Shih-Ann Chen

National Yang Ming University, T’ai-pei, Taipei, Taiwan

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Publications (430)1686.85 Total impact

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    ABSTRACT: Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is an inherited genetic disease caused by defective desmosomal proteins, and it has typical histopathological features characterized by predominantly progressive fibro-fatty infiltration of the right ventricle. Clinical presentations of ARVD/C vary from syncope, progressive heart failure (HF), ventricular tachyarrhythmias, and sudden cardiac death (SCD). The 2010 modified Task Force criteria were established to facilitate the recognition and diagnosis of ARVD/C. An implantable cardiac defibrillator (ICD) remains to be the cornerstone in prevention of SCD in patients fulfilling the diagnosis of definite ARVD/C, especially among ARVD/C patients with syncope, hemodynamically unstable ventricular tachycardia (VT), ventricular fibrillation, and aborted SCD. Further risk stratification is clinically valuable in the management of patients with borderline or possible ARVD/C and mutation carriers of family members. However, given the entity of heterogeneous penetrance and non-uniform phenotypes, the standardization of clinical practice guidelines for at-risk individuals will be the next frontier to breakthrough. Antiarrhythmic drugs are prescribed frequently to patients experiencing frequent ventricular tachyarrhythmias and/or appropriate ICD shocks. Amiodarone is the recommended drug of choice. Radiofrequency catheter ablation (RFCA) has been demonstrated to effectively eliminate the drug-refractory VT in patients with ARVD/C. However, the efficacy and clinical prognosis of RFCA via endocardial approach alone was disappointing prior to the era of epicardial approach. In recent years, it has been proven that the integration of endocardial and epicardial ablation by targeting the critical isthmus or eliminating abnormal electrograms within the diseased substrates could yield higher acute success and lower recurrence of ventricular tachyarrhythmias during long-term follow-up. Heart transplantation is the final option for patients with extensive disease, biventricular HF with uncontrollable hemodynamic compromise, and refractory ventricular tachyarrhythmias despite aggressive medical and ablation therapies. Copyright © 2015 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
    Journal of Cardiology 03/2015; DOI:10.1016/j.jjcc.2014.12.023 · 2.57 Impact Factor
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    ABSTRACT: Non-steroidal anti-inflammatory drugs (NSAIDs) increase the risk of atrial fibrillation (AF). This study investigated whether selective and non-selective NSAIDs differentially regulate the arrhythmogenesis of pulmonary veins and atria. Conventional microelectrodes were used to record action potentials (APs) in isolated rabbit PVs, sinoatrial node (SAN), left atrium (LA), and right atrium (RA) preparations before and after celecoxib or indomethacin administration. A whole-cell patch clamp was used to record the sodium-calcium exchanger (NCX) current, L-type calcium current (ICa-L), and late sodium current (INa-late) before and after celecoxib administration in isolated PV cardiomyocytes. Celecoxib (0.3, 1, and 3μM) reduced PV spontaneous beating rates, and induced delayed afterdepolarizations and burst firings in four of eight PV preparations (50%, p<0.05). Celecoxib also reduced SAN beating rates and decreased AP durations (APDs) in RA and LA, but did not change the resting membrane potential. Indomethacin (0.3, 1, 3, and 10μM) changed neither the PV or SAN beating rates nor RA APDs, but it reduced LA APDs. Celecoxib (3μM) significantly increased the NCX current and decreased the ICa-L, but did not change the INa-late. Ranolazine (10μM) suppressed celecoxib (3μM)-induced PV burst firings in 6 (86%, p<0.05) of 7 PVs. KB-R7943 (10μM) suppressed celecoxib (3μM)-induced PV burst firings in 5 (71%, p<0.05) of 7 PVs. Selective and non-selective NSAIDs differentially modulate PV and atrial electrophysiological characteristics. Celecoxib increased PV triggered activity through enhancement of the NCX current, which contributed to its arrhythmogenesis. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
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    ABSTRACT: Although the CHA2DS2-VASc (congestive heart failure, hypertension, age 75 years or older, diabetes mellitus, previous stroke or transient ischemic attack, vascular disease, age 65 to 74 years, female) score is recommended by both American and European guidelines for stroke risk stratification in atrial fibrillation (AF), the treatment recommendations for a CHA2DS2-VASc score of 1 are less clear. This study aimed to investigate the risk of ischemic stroke in patients with a single additional stroke risk factor (i.e., CHA2DS2-VASc score = 1 [males] or 2 [females]) and the impact of different component risk factors. We used the National Health Insurance Research Database in Taiwan. Among 186,570 AF patients not on antiplatelet or anticoagulant therapy, we evaluated males with a CHA2DS2-VASc score of 1 and females with a CHA2DS2-VASc score of 2. The clinical endpoint was the occurrence of ischemic stroke. Among 12,935 male AF patients with a CHA2DS2-VASc score of 1, 1,858 patients (14.4%) experienced ischemic stroke during follow-up (5.2 ± 4.3 years), with an annual stroke rate of 2.75%. Ischemic stroke risk ranged from 1.96%/year for men with vascular disease to 3.50%/year for those 65 to 74 years of age. For 7,900 females with AF and a CHA2DS2-VASc score of 2, 14.9% experienced ischemic stroke for an annual stroke rate of 2.55%. Ischemic stroke risk increased from 1.91%/year for women with hypertension to 3.34%/year for those 65 to 74 years of age. Not all risk factors in CHA2DS2-VASc score carry an equal risk, with age 65 to 74 years associated with the highest stroke rate. Oral anticoagulation should be considered for AF patients with 1 additional stroke risk factor given their high risk of ischemic stroke. Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
    Journal of the American College of Cardiology 02/2015; 65(7):635-642. DOI:10.1016/j.jacc.2014.11.046 · 15.34 Impact Factor
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    ABSTRACT: Ablations of atrial fibrillation (AF) have become more widely performed, and the strategy about long-term usage of oral anticoagulants (OACs) after catheter ablation is an important issue, especially for patients without obvious evidences of recurrences. The annual rate of thromboembolic (TE) event after catheter ablation was less than 1%. CHADS2 and CHA2DS2-VASc scores could be used to identify patients at the risk of TE events after ablations who should continue OACs regardless of the status of recurrence. Despite the improvement in understanding of AF and advancement of technology in catheter ablation, the long-term successful rates of paroxysmal and non-paroxysmal AF are around 50% and 30%, respectively. Patients with a high CHADS2 score are at a high risk of recurrence which could continuously occur after the catheter ablation without reaching a plateau. Among the patients with a CHADS2 score of ≥3, 26.9% of the recurrences happened 2 years post catheter ablation. Compared to the episodes of AF before catheter ablation, the AF episodes after ablation procedures are less symptomatic and shorter in duration. Therefore, it may not be safe to stop OACs for patients with a high risk score since the AF episodes are difficult to be detected after ablation procedures, but remain dangerous. In conclusion, the decision about the long-term strategy of OACs should be based on patients' baseline clinical risk scores, such as CHADS2 and CHA2DS2-VASc scores, rather than the status of recurrence.
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    ABSTRACT: Resveratrol has shown benefits in reducing ventricular remodeling and arrhythmias. This study aimed to assess the therapeutic efficacy of resveratrol in reducing atrial fibrillation (AF) in a heart failure (HF) model and explore underlying mechanisms. HF rabbits were created 4 weeks after undergoing coronary ligation. Group 1 (n = 6) included (a) normal; (b) HF sham; (c) HF rabbits treated for 1 week with intraperitoneal injections of resveratrol; (d) resveratrol + wortmannin, and (e) resveratrol + diphenyleneiodonium chloride (DPI). All rabbits underwent epicardial catheter stimulation. Collagen content, mRNA and protein expression in ionic channels, and PI3K/AKT/eNOS signaling pathways were studied in left atrial appendage (LAA) preparations. To investigate acute drug effects on left atrial (LA) electrophysiology, Groups 2 a-e (n = 6) were subjected to Langendorff perfusion. Higher AF inducibility was found in the HF group and groups that were administered PI3K and eNOS inhibitors than in the normal and resveratrol-treated groups (P < 0.001). Histological analysis of LAA revealed a decrease in fibrosis in resveratrol-treated groups compared with the HF group (8.95% ± 1.53% vs. 26.62% ± 2.19%, P < 0.001). In real-time PCR analysis, ionic channels including Kv1.4, Kv1.5, KvLQT1, Kir2.1, Nav1.5, Cav1.2, NCX, SERCA2a, and PLB were upregulated by resveratrol. PI3K, AKT, and eNOS mRNA and protein expressions were upregulated by resveratrol but were inhibited by the co-administration of wortmannin and DPI. Resveratrol decreases LA fibrosis and regulates variation in ionic channels to reduce AF through the PI3K/AKT/eNOS signaling pathway. Copyright © 2015. Published by Elsevier Inc.
    Heart rhythm: the official journal of the Heart Rhythm Society 01/2015; DOI:10.1016/j.hrthm.2015.01.044 · 4.56 Impact Factor
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    ABSTRACT: Atrial fibrillation (AF) is the most common cardiac arrhythmia. However, the development of preventative therapies for AF has been disappointing. The infiltration of immune cells and proteins that mediate the inflammatory response in cardiac tissue and circulatory processes is associated with AF. Furthermore, the presence of inflammation in the heart or systemic circulation can predict the onset of AF and recurrence in the general population, as well as in patients after cardiac surgery, cardioversion, and catheter ablation. Mediators of the inflammatory response can alter atrial electrophysiology and structural substrates, thereby leading to increased vulnerability to AF. Inflammation also modulates calcium homeostasis and connexins, which are associated with triggers of AF and heterogeneous atrial conduction. Myolysis, cardiomyocyte apoptosis, and the activation of fibrotic pathways via fibroblasts, transforming growth factor-β and matrix metalloproteases are also mediated by inflammatory pathways, which can all contribute to structural remodelling of the atria. The development of thromboembolism, a detrimental complication of AF, is also associated with inflammatory activity. Understanding the complex pathophysiological processes and dynamic changes of AF-associated inflammation might help to identify specific anti-inflammatory strategies for the prevention of AF.
    Nature Reviews Cardiology 01/2015; DOI:10.1038/nrcardio.2015.2 · 10.40 Impact Factor
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    ABSTRACT: Noncompliant patients might be at risk of thromboembolism because of the short half-life and rapid offset of dabigatran etexilate. The assessment and management of dabigatran noncompliance should be optimized. A total of 150 nonvalvular atrial fibrillation patients receiving dabigatran were prospectively enrolled and followed for drug compliance and persistence. Noncompliance was identified by questionnaires and interviews. The hemoclot thrombin inhibitor (HTI) assay was used for monitoring the plasma dabigatran levels. Sixteen patients were noncompliant (10.7%). None of the clinical characteristics were significantly relevant to noncompliance after multivariate analysis. The dabigatran plasma level based on HTI was the only independent predictor of noncompliance (odds ratio: 0.97 per ng/mL, P = 0.003). The prothrombin time (PT), international normalized ratio of PT (INR [PT]), and activated partial thromboplastin time did not differ between compliant and noncompliant patients. During the follow-up, the persistent prescription of dabigatran was noted in 75% of noncompliant patients without improvement in compliance. The drug discontinuation rate was higher in the noncompliant than compliant patients (6.7% vs. 25%, P = 0.035). None of the patients in either group received warfarin after discontinuing dabigatran. The assessment and management of dabigatran noncompliance is generally ignored in clinical practice. The measurement of dabigatran plasma levels by HTI could be a reliable and simple method to identify noncompliant patients. ©2015 Wiley Periodicals, Inc.
    Pacing and Clinical Electrophysiology 01/2015; DOI:10.1111/pace.12575 · 1.75 Impact Factor
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    ABSTRACT: Atrial fibrillation (AF) is prevalent in end-stage renal disease (ESRD) patients and negatively impacts patient outcomes. We explored the incidence and risk factors for new-onset AF among patients with ESRD undergoing renal replacement therapy, without a prior history of AF, retrieved from Taiwan's National Health Insurance Research Database (NHIRD). For each of 134,901 patients with ESRD, one age- and gender-matched control and one similarly matched patient with chronic kidney disease (CKD), a total of 404,703 patients, were selected from the NHIRD. The study endpoint was the occurrence of new-onset AF and patients were followed an average of 5.1 years. The incidence rates of AF were 12.1, 7.3, and 5.0 per 1000 person-years for ESRD, CKD, and control patients, respectively. Among patients with ESRD, age, hypertension, heart failure, coronary artery disease, peripheral arterial occlusive disease, and chronic obstructive pulmonary disease were significant risk factors for new-onset AF. Thus, patients with ESRD had a significantly higher risk of new-onset AF. The presence of multiple risk factors was associated with a higher possibility of AF occurrence.Kidney International advance online publication, 14 January 2015; doi:10.1038/ki.2014.393.
    Kidney International 01/2015; DOI:10.1038/ki.2014.393 · 8.52 Impact Factor
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    ABSTRACT: Multiform premature ventricular complexes (PVCs) are common electrocardiographic abnormalities in patients with structurally normal hearts. However, the prognostic value of these complexes remains unclear. This study aimed to clarify the role of PVC polymorphism in predicting adverse outcomes. We examined the database for 24-hour electrocardiography monitoring between January 1, 2002 and December 31, 2004. We analyzed 3351 individuals with apparently normal hearts. Kaplan-Meier curves and multivariate Cox proportional hazards models were employed to estimate the effect of multiform PVC and uniform PVC on the number of incident adverse events. Average follow-up time was 10±1years. Patients with multiform PVC were older and had a higher prevalence of comorbidities. In multivariate analysis, patients with multiform PVC had an increased incidence of mortality (hazard ratio [HR]: 1.642, 95% confidence interval [CI]: 1.327-2.031), hospitalization (HR: 1.196, 95% CI: 1.059-1.350), cardiovascular hospitalization (HR: 1.289, 95% CI: 1.030-1.613), new-onset heart failure (HF; HR: 1.456, 95% CI: 1.062-1.997), transient ischemic accident (HR: 1.411, 95% CI 1.063-1.873), and new-onset atrial fibrillation (AF; HR: 1.546, 95% CI: 1.058-2.258) compared to the group without PVC. Patients with multiform PVC had a higher rate of mortality (HR: 1.231, 95% CI: 1.033-1.468) and all cause-hospitalization (HR: 1.147, 95% CI: 1.025-1.283) compared with patients with uniform PVC. The presence of multiform PVC was associated with a higher incidence of mortality, hospitalization, transient ischemic attack, new-onset AF, and new-onset HF independent of other clinical risk factors. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
    International Journal of Cardiology 11/2014; 180C:80-85. DOI:10.1016/j.ijcard.2014.11.110 · 6.18 Impact Factor
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    ABSTRACT: A new scoring system, the anticoagulation and risk factors in atrial fibrillation (ATRIA) score, was proposed for risk stratification in patients with atrial fibrillation (AF). Whether the ATRIA scheme can adequately identify patients who are at low risk of ischemic stroke remains unknown.
    Journal of the American College of Cardiology 10/2014; 64(16):1658-65. DOI:10.1016/j.jacc.2014.06.1203 · 15.34 Impact Factor
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    ABSTRACT: Pulmonary veins (PVs) play a critical role in the pathophysiology of atrial fibrillation (AF). Histone deacetylases (HDACs) are vital to calcium homeostasis and AF genesis. However, the electrophysiological effects of HDAC inhibition were unclear. This study evaluated whether HDAC inhibition can regulate PV electrical activity through calcium modulation. Whole-cell patch-clamp, confocal microscopic with fluorescence, and Western blot were used to evaluate electrophysiological characteristics and Ca(2+) dynamics in isolated rabbit PV cardiomyocytes with and without MPT0E014 (a pan HDAC inhibitor), MS-275 (HDAC1 and 3 inhibitor), and MC-1568 (HDAC4 and 6 inhibitor) for 5~8h. Atrial electrical activity and induced-AF (rapid atrial pacing and acetylcholine infusion) were measured in rabbits with and without MPT0E014 (10mg/kg treated for 5hours) in vivo. MPT0E014 (1μM)-treated PV cardiomyocytes (n=12) had slower beating rates (2.1±0.2 vs. 2.8±0.1Hz, p<0.05) than control PV cardiomyocytes. However, control (n=11) and MPT0E014 (1μM)-treated (n=12) SAN cardiomyocytes had similar beating rates (3.2±0.2 vs. 2.9±0.3Hz). MS-275-treated PV cardiomyocytes (n=12, 2.3±0.2Hz), but not MC-1568-treated PV cardiomyocytes (n=14, 3.1±0.3Hz) had slower beating rates than control PV cardiomocytes. MPT0E014-treated PV cardiomyocytes (n=14) had a lower frequency (2.4±0.6 vs. 0.3±0.1 spark/mm/s, p<0.05) of Ca(2+) sparks than control PV (n=17) cardiomyocytes. As compared to control, MPT0E014-treated PV cardiomyocytes had reduced Ca(2+) transient amplitudes, sodium-calcium exchanger currents, and ryanodine receptor expressions. Moreover, MPT0E014-treated rabbits had less AF and shorter AF duration than control rabbits. In conclusions, HDAC inhibition reduced PV arrhythmogenesis and AF inducibility with modulation on calcium homeostasis. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
    International Journal of Cardiology 10/2014; 177(3):982-989. DOI:10.1016/j.ijcard.2014.09.175 · 6.18 Impact Factor
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    ABSTRACT: Background The implantation of permanent pacemaker (PPM) is life-saving for patients with life-threatening bradycardia. However, the effectiveness and prognosis of PPM implantations for extremely old patients (> 90 years old) have not been investigated before. Methods From 2001-2012, a total of 108 patients older than 90 years were identified from 2,630 consecutive patients receiving PPM implantations in our hospital as the study group. For each study patient, four age-, gender- and comorbidity-matched subjects who did not have the diagnoses of bradyarrhythmias indicated for PPM implantations were selected from the “Taiwan National Health Research Database” to constitute the control group (n = 432). The study endpoint was all-cause mortality. Results The median age of the study population was 91 (inter-quartile range = 90-93) years. Among the PPM group, 45 patients died during the follow-up with an annual mortality rate of 18.7%. The risk of mortality did not differ significantly between the study and control groups with a hazard ratio of 1.020 (95% confidence interval = 0.724-1.437, p value = 0.912) after the adjustment for age and gender. Procedure-related complications occurred in 7.4% of the patients receiving PPM implants, and pocket hematoma was the most common one. The pre-implantation history of heart failure and cerebrovascular accident, rather than age, were significant predictors of mortality among PPM recipients. Conclusions Nonagenarians with severe bradyarrhythmias could retain the same life expectancies as those without bradyarrhythmias through PPM implantations. Extremely old age (> 90 years) should not be a barrier for PPM implants when indications were present.
    The Canadian journal of cardiology 10/2014; 30(10). DOI:10.1016/j.cjca.2014.04.010 · 3.12 Impact Factor
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    ABSTRACT: Background Digoxin and related cardiac glycoside have been used for almost 100 years in atrial fibrillation (AF). However, recent 2 analyses of the “AFFIRM” trial showed non-consistent results about the risk of mortality associated with digoxin use. The goal of the present study is to investigate the relationship between digoxin and the risk of ischemic stroke and mortality in Asians. Methods This study used the “National Health Insurance Research Database” in Taiwan. A total of 4,781 AF patients who did not receive any antithrombotic therapy were selected as the study population. Among the study population, 829 subjects (17.3%) received the digoxin treatment. The risks of ischemic stroke and mortality of patients with or without digoxin use were compared. Results The use of digoxin was associated with an increased risk of clinical events with an adjusted hazard ratio of 1.41 (95% CI =1.17-1.70) for ischemic stroke and 1.21 (95% CI =1.01-1.44) for all-cause mortality. In the subgroup analysis based on the coexistence with heart failure or not, digoxin was a risk factor of adverse events for patients without heart failure, but not for those with heart failure (interaction p<0.001 for either endpoint). Among AF patients without heart failure, the use of beta-blockers was associated with better survival with an adjusted hazard ratio of 0.48 (95% CI = 0.34-0.68). Conclusions Digoxin should be avoided for AF patients without heart failure since it was associated with an increased risk of clinical events. Beta-blockers may be a better choice for controlling ventricular rate.
    The Canadian journal of cardiology 10/2014; 30(10). DOI:10.1016/j.cjca.2014.05.009 · 3.12 Impact Factor
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    ABSTRACT: Chronic kidney disease (CKD) is associated a higher incidence of atrial fibrillation (AF) with unclear mechanisms. Indoxyl sulfate (IS) accumulates in CKD patients. IS increases oxidative stress, which contributes to the genesis of AF. The arrhythmogenic effect of IS is unclear.
    Journal of Cardiovascular Electrophysiology 09/2014; 26(2). DOI:10.1111/jce.12554 · 3.48 Impact Factor
  • Shih-Lin Chang, Shih-Ann Chen
    Cardiac electrophysiology clinics 09/2014; DOI:10.1016/j.ccep.2014.05.004
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    ABSTRACT: Background: This study aimed to investigate the mechanism by which colchicine suppresses atrial fibrillation (AF) in a rabbit heart failure (HF) model. Methods and results: HF was induced by coronary ligation. Using the Langendorff perfusion system, monophasic action potentials were recorded in =the left atrial appendage (LAA) of normal rabbits (n = 6) and HF rabbits (n = 6) treated with colchicine (100 mu M) followed by colchicine (100 mu M) plus paclitaxel (5 RIM). Collagen content and mRNA and protein expression of ion channels through the PI3K/AKT/eNOS signaling pathway were evaluated in LAA of normal rabbits (n = 6) and HF rabbits treated with vehicle (n =6) or colchicine (n = 6) intraperitoneal injection for 2 clays. Colchicine decreased action potential duration (74.1 +/- 2.6 vs 91.8 +/- 3.3 ms, P < 0.001), effective refractory period, and maximum slope of the restitution curve in HF LAA. However, these effects were reversed by paclitaxel. The incidence of early afterdepolarizations, delayed afterdepolarizations, and AF inducibility was significantly lower after colchicine perfusion than at baseline or after colchicine plus paclitaxel perfusion. Cardiac function increased and LA fibrosis decreased after colchicine treatment, mRNA and protein expression of Kir2.1, Kv1.4, Kv1.5, Kv7.1, Cav1.2, and SERCA2a were upregulated after colchicine treatment, as was mRNA expression of PI3K, AKT, and eNOS. Conclusion: Colchicine regulates ion channel gene expression and activates the PI3K/AKT/eNOS signaling pathway in HF rabbits, which may reverse atrial remodeling and suppress AF.
    International Journal of Cardiology 08/2014; 176(3). DOI:10.1016/j.ijcard.2014.07.069 · 6.18 Impact Factor
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    ABSTRACT: A 44-year-old man with structurally normal heart underwent catheter ablation of left ventricular summit tachycardia. The initial mapping revealed the origin of tachycardia at the junction of great cardiac vein and anterior interventricular vein. During ablation the exit site shifted to the nearby regions, which was recognized by subtle changes of 12-lead ECG. Mapping and ablating at different exit sites rendered the tachycardia noninducible. This article is protected by copyright. All rights reserved.
    Journal of Cardiovascular Electrophysiology 08/2014; 26(1). DOI:10.1111/jce.12506 · 2.88 Impact Factor
  • International Journal of Cardiology 08/2014; 176(3). DOI:10.1016/j.ijcard.2014.07.250 · 6.18 Impact Factor
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    ABSTRACT: BACKGROUND The risk of acute myocardial infarction (AMI) in patients with atrial fibrillation (AF) with a CHA(2)DS(2)-VASc score of 0 (for men) or 1 (for women) has not been previously investigated. OBJECTIVE The objective of the present study was to compare the risk of AMI in AF and non-AF subjects with a Low (0 or 1) CHA(2)DS(2)VASc score. METHODS By using the National Health Insurance Research Database in Taiwan, we identified 7254 men with AF (with a CHA(2)DS(2)VASc score of 0) and 4860 women with AF (with a CHA(2)DS(2)-VASc score of 1). For each study patient, 1 age-, sex-, and CHA(2)DS(2)-VASc score-matched subject without AF was randomly selected to constitute the control group (n = 12,114). The clinical end point was the occurrence of AMI. RESULTS During a mean follow-up period of 5.7 L- 3.6 years, 258 patients (1.1%) suffered an AMI, with an annual incidence of 0.29% and 0.100/0 for patients with and without AF. AF was an independent risk factor of AMI, with an adjusted hazard ratio (HR) of 2.93 (95% confidence interval 2.21-3.87; P <.001). The risk of AMI was higher in men with AF than in women with AF, with a hazard ratio of 2.24 (95% confidence interval 1.61-3.11; P <.001) after adjustment for age and other comorbidities. CONCLUSION In patients with a CHA(2)DS(2)-VASc score of 0 or 1, AF was an independent risk factor of AMI. The risk of AMI was higher in men with AF than in women with AF. Cardiovascular risk prevention should be performed as part of the holistic management of AF to minimize the risks of AMI associated with AF.
    Heart rhythm: the official journal of the Heart Rhythm Society 08/2014; 11(11). DOI:10.1016/j.hrthm.2014.08.003 · 4.56 Impact Factor
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    ABSTRACT: Endocardial Unipolar Peak-Negative Voltage Predicts Abnormal Epicardial Substrates. Introduction: The characteristics of endocardial electrograms needed to detect the overlying abnormal epicardial substrates in arrhythmogenic right ventricular cardiomyopathy with epicardial ventricular tachycardia (VT) remain unclear. This study investigated which of the endocardial electrogram characteristics could predict the overlying abnormal epicardial substrates. Methods and Results: In 20 consecutive patients (median age: 46 years, 11 men) undergoing epicardial VT ablation, detailed endocardial and epicardial mappings were obtained by using the CARTO 3 system. The endocardial electrographic characteristics (unipolar peak-to-peak voltage, unipolar peak-negative-voltage, bipolar voltage, and bipolar electrogram duration) of the opposite endocardium and epicardium in RV were retrospectively investigated (N = 1,697 paired points, 84 +/- 60 pairs/patient). Endocardial predictors of the presence of epicardial dense scar (<0.5 mV), low voltage zones (LVZ; <= 1.5 mV), and ablation targets (by using activation mapping, entrainment mapping, and pace mapping) were analyzed. Results: In the multivariable analysis, (1) unipolar peak-negative voltage independently predicted the presence of epicardial LVZ, epicardial dense scar, and ablation targets; (2) bipolar voltage could not predict epicardial lesions; and (3) bipolar electrogram duration predicted epicardial LVZ, but not dense scar or ablation targets. The endocardial unipolar peak-negative voltage of <1.66 mV (89% sensitivity and 53% specificity) was the optimal cutoff point for predicting epicardial dense scar. Conclusions: In patients with RV epicardial VT, the presence of unipolar peak-negative voltage of <1.66 mV in the endocardium predicted the presence of epicardial dense scar (<0.5 mV) and potential ablation targets in the overlying epicardium.
    Journal of Cardiovascular Electrophysiology 07/2014; 25(12). DOI:10.1111/jce.12495 · 2.88 Impact Factor

Publication Stats

8k Citations
1,686.85 Total Impact Points


  • 1996–2015
    • National Yang Ming University
      • • School of Medicine
      • • Institute of Clinical Medicine
      T’ai-pei, Taipei, Taiwan
  • 1992–2015
    • Taipei Veterans General Hospital
      • Cardiology Division
      T’ai-pei, Taipei, Taiwan
  • 2012
    • Johns Hopkins Medicine
      Baltimore, Maryland, United States
  • 2011
    • Buddhist Tzu Chi General Hospital
      T’ai-pei, Taipei, Taiwan
    • National Defense Medical Center
      T’ai-pei, Taipei, Taiwan
  • 2009
    • University of the Ryukyus
      • Faculty of Medicine
      Okinawa, Okinawa, Japan
    • Chiang Mai University
      • Department of Internal Medicine
      Chiang Mai, Chiang Mai Province, Thailand
  • 2003–2008
    • Chung Shan Medical University
      • Institute of Medicine
      Taichung, Taiwan, Taiwan
  • 2000–2008
    • Shin Kong Wu Ho-Su Memorial Hospital
      T’ai-pei, Taipei, Taiwan
  • 2007
    • Taipei Medical University
      • Division of Cardiovascular Medicine
      T’ai-pei, Taipei, Taiwan
    • Indiana University-Purdue University Indianapolis
      • Department of Medicine
      Indianapolis, IN, United States
  • 2004–2005
    • Fu Jen Catholic University
      • School of Medicine
      T’ai-pei, Taipei, Taiwan
    • Kuang Tien General Hospital
      臺中市, Taiwan, Taiwan
    • Mackay Memorial Hospital
      • Department of Internal Medicine
      T’ai-pei, Taipei, Taiwan
  • 2002–2003
    • Wan Fang Hospital
      T’ai-pei, Taipei, Taiwan
  • 1995
    • Singapore General Hospital
      • Department of Cardiology
      Tumasik, Singapore