BackgroundActive fixation leads have provided stable atrial and ventricular pacing; however, long-term follow-up data have not been satisfactory. The purpose of this study was to investigate the long-term reliability of active fixation leads and their electrical characteristic stability.MethodsA total of 1196 pacing leads were implanted in 830 patients consecutively between 2002 and 2013. In this retrospective study, we were able to trace 1092 leads in 750 patients to investigate the prognosis of implanted leads. The measurement values (including pacing thresholds, sensing amplitudes, and lead impedances of both the atrial and ventricular leads) were obtained from medical records at the time of implantation and during follow up at the outpatient device clinic. All pacing leads were FINELINE II Sterox EZ Leads (Boston Scientific, MN, USA), which are sweet-tip type screw-in active fixation leads, except for the shock leads in patients with implantable cardioverter defibrillator.ResultsThe mean follow-up period was 51.3±29.2 months (median, 48 months). A total of 1092 leads were implanted in either the atrium (682 leads) or the ventricle (410 leads). Venous access was achieved through cephalic vein cut down (CVC) method (914 leads) or the subclavian vein puncture (SVP) method (178 leads). The overall lead survival rate was 99.6% at both 5 and 10 years. Lead fracture was observed in 4 of 1092 leads (0.37%), all of which were implanted by the SVP method. No lead fracture occurred among patients wherein CVC method was applied (p<0.01). Device-related infection was observed in four patients (0.53%).ConclusionsThe overall reliability and stability of sweet-tip type screw-in leads were satisfactory throughout the long-term follow-up period (median, 4 years). Because it was associated with less lead fractures, cut-down access from the cephalic vein may be recommended as the first-line approach when considering the importance of long-term durability of pacing leads.
Thrombocytopenia is a frequent complication in patients requiring intra-aortic balloon pumping (IABP) counterpulsation. However, its prognostic impact has not been fully addressed. The objective of this study is to evaluate the impact of the change in the platelet number during IABP use on the prognosis after device removal. This is a retrospective observational study. Patients in the intensive cardiac care unit at three Juntendo University hospitals who underwent percutaneous implantation of IABP with or without veno-arterial extracorporeal membrane oxygenation (V-A ECMO), since 2012-2016, were enrolled in the study (n = 439). Patients who died during mechanical circulatory support (n = 47) were excluded. We evaluated the prognostic impact of the ratio of platelet reduction from the baseline (% PLT reduction) during IABP use on cardiovascular mortality after device removal. The median and the range of follow-up period were 298 days and 0-1,869 days, respectively. Unadjusted Kaplan-Meier analysis demonstrated that patients with a higher % PLT reduction had higher cardiovascular (CV) mortality. An adjusted Cox proportional hazard analysis demonstrated that a 10% higher % PLT reduction was associated with higher cardiovascular (CV) mortality (Hazard ratio: 1.3, 95% Confidence interval: 1.1-1.6, P < 0.001). Moreover, % PLT reduction and the maximum C-reactive protein (CRP) level during IABP use were positively correlated (r = 0.326, P < 0.001). The reduced number of platelets during IABP use was associated with an increased risk of CV mortality.
Background Inflammation in atrial tissue underlies structural remodeling of left atrium, which is a hallmark of atrial fibrillation (AF). Activated monocytes mediate inflammation; however, the role of monocytes in AF pathogenesis has not been extensively examined. In this study, we thus investigated the association between structural remodeling of left atrium, represented by left atrial dimension (LAD), and characteristics of peripheral monocytes in patients with AF. Methods Blood samples were collected from patients undergone catheter ablation between July 2017 and October 2018, including AF patients (n=152) and paroxysmal supraventricular tachycardia (PSVT) patients, which serves as a control non-AF group (n=22). AF patients were further divided into two groups by the median of LAD (normal LAD group: LAD <40 mm, n=77, large LAD group: LAD ≥40 mm, n=75). Peripheral blood mononuclear cells (PBMC) were isolated to analyze monocyte subsets by flow cytometry. In a subset of patients, we further isolated monocytes from PBMC by using magnetic bead-based negative selection method then gene products associated with inflammation or monocyte functions were evaluated. We also examined migratory activity of monocytes toward monocyte chemotactic protein-1, a ligand for CC chemokine receptor 2 (CCR2), using a modified Boyden chamber method. Finally, we performed immunofluorescence staining of monocytes and macrophages in left atrial appendages resected from patients underwent coronary bypass graft surgery (CABG) complicated by AF. Results There were no differences in age, body mass index and high-sensitivity C-reactive protein levels among three groups, including non-AF, normal LAD and large LAD groups, except that more female subjects were included in non-AF group. We found that proportions of classical CD14++CD16- and nonclassical CD14+CD16++ monocytes were higher (non-AF: 71.2±7.3% vs. AF: 75.5±8.3%, p<0.05) and lower (non-AF: 16.4±5.9% vs. AF: 13.2±5.5%, p<0.05), respectively, in all AF patients compared with those in non-AF group, while no significant difference was observed between normal and large LAD groups. In monocytes from large LAD group, mRNA levels of CCR2, a receptor to mediate monocyte chemotaxis, were significantly higher compared to those in normal LAD group (Figure A, p<0.05). Furthermore, monocytes isolated from large LAD group exhibited higher migratory capacity compared to normal LAD group (Figure B, p<0.01). Finally, higher monocyte/macrophage infiltrations to left atrial appendages were implicated in patients with large LAD, shown by immunofluorescence staining. Conclusions Monocytes in AF patients with enlarged left atrium expressed higher CCR2 mRNA and were more active in chemotaxis to MCP-1, suggesting the proactive roles of activated monocytes in the pathogenesis of arterial remolding in AF.
Background The clinical significance of high-density lipoprotein (HDL) function, represented by cholesterol efflux capacity (CEC), in addition to serum HDL cholesterol (HDL-C) levels, has been recognized in the pathogenesis and prognosis in patients with atherosclerotic cardiovascular diseases. However, the roles of HDL in the development and the progression of atrial fibrillation (AF), has been rarely evaluated. In this study, we thus hypothesized that the compromised HDL function may be associated with the progression of pathological structural remodeling in left atrium (LA). Objective We explored the association between CEC of HDL and the left atrial dimension (LAD), a maker of structural remodeling in the LA, in patients with AF and control. Methods This is a single center case-control study including consecutive 260 AF patients (AF group) and 34 paroxysmal supraventricular tachycardia (PSVT) patients (PSVT group, served as a control group), who underwent catheter ablation from July 2017 to December 2018. Blood samples were collected before catheter ablation procedure. CEC of HDL was measured by using ex vivo radiotracer system that involved incubation of [3H] cholesterol-loaded J774.1 murine macrophage-like cells with apoB-depleted serum. Results Serum HDL-C level was lower in AF group compared to those of PSVT group (55.3±15.3mg/dl vs 61.7±13.3mg/dl: p=0.024). As a marker of HDL function, CEC of HDL was significantly lower in patients with AF group compared to those in PSVT patients (4.74±0.84% vs 5.20±0.99%: p=0.005, Fig 1). In all patients including both groups, CEC of HDL was inversely correlated with LAD (r=−0.25; p<0.001, Fig 2), indicating the inverse association between HDL function and the progression of structural remodeling in AF. Moreover, multivariate logistic regression analysis adjusted by age, gender, body mass index, ejection fraction, and HDL-C demonstrated that increase in CEC of HDL was associated with the lower risk to be highest quartiles of LAD (>42mm), even adjusted by serum HDL-C levels (odds ratio of 1-SD elevation in CEC of HDL for LAD>42mm: 0.63; 95% confidence interval: 0.40–0.97, p=0.037), which implicated the link between HDL function and progression of left atrial structural remodeling. Conclusion Findings in this study may suggest that compromised HDL functionality is associated with the pathogenesis of left atrial structural remodeling in AF patients.
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