Publications by authors named "Hsiang-Tai Chou"

This case-control study was carried out to investigate the possible relationship between the gene frequencies of HLA-DRB1, -DQA1 and -DQB1 alleles/haplotypes and rheumatic heart disease (RHD) among the Chinese population in Taiwan. A group of 115 patients with RHD documented by echocardiography, and a group of 115 normal controls were studied. The HLA-DRB1, -DQA1 and -DQB1 allele frequencies were determined by polymerase chain reaction and sequence-specific oligonucleotide probe.

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Inflammation and genetics may play a role in the pathogenesis of rheumatic heart disease (RHD). The aim of this study was to test whether interleukin (IL)-1beta, IL-1 receptor antagonist (IL-1Ra), IL-4, or IL-10 gene polymorphisms could be used as markers of susceptibility to or severity of RHD among the Chinese population in Taiwan. A group of 115 patients with RHD diagnosed by echocardiography, and 163 age- and sex-matched normal control subjects were studied.

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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.

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Scarring and collagen deposition in the valves and destruction of myocytes may result from the combined effects of a smoldering rheumatic process and a constant trauma to the mitral valve or aortic valve by the turbulent flow in rheumatic heart disease (RHD). It has been suggested that angiotensin I-converting enzyme (ACE) may be responsible for the increased valvular fibrosis and calcification in the pathogenesis of RHD. However, the role of ACE genetic variant in RHD has not been studied among the Chinese population in Taiwan.

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Background: Abnormalities of collagen and elastic fibers were found in floppy mitral valves (FMV). Urokinase-plasminogen activator (PLAU) was suggested to be involved in the pathogenesis of elastin and collagen degradation in arterial aneurysm. The role of PLAU genetic variant in mitral valve prolapse (MVP) has not been studied.

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Background: Scarring and collagen deposition in the valves and destruction of myocytes may result from the combined effects of a smoldering rheumatic process and a constant trauma to the mitral valve or aortic valve by the turbulent flow in rheumatic heart disease (RHD). Transforming growth factor-beta1 (TGF-beta1) may be responsible for the increased valvular fibrosis and calcification in the pathogenesis of RHD. However, the role of TGF-beta1 genetic variant in RHD has not been studied.

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Background: Collagen structure is a key element in mitral valves. Collagen defects were proposed as the primary events causing floppy mitral valves (FMV). The role of collagen genetic variant in floppy mitral valve/mitral valve prolapse (FMV/MVP) has not been well studied.

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Multiple intracardiac catheters are often necessary for electrophysiological study (EPS) and radiofrequency (RF) ablation therapy. Therefore, multiple venous sheath placement in one femoral vein is always required for multiple intracardiac catheter insertion. The vascular complications incurred by placement of multiple sheaths have not been fully studied.

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Abnormalities of proteoglycan, collagen, and elastic fibers were found in floppy mitral valves. Perlecan is one of the three major classes of heparan sulfate proteoglycans within the cardiovascular system. The role of perlecan genetic variant in mitral valve prolapse (MVP) has not been studied.

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Background: 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.

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Background And Aim Of The Study: Fibrillin is one of the structural components of the elastin-associated microfibrils found in the mitral valve. Abnormalities of elastic fiber were found in floppy mitral valves. The role of fibrillin genetic variant in isolated mitral valve prolapse (MVP) has not been studied.

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Background And Aims Of The Study: Inflammation and genetics may play a role in the pathogenesis of mitral valve prolapse (MVP). The study aim was to test whether interleukin-1beta (IL-1beta), IL-1 receptor antagonist (IL-1Ra), IL-4 or IL-10 gene polymorphisms could be used as markers of susceptibility or severity in MVP among the Chinese population in Taiwan.

Methods: A group of 100 patients with MVP diagnosed echocardiographically, and 103 age- and sex-matched normal control subjects was studied.

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A germline mutation of the thyroid-stimulating hormone receptor (TSHR) gene has been reported to be associated with thyrotoxicosis and mitral valve prolapse syndrome (MVPS) in a Chinese family. The role of TSHR genetic variants in MVPS has not been well studied. This study investigated the possible relationship between the polymorphisms of codon 727 and 52 of the TSHR gene and MVPS among the Chinese population in Taiwan.

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Background: Some studies have reported that patients with mitral valve prolapse syndrome (MVPS) also have a disorder in the autonomic or neuroendocrine function, which can cause a host of related symptoms. A potential role of the renin-angiotensin system in the pathogenesis of MVPS has been addressed. However, the role of angiotensin I-converting enzyme (ACE) genetic variant in MVPS has not been studied.

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Background And Aim Of The Study: It has been reported that patients with mitral valve prolapse syndrome (MVPS) also have a disorder in autonomic or neuroendocrine function which can cause many related symptoms. Although a potential role of the reninangiotensin system in the pathogenesis of MVPS has been addressed, the role of the angiotensinogen (AGT) genetic variant in MVPS has not been studied. Thus, a case-controlled study was performed to investigate the possible relationship between AGT gene polymorphisms and MVPS.

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Background And Aims Of The Study: A role of collagen abnormality in the pathogenesis of mitral valve prolapse (MVP) has been addressed. It is considered that transforming growth factor-beta1 (TGF-beta1) may be responsible for the increased deposition of extracellular matrix in hypertensive blood vessels, and increased myocardial collagen expression and myocardial fibrosis in human aortic valve disease. However, the role of a TGF-beta1 genetic variant in MVP has not been studied.

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Introduction: Cellular mechanisms of adenosine include a direct effect on the activation of the adenosine-sensitive potassium current (I(K,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 I(K,Ado) potassium current, rather than indirectly by reversing the catecholamine effects, then pretreatment with beta-adrenergic blockade would not potentiate the effects of adenosine in terminating AV nodal-dependent supraventricular tachycardia (SVT).

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The adenine/cytosine1166 (A/C1166) polymorphism of the angiotensin-II type 1 receptor (AGTR1) gene is presumed to be associated with mitral valve prolapse syndrome (MVPS) in Caucasians. To investigate whether a similar association exists among the Chinese population in Taiwan, 100 patients with MVP diagnosed by echocardiography and 100 normal subjects were studied by polymerase chain reaction-based restriction analysis. The difference in genotype (chi2=0.

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