coronary artery stenosis, which can be reduced by PCI. Tpe can be a new index for evaluating myocardial ischemia in CHD patients.

[Clinical assessment of Tpeak-end interval for prediction of myocardial infarction].

OBJECTIVE: To assess the value of Tpeak-end interval (Tpe) in predicting myocardial infarction (MI). METHODS: Tpe and Tpeak-end internal after correcting the heart rate (TpeRR) were measured and analyzed in 234 MI patients, who were followed-up for an average of 32 ± 10 months. RESULTS: Clinical events occurred in 45 (19.2%) patients at the end TpeRR of the follow-up. Tpe and of the patients with clinical events were significantly higher than those in patients without the clinical events (P < 0.001). The incidence of clinical events in patients with Tpe > 140 ms were significantly higher than that in patients with Tpe ≤ 140 ms by Kaplan-Meier analysis (P < 0.001). With clinical event as the end point, the proportional hazards rate was 2.48 in univariate COX analysis (P < 0.01). After controlling for risk factors, the hazards rate was 2.66 by multvariate COX regression (P < 0.01). CONCLUSION: Tpe is positively correlated to the prognosis of MI and serves as an new index for predicting the clinical events in MI patients.

[Comparison of right atrial matrix metalloproteinase expression between patients with unstable angina and myocardial infarction].

OBJECTIVE: To compare right atrial structural remodeling and the expression of matrix metalloproteinase (MMP) and tissue inhibitors (TIMP) between patients with unstable angina (UA) and myocardial infarction (MI). METHODS: Right atrial appendages were obtained from 18 patients with UA and 22 patients with MI undergoing coronary artery bypass grafting (CABG) operations. MMP-1, -3, -7, -9 and TIMP-1 protein expressions were detected by immunohistochemistry and RT-PCR. Echocardiography was performed before CABG. RESULTS: The left and right atrial diameter, left ventricular diameter and mRNA levels of MMP-3, MMP-9 and TIMP-1 were significantly higher in MI group than those in UA group [LAD: (40.8 +/- 4.2) mm vs. (33.1 +/- 5.1) mm, P < 0.01; RAD: (44.1 +/- 6.8) mm vs. (28.8 +/- 6.0) mm, P < 0.01; LVEDD: (48.9 +/- 6.0) mm vs. (39.7 +/- 7.1) mm, P < 0.05; MMP-3: 0.39 +/- 0.18 vs. 0.28 +/- 0.07, P < 0.05; MMP-9: 0.81 +/- 0.21 vs. 0.55 +/- 0.20, P < 0.01; TIMP-1: 1.79 +/- 0.89 vs. 0.94 +/- 0.47, P < 0.01]. MMP-1, MMP-7 levels were similar between the 2 groups (MMP-1: 0.14 +/- 0.06 vs. 0.10 +/- 0.08, P > 0.05; MMP-7: 0.25 +/- 0.05 vs. 0.23 +/- 0.06, P > 0.05). CONCLUSION: Right atrial up-regulation of MMP-3, MMP-9 and TIMP-1 levels may contribute to the right atrial structural remodeling in MI patients.

[Role of matrix metalloproteinase and tissue inhibitor of metalloproteinase in atrial structural remodeling in patients with atrial fibrillation].

OBJECTIVE: To study the relationship between atrial structural remodeling and the expressions of matrix metalloproteinase (MMPs) and their tissue inhibitors (TIMPs) in atrial fibrillation (AF). METHODS: Biopsy samples of the right atrial appendages were collected from 20 patients with sinus rhythm and 30 with AF undergoing heart valve replacement surgery for rheumatic heart diseases. All the patients received echocardiographic examination preoperatively. MMP-1, -3, -7, -9 and TIMP-1, -2, -3, -4 protein expressions were detected by immunohistochemistry and RT-PCR. RESULTS: Compared with those in patients with sinus rhythm, the AF patients had significantly increased left and right atrial diameters and mRNA levels of MMP-3, -7, -9 and TIMP-1, -2, -3, -4 (P<0.01). MMP-1 expression also showed an increase in AF patients, but the difference was no statistically significant from that in patients with sinus rhythm. CONCLUSION: The expressions of MMP-1, -3, -7, -9 and TIMP-1, -2, -3, -4 increase in fibrillating atrial tissue, which may contribute to atrial structural remodeling and atrial dilatation in AF patients.

[Correlation of heart rate turbulence to coronary lesions and its changes following percutaneous transluminal coronary angioplasty].

OBJECTIVE: To investigate the correlation between heart rate turbulence (HRT) and coronary lesion and the effects of percutaneous transluminal coronary angioplasty (PTCA) on HRT. METHODS: This study involved 150 patients undergoing 24-hour ambulatory electrocardiography (AECG) and elective coronary angiography (CAG). AECG was monitored on the first day and 7 days after PTCA in 108 patients with positive CAG findings, and the variation of HRT and cardiac functions were observed. The turbulence onset (TO), turbulence slope (TS) and turbulence timing (TT) of each section of HRT were calculated, analyzed and compared. RESULTS: The values of TO and TT were significantly higher and TS significantly lower in CAG-positive group than in CAG-negative group (P<0.05 or 0.001). Significant difference was found in TO, TS and TT between patients with single and multiple coronary lesions (P<0.05 and 0.001). The values of TO, TS and TT on the first day after PTCA improved significantly in comparison with the those before PTCA in patients with single and multiple coronary lesions (P<0.001). Postoperative follow-up of the patients revealed obviously attenuated HRT in patients with left cardiac insufficiency compared with the patients with normal cardiac function (P<0.05). CONCLUSION: HRT is correlated to the severity of the coronary lesions and shows significant improvement after PTCA. Cardiac function insufficiency is an important factor affecting the HRT attenuation.

[Efficacy and safety of segmental pulmonary vein isolation and circumferential pulmonary vein isolation in patients with atrial fibrillation: a comparative study].

OBJECTIVE: To compare the efficacy and safety of segmental pulmonary vein isolation (SPVI) and circumferential pulmonary vein isolation (CPVI) guided by EnSite NavX system in patients with atrial fibrillation (AF). METHODS: Eighty-five patients with paroxysmal AF and persistent AF were enrolled in this study. Forty patients (30 with paroxysmal AF and 10 with persistent AF) underwent SPVI procedure, and 45 (31 with paroxysmal AF and 14 with persistent AF) underwent CPVA guided by EnSite NavX three-dimensional electrophysiological mapping system. All the patients were followed up for over six months. RESULTS: The success rate was 65% in the SPVI group and 84.4% in the CPVI group (P=0.0332), with incidence of major complications of 17.5% and 6.7%, respectively (P=0.0845). In the SPVI group, 12.5% patients had pulmonary vein stenosis after the operation, which occurred in none of the patients in the CPVI group (P=0.0312). The total procedure time was 200.4+/-37.0 min in the SPVI group, significantly shorter than that in the CPVI group (226.5+/-26.1 min, P=0.002). The fluoroscopy time in the SPVI group was obviously longer than that in the CPVI group (54.7+/-9.7 vs 27.1+/-3.1 min, P<0.001). CONCLUSIONS: CPVI guided by EnSite NavX system is more effective than SPVI for treatment of atrial fibrillation with significantly shortened fluoroscopy time but prolonged procedure time. The two procedures results in comparable incidences of major complications, but CPVI is associated with reduced rate of pulmonary vein stenosis in comparison with SPVI.

[Therapeutical efficacy of routine intra-aortic balloon pump support in patients with high-risk acute myocardial infarction undergoing percutaneous coronary intervention].

OBJECTIVE: To assess the value of routine intra-aortic balloon pump (IABP) support in patients with high-risk acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI). METHODS: The clinical data of 41 patients with high-risk AMI undergoing emergency PCI with routine IABP support were retrospectively reviewed, and 38 patients paired with the former group receiving emergency PCI for high-risk AMI without IABP support at the same time were included as the control group. Thirty days after the operation, the two groups were compared for myocardial ischemic events, left ventricular function and major adverse cardiac events (MACE). RESULTS: Patients receiving IABP support had a significantly lower incidence of myocardial ischemic events than those without IABP (4.9% vs 15.8%, P<0.05), and showed greater improvement in the left ventricular function. Significant differences were also observed in the mortality rate, incidence of reinfarction and revascularization rate between the two groups, but not in the rate of MACE. CONCLUSION: Patients undergoing PCI for high-risk acute AMI can benefit from routine IABP support in terms of improvement of left ventricular function and reduce myocardial ischemic events and the rate of MACE. These results, however, still await further confirmation by large-scale clinical trials.

[Relation of plasma brain natriuretic peptide to serum creatine kinase MB level in patients with acute myocardial infarction following primary percutaneous coronary intervention].

OBJECTIVE: To study the relation between plasma brain natriuretic peptide (BNP) and serum creatine kinase MB (CK-MB) level in patients with acute myocardial infarction (AMI) following primary percutaneous coronary intervention (PCI). METHODS: Sixty-three consecutive patients with AMI were divided into two groups according to the timing of PCI, namely direct PCI and indirect PCI groups. Plasma BNP levels were measured in all patients on admission and at 4, 24 and 48 h after admission. The CK-MB level was measured every 3 h on the first day of hospitalization, every 6 h on the second day and every 12 h on the third day. RESULTS: BNP level increased gradually following admission and began to decrease 48 h after admission in the two groups of patients. The peak BNP level occurred at 24 h after admission, and the BNP levels in patients of indirect PCI group were significantly higher than that of direct PCI group at 4, 24 and 48 h after admission. The peak CK-MB level of the direct PCI group occurred significantly earlier than that of the indirect group. CONCLUSION: Plasma BNP level may serve as an important objective indicator for recanalization of the infarct-related arteries following PCI in the early stage of AMI, which can help in the decision on clinical treatment plans for AMI.