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Objective: To study the expression pattern of apolipoprotein J (Apo J) in rat's model of vascular restenosis after cartid balloon dilation. Methods: A total of 40 Wistar rats were randomly divided into 2 groups: Experimental group, the rat's model of carotid artery injury was established by 2 F Fogarty balloon catheter scratching in right carotid artery and Control group, the rats received sham operation without catheter scratching. n=20 in each group. Right carotid artery tissue was taken at 1, 2, 3, 4 weeks after the operation respectively and 5 rats were used for each time point. The morphological changes were measured by HE staining, protein and gene expressions of Apo J were examined by immunohistochemistry and qRT-PCR. Results: Compared with Control group, at each time point Experimental group had obvious intimal hyperplasia and up-regulated protein and gene expressions of Apo J, P<0.05. In Experimental group, with prolonged time of injury, consistent endometrial hyperplasia was observed and it reached the maximum at 4 weeks after operation; the peak protein and gene expressions of Apo J was found at 3 weeks after operation, then decreased at certain point at 4 weeks after operation, P<0.05. Conclusion: Apo J might be closely related to intimal hyperplasia after vascular injury, high expression of vascular Apo J was mainly derived from vascular smooth muscle cell synthesis, it could be a kind of compensation with protective role and might be used as a new biological target for treating vascular retenosis after percutaneous coronary intervention.
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<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>
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Objective: To observe the automatic ventricular capture management (VCM) conifrmed by paced depolarization integral (PDI) evoked response detection via the follow-up study in patients with Zephyr5826 pacemaker implantation. Methods: A total of 102 relevant patients were enrolled. In order to conduct PDI calculation, pacemakers were set by bipolar sensing and bipolar pacing at immediately after implantation. VCM functions were observed at 1 day, 7 days and 1 month, 3, 6, 12 months after implantation, the ventricular threshold by VCM test and manual test were compared. The symptoms of pectoralis major stimulus, diaphragm stimulus and palpitation were observed in all follow-up patients. Results: There was 1 patient died by MI at 1 month after Zephyr5826 pacemaker implantation, the rest 101 patients were followed-up for 12 months. VCM function was successfully turned-on at immediately after implantation in all patients, no pectoralis major stimulus and diaphragm stimulus occurred. VCM function was turned-off in 6/101 (5.9%) patients at 7 days after implantation due to intolerable palpitation caused by daily automatic VCM, instead they received manual test at follow-up visit. The coincidence rate of ventricular thresholds between VCM test and manual test were 100%. Ventricular pacing output voltage by VCM was (0.99 ± 0.48) V,n=608. Compared with regular pacing output voltage (2.5V, 0.4ms), VCM function may save 84% of energy consumption; compared to high pacing output voltage (3.5V, 0.4ms), VCM may save 92%. Loss of ventricular capture and poor sensation were not found by ECG and 24 h dynamic monitoring. Conclusion: Zephyr5826 pacemaker may conduct bipolar pacing and scanning with VCM function, it can be effectively and safely operated by low energy output. A few patients may not use VCM function due to intolerable palpitation.
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Objective To investigate the predictive value of the non-invasive indicator deceleration capacity of heart rate (DC) in the sudden cardiac death (SCD) after acute myocardial infarction. Methods A total of 417 myocardial infarc?tion patients with ST-segment elevation in sinus rhythm were enrolled in this study. DC was assessed from data of 24-hour ECG Holter. Regular follow-ups were carried out within 12 months. The SCD events were recorded and compared with pa?tients without SCD. Results During 12 months of follow-up, 20 patients were died due to SCD (4.8%). Compared with sur?vival group, patients showed significantly lower left ventricular ejection fraction (LVEF, 0.393 ± 0.065 vs 0.528 ± 0.042, P<0.05) and DC [(2.85±1.66) ms vs (5.49±1.71) ms,P<0.05]in SCD group. Multivariate Cox proportional hazard regression analysis showed that lower LVEF(<0.35)[RR: 2.167(1.384-4.661), P=0.013]and DC (DC<4.5 ms)[RR: 3.706(2.709-5.374),P=0.020]were risk factors for the occurrence of SCD. The prediction sensitivity by the decreased LVEF and DC was 52.1%and 76.4%respectively, and the specificity was 84.5%and 86.1%respectively. Conclusion The decreased value of DC after acute myocardial infarction can predict the SCD events.
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<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>
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Adiponectin , Blood , Genetics , Coronary Artery Disease , Blood , Genetics , Gene Frequency , Genotype , Lipoproteins, LDL , Blood , Polymorphism, Single Nucleotide , Risk FactorsABSTRACT
<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>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Adiponectin , Blood , Coronary Restenosis , Blood , Pathology , Drug-Eluting Stents , Treatment OutcomeABSTRACT
<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>