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Juey-Jen Hwang

Publications and source records attributed to Juey-Jen Hwang.

29 records · Page 2Linked to original sources
PubMed2004

Renin-angiotensin system gene polymorphisms and atrial fibrillation.

BACKGROUND: The activated local atrial renin-angiotensin system (RAS) has been reported to play an important role in the pathogenesis of atrial fibrillation (AF). We hypothesized that RAS genes might be among the susceptibility genes of nonfamilial structural AF and conducted a genetic case-control study to demonstrate this. METHODS AND RESULTS: A total of 250 patients with documented nonfamilial structural AF and 250 controls were selected. The controls were matched to cases on a 1-to-1 basis with regard to age, gender, presence of left ventricular dysfunction, and presence of significant valvular heart disease. The ACE gene insertion/deletion polymorphism, the T174M, M235T, G-6A, A-20C, G-152A, and G-217A polymorphisms of the angiotensinogen gene, and the A1166C polymorphism of the angiotensin II type I receptor gene were genotyped. In multilocus haplotype analysis, the angiotensinogen gene haplotype profile was significantly different between cases and controls (chi2=62.5, P=0.0002). In single-locus analysis, M235T, G-6A, and G-217A were significantly associated with AF. Frequencies of the M235, G-6, and G-217 alleles were significantly higher in cases than in controls (P=0.000, 0.005, and 0.002, respectively). The odds ratios for AF were 2.5 (95% CI 1.7 to 3.3) with M235/M235 plus M235/T235 genotype, 3.3 (95% CI 1.3 to 10.0) with G-6/G-6 genotype, and 2.0 (95% CI 1.3 to 2.5) with G-217/G-217 genotype. Furthermore, significant gene-gene interactions were detected by the multifactor-dimensionality reduction method and multilocus linkage disequilibrium tests. CONCLUSIONS: This study demonstrates the association of RAS gene polymorphisms with nonfamilial structural AF and may provide the rationale for clinical trials to investigate the use of ACE inhibitor or angiotensin II antagonist in the treatment of structural AF.

Aged↗
PubMed2004

Retrograde wire-assisted percutaneous transcatheter closure of persistent ductus arteriosus with Amplatzer duct occluder in the elderly: A new application.

Percutaneous transcatheter closure of persistent ductus arteriosus (PDA) has been well established in the pediatric field. For moderate- to large-sized PDA, the newly developed Amplatzer duct occluder had offered a good solution, but it depends on stiff wire and delivery sheath. We reported two elderly patients of PDA with vascular anatomy too difficult to be antegradely approached and were closed by a retrograde technique by an assisting wire from the descending aorta. The wire served as a guide and tracked the delivery system to cross the ductus from the venous side smoothly. This retrograde wire-assisted technique could be utilized to overcome the PDA of difficult vascular anatomy, which could not be easily fulfilled by conventional antegrade venous approach.

Aged↗
PubMed2004

Restoration of heart rate turbulence by titrated beta-blocker therapy in patients with advanced congestive heart failure: positive correlation with enhanced vagal modulation of heart rate.

INTRODUCTION: Heart rate turbulence (HRT) is a powerful novel predictor for cardiovascular mortality. Chronic congestive heart failure is associated with abnormal HRT. Whether antiadrenergic beta-blocker therapy can restore control of HRT in patients with chronic congestive heart failure is unknown. METHODS AND RESULTS: A 24-hour Holter ECG recording was obtained before and 1 and 3 months after titrated addition of atenolol therapy in 10 consecutive patients with advanced congestive heart failure. Two parameters derived from HRT, turbulence slope (TS) and turbulence onset (TO), and time- and frequency-domain heart rate variability (HRV) parameters (SDNN, RMSSD, VLF, LF, HF) from 24-hour ECG were compared before and after beta-blocker therapy, together with the same parameters in age-matched normal control. Results showed that TS (3.1 +/- 2.2 vs 6.2 +/- 3.0; P = 0.001) and all HRV parameters were increased after 3 months of atenolol treatment. No changes in TO were evident (0.6 +/- 0.5 vs -0.2 +/- 1.3; P = 0.13). The improvement of TS and the vagally mediated parameters of mean R-R interval, RMSSD, and the HF component of HRV were positively correlated. CONCLUSION: Abnormal HRT caused by chronic congestive heart failure can be restored by beta-blocker therapy. The evolution of TS was positively correlated with measures of vagal modulation of heart rate.

Adrenergic beta-Antagonists↗
PubMed2004

Functional genomic study on atrial fibrillation using cDNA microarray and two-dimensional protein electrophoresis techniques and identification of the myosin regulatory light chain isoform reprogramming in atrial fibrillation.

INTRODUCTION: Functional and structural changes of atrial tissue occur during the natural course of atrial fibrillation (AF), and these changes may contribute to further AF. We investigated the changes in AF tissue using cDNA microarray and two-dimensional protein electrophoresis techniques. METHODS AND RESULTS: We established a porcine model of AF by rapid right atrial appendage pacing at a rate of 600/min. Atrial tissue was obtained after rapid atrial depolarization for 6 weeks. Microarrays containing 6,035 cDNA clones were used to evaluate the alterations of mRNA. Two-dimensional protein electrophoresis was performed to compare protein patterns. In cDNA microarray studies, we identified 387 genes with significant change in the left atrium and 81 genes in the right atrium. Among the genes, the ventricular isoform of the myosin regulatory light chain (MLC-2V) showed the greatest fold of change (9.4 and 7.3 in the left and right atrium, respectively). In protein electrophoresis, the expression levels of three protein spots spanning from 18 to 20 kDa in the acidic region (PI 4.5-5.0) were specifically elevated in the AF group. Interestingly, through tandem mass spectrometric analysis, these three spots were identified as MLC-2V. Thus, MLC-2V expression at the mRNA and protein levels corresponded well, and both indicated a significant increase in AF. CONCLUSION: Both cDNA microarray and two-dimensional polyacrylamide protein electrophoresis studies revealed characteristic changes in AF tissue. We demonstrated the reprogramming of myosin regulatory light chain isoform composition, with a significant increase of its ventricular isoform (MLC-2V).

Animals↗
PubMed2004

Surgical treatment of tracheoesophageal fistula in a patient with severe acute respiratory syndrome complicated with extensive pulmonary fibrosis.

Tracheoesophageal fistula is an uncommon complication usually associated with chronic usage of ventilator and pressure necrosis of the tracheoesophageal wall. A 56-year-old female patient with severe acute respiratory syndrome (SARS) with tracheoesophageal fistula is reported. She was intubated for ventilatory support 3 days after admission because of progressive respiratory distress. Methylprednisolone pulse therapy followed by a maintenance dosage was given due to persistence of bilateral pulmonary fibrosis. Thirty three days after admission, she underwent tracheostomy because of difficulty in weaning from the ventilator. Ten days after tracheostomy, she developed tracheoesophageal fistula, which was confirmed by bronchoscopy and panendoscopy. Tracheal resection and primary repair for the esophageal defect was performed via a cervical incision combined with partial sternotomy. She was weaned from the ventilator soon after the surgery and discharged 34 days after the operation. In SARS patients with persistent pulmonary fibrosis and under prolonged corticosteroid treatment, special care should be given to avoid intubation-related tracheal injury during the period of ventilatory support. The tracheoesophageal fistula, once developed, can be repaired in a single stage after improvement of the nutritional status.

Female↗
PubMed2003

Methylene 3, 4 dioxymethamphetamine-induced acute myocardial infarction.

Methylene 3, 4 dioxymethamphetamine (MDMA) has been gaining popularity as a recreational drug over the past few decades around the globe. Although once thought to be safer than its mother compound, amphetamine, several life-threatening adverse reactions have been reported. Among the cardiovascular toxicities documented, MDMA commonly causes various forms of arrhythmia and heart failure. However, MDMA-induced acute myocardial infarction is rarely reported. We report a case of acute myocardial infarction in a young man shortly after taking MDMA. Massive thrombosis over the right coronary artery was demonstrated by means of emergency angiography. After treatment with intravenous glycoprotein IIb/IIIa inhibitor and intracoronary urokinase infusion, the coronary artery was shown to be patent without any apparent stenotic lesions. The mechanism of MDMA-induced acute myocardial infarction was discussed.

Administration, Oral↗
PubMed2003

Angiotensinogen gene haplotype and hypertension: interaction with ACE gene I allele.

There are many reports demonstrating the association of renin-angiotensin system gene polymorphisms with hypertension in different populations. In the present study, we used haplotype analyses of the angiotensinogen gene with a new permutation-based hypothesis testing method to determine the association between multilocus angiotensinogen gene polymorphisms and hypertension in a relatively homogeneous Taiwanese population. We also genotyped angiotensin-converting enzyme gene insertion/deletion polymorphism and angiotensin II type 1-receptor gene A1166C polymorphism to detect epistatic gene-gene interactions. There were 408 patients with hypertension (hypertensives) and 286 controls. The angiotensinogen gene haplotype frequencies were significantly different between hypertensives and controls, and this finding was only present in subjects with angiotensin-converting enzyme gene II genotypes when the analysis was stratified by genotype of this polymorphism. In addition, the angiotensinogen gene haplotype structure of hypertensives was more heterogeneous than that of controls. Our results showed that angiotensinogen gene haplotypes were associated with hypertension and might act synergistically with I allele of the angiotensin-converting enzyme gene.

Alleles↗
PubMed2002

Microarray gene expression profiles in dilated and hypertrophic cardiomyopathic end-stage heart failure.

Despite similar clinical endpoints, heart failure resulting from dilated cardiomyopathy (DCM) or hypertrophic cardiomyopathy (HCM) appears to develop through different remodeling and molecular pathways. Current understanding of heart failure has been facilitated by microarray technology. We constructed an in-house spotted cDNA microarray using 10,272 unique clones from various cardiovascular cDNA libraries sequenced and annotated in our laboratory. RNA samples were obtained from left ventricular tissues of precardiac transplantation DCM and HCM patients and were hybridized against normal adult heart reference RNA. After filtering, differentially expressed genes were determined using novel analyzing software. We demonstrated that normalization for cDNA microarray data is slide-dependent and nonlinear. The feasibility of this model was validated by quantitative real-time reverse transcription-PCR, and the accuracy rate depended on the fold change and statistical significance level. Our results showed that 192 genes were highly expressed in both DCM and HCM (e.g., atrial natriuretic peptide, CD59, decorin, elongation factor 2, and heat shock protein 90), and 51 genes were downregulated in both conditions (e.g., elastin, sarcoplasmic/endoplasmic reticulum Ca2+-ATPase). We also identified several genes differentially expressed between DCM and HCM (e.g., alphaB-crystallin, antagonizer of myc transcriptional activity, beta-dystrobrevin, calsequestrin, lipocortin, and lumican). Microarray technology provides us with a genomic approach to explore the genetic markers and molecular mechanisms leading to heart failure.

Adult↗
PubMed2002

Association of the human minK gene 38G allele with atrial fibrillation: evidence of possible genetic control on the pathogenesis of atrial fibrillation.

BACKGROUND: Human minK protein is the beta-subunit of I(Ks) potassium channel and plays an important role in cardiac cellular electrophysiology. We investigated the association between human atrial fibrillation and the polymorphism of minK gene (38G or 38S) with a case-control study. METHODS: We included 108 patients with atrial fibrillation and 108 control subjects. The case patients and control subjects were matched regarding age, sex, presence of valvular heart disease, and presence of left ventricular dysfunction. The genotype of minK was determined with polymerase chain reaction and restriction fragment analysis. RESULTS: The results showed an association between the minK 38G allele and atrial fibrillation. The odds ratios for atrial fibrillation in patients with 1 and 2 minK 38G alleles were 2.16 (95% CI 0.81-5.74) and 3.58 (95% CI 1.38-9.27), respectively, when compared with patients without minK 38G allele. In a logistic regression model, the odds ratio for atrial fibrillation was 1.80 (95% CI 1.20-2.71, P <.0046) for patients with 1 more minK 38G allele. CONCLUSION: We report the association between the minK 38G allele and clinical atrial fibrillation. Our findings suggest possible genetic control on the pathogenesis of atrial fibrillation.

Alleles↗
PubMed2002

The 27-bp tandem repeat polymorphism in intron 4 of the endothelial nitric oxide synthase gene is not associated with coronary artery disease in a hospital-based Taiwanese population.

We studied whether the 27 base pair (bp) tandem repeat polymorphism in intron 4 of the endothelial nitric oxide synthase (eNOS) gene was associated with coronary artery disease (CAD) in a hospital-based Taiwanese population. We included 219 consecutive patients who underwent coronary angiography at our institution. Two alleles, containing 4 (eNOS4a) and 5 repeats (eNOS4b), were identified after polymerase chain reaction amplifying intron 4 of the eNOS gene. The genotype frequencies for eNOS4b/b, eNOS4a/b and eNOS4a/a were 77.9, 21.5 and 0.6% in CAD subjects, and 80, 20 and 0% in control subjects (Fisher's exact test, p = 0.90), respectively. The odds ratio (OR) for CAD in patients with at least one eNOSa allele was 1.2 (0.5-2.9) after adjustment for classical CAD risk factors. The eNOS4a allele was not associated with the severity of CAD (Fisher's exact test, p = 0.90) and the occurrence of acute myocardial infarction (AMI) or unstable angina (adjusted OR 0.6, 0.3-1.6) in patients with CAD. In conclusion, the 27-bp repeat polymorphism of the eNOS gene was not associated with CAD and the occurrence of AMI or unstable angina in a hospital-based Taiwanese population.

Aged↗