Browsing by Author "Hu, Yu-Feng"

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A Novel and Simple Algorithm Using Surface Electrocardiogram That Localizes Accessory Conduction Pathway in Wolff-Parkinson-White Syndrome in Pediatric Patients
(2019-09-01)
Li, Hsing-Yuan
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Chang, Shih-Lin
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Chuang, Chi-Hsi
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Lin, Ming-Chih
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Lin, Yenn-Jiang
Background: The location of the accessory pathway (AP) can be precisely identified on surface electrocardiography (ECG) in adults with Wolff-Parkinson-White (WPW) syndrome. However, current algorithms to locate the AP in pediatric patients with WPW syndrome are limited. Objective: To propose an optimal algorithm that localizes the AP in pediatric patients with WPW syndrome. Methods: From 1992 to 2016, 180 consecutive patients aged below 18 years with symptomatic WPW syndrome were included. After the exclusion of patients with non-descriptive electrocardiography (ECG), multiple APs, congenital heart diseases, non-inducible tachycardia, and those who received a second ablation, 104 patients were analyzed retrospectively. Surface ECG was obtained before ablation and evaluated by using previously documented algorithms, from which a new pediatric algorithm was developed. Results: Previous algorithms were not highly accurate when used in pediatric patients with WPW syndrome. In the new algorithm, the R/S ratio of V1 and the polarity of the delta wave in lead I could distinguish right from the left side AP with 100% accuracy. The polarity of the delta wave of lead V1 could distinguish free wall AP from septal AP with an accuracy of 100% in left-side AP, compared to 88.6% in leads III and V1 for right-side AP. The overall accuracy was 92.3%. Conclusions: This simple, novel algorithm could differentiate left from right AP and septal from free wall AP in pediatric patients with WPW syndrome.
Effects of long-term exercise on arrhythmogenesis in aged hypertensive rats
(2018-11-01)
Sung, Yen-Ling
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Wu, Chih-En
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Syu, Jhen-Yang
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Kuo, Terry B. J.
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Li, Jai-Yi
Chronic hypertension is a multifactorial disease that is highly associated with cardiovascular disorders. Physical activity, such as long-term exercise, is advocated as a treatment for hypertension, but the responses of different age groups to long-term exercise are unknown. We used aged spontaneous hypertensive rats (SHRs, 80 weeks old) to test the hypothesis that long-term exercise compensated for deficient autonomic control and reduced susceptibility to ventricular tachycardia (VT) and ventricular fibrillation (VF) in this animal model. The aged SHRs were divided into control and voluntary exercise groups. Ambulatory electrocardiography was recorded for the heart rate variability (HRV) analysis. Programmed stimulation was applied to exposed hearts to induce ventricular arrhythmia in situ. Then, the hearts were isolated for an optical mapping study. The results showed that increased HRV indices were broadly related to vagal dominance in the high-intensity exercise group. Exercise altered the electrical propagation dynamic properties, such as the action potential duration restitution (APDR). Furthermore, the VF inducibility decreased with increased exercise intensity. Taken together, our results suggest that long-term exercise reduces the risk of arrhythmogenesis in aged SHRs through enhanced vagal control and stabilized electrical dynamics.
Interleukin-17 enhances cardiac ventricular remodeling via activating MAPK pathway in ischemic heart failure
(2018-09-01)
Chang, Shih-Lin
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Hsiao, Ya-Wen
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Tsai, Yung-Nan
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Lin, Shien-Fong
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Liu, Shuen-Hsin
Background: We aimed to investigate the impact of interleukin (IL)-17 on ventricular remodeling and the genesis of ventricular arrhythmia (VA) in an ischemic heart failure (HF) model. The expression of the proinflammatory cytokine IL-17 is upregulated during myocardial ischemia and plays a fundamental role in post-infarct inflammation. However, the influence of IL-17 on the genesis of VA has not yet been studied. Methods and results: The level of inflammation and Th17 cell (CD4(+)IL-17(+)) expression in the rabbit model of ischemic HF were studied by flow cytometry, quantitative polymerase chain reaction (qPCR), and enzyme-linked immunosorbent assay (ELISA). The effect of IL-17 on VA induction following acute and chronic administration of IL-17 was determined using electrophysiological techniques and optical mapping. The expression of IL-17 target genes and related cytokines and chemokines in vivo and in vitro were measured using qPCR, ELISA, and immunoblotting. Th17 cells were markedly increased in the ischemic HF rabbit model. IL-17 directly induced VA in vivo and in vitro in a dose-dependent manner. IL-17 decreased conduction velocity, lengthened action potential duration, and increased the slope of the left ventricle (LV) restitution curve. IL-17 treatment led to fibrosis, collagen production and apoptosis in the LV. Furthermore, increased IL-17 signaling activated mitogen-activated protein kinase and increased the expression of downstream target genes, IL-6, TNF, CCL20, and CXCL1. An anti IL -17 neutralizing antibody abolished the effects of IL-17. Conclusions: The expression of IL-17 and its downstream target genes may play fundamental roles in inducing VA in ischemic HF.
Large-scale Classification of 12-lead ECG with Deep Learning
(2019-01-01)
Chen, Yu-Jhen
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Liu, Chien-Liang
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Tseng, Vincent S.
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Hu, Yu-Feng
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Chen, Shih-Ann
The 12-lead Electrocardiography(ECG) is the gold standard in diagnosing cardiovascular diseases, but most previous studies focused on 1-lead or 2-lead ECG. This work uses a large data set, comprising 7,704 12-lead ECG samples, as the data source, and the goal is to develop a classification model for six common types of urgent arrhythmias. We consider the characteristics of multivariate time-series data to design a novel deep learning model, combining convolutional neural network (CNN) and long short-term memory (LSTM) to learn feature representations as well as the temporal relationship between the latent features. The experimental results indicate that the proposed model achieves promising results and outperforms the other alternatives. We also provide brief analysis about the proposed model.
Methodological considerations in calculating heart rate variability based on wearable device heart rate samples
(2018-11-01)
Chen, Hung-Kai
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Hu, Yu-Feng
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Lin, Shien-Fong
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交大名義發表
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電機工程學系
Heart rate variability (HRV) analysis has recently been incorporated into wearable device application. The data source of HRV is the time series of heart beat intervals extracted from electrocardiogram or photoplethysmogram. These intervals are non-uniformly sampled signals and not suitable for spectral HRV analysis, which usually uses uniformly resampled heart beat intervals before calculating the spectral domain parameters. Such a practice is not applicable to heart rate data obtained from wearable devices that usually display and export the beat per minute (BPM) time series data at 1 Hz. The preferred resampling rate to calculate spectral domain parameters is 4 Hz. We compare the spectral HRV results with the 1 Hz and 4 Hz resampling rates in order to validate the use of 1 Hz resampled-RRI data to represent wearable devices BPM time series data for HRV analysis. Our results show that, using a specific combination of signal processing techniques, the lowest mean relative error in spectral domain parameters of normalized low-frequency power (LFnu), normalized high-frequency power (HFnu) and the ratio of normalized low-frequency power to normalized high-frequency power (LFnu/HFnu) between 1 Hz and 4 Hz are 3.7%, 15.3% and 16.4%, respectively. We conclude that using the heart rate data sampled at 1 Hz produces a reasonable estimation of sympathetic activity but a poor estimation of parasympathetic activity.
Pleiotropic Effects of Myocardial MMP-9 Inhibition to Prevent Ventricular Arrhythmia
(2016-12-14)
Weng, Ching-Hui
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Chung, Fa-Po
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Chen, Yao-Chang
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Lin, Shien-Fong
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Huang, Po-Hsun
Observational studies have established a strong association between matrix metalloproteinase-9 (MMP-9) and ventricular arrhythmia. However, whether MMP-9 has a causal link to ventricular arrhythmia, as well as the underlying mechanism, remains unclear. Here, we investigated the mechanistic involvement of myocardial MMP-9 in the pathophysiology of ventricular arrhythmia. Increased levels of myocardial MMP-9 are linked to ventricular arrhythmia attacks after angiotensin II (Ang II) treatment. MMP-9-deficient mice were protected from ventricular arrhythmia. Increased expressions of protein kinase A (PKA) and ryanodine receptor phosphorylation at serine 2808 (pS2808) were correlated with inducible ventricular arrhythmia. MMP-9 deficiency consistently prevented PKA and pS2808 increases after Ang II treatment and reduced ventricular arrhythmia. Calcium dynamics were examined via confocal imaging in isolated murine cardiomyocytes. MMP-9 inhibition prevents calcium leakage from the sarcoplasmic reticulum and reduces arrhythmia-like irregular calcium transients via protein kinase A and ryanodine receptor phosphorylation. Human induced pluripotent stem cell-derived cardiomyocytes similarly show that MMP-9 inhibition prevents abnormal calcium leakage. Myocardial MMP-9 inhibition prevents ventricular arrhythmia through pleiotropic effects, including the modulation of calcium homeostasis and reduced calcium leakage.
SVAD: A genetic database curates non-ischemic sudden cardiac death-associated variants
(2020-08-19)
Huang, Wei-Chih
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Huang, Hsin-Tzu
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Chen, Po-Yuan
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Wang, Wei-Chi
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Ko, Tai-Ming
Sudden cardiac death (SCD) is an important cause of mortality worldwide. It accounts for approximately half of all deaths from cardiovascular disease. While coronary artery disease and acute myocardial infarction account for the majority of SCD in the elderly population, inherited cardiac diseases (inherited CDs) comprise a substantial proportion of younger SCD victims with a significant genetic component. Currently, the use of next-generation sequencing enables the rapid analysis to investigate relationships between genetic variants and inherited CDs causing SCD. Genetic contribution to risk has been considered an alternate predictor of SCD. In the past years, large numbers of SCD susceptibility variants were reported, but these results are scattered in numerous publications. Here, we present the SCD-associated Variants Annotation Database (SVAD) to facilitate the interpretation of variants and to meet the needs of data integration. SVAD contains data from a broad screening of scientific literature. It was constructed to provide a comprehensive collection of genetic variants along with integrated information regarding their effects. At present, SVAD has accumulated 2,292 entries within 1,239 variants by manually surveying pertinent literature, and approximately one-third of the collected variants are pathogenic/likely-pathogenic following the ACMG guidelines. To the best of our knowledge, SVAD is the most comprehensive database that can provide integrated information on the associated variants in various types of inherited CDs. SVAD represents a valuable source of variant information based on scientific literature and benefits clinicians and researchers, and it is now available on.