Jan-Yow Chen

Comparing Survival between Peritoneal Dialysis and Hemodialysis Patients with Subclinical Peripheral Artery Disease: a 6-Year Follow-Up

Peripheral artery disease (PAD) is known to be an increased mortality risk in patients with end-stage renal disease (ESRD). The aim of this study was to compare patient survival between patients with subclinical PAD undergoing peritoneal dialysis (PD) and hemodialysis (HD). Subclinical peripheral artery was defined as an ankle-brachial index of less than 0.9. This study was conducted from April 2005, and the observation period ended on 30 June 2011. At the end of the follow-up, the status of all patients was assessed and data on mortality were obtained for the entire cohort. A total of 91 patients (61 HD and 30 PD) were included for analyses in this study. Mortality rate was 60.0% (18/30) for PD and 52.5% (32/61) for HD. Kaplan-Meier estimate demonstrate that PD patients had a higher mortality rate than those underwent HD (log-rank p = 0.0039). Cox regression model demonstrated that PD was an independent predictor for further mortality in ESRD patients with subclinical peripheral artery disease.(p = 0.012, HR: 1.776, 95% CI: 1.136-2.775). In multivariate analysis, the HD group still had a greater survival than PD group (p = 0.005, HR:1.916, 95% CI: 1.218-3.015). In patients with subclinical peripheral artery disease, the patient survival is better in HD patients as compared with PD patients.

Promoter Polymorphism G-6A, which Modulates Angiotensinogen Gene Expression, Is Associated with Non-Familial Sick Sinus Syndrome

Background It is well known that familial sick sinus syndrome (SSS) is caused by functional alterations of ion channels and gap junction. Limited information is available on the mechanism of age-related non-familial SSS. Although evidence shows a close link between arrhythmia and the renin-angiotensin system (RAS), it remains to be determined whether the RAS is involved in the pathogenesis of non-familial SSS. Methods In this study, 113 patients with documented non-familial SSS and 125 controls were screened for angiotensinogen (AGT) and gap junction protein-connexin 40 (Cx40) promoter polymorphisms by gene sequencing, followed by an association study. A luciferase assay was used to determine the transcriptional activity of the promoter polymorphism. The interaction between nuclear factors and the promoter polymorphism was characterized by an electrophoretic mobility shift assay (EMSA). Results Association study showed the Cx40 -44/+71 polymorphisms are not associated with non-familial SSS; however, it indicated that four polymorphic sites at positions -6, -20, -152, and -217 in the AGT promoter are linked to non-familial SSS. Compared to controls, SSS patients had a lower frequency of the G-6A AA genotype (OR 2.88, 95% CI 1.58–5.22, P = 0.001) and a higher frequency of the G allele at -6 position (OR 2.65, 95% CI 1.54–4.57, P = 0.0003). EMSA and luciferase assays confirmed that nucleotide G at position -6 modulates the binding affinity with nuclear factors and yields a lower transcriptional activity than nucleotide A (P<0.01). Conclusion G-6A polymorphism, which modulates the transcriptional activity of the AGT promoter, may contribute to non-familial SSS susceptibility.

Feasibility and Accuracy of Pre-procedure Imaging of the Proximal Cephalic Vein by Duplex Ultrasonography in Pacemaker and Defibrillator Implantation

AbstractBackground: Failure of the cephalic venous approach in pacemaker and defibrillator implantation is always due to the small size and difficulty in isolation of the cephalic vein. We propose that pre-procedure imaging of the proximal cephalic vein is valuable to achieve successful access of cephalic vein. However, the feasibility and accuracy of duplex ultrasonographic imaging of the proximal cephalic vein are unknown. Methods: The study enrolled 30 consecutive patients who underwent new implantation of permanent pacemakers or defibrillators at our institute. An ultrasound probe scanned along the plane 2 cm beneath the inferior margin of the clavicle to locate the cephalic vein before device implantation. If the vein was well visualized, the venous diameter and the vertical depth were measured. The corresponding surface location of the vein on the chest wall was also identified and recorded by duplex ultrasonography. The echo-derived vertical depths and vascular findings were compared with those measured during surgery. Results: All proximal cephalic veins were well visualized in the infraclavicular region by duplex ultrasonography. They were compressible, patent in color Doppler ultrasound imaging, and displayed phasic change of Doppler signal during respiration, indicating patency in all study veins. The average diameter of the target cephalic vein was 7.7 ± 1.6 mm (range, 5.0–11.1 mm). The echo-derived vertical depth of the proximal cephalic veins was highly correlated with the depth measured during surgery (28.4 ± 5.5 vs. 28.4 ± 5.6 mm, r = 0.93, P < 0.0001). All target cephalic veins were isolated after exploration via the estimated surface location of the chest wall by pre-procedure duplex ultrasonography. Seven (23%) of the studied patients did not have their cephalic vein cannulated successfully. Conclusion: The target proximal cephalic vein in pacemaker and defibrillator implantation can be precisely imaged and localized by duplex ultrasonography. Although further studies are needed, our findings pave a way to further study and clarify the implantation problems of cephalic vein approach.

Ultrasonographic Predictors of Unsuccessful Cephalic Vein Approach During Pacemaker or Defibrillator Lead Implantation

Background: The cephalic vein approach is a preferred route for endocardial lead implantation; however, it is associated with a significant failure rate. Anatomic abnormalities likely play an important role, but specific features have not been well characterized.

Pre-procedure duplex ultrasonography to assist cephalic vein isolation in pacemaker and defibrillator implantation

Background: Difficulty in isolating the cephalic vein contributes to failed pacemaker and intracardiac cardioverter-defibrillator (ICD) implantation via the cephalic venous approach. The deltopectoral groove is used as a rough landmark, but the vein is often not found here. We evaluated the benefit of pre-procedural duplex ultrasonography in isolating the cephalic vein.Methods: We enrolled 80 consecutive patients undergoing new pacemaker or defibrillator implantation and performed duplex ultrasonography to localize the cephalic vein before implantation. The corresponding surface location in the infraclavicular region and the depth of the cephalic vein were identified and recorded if the vein was well visualized. Using the imaging results, we dissected the skin over the predicted location until the cephalic vein was isolated. We determined the depth and corresponding surface location of the proximal cephalic vein during surgery. Afterward, we compared localization of the vein using imaging, surgery, and the deltopectoral-groove method. The relationship between cephalic vein depth and body parameters was also evaluated after the procedure.Results: All proximal cephalic veins were successfully isolated under the assistance of pre-procedural duplex ultrasonography. When the corresponding surface locations were compared, the location depicted on sonograms was closer to the surgical finding than the location determined by using the deltopectoral-groove method (0.5 ± 3.9 vs. 4.9 ± 9.6 mm; P < .001). The depth of the cephalic vein derived from duplex sonograms showed excellent correlation with the surgical findings (r = 0.93, P < 0.001). The cephalic vein depth and body mass index (BMI) also showed a linear relationship with good correlation (r = 0.70, P < 0.001).Conclusion: Pre-procedural duplex ultrasonography helped in localizing the proximal cephalic vein and isolating the cephalic vein. Surface localization of the proximal cephalic vein was superior with sonography than with the deltopectoral-groove method. There was a linear relationship with good correlation between BMI and cephalic vein depth.

Interactions of Esmolol and Adenosine in Atrioventricular Nodal-Dependent Supraventricular Tachycardia: Implication for the Cellular Mechanisms of Adenosine

Introduction: Cellular mechanisms of adenosine include a direct effect on the activation of the adenosine-sensitive potassium current (IK,Ado) and an indirect effect on antagonism of catecholamine-stimulated adenylate cyclase activity. However, previous studies evaluating the influence of catecholamine activity on the electrophysiologic effects of adenosine have yielded conflicting results. We tested the hypotheses that if adenosine exerts its atrioventricular (AV) nodal blocking effects directly by activating the IK,Ado potassium current, rather than indirectly by reversing the catecholamine effects, then pretreatment with β-adrenergic blockade would not potentiate the effects of adenosine in terminating AV nodal-dependent supraventricular tachycardia (SVT). Methods and Results: During sustained AV nodal reentrant tachycardia (AVNRT) or AV reentrant tachycardia (AVRT) in 28 patients, adenosine was rapidly injected in incremental doses of 1.5, 3, 6, 9, 12 and 18 mg to determine the lowest effective dose required for tachycardia termination before and immediately after the end of esmolol infusion. Esmolol infusion was started with loading doses of 500 µg/kg/min for 1 min and 150 µg/kg/min for 4 min, followed by a maintenance infusion of 50–100 µg/kg/min. Esmolol infusion was continued until the tachycardia was terminated or the maximal dose of 100 mg was reached. Adenosine was effective in terminating SVT in all 28 patients with a mean lowest effective dose of 96 ± 54 µg/kg before esmolol. During esmolol infusion, tachycardia was reproducibly terminated in 8 patients (6 with AVNRT, 2 with AVRT) with a mean dose of 67 ± 23 mg. In the other 20 patients with persistent tachycardia after 100 mg of esmolol infusion, the lowest effective dose of adenosine could be determined in 19 patients. In the remaining patient with AVRT, the maximal dose of adenosine (18 mg) was unable to terminate the tachycardia immediately after the end of esmolol infusion. In these 19 patients, esmolol infusion caused significant lengthening of the tachycardia cycle length from 338 ± 36 to 372 ± 51 ms (p < 0.0001) and reduction of the mean arterial blood pressure from 96 ± 15 to 88 ± 18 mm Hg (p = 0.034). Compared to the dosage that was determined before esmolol infusion, the lowest effective dose of adenosine remained the same in 13 patients after the end of esmolol infusion, whereas the dose increased in 5 and decreased in 1 patient. The mean lowest effective dose of adenosine was not significantly different before (98 ± 54 µg/kg) and immediately after (115 ± 56 µg/kg) the end of esmolol infusion (p = 0.054). Conclusions: Intravenous esmolol infusion (up to 100 mg total dose) usually fails to terminate AV nodal-dependent SVT. In the esmolol-resistant tachycardia, esmolol pretreatment does not produce a positive synergistic effect on the efficacy of adenosine-induced termination of SVT. Therefore, in this tachycardia adenosine may exert its effects on AV nodal conduction directly by activation of the IK,Ado potassium current, rather than by antagonizing the β-adrenergic system.

Unexpected Loss of Atrial Tracking Caused by Interaction Between Temporary and Permanent Right Ventricular Leads During Implantation of a Biventricular Pacemaker

This report describes a patient who underwent implantation of an atriobiventricular pacemaker following AV junction ablation and insertion of a temporary right ventricular (RV) pacemaker. During implantation, intermittent loss of sinus P wave tracking occurred when the three permanent leads were connected to the generator. Analysis of marker annotation disclosed intermittent abnormal ventricular sensing that reinitiated postventricular atrial blanking and caused failure of P wave tracking. This phenomenon disappeared after removing the temporary RV lead, but not by turning off the temporary pacemaker. We assume that mechanical contact between the temporary and the permanent RV leads is the underlying mechanism. (PACE 2004; 27:998–1001)

Transforming Growth Factor-β1 T869C Gene Polymorphism Is Associated with Acquired Sick Sinus Syndrome via Linking a Higher Serum Protein Level.

Background Familial sick sinus syndrome is associated with gene mutations and dysfunction of ion channels. In contrast, degenerative fibrosis of the sinus node tissue plays an important role in the pathogenesis of acquired sick sinus syndrome. There is a close relationship between transforming growth factor-β1 mediated cardiac fibrosis and acquired arrhythmia. It is of interest to examine whether transforming growth factor-β1 is involved in the pathogenesis of acquired sick sinus syndrome. Methods Overall, 110 patients with acquired SSS and 137 age/gender-matched controls were screened for transforming growth factor-β1 and cardiac sodium channel gene polymorphisms using gene sequencing or restriction fragment length polymorphism methods. An enzyme-linked immunosorbent assay was used to determine the serum level of transforming growth factor-β1. Results Two transforming growth factor-β1 gene polymorphisms (C-509T and T+869C) and one cardiac sodium channel gene polymorphism (H588R) have been identified. The C-dominant CC/CT genotype frequency of T869C was significantly higher in acquired sick sinus syndrome patients than in controls (OR 2.09, 95% CI 1.16–3.75, P = 0.01). Consistently, the level of serum transforming growth factor-β1 was also significantly greater in acquired sick sinus syndrome group than in controls (5.3±3.4 ng/ml vs. 3.7±2.4 ng/ml, P = 0.01). In addition, the CC/CT genotypes showed a higher transforming growth factor-β1 serum level than the TT genotype (4.25 ± 2.50 ng/ml vs. 2.71± 1.76 ng/ml, P = 0.028) in controls. Conclusion Transforming growth factor-β1 T869C polymorphism, correlated with high serum transforming growth factor-β1 levels, is associated with susceptibility to acquired sick sinus syndrome.

Sinus node dysfunction as an initial presentation of adult systemic lupus erythematosus

Cardiac involvement in systemic lupus erythematosus (SLE) has been well described. However, sinus node involvement with profound sinus bradycardia as an early manifestation of adult SLE has not been reported. A 27-year-old previously healthy female was admitted due to intermittent fever for 4 days. SLE was diagnosed based on clinical manifestations and laboratory data. Profound sinus bradycardia (heart rate = 41/min) with weakness was noted during hospitalization. ECG abnormalities completely resolved after a high-dose intravenous steroid infusion. Sinus node involvement with significant bradycardia is one of the possible complications in the early stage of adult SLE. Close cardiovascular monitoring and serial ECGs are suggested for early detection of this serious complication of adult SLE.

The Shortest QRS Duration of an Electrocardiogram Might Be an Optimal Electrocardiographic Predictor for Response to Cardiac Resynchronization Therapy

QRS duration has been associated with the response to cardiac resynchronization therapy (CRT). However, the methods for defining QRS duration to predict the outcome of CRT have discrepancies in previous reports. The aim of this study was to determine an optimal measurement of QRS duration to predict the response to CRT.Sixty-one patients who received CRT were analyzed. All patients had class III-IV heart failure, left ventricular ejection fraction not more than 35%, and complete left bundle branch block. The shortest, longest, and average QRS durations from the 12 leads of each electrocardiogram (ECG) were measured. The responses to CRT were determined using the changes in echocardiography after 6 months. Thirty-five (57.4%) patients were responders and 26 (42.6%) patients were non-responders. The pre-procedure shortest, average, and longest QRS durations and the QRS shortening (ΔQRS) of the shortest QRS duration were significantly associated with the response to CRT in a univariate logistic regression analysis (P = 0.002, P = 0.03, P = 0.04 and P = 0.04, respectively). Based on the measurement of the area under curve of the receiver operating characteristic curve, only the pre-procedure shortest QRS duration and the ΔQRS of the shortest QRS duration showed significant discrimination for the response to CRT (P = 0.002 and P = 0.038, respectively). Multivariable logistic regression showed the pre-procedure shortest QRS duration is an independent predictor for the response to CRT.The shortest QRS duration from the 12 leads of the electrocardiogram might be an optimal measurement to predict the response to CRT.