Feasibility of Atrial AutoCapture™ to Detect Atrial Evoked Response: Experience from 102 Patients Implanted with Dual-chamber Pacemakers.

BACKGROUND: Atrial AutoCapture™ (ACap™) was a new technological development that confirmed atrial capture by analyzing evoked response (ER) with a new method - paced depolarization integral ER detection - and optimized energy output to changes in the stimulation threshold. The purpose of this study was to evaluate the clinical performance of ACap™ function. METHODS: This was a prospective, observational, nonrandomized two-center study. Between November 2008 and August 2014, 102 patients were enrolled from two different institutions. Data were collected by case report forms at enrollment, hospital discharge, and in-office follow-ups scheduled at 1, 2, 3, 6, and 12 months postimplantation. RESULTS: Ambulatory ACap™ function started to become available for 20.6% of patients at 1 day, then progressed to 30.4% at 7 days, 38.6% at 1 month, 41.6% at 2 months, 47.5% at 3 months, 53.5% at 6 months, and 63.4% at 1 year. The cause of the unsuccessful attempts to perform ACap™ threshold was ER/polarization <2:1. Availability for SD, BND, and HOCM indications had shown better results than AVB indication. For SD indication cases, feasibility was significantly better for SD with paroxysmal atrial fibrillation (pAF) than SD without pAF (78.4% vs. 35.0% at 1 year, n = 71, P< 0.001). At each stage of the clinical follow-ups, there had been a strict correlation between ACap™ measurements and those conducted manually with P 0.001 (n = 299). CONCLUSIONS: It has been concluded that ACap™ function was safe and effective to confirm atrial threshold and reduce energy output automatically. ACap™ function is unavailable for some patients at early stages of the implantation; however, availability has been progressively increasing during follow-up.

[Association between plasma adiponectin and small, dense low density lipoprotein in patients with coronary artery disease].

OBJECTIVE: To observe the association between adiponectin and small dense low-density lipoprotein (sLDL-c) in coronary artery disease (CAD) patients. Furthermore, we sought to determine the association between single nucleotide polymorphisms (SNP) rs1501299 (+276G/T), rs266729 (-11365C/G) and the incidence of CAD. METHODS: Consecutive subjects with chest discomfort were examined by coronary angiography and divided into non-CAD [n = 250, 147 male, mean age (60.26 ± 7.52) years] and CAD [n = 267, 153 male, mean age (60.79 ± 9.63) years] groups. Blood samples were collected from all participants following an overnight fasting for at least 12 hours. Plasma adiponectin levels were measured by competitive enzyme-linked immunosorbent assay (ELISA). The serum levels of sLDL-C and oxidized low-density lipoprotein (ox-LDL) were determined by ELISA. Genotypes in rs1501299 and rs266729 of the adiponectin were determined by polymerase chain reaction (PCR). RESULTS: 1. The adiponectin levels were significantly lower [(306.17 ± 74.52) mg/L vs. (321.78 ± 86.28) mg/L], whereas sLDL-C and ox-LDL levels were significantly higher [(276.30 ± 45.55) ng/L vs. (249.00 ± 32.02) ng/L and (545.06 ± 115.46) µg/L vs. (497.74 ± 106.09) µg/L, P < 0.05] in CAD group than non-CAD group. 2. Adiponectin level was negatively associated with sLDL-C, whereas sLDL-C positively correlated with ox-LDL in all subjects. 3. Genotype distribution and allele frequencies of rs1501299 and rs266729 were similar between CAD and non-CAD subjects and not related to the serum levels of adiponectin, sLDL-C and ox-LDL. CONCLUSIONS: Reduced adiponectin and increased sLDL-C were independent risk factors for coronary artery disease. Genetic polymorphisms in rs1501299 and rs266729 were not linked with coronary artery disease.

[Association between plasma adiponectin level and in-stent restenosis after coronary stenting].

OBJECTIVE: The purpose of the present study was to identify the relationship between the plasma level of adiponectin and in-stent restenosis of patients with coronary heart disease after coronary stenting. METHOD: The study population comprised 119 individuals (92 men) who underwent stent implantation, including 65 subjects without in-stent restenosis (group A) and 54 patients with in-stent restenosis (group B). The level of plasma adiponectin was measured using ELISA. Coronary angiography was performed immediately before and after implanting stent and 9 - 12 months later. RESULTS: Baseline characteristics including drug use after PCI were similar between the groups. The rate of implanting bare metal stent is 8 (12.31%) and 6 (11.11%), TAXUS drug-eluting stent is 11 (16.92%) and 10 (18.52%) and CYPHER drug-eluting stent is 46 (70.77%) and 38 (70.37%) respectively (all P > 0.05). Plasma level of adiponectin in patient of group A was significantly higher than that in group B [(15.16 +/- 5.02) mg/L vs. (10.01 +/- 4.93) mg/L, P < 0.05]. The quantitative coronary angiography (QCA) showed that lesion length was similar between groups [(15.82 +/- 6.67) mm vs. (13.40 +/- 4.20) mm, P > 0.05], minimum lumen diameter (MLD) and stenosis rate were also similar before and after implanting stent (P > 0.05) and acute gain was (1.48 +/- 0.65) mm vs. (1.19 +/- 0.37) mm (P > 0.05). MLD was higher in group A than that in group B [(2.55 +/- 0.53) mm vs. (0.57 +/- 0.60) mm, P < 0.01] at 9 - 12 months follow up. Restenosis rate [(24.2 +/- 11.2)% vs.(81.0 +/- 19.1)%, P < 0.01] and late lumen loss [(0.50 +/- 0.34) mm vs. (1.60 +/- 0.54) mm, P < 0.01] were lower in group A than in group B. CONCLUSIONS: The lower plasma adiponectin level might be associated with in-stent restenosis after coronary stenting.

[Association of paraoxonase polymorphisms and serum homocysteine thiolactone complex with coronary heart disease].

OBJECTIVE: To investigate the relationship between paraoxonase (PON) polymorphisms and serum homocysteine thiolactone (HTL) and coronary heart diseases. METHOD: In this prospective study, serum complex of HTL levels using ELISA, and the lever of serum Hcy using high pressure liquid chromatography (HPLC), determined the PON1/T(-107)C and PON2/C311S genotypes using PCR-restriction fragment length polymorphisms 203 were measured in patients with angiographic documented coronary heart disease (CAD) and 117 controls. RESULTS: Serum levels of Hcy and the complex of HTL in CAD patients were significantly higher than that in controls (P < 0.05). No significant difference was found in frequencies of PON1/T(-107)C genotypes and alleles (P > 0.05) between CAD patient and controls. The PON2/C311S (SS) genotype was lower in CAD patients than that in controls (P < 0.05), while the frequency of allele was similar between the two groups (P > 0.05). The T allele of PON1/T(-107)C and S alleles of PON2/C311S polymorphism were associated with lower plasma Hcy and HTL complex [Hcy (11.83 +/- 4.76) micromol/L vs (15.32 +/- 10.32) micromol/L, P < 0.05; HTL complex (24.36 +/- 9.30) U/ml vs (32.05 +/- 10.44) U/ml, P < 0.05]. The genetype PON2 and allele C were higher in CAD patients with type 2 diabetes than that in CAD patients without type 2 diabetes and controls (P < 0.005). CONCLUSIONS: The elevation of serum Hcy and the complex of HTL were associated with increased risk of coronary heart disease. The allele PON1/(-107)T and PON2/311S might be protective for the development of atherosclerosis.

[Association of matrix metalloproteinase-9 and platelet membrane glycoprotein VI polymorphisms with acute coronary syndrome].

OBJECTIVE: To investigate serum level and gene polymorphisms of matrix metalloproteinase 9 (MMP-9), and platelet glycoprotein VI (GPVI) in patients with acute coronary syndrome (ACS). METHODS: In a prospective study of 179 patients with documented ACS and 164 controls, we measured baseline serum MMP-9 levels using ELISA and determined the MMP-9/C-1562T and MMP-9/G5564A genotypes using PCR-restriction fragment length polymorphism. Fib serum level was measured by Clauss assay. We also analyzed the Fib/Bbeta-148C/T and GPVI/T13254C polymorphisms. RESULTS: Serum levels of MMP-9 and Fib in ACS patients were significantly higher than in controls (P < 0.001), and serum level of Fib in the acute myocardial infarction group was higher than in patients with unstable angina (P < 0.05). No significant difference between ACS patients and controls was found in frequencies of MMP-9/C-1562T, MMP-9/G5564A, Fib/Bbeta-148C/T, and GPVI/T13254C genotypes and alleles (P > 0.05). The T allele of the Fib/Bbeta-148T polymorphism was associated with increased plasma Fib level (P < 0.05). There was a strong positive correlation between serum level of MMP-9 and Fib (r = 0.289, P < 0.01). CONCLUSION: Serum levels of MMP-9 and Fib were independent risk factors of ACS. There was an obvious relationship between the Bbeta-148C/T mutation and high Fib level. No significant difference between controls and ACS patients was found in the frequencies of MMP-9 C-1562T and G5564A, Fib Bbeta-148C/T and GPVI T13254C genotypes and alleles (P > 0.05).

[Metabolic syndrome strongly linked to stroke in Chinese].

OBJECTIVE: To assess the association of the metabolic syndrome with stroke in Chinese using the definition of ATP III, and revised definition according to Chinese criteria for abdominal obesity. METHODS: Multi-center case control study, 1934 first-ever-stroke patients (Atherothrombosis, lacunar infarction, and intracerebral hemorrhage) aged 30 to 74 years were sequentially recruited. And 1839 age, gender and geographically matched subjects were included as controls. RESULTS: The prevalence of metabolic syndrome defined by either ATP III or Chinese criteria was significantly increasing in patients with lacunar infarction, cerebral atherosclerosis, or intracerebral hemorrhage than control subjects. After age- and sex-adjusted and further adjusted age, sex, total cholesterol, smoking, drinking, and education levels, the metabolic syndrome defined by ATP III criteria was associated with a 2.7 to 4.3 fold and 2.5 to 4.0 fold higher risk of the three stroke subtypes, respectively. CONCLUSION: the metabolic syndrome defined by ATP III and revised according to Chinese criteria of abdominal obesity was positively associated with the risk of stroke in our case control study. This study underscores the need for well-designed prospective study in Chinese to give further evidence to the link between metabolic syndrome and stroke.

[Alpha-adducin gene G/W460 polymorphism is associated with intracerebral hemorrhage in Chinese].

OBJECTIVE: To explore the association between alpha-adducin (ADD1) G/W460 and intracerebral hemorrhage (ICH) in Chinese. METHODS: Samples of peripheral blood were collected from 456 patients with ICH diagnosed by CT or MRI from 7 clinical centers in China and 454 age, sex, and geographically matched subjects as controls. The ADD1 G/W460 polymorphism was detected by PCR. Information about prior exposure to various potential risk factors was collected by questionnaire survey. RESULTS: The distribution of ADD1gene G460W polymorphisms in the ICH patients and controls were in agreement with the Hardy-Weinberg proportion. The prevalence of 460W allele among ICH cases was 82.2%, higher than that in the controls (76.0%, crude odds ratio, 1.46; 95% CI, 1.05 to 2.05). The ADD1 460W allele was still significantly associated with ICH after adjustment for hypertension and other ICH putative risk factors (adjusted odds ratio, 1.38; 95% CI, 1.01 to 1.88). CONCLUSION: Alpha-adducin gene G/W 460 polymorphism is significantly associated with the risk of ICH. This association does not appear to be mediated by established ICH risk factors, specifically hypertension status.

[Correlation of thrombospondin-1 G1678A polymorphism to stroke: a study in Chinese population].

OBJECTIVE: To assess whether thrombospondin-1 (THBS-1) gene G1678A polymorphism is associated with stroke. METHODS: Samples of venous blood were collected from 1634 patients with stroke, including cerebral thrombosis, lacunar cerebral infarction, and cerebral hemorrhage confirmed by CT or MRI, and sex-, and age-matched 1171 controls without cerebrovascular diseases. Genotypes were determined with polymerase chain reaction and allele-specific restriction enzyme analysis. RESULTS: The frequency of the THBS-1 gene 1678 AA genotype (0.503 vs. 0.441) was significantly higher in the cerebral thrombosis group than in the controls (P = 0.008). The frequency of the G allele (0.299 vs. 0.339) was significantly lower in the cerebral thrombosis group than in the controls (P = 0.009). No significant difference was seen in THBS-1 gene 1678 AA polymorphism either between the lacunar cerebral infarction group and the control group or between the cerebral hemorrhage group and the control group (all P > 0.05). Multiple logistic regression analysis showed that the AA genotype of THBS-1 gene G1678A carriers had a higher risk of cerebral thrombosis (OR: 1.4; 95% CI 1.083 - 1.693; P = 0.008) after adjustment for age, sex, SBP, DBP, BMI, smoking, TC, TG, HDL-C, LDL-C and Glu. CONCLUSION: AA genotypes in THBS-1 gene G1678A polymorphism may be a genetic risk factor of cerebral thrombosis in Chinese population.

[Association of small, dense low density lipoprotein with stroke].

OBJECTIVE: To investigate the relationship between small, dense LDL (sLDL) and stroke in Chinese population. METHODS: The plasma level of sLDL was examined by 2% - 16% nondenatured gradient gel electrophoresis in 204 patients with stroke, including 103 cases of ischemic cerebral infarction (ICI), 51 cases of lacunar infarction (LI), and 50 cases of subcortical hemorrhage (SH), and in 341 sex- and age-matched controls in China. Traditional risk factors for stroke were investigated as well. RESULTS: The plasma level of sLDL was significantly higher in patients with ICI and LI (54 +/- 8% and 52 +/- 7%) than in the controls (47 +/- 11%, both P < 0.01). However, the plasma sLDL of the CH patients was 50 +/- 9%, not significantly different from that of the controls (P > 0.05). Multiple stepwise regression analysis showed that sLDL was significantly associated with systolic blood pressure, age, and the levels of triglyceride, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol (all P < 0.05). Multivariate logistic regression analysis showed that those with sLDL > 50% had increase of risk of ischemic cerebral infarction (OR = 3.1, 95% CI 1.649 - 5.691, P < 0.001) independent of other risk factors. The relationship between sLDL abnormality and LI and between sLDL abnormality and SH had no statistical significance (both P > 0.05). CONCLUSION: sLDL is significantly associated with ischemic cerebral infarction independent of other risk factors in Chinese population. sLDL may be a new marker for stroke at least in this Chinese population.