Feasibility of Atrial AutoCapture™ to Detect Atrial Evoked Response: Experience from 102 Patients Implanted with Dual-chamber Pacemakers / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSIONS</b>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.</p>

Association between plasma adiponectin and small, dense low density lipoprotein in patients with coronary artery disease / 中华心血管病杂志

<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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).</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSIONS</b>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.</p>

Association between plasma adiponectin level and in-stent restenosis after coronary stenting / 中华心血管病杂志

<p><b>OBJECTIVE</b>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.</p><p><b>METHOD</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSIONS</b>The lower plasma adiponectin level might be associated with in-stent restenosis after coronary stenting.</p>

Association of paraoxonase polymorphisms and serum homocysteine thiolactone complex with coronary heart disease / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the relationship between paraoxonase (PON) polymorphisms and serum homocysteine thiolactone (HTL) and coronary heart diseases.</p><p><b>METHOD</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSIONS</b>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.</p>

Association of matrix metalloproteinase-9 and platelet membrane glycoprotein VI polymorphisms with acute coronary syndrome / 中华心血管病杂志

<p><b>OBJECTIVE</b>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).</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSION</b>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).</p>