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   2016| July-September  | Volume 1 | Issue 3  
    Online since December 26, 2018

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Asian expert consensus for the diagnosis and treatment of hypertension-associated left ventricular hypertrophy
Ningling Sun, Jaw-Wen Chen, Jiguang Wang, Liangdi Xie, Luyuan Chen, Jianjun Mu, Yuemin Sun, Chern-En Chiang, Cheuk-Man Yu, Huay Cheem Tan, Razali Omar, Yong Huo
July-September 2016, 1(3):37-47
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Percutaneous retrieval of a dislodged watchman left atrial appendage closure device
Jiangtao Yu, Shaofeng Guan, Manuela Muenzel, Erich Duenninger
July-September 2016, 1(3):48-50
A 46-year-old female underwent left atrial appendage closure (LAAC) with a Watchman LAAC device. During the procedure, the device embolized into the descending aorta. A new device was implanted to the left atrial appendage complete the closure. The displaced device was successfully snared and removed by Amplatz Goose Neck™ Snare Kit. The patient recovered well and suffered from no clinical sequelae.
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The role of Galectin-3 in cardiac remodeling
Jingni He, Zaixin Yu
July-September 2016, 1(3):28-36
Galectin-3 is a member of the β-galactoside-binding galectins and is characterized by a carbohydrate recognition domain. Galectin-3 regulates the various biological processes such as cell growth, differentiation, immune function, cancer metastasis, apoptosis, inflammation, and fibrosis. Current clinical and experimental evidence repeatedly suggest that galectin-3 expression is upregulated in various stages of cardiac remodeling in cardiovascular diseases. Studies also find that either genetic or pharmacological inhibition of galectin-3 can slow the progression of myocardial inflammation, reduce collagen production, attenuate cardiac remodeling, and ameliorate cardiac function. Altogether these data support further scientific attention for galectin-3 to clarify its precise mechanisms in causing or aggravating cardiac remodeling in cardiovascular diseases. This reviews presents a general survey on galectin-3 as a regulatory molecule affecting the various stages from acute to chronic inflammation and cardiac fibrogenesis in common types of cardiovascular diseases, as well as its potential role in the diagnosis, risk stratification, and treatment of cardiovascular diseases.
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First clinical experience with new left atrial appendage closure device: WATCHMAN FLX® System
Xin Xue, Erich Duenninger, Manuela Muenzel, Adam Fazakas, Nina Schneider, Jing Chang, Jiangtao Yu
July-September 2016, 1(3):9-12
Background: Percutaneous left atrial appendage closure (LAAC) with WATCHMAN (WM) has been recognized as a new interventional routine, but the development of device is continuing. The WATCHMAN FLX® system (WMF) is a new equipment for LAAC which was used in patients since December 2015 until now; however, there is still lack of WMF clinical experience. We therefore evaluate selection of patient, safety, feasibility, and the early results of LAAC with WMF in a single hospital. Results: LAAC was performed using WMF in 16 nonvalvular atrial fibrillation (NVAF) patients mostly with long-term oral anticoagulant contraindication. Mean age at LAAC was 75 ± 5 years, and 70.6% were male. Hypertension, diabetes, and stroke before operation were present in 87.5%, 25%, and 18.8%, respectively. Mean CHADS2, CHA2DS-VASc, and HASBLED scores were 3.0 ± 1.1, 4.0 ± 1.5, and 3.0 ± 1.2, respectively. The success rate of device implantation was 100%, and there were no severe major procedural complications. Transesophageal echocardiography (TEE) was performed in the first 6 weeks and 6 months after LAAC; 100% of patients finished 6 weeks follow-up. No device-related death was recorded. No ischemic stroke/transient ischemic attack was observed. However, three cases experienced device dislocation. WMF devices were out of left appendage, two at descending aorta and one at ascending aorta. Fortunately, all the lost devices were found and successfully captured with Caesar Grasping Forceps System via arteria femoralis (18F sheath). Twelve patients have already accepted 6 months TEE, with one patient detected thrombosis on the WMF surface. Conclusions: LAAC with WM is a safe and effective therapy to prevent stroke in NVAF patients. The WMF is upgrading novel and updated version of the WATCHMAN device, but not the final device. It still needs accumulating clinical experience with WMF, product, and device dislocation should be also be closely monitored.
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In-depth analysis of confusion and argument focusing on left atrial appendage closure
Jiangtao Yu, Lisheng Jiang, Xin Xue
July-September 2016, 1(3):4-8
Left atrial appendage closure (LAAC) technology has been developing over 10 years from its research and development to routine clinical application and has acquired solid evidence-based support through the Protection in Patients with Atrial Fibrillation, PREVAIL, and other registered studies. However, this technology still faces misinterpretation and confusion over its concept and acceptance as a universal clinical application. In this review, we try to provide an in-depth analysis of current perceptions and arguments focused on LAAC from its concept, operation, and other important issues.
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Acceleration of chest pain center construction and improvements for the treatment of acute myocardial infarction in China
Yong Huo, Junbo Ge
July-September 2016, 1(3):1-3
At present, cardiovascular disease (CVD) prevention and control in China is in crisis. The level of acute coronary syndrome treatment and the establishment of modern treatment guidelines in China lag behind those other developed countries. The Chinese Medical Association, the Chinese Association of Cardiovascular Health, and the Cardiovascular Health Alliance have developed a program to accelerate the construction of China Chest Pain Centers (CCPC) and stringent certification requirements. The program includes (1) establishing demonstration centers in 60 cities throughout China, (2) development of guidelines for the construction and certification of regional and primary chest pain centers, (3) expansion of the number of training instructors and certification experts, (4) expansion of the scale and frequency of training, (5) quality improvements to the overall training system, and (6) quality improvements to key assessment indicators information systems and related initiatives. We propose the establishment of 40 chest pain center demonstration bases through the provision of guidance and training to 2500 hospitals toward the goals of promotion, construction, and certification of 1000 chest pain centers in China between 2016 and 2018.
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Amiodarone treatment investigation on the correlation between the drug sensitivity for paroxysmal atrial fibrillation and gene polymorphism
Shuxin Hou, Yingmin Lu, Damin Huang, Zhaoxia Wang, Xiaohan Luo, Jinchun Zhang, Jian Ji, Lei Song, Zhihua Li, Caiwen Wei, Zengyan Zhao, Weiping Xu
July-September 2016, 1(3):13-19
Objective: To investigate the correlation between the sensitivity to amiodarone therapy and the polymorphism of KCNN3 gene rs13376333 site and ZFHX3 gene rs7193343 site in patients with paroxysmal atrial fibrillation (AF). Materials and Methods: A total of 100 patients comprised 57 men and 43 women with paroxysmal AF hospitalized in Xinhua Hospital were selected between November 1, 2014, and April 30, 2016. Their clinical data and peripheral venous blood samples were collected for case–control study. Patients with recovered to sinus rhythm that was maintained for 6 months in response to amiodarone treatment were included in the observational group. Patients whose rhythm could not be converted to sinus rhythm after amiodarone treatment or who had recurrence within 6 months were included in the control group. DNA of the white blood cells collected from the peripheral venous blood was extracted for each group. The polymerase chain reaction-restriction fragment length polymorphism method and gene sequencing were used to detect the genotype of KCNN3 gene rs13376333 site and ZFHX3 gene rs7193343 site in all the patients. The polymorphism in KCNN3 gene rs13376333 site and ZFHX3 gene rs7193343 was analyzed between the observational and control groups. Results: Three genotypes for KCNN3 gene rs13376333 in the observational and control groups were identified: TT, TC, and CC. The genotype frequency was 26% versus 20% for TT, 40% versus 36% for TC, and 34% versus 44% for CC and 46% versus 38% for T allele and 54% versus 62% for C allele, respectively. However, differences were not statistically significant (P > 0.05). More patients in the observational group carried T allele than that in the control group. Logistic regression indicated a 1.21-fold increase in sensitivity to amiodarone by T allele for the treatment of paroxysmal AF (odds ratio [OR] =1.21, P > 0.05). However, this result was not statistically significant. There were three genotypes for ZFHX3 gene rs7193343 site in both groups: 28% versus 42% for TT, 42% versus 42% for TC and 30% versus 16% for CC and 49% versus 63% for T allele and 51% versus 37% for C allele, respectively. More patients in the observational group carried C allele than that in the control group. Logistic regression indicated a 1.32-fold increase in the sensitivity to amiodarone by the C allele for the treatment of paroxysmal AF (OR = 1.32, P < 0.05). Conclusion: Gene polymorphism was present at KCNN3 gene rs13376333 site and ZFHX3 gene rs7193343 in the observational and control groups, respectively. However, there was no statistical difference in the genotype and allele frequency of KCNN3 gene rs13376333 between the two groups. The effect on the sensitivity to amiodarone in the treatment of paroxysmal AF could not yet be determined. The C allele at ZFHX3 gene rs7193343 site significantly increased the sensitivity to amiodarone for paroxysmal AF.
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Role of the cathepsin K/Calcineurin/Nuclear factor of activated T-cells axis in the pathogenesis and management of diabetic cardiomyopathy
Rui Guo, Sreejayan Nair, Jun Ren
July-September 2016, 1(3):20-27
Diabetes mellitus has become a devastating global epidemic. Patients with diabetes suffer a high prevalence of diabetic cardiomyopathy (DCM). DCM is a type of cardiac problem independent of any preexisting macro- and micro-vascular diseases. The pathophysiological basis underlying diabetes-induced cardiac damage is rather complex and multifactorial. Although a number of risk factors including oxidative stress, apoptosis, and aberrant intracellular Ca2+ metabolism have been postulated to play a role in the onset and development of cardiac anomalies within diabetes, the precise mechanisms responsible for DCM remain elusive. This mini-review discusses the latest findings of mechanisms involved in the progression of cardiomyopathy in diabetes. We emphasize the role of the lysosomal cysteine protease, cathepsin K, and its downstream calcineurin/nuclear factor of activated T-cells signaling in the prevention and treatment of DCM.
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