Chiung-Zuan Chiu

Publications (11)25.98 Total impact

• Article: Use of atorvastatin to inhibit hypoxia-induced myocardin expression.

  Chiung-Zuan Chiu, Bao-Wei Wang, Kou-Gi Shyu
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  ABSTRACT: Hypoxia induces the formation of reactive oxygen species (ROS), myocardin expression and cardiomyocyte hypertrophy. The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have been demonstrated to have both antioxidant and antihypertrophic effects. We evaluated the pathways of atorvastatin in repressing ROS and myocardin after hypoxia to prevent cardiomyocyte hypertrophy. Cultured rat neonatal cardiomyocytes were subjected to hypoxia, and the expression of myocardin and ROS were evaluated. Different signal transduction inhibitors, atorvastatin and N-acetylcysteine (NAC) were used to identify the pathways that inhibited myocardin expression and ROS. Electrophoretic motility shift assay (EMSA) and luciferase assay were used to identify the binding of myocardin/serum response factor (SRF) and transcription to cardiomyocytes. Cardiomyocyte hypertrophy was assessed by (3)H-proline incorporation assay. Myocardin expression after hypoxia was inhibited by atorvastatin, RhoA/Rho kinase inhibitor (Y27632), extracellular signal-regulated kinase (ERK) small interfering RNA (siRNA)/ERK pathway inhibitor (PD98059), myocardin siRNA and NAC. Bindings of myocardin/SRF, transcription of myocardin/SRF to cardiomyocytes, presence of myocardin in the nuclei of cardiomyocytes and protein synthesis after hypoxia were identified by EMSA, luciferase assay, confocal microscopy and (3)H-proline assay and were suppressed by atorvastatin, Y27632, PD98059 and NAC. Hypoxia in neonatal cardiomyocytes increases myocardin expression and ROS to cause cardiomyocyte hypertrophy, which can be prevented by atorvastatin by suppressing ROS and myocardin expression.
  European Journal of Clinical Investigation 11/2011; 42(5):564-71. · 3.02 Impact Factor
• Article: Gastrointestinal bleeding and outcomes after percutaneous coronary intervention for ST-segment elevation myocardial infarction.

  Su-Kiat Chua, Chao-Sheng Liao, Huei-Fong Hung, Jun-Jack Cheng, Chiung-Zuan Chiu, Che-Ming Chang, Shih-Huang Lee, Sheng-Chang Lin, Jer-Young Liou, Huey-Ming Lo, Peiliang Kuan, Kou-Gi Shyu
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  ABSTRACT: Gastrointestinal bleeding is a hemorrhagic complication after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction (STEMI). To determine predictors of gastrointestinal bleeding and the impact of gastrointestinal bleeding on outcomes in STEMI patients undergoing primary percutaneous coronary intervention. Gastrointestinal bleeding occurred in 18 (3.5%) of 519 consecutive patients with STEMI undergoing primary percutaneous coronary intervention. Univariate predictors of gastrointestinal bleeding were previous gastrointestinal bleeding (33% vs 4%, P < .001), impaired renal function (89% vs 37%, P<.001), Killip class IV at presentation (61% vs 18%, P<.001), higher peak creatinine kinase level (mean [SD], 3801.6 [3280.2] vs 2721.3 [2286.6] IU/L, P=.05), and mechanical ventilator support (44% vs 12%, P<.001). Coprescription of proton-pump inhibitors did not reduce the risk of gastrointestinal bleeding (22.2% vs 13.4%, P=.22). Multivariate analysis showed an odds ratio (95% confidence interval) for gastrointestinal bleeding of 22.1 (5.6-86.89, P<.001) for previous gastrointestinal bleeding, 6.74 (1.30-34.89, P=.02) for impaired renal function, and 4.68 (1.35-16.2, P=.01) for Killip class IV at presentation. Gastrointestinal bleeding was associated with longer intensive care unit stay (mean [SD], 5.4 [6.7] vs 3.6 [3.6] days, P=.04), and higher in-hospital (44% vs 9%, P<.001) and overall (44% vs 13%, P<.001) mortality rate. Although rare, gastrointestinal bleeding in patients with STEMI significantly prolongs intensive care unit stay and increases mortality. Previous gastrointestinal bleeding, impaired renal function, and Killip class IV at presentation are associated with higher incidence of gastrointestinal bleeding.
  American Journal of Critical Care 05/2011; 20(3):218-25. · 1.66 Impact Factor
• Article: Long-term clinical outcomes following elective stent implantation for unprotected left main coronary artery disease.

  Wei-Syun Hu, Shih-Huang Lee, Chiung-Zuan Chiu, Kou-Gi Shyu, Shen-Chang Lin, Huei-Fong Hung, Jer-Young Liou, Jun-Jack Cheng
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  ABSTRACT: Percutaneous coronary intervention (PCI) has been increasingly adopted for unprotected left main coronary artery (LMCA) disease. The aim of this study was to evaluate the predictors of long-term clinical outcomes in patients after elective stent implantation for unprotected LMCA disease. A total of 122 patients with medically refractory angina who received coronary stenting for unprotected LMCA disease between August 1997 and December 2008 were included. During the follow-up period of 45 ± 35 months (range: 1-137 months), the incidence of repeated PCI and/or coronary artery bypass grafting (CABG), and cardiovascular and total mortality were 28% (34 patients), 20% (24 patients), and 25% (31 patients), respectively. Multivariate analysis revealed that young age [p = 0.02; hazard ratio (HR): 2.19, 95% confidence interval (CI): 1.11-4.30] and bare-metal stent (BMS) use (p = 0.02; HR: 5.35, 95% CI: 1.27-22.57) were the independent predictors of repeated PCI and/or CABG. Only lower left ventricular ejection fraction (LVEF) could predict both cardiovascular mortality (p = 0.003; HR: 4.25, 95% CI: 1.63-11.08) and total mortality (p = 0.002; HR: 3.95, 95% CI: 1.65-9.45). Lower LVEF (p = 0.001; HR: 0.31, 95% CI: 0.16-0.61) and small stent size (p = 0.01; HR: 5.95, 95% CI: 1.43-24.80) could predict the composite endpoint, including target vessel revascularization and total mortality. We showed that young age and BMS implantation could predict repeated PCI and/or CABG after stent implantation for unprotected LMCA disease. Only lower LVEF could predict both cardiovascular and total mortality. Lower LVEF and small stent size but not BMS implantation could predict composite target vessel revascularization/total mortality.
  Journal of the Formosan Medical Association 01/2011; 110(1):19-26. · 1.13 Impact Factor
• Article: Incidence, predictors and outcomes of subacute stent thrombosis following primary stenting for ST-elevation myocardial infarction.

  Su-Kiat Chua, Huei-Fong Hung, Jun-Jack Cheng, Jen-Hsiang Wang, Huey-Ming Lo, Peiliang Kuan, Shih-Huang Lee, Sheng-Chang Lin, Jer-Young Liou, Che-Ming Chang, Chiung-Zuan Chiu, Kou-Ci Shyu
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  ABSTRACT: Knowledge concerning subacute stent thrombosis (SST) following primary stenting for ST-elevation myocardial infarction (STEMI) is not widely available. We studied the incidence, predictors, and clinical outcomes of SST following STEMI. We analyzed data from 455 consecutive patients who underwent primary stenting for STEMI. Baseline clinical characteristics, coronary angiographic features, medication and outcome were compared in patients with and without SST. SST occurred in 17 patients, and the incidence was 3.7%. Univariate predictors of SST were being a current smoker (53.0%vs. 82.4%, p = 0.01), Killip class >or= II (38.4%vs. 58.8%, p = 0.05), no coronary re-flow after stenting (6.2%vs. 17.6%, p = 0.05) and lack of coprescription with a statin (39.5%vs. 5.9%, p<0.01). After multivariate analysis, being a current smoker (odds ratio = 4.76; 95% confidence interval 1.20-18.95) and using statin therapy (odds ratio = 0.09; 95% confidence interval = 0.01-0.75) were independent correlates of SST. Patients with SST were associated with higher 30-day mortality (37.5%vs. 3.1%, p<0.01) and all-cause mortality (23.5%vs. 5.3%, p = 0.01) at long-term follow-up. Although SST is rare in patients with STEMI treated by primary stenting, it imparts a significantly higher mortality at short-term and long-term follow-up. Being a current smoker and the lack of co-prescription with a statin were associated with higher incidence of SST. Our results suggest initiation of statin therapy in patients with STEMI should be considered before discharge.
  Journal of the Formosan Medical Association 06/2010; 109(6):430-7. · 1.13 Impact Factor
• Source

  Available from: PubMed Central

  Article: Angiotensin II and the ERK pathway mediate the induction of myocardin by hypoxia in cultured rat neonatal cardiomyocytes.

  Chiung-Zuan Chiu, Bao-Wei Wang, Tun-Hui Chung, Kou-Gi Shyu
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  ABSTRACT: Hypoxic injury to cardiomyocytes is a stress that causes cardiac pathology through cardiac-restricted gene expression. SRF (serum-response factor) and myocardin are important for cardiomyocyte growth and differentiation in response to myocardial injuries. Previous studies have indicated that AngII (angiotensin II) stimulates both myocardin expression and cardiomyocyte hypertrophy. In the present study, we evaluated the expression of myocardin and AngII after hypoxia in regulating gene transcription in neonatal cardiomyocytes. Cultured rat neonatal cardiomyocytes were subjected to hypoxia, and the expression of myocardin and AngII were evaluated. Different signal transduction pathway inhibitors were used to identify the pathway(s) responsible for myocardin expression. An EMSA (electrophoretic mobility-shift assay) was used to identify myocardin/SRF binding, and a luciferase assay was used to identify transcriptional activity of myocardin/SRF in neonatal cardiomyocytes. Both myocardin and AngII expression increased after hypoxia, with AngII appearing at an earlier time point than myocardin. Myocardin expression was stimulated by AngII and ERK (extracellular-signal-regulated kinase) phosphorylation, but was suppressed by an ARB (AngII type 1 receptor blocker), an ERK pathway inhibitor and myocardin siRNA (small interfering RNA). AngII increased both myocardin expression and transcription in neonatal cardiomyocytes. Binding of myocardin/SRF was identified using an EMSA, and a luciferase assay indicated the transcription of myocardin/SRF in neonatal cardiomyocytes. Increased BNP (B-type natriuretic peptide), MHC (myosin heavy chain) and [(3)H]proline incorporation into cardiomyocytes was identified after hypoxia with the presence of myocardin in hypertrophic cardiomyocytes. In conclusion, hypoxia in cardiomyocytes increased myocardin expression, which is mediated by the induction of AngII and the ERK pathway, to cause cardiomyocyte hypertrophy. Myocardial hypertrophy was identified as an increase in transcriptional activities, elevated hypertrophic and cardiomyocyte phenotype markers, and morphological hypertrophic changes in cardiomyocytes.
  Clinical Science 05/2010; 119(7):273-82. · 4.61 Impact Factor
• Article: Acute ST-elevation myocardial infarction in young patients: 15 years of experience in a single center.

  Su-Kiat Chua, Huei-Fong Hung, Kou-Gi Shyu, Jun-Jack Cheng, Chiung-Zuan Chiu, Che-Ming Chang, Sheng-Chang Lin, Jer-Young Liou, Huey-Ming Lo, Peiliang Kuan, Shih-Huang Lee
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  ABSTRACT: There have been few studies done regarding young patients with ST-elevation myocardial infarction (STEMI). The purpose of this study was to investigate the clinical characteristics and coronary angiographic features in young patients with STEMI. We collected data on 849 consecutive patients with STEMI from 1992 to 2006. Baseline clinical characteristics, coronary anatomy, and outcome were compared in young (< or =45 yrs) and older patients (>45 yrs). Young patients presented 11.6% of all patients with STEMI. These patients were predominantly male (92.9% vs 80.3%, P < 0.001), more likely to smoke (75.8% vs 47.2%, P < 0.001), obese (48.2% vs 27.9%, P = 0.002), have higher triglyceride levels (176.9 +/- 153.8 mg/dL vs 140.7 +/- 112.7 mg/dL, P = 0.005), and lower high-density lipoprotein cholesterol (37.1 +/- 7.9 mg/dL vs 42.8 +/- 14.3 mg/dL, P = 0.005) than older patients. Also, younger patients had a shorter hospital stay (7.1 +/- 4.9 d vs 8.5 +/- 6.7 d, P = 0.04), less in-hospital morbidity (29.3% vs 39.7%, P = 0.02), and mortality (3.0% vs 12.3%, P = 0.002). Killip class III or IV could predict in-hospital morbidity and mortality in young patients. Both groups had similar rates of repeated percutaneous coronary intervention (PCI; 45.5% vs 41.5%, P = 0.23) and reinfarction (6.1% vs 3.2%, P = 0.32). Mortality rate during follow-up was significantly lower in younger patients (3.0% vs 19.6%, P < 0.001). Cigarette smoking, obesity, and dyslipidemia were the most important modifiable risk factors in young patients with STEMI. These patients had a better outcome than older patients without differences in repeated PCI and reinfarction between them. Only Killip class III or IV could predict in-hospital morbidity and mortality in young patients with STEMI.
  Clinical Cardiology 03/2010; 33(3):140-8. · 2.15 Impact Factor
• Article: Significance of left circumflex artery-related acute myocardial infarction without ST-T changes.

  Su-Kiat Chua, Kou-Gi Shyu, Jun-Jack Cheng, Jer-Young Liou, Sheng-Chang Lin, Huei-Fong Hung, Shih-Huang Lee, Chiung-Zuan Chiu, Huey-Ming Lo
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  ABSTRACT: Left circumflex (LC)-related acute myocardial infarction (AMI) presenting without ST-T changes has been underdiagnosed in the emergency department. There is little information on its clinical features and significance. The aims of the study were to investigate the clinical characteristics and outcomes of LC-related AMI without ST-T changes. Ninety-six patients were admitted for LC-related AMI. Comparisons between those with and without ST-T changes were analyzed. Twenty-two patients (23%) did not have ST-T changes, whereas 74 patients (77%) had them. Patients without ST-T changes had younger age (55.6 + or - 16.8 vs 62.6 + or - 12.0 years, P = .03), fewer presented as Killip III/IV (4.5% vs 27.4%, P = .02) and with lower creatine kinase (1647.3 + or - 1602.2 vs 2778.2 + or - 2343.3 IU/L, P = .037) and creatine kinase-MB (136.8 + or - 130.3 vs 247.7 + or - 200.0 IU/L, P = .017), and more were with concurrent culprit lesion in the middle or distal LC and right- or balanced-dominant coronary circulation (86.4% vs 44.6%, P < .001). During follow-up, the need for repeat percutaneous coronary intervention (48.6% vs 45.5%, P = .40) and recurrent infarction (13.5% vs 13.6%, P = .62) were similar between the 2 groups. The 30-day mortality (0% vs 5.4%, P = .35) and overall mortality rate (4.5% vs 12.2%, P = .28) between them were not different statistically. The relatively lower prevalence of LC-related AMI without ST-T changes in the study might be underestimated. These patients have smaller infarct size than patients with ST-T changes without differences in the short- and long-term outcomes between them.
  The American journal of emergency medicine 02/2010; 28(2):183-8. · 1.54 Impact Factor
• Article: Angiographic and clinical manifestations of coronary fistulas in Chinese people: 15-year experience.

  Chiung-Zuan Chiu, Kou-Gi Shyu, Jun-Jack Cheng, Shen-Chang Lin, Shih-Huang Lee, Huei-Fong Hung, Jer-Young Liou
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  ABSTRACT: Coronary artery fistula (CAF) is an anomaly resulting in the steal phenomenon of coronary blood flow, which may cause morbidity or mortality. CAFs in Chinese patients after long-term follow-up of 15 years were retrospectively analyzed. From September, 1992 to August, 2007, 152 CAFs were detected in 28,210 coronary angiograms from 125 patients. Clinical and angiographic data of all patients were analyzed retrospectively. Two types of CAFs were characterized: type I in 99 patients with 124 solitary coronary to cardiac chamber or great vessel fistula; type II: 26 patients with 28 coronary artery--left ventricular multiple microfistulas. Single-, double-, and triple-CAFs were detected in 79%, 20%, and 1% of patients, respectively. Coexistent coronary lesions were noted in 41% of patients. Fistula-related symptoms included stable angina in 55, myocardial infarction in 2, heart failure in 2, sudden death with ventricular fibrillation in 1, and syncope in 1. Twenty-four patients had coexistent congenital anomalies. Only 9 patients underwent coronary intervention or/and surgery for CAFs. CAFs may cause trivial or lethal cardiac events, and may coexist with coronary lesion or congenital anomaly. Coronary to cardiac chamber or great vessel fistula and coronary-left ventricular multiple microfistulas have different morphologic and pathological phenomena.
  Circulation Journal 08/2008; 72(8):1242-8. · 3.77 Impact Factor
• Source

  Available from: Ko-Nien Shih

  Article: Predictors of long-term outcomes in patients after elective stent implantation for unprotected left main coronary artery disease.

  Ren-Jen Lee, Ko-Nien Shih, Shih-Huang Lee, Kou-Gi Shyu, Chiung-Zuan Chiu, Shen-Chang Lin, Huei-Fong Hung, Jer-Young Liou, Jun-Jack Cheng, Peiliang Kuan
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  ABSTRACT: The purpose of this study was to investigate the predictor of long-term outcomes in patients after stent implantation for unprotected left main coronary artery (LMCA) disease. Coronary stenting has recently been advocated as an alternative procedure for LMCA disease. Information on the predictors of long-term outcomes in patients after stent implantation for unprotected LMCA disease is not clear. Seventy six patients (51 men and 25 women, age 68 +/- 10 years) with medically refractory angina received coronary stenting for unprotected LMCA disease. During a follow-up period of 40 +/- 26 months, 7 patients (9%) died because of cardiovascular disease in 5 (7%) and noncardiovascular disease in 2 (3%). In the other 69 patients, 19 patients (25%) needed repeated percutaneous coronary intervention (PCI) and/or coronary artery bypass grafting (CABG). In a univariate analysis, only female sex was related to the repeated PCI and/or CABG (P = 0.04). A history of cerebral vascular attack (CVA) (P = 0.005), anemia (P = 0.03) and lower left ventricular ejection fraction (LVEF) (P = 0.008) were related to the cardiovascular mortality. A history of myocardial infarction (P = 0.03), a history of CVA (P = 0.02), anemia (P = 0.02), and lower LVEF (P = 0.002) were related to the total mortality. In a multivariate analysis, female sex (P = 0.007; odds ratio 5.29, 95% confidence interval [CI] 1.57-17.80) and young age (P = 0.025; odds ratio 3.92, 95% CI 1.19-12.98) could predict the repeated PCI and/or CABG. Only a history of CVA could predict the cardiovascular mortality (P = 0.027; odds ratio 34.18, 95% CI 1.49-783) and only lower LVEF could predict the total mortality (P = 0.027; odds ratio 13.26, 95% CI 1.34-131). Female sex and young age could predict the repeated PCI and/or CABG in patients after stent implantation for unprotected LMCA disease. Furthermore, a history of CVA could predict the cardiovascular mortality and lower LVEF could predict the total mortality.
  Heart and Vessels 03/2007; 22(2):99-103. · 2.05 Impact Factor
• Article: Prevention of left ventricular remodeling by long-term corticosteroid therapy in patients with cardiac sarcoidosis.

  Chiung-Zuan Chiu, Satoshi Nakatani, Guican Zhang, Teruo Tachibana, Fumio Ohmori, Masakazu Yamagishi, Masafumi Kitakaze, Hitonobu Tomoike, Kunio Miyatake
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  ABSTRACT: Forty-three patients with cardiac sarcoidosis were studied echocardiographically before and after (mean follow-up 88 months) steroid therapy to determine the effectiveness of corticosteroids to prevent left ventricular (LV) remodeling and improve LV contractility. In patients with initial LV ejection fractions (LVEFs) >or=55%, long-term steroid therapy showed preventive effects for LV remodeling and LV function. Patients with LVEF <54% showed significant reductions of LV volumes and LVEF improvement. However, in patients with LVEFs <30%, steroid therapy resulted in neither LV volume reductions nor improved LVEFs. In the early or middle stage of the disease, steroid therapy may be protective or therapeutic in preventing LV remodeling and preserving LV function. However, it may not be as effective in the late stage.
  The American Journal of Cardiology 02/2005; 95(1):143-6. · 3.37 Impact Factor
• Source

  Available from: Chiung-Tong Chen

  Article: Central pressor effects of CART peptides in anesthetized rats.

  Ling-Ling Hwang, Chiung-Tong Chen, Tzu-Ling Li, Chiung-Zuan Chiu, Shih-Fang Chi
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  ABSTRACT: Interrelationships between energy homeostasis and regulation of cardiovascular functions have been suggested by previous observations [Am. J. Physiol. 278 (2000) R692; Regul. Pept. 104 (2002) 75; Am. J. Physiol. 277 (1999) R1780]. Cocaine- and amphetamine-regulated transcript (CART) was first discovered in the striatum of rats treated with cocaine or amphetamine. The CART peptides were later found in the hypothalamus and functioned as anorectic peptides. We observed that intracisternally (I.C.) administered CART peptide fragments (CART 61-102 and CART 55-102) dose-dependently (1-4 nmol) increased heart rate and blood pressure in urethane-anesthetized adult male Sprague-Dawley rats. Intrathecal (levels T2-T3) and intravenous administrations of these peptides, however, showed little or no effects on the heart rate and blood pressure in the rat. Furthermore, an increase of c-Fos-like immunoreactivity in the rat rostral ventrolateral medulla (RVLM) following an I.C. CART 61-102 was observed. The results suggest that central pressor effects of anorectic CART peptides may involve in activation of the medullary sympathetic systems in the rat. Our observations support the hypothesis that energy homeostasis and cardiovascular regulations are closely related and regulated.
  Neuropeptides 38(2-3):69-76. · 1.55 Impact Factor