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Chau-Chung Wu

Publications and source records attributed to Chau-Chung Wu.

13 recordsLinked to original sources

Dyslipidemia is associated with ventricular tachyarrhythmia in patients with acute ST-segment elevation myocardial infarction.

BACKGROUND: Ventricular tachyarrhythmia developing in the acute stage of myocardial infarction (MI) is an important cause of sudden cardiac death. The aim of this study was to determine whether dyslipidemia is associated with the occurrence of ventricular tachycardia/fibrillation (VT/VF) during the acute stage of ST-segment elevation MI (STEMI). METHODS: A total of 58 patients experiencing VT/VF within 24 hours after the onset of MI were selected as the study group. A group of 58 patients with MI but without VT/VF was selected as the control group matched for sex (overall, 104 males), age (overall, 58 +/- 10 years), and the use of thrombolytic therapy (n = 82). The lipid profiles including total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglyceride were measured during the first week and at the third month after the index MI. Other coronary risk factors, and clinical, hemodynamic and angiographic characteristics were also included in the assessment. RESULTS: During the acute stage, patients with VT/VF had higher levels of LDL-C and lower blood pressure on initial arrival at our hospital. At the 3-month follow-up, those patients with VT/VF showed higher levels of TC, LDL-C and triglyceride. Multivariate analysis revealed that LDL-C (p < 0.001) at the 3-month follow-up, mean blood pressure on arrival (p < 0.01), and the difference in triglyceride levels between the first week and the third month (p < 0.05) were independent predictors for the occurrence of VT/VF in the acute stage of MI. CONCLUSION: This study suggests that dyslipidemia imposes a higher risk of developing tachyarrhythmia in the acute phase of STEMI.

Aged↗

Immediate impairment of left ventricular mechanical performance and force-frequency relation by rate-responsive dual-chamber, but not atrial pacing: Implications from intraventricular isovolumic relaxation flow.

BACKGROUND: Despite the maintenance of atrioventricular (AV) synchrony, the detrimental effect of left ventricular asynchronization on mechanical performance and intraventricular flow by nonphysiologic right ventricular apical pacing in dual-chamber pacing, with and without rate adaptation, is not clear. METHOD: Twenty-seven consecutive patients receiving permanent pacemakers for symptomatic bradyarrhythmias (18 with DDD and 9 with AAI mode pacemakers) were evaluated with standard and tissue Doppler echocardiography before and 24 h after pacemaker implantation. The rate-response effect of pacing was studied by programmed rate with increments of 20, from 60 to 100/min. RESULTS: Color M-mode echocardiography demonstrated that much more DDD patients developed new biphasic intraventricular flow during isovolumic relaxation period than AAI patients (13/18 versus 0/9, P<0.001). In DDD patients, the ventricular relaxation represented by mitral annulus velocity in early diastole significantly attenuated (before vs. after DDDR, 8.5+/-2.8 vs. 5.2+/-1.2 cm/s, P<0.05), and also the mitral flow propagation velocity (33+/-11 vs. 25+/-5 cm/s, P<0.01). The myocardial performance index increased after DDD (0.70+/-0.15 vs. 0.79+/-0.24, P<0.05) but not after AAI (0.61+/-0.1 vs. 0.59+/-0.08, P=NS). For both pacing groups, the accelerated pacing rate prolonged the isovolumic relaxation time and shortened the diastole period (P<0.001). However, only DDD patients had a decreased mitral flow propagation velocity (P=0.026) and an attenuated force-frequency relation in programmed rate acceleration. CONCLUSION: Despite the AV synchrony, right ventricular apical pacing immediately attenuates the left ventricular contraction and relaxation performance, which deteriorated further and suppressed the physiologically positive force-frequency relation after accelerated pacing rate.

Aged↗

Downregulated myocardial connexin 43 and suppressed contractility in rabbits subjected to a cholesterol-enriched diet.

The effects of hypercholesterolemia on the myocardium per se include electrophysiological and mechanical alterations. Since gap junctions are essential in electromechanical coupling throughout the heart, we examined the correlation between the temporal expression of cardiac connexin 43 (Cx43), contractile function, and conduction velocity in cholesterol-fed rabbits. After a 12-week feeding period, serum cholesterol levels gradually increased (P<0.001). In contrast, expression of cardiomyocyte Cx43 protein progressively decreased (60% reduction at 12 weeks, P<0.001). Such a reduction was also demonstrated by immunoconfocal microscopy, which further showed redistribution of Cx43 gap junctions at the lateral cell membrane. The downregulation of Cx43 protein was associated with increased levels of Cx43 mRNA (3.5 -fold at 12 weeks, P<0.001) and phosphorylated c-Jun N-terminal kinase (three-fold at 12 weeks, P=0.001). Functionally, although fractional shortening of the left ventricle remained unchanged throughout the feeding protocol, the cholesterol-fed rabbits had a reduced cardiac cycle-dependent variation of integrated backscatters, a decreased mitral ring systolic velocity, and an increased modified Tei index (all P<0.001), all of which indicated impaired intrinsic myocardial contractility and attenuated ventricular systolic performance. In Langendorff-perfused hearts of cholesterol-fed rabbits, decreased conduction velocity was observed (P<0.005). Withdrawal of the cholesterol-enriched diet for 18 weeks restored the contractile parameters and Cx43 protein expression. These findings suggest that Cx43 is highly involved in the molecular mechanism of hypercholesterolemia-induced cardiac contractile dysfunction and dysrhythmias.

Animals↗

The relation between myocardial cyclic variation of integrated backscatter and serum concentrations of procollagen propeptides in hypertensive patients.

Cyclic variation of integrated backscatter (IBS), or CVIBS, provides a noninvasive method to measure myocardial collagen deposition and ischemia in hypertensive patients. We hypothesized that serum procollagen propeptides can offer additional values to CVIBS for evaluating cardiac changes related to fibrosis or ischemia. A total of 21 patients were enrolled in this study and were divided into three groups according to the presence of hypertension and serum carboxyterminal propeptide of type I procollagen (PICP) concentration; these were: 7 hypertensive patients with PICP > or = 127 microg/L (group 1), 7 hypertensive patients with PICP < 127 microg/L (group 2), 7 normotensive subjects with PICP < 127 microg/L (group 3). In addition to PICP, serum aminoterminal propeptide of type III procollagen (PIIINP), stress 201thalium scintigraphy and CVIBS were examined. Phase-compensated amplitudes of CVIBS at mid posterior and mid anteroseptal segments were significantly lower in group 1 (p < 0.05). Patients with fixed 201thallium perfusion defects had lower phase-compensated amplitudes of CVIBS at mid anteroseptal segment and higher PIIINP concentrations (p < 0.05). In conclusions, decrease of myocardial phase-compensated amplitude accompanied with increase of serum PICP concentration may be indicative of the underlying fibrotic process of hypertensive myocardium. Decrease of this CVIBS parameter with increase of serum PIIINP implies concomitant myocardial ischemia.

Biomarkers↗

Sympathetic nerve sprouting, electrical remodeling, and increased vulnerability to ventricular fibrillation in hypercholesterolemic rabbits.

Whether hypercholesterolemia (HC) can induce proarrhythmic neural and electrophysiological remodeling is unclear. We fed rabbits with either high cholesterol (HC, n=10) or standard (S, n=10) chows for 12 weeks (protocol 1), and with HC (n=12) or S (n=10) chows for 8 weeks (protocol 2). In protocol 3, 10 rabbits were fed with various protocols to observe the effects of different serum cholesterol levels. Results showed that the serum cholesterol levels were 2097+/-288 mg/dL in HC group and 59+/-9 mg/dL in S group for protocol 1 and were 1889+/-577 mg/dL in HC group and 50+/-21 mg/dL in S group for protocol 2. Density of growth-associated protein 43- (GAP43) and tyrosine hydroxylase- (TH) positive nerves in the heart was significantly higher in HC than S in protocol 1. Compared with S, HC rabbits had longer QTc intervals, more QTc dispersion, longer action potential duration, increased heterogeneity of repolarization and higher peak calcium current (ICa) density (14.0+/-3.1 versus 9.1+/-3.4 pA/pF; P<0.01) in protocol 1 and 2. Ventricular fibrillation was either induced or occurred spontaneously in 9/12 of hearts of HC group and 2/10 of hearts in S group in protocol 2. Protocol 3 showed a strong correlation between serum cholesterol level and nerve density for GAP43 (R2=0.94; P<0.001) and TH (R2=0.91; P<0.001). We conclude that HC resulted in nerve sprouting, sympathetic hyperinnervation, and increased ICa. The neural and electrophysiological remodeling was associated with prolonged action potential duration, longer QTc intervals, increased repolarization dispersion, and increased ventricular vulnerability to fibrillation.

Action Potentials↗

Left ventricular dysfunction is associated with CD4 lymphocyte count rather than opportunistic infection in human immunodeficiency virus infection.

BACKGROUND AND PURPOSE: Left ventricular (LV) dysfunction is often found in the early stage of human immunodeficiency virus (HIV) infection and deteriorates with disease progression. CD4 lymphocyte count and opportunistic infection are the major indicators for the clinical staging of HIV infection. This study investigated the association of these indicators with LV dysfunction in the clinical course of HIV infection. METHODS: HIV-positive patients without cardiac manifestations consecutively admitted from May 1998 to April 1999 were enrolled in the study. Echocardiographic LV function evaluation and measurement of CD4 lymphocyte count were performed. Parameters for LV systolic and diastolic functions were compared between patients with CD4 lymphocyte count >or= 200/microL and those with CD4 < 200/microL. In patients with CD4 < 200/microL, LV function was further correlated with the presence or absence of opportunistic infections. RESULTS: Ninety eight HIV-positive patients including 52 with CD4 >or= 200/microL and 46 with CD4 < 200/microL were studied. One half of the 46 patients with CD4 < 200/microL had active opportunistic infections. We found that LV fractional shortening, ejection fraction, and isovolumic relaxation time were all significantly lower in the patients with CD4 < 200/microL compared with those with CD4 >or= 200/microL. Moreover, these LV systolic and diastolic dysfunctions were positively correlated with decreased CD4 lymphocyte count. In contrast, no difference was found in these parameters between patients with and without opportunistic infections. In multiple regression analysis, CD4 lymphocyte count was found to be the only factor for predicting the LV systolic and diastolic dysfunction. CONCLUSIONS: Both LV systolic and diastolic function deteriorate as the CD4 lymphocyte count decreases in HIV infection. Opportunistic infection seems to have a limited role in the pathogenesis of LV dysfunction in advanced HIV infection.

AIDS-Related Opportunistic Infections↗

Assessment of menopause-induced myocardial changes by integrated backscatter during inotropic stimulation and atropine injection.

Estradiol has been considered as an L-type calcium channel blocker in animal studies. The concentration of estradiol decreases after menopause. Therefore, we hypothesized that human myocardial functional changes developed after menopause, and those changes could be evaluated through the use of cyclic variation of integrated backscatter (CVIBS). A total of 16 patients with menopause (native and surgical menopause), follicular stimulating hormone > 40 IU/L and estradiol < 20 pg/mL underwent dobutamine stress IBS examination (study group). Another 12 women with normal menstruation, follicular stimulating hormone < 40 IU/L and estradiol > 20 pg/mL were enrolled as a control group. All patients had a low likelihood of coronary artery disease and negative results of dobutamine stress echocardiography and (201)thallium scintigraphy. To avoid the phenomenon of anisotropy, the amplitude and phase of IBS were acquired only in the midanteroseptal segment from the parasternal short axis view. The baseline amplitudes of CVIBS differed between the control and study groups (5.9 +/- 1.2 dB vs. 8.1 +/- 2.1 dB; p = 0.007). The amplitudes during low-dose (20 microg/kg-min) and peak-dose (40 microg/kg-min) dobutamine infusion were also different between these 2 groups (5.7 +/- 0.9 dB vs. 8.4 +/- 1.7 dB; p < 0.001; 6.0 +/- 1.0 dB vs. 7.7 +/- 2.4 dB; p = 0.026). However, there were no significant differences in amplitudes between these two groups after atropine injection (control group 4.5 +/- 1.2 dB, study group 5.3 +/- 1.0 dB; p = NS). No significant differences of phase were found either at baseline or under dobutamine infusion between the two groups. Multivariate linear regression analysis showed that only menopause status associated significantly with the amplitudes at different doses of dobutamine infusion (p < 0.05). In conclusion, human myocardial functional changes are observed by CVIBS after menopause. Postmenopausal women have higher values of amplitude than premenopausal women. These phenomena persist during low and peak doses of dobutamine infusion, but are abolished by atropine injection.

Adult↗

Suppression of cyclic coronary flow variation and reduction of restenosis with abciximab for morphologically high-risk lesions undergoing percutaneous coronary intervention.

Cyclic coronary flow variation (CCFV), a phenomenon related to repetitive accumulation of platelet aggregates at sites with endothelial injury, was reported to predict the acute ischemic complication after percutaneous coronary intervention. Platelet activation also stimulates neointimal proliferation, which is essential in the late restenosis process. Abciximab, a nonspecific antagonist to the platelet membrane glycoprotein IIb/IIIa as well as other integrins, may eliminate CCFV. A randomized study was conducted to evaluate the effect of abciximab on CCFV and restenosis in morphologically high-risk lesions. Forty-six coronary arteries with objective ischemia on the corresponding vascular territories were successfully treated. The use of abciximab successfully suppressed the occurrence of CCFV (p < or = 0.001) after balloon dilatation. In the follow-up study 3 months later, the use of abciximab predicted a lower loss index and less clinical recurrence (p = 0.008 and 0.03, respectively). The occurrence of CCFV, however, did not affect the angiographic or clinical outcome. The reduction of restenosis and clinical recurrence by the use of abciximab may thus be related to its nonglycoprotein IIb/IIIa effects, in addition to platelet inhibition.

Abciximab↗

Comparing the efficacy and safety of atorvastatin and simvastatin in Asians with elevated low-density lipoprotein-cholesterol--a multinational, multicenter, double-blind study.

BACKGROUND AND PURPOSE: There have been few reports on the efficacy and safety of statins in the Asian population. The study objectives were to compare the efficacy and safety of atorvastatin and simvastatin in Asian people. MATERIALS AND METHODS: This was a 16-week, double-blind, double-dummy, randomized, multicenter study involving eight medical centers in six Asian countries or areas. After a 6-week, diet-controlled, placebo lead-in period, 157 patients with low-density lipoprotein cholesterol (LDL-C) of between 160 and 250 mg/dL and serum triglyceride (TG) of less than 400 mg/dL were randomized to receive 10 mg of either atorvastatin (n = 79) or simvastatin (n = 78). After 8 weeks of treatment, all patients had the dose of study medication increased to 20 mg, irrespective of LDL-C concentration. Data obtained by monitoring lipid profiles, adverse events, and laboratory tests during the 16 weeks of study were used to assess the efficacy and safety of both treatments. RESULTS: After 8 weeks of treatment, LDL-C concentrations were reduced by 42.5% from baseline in patients receiving atorvastatin and 34.8% in those receiving simvastatin (p = 0.0006). Patients treated with atorvastatin also had a significantly greater reduction in very-low-density lipoprotein cholesterol (VLDL-C), TG, and total cholesterol (TC) after 8 weeks of treatment. The significantly greater reductions in LDL-C, VLDL-C, TG, and TC from baseline achieved with atorvastatin were still observed after an additional 8 weeks of treatment with 20 mg study medication. Both drugs increased high-density lipoprotein cholesterol (HDL-C) concentrations after 16 weeks of treatment, with no significant difference between the two treatments. After 16 weeks of treatment, 93% of atorvastatin and 85% of simvastatin patients had achieved their National Cholesterol Education Program LDL-C goals. No deaths occurred in the study population and the incidence of treatment-emergent adverse events was the same in the two groups (28%). Only one patient who was treated with simvastatin had a transaminase or creatine phosphokinase concentration that was more than three-fold the upper limit of normal. CONCLUSIONS: Asian people with primary hypercholesterolemia treated with atorvastatin had lower LDL-C, VLDL-C, TG, and TC after 8 weeks and 16 weeks of treatment than those treated with simvastatin. Both drugs demonstrated acceptable safety profiles.

Adult↗

Effect of hypercholesterolemia on myocardial function in New Zealand white rabbits.

Although hypercholesterolemia is a well-known risk factor for atherosclerosis, little is known about the effect of hypercholesterolemia on cardiac contractile function. The objective of this study was to examine the effect of hypercholesterolemia on myocardial contractility. Fifteen New Zealand white rabbits were fed standard chow (control group) and another 15 were fed a cholesterol-enriched diet (HC group) for 12 weeks. The contractile response of ventricular muscle strips was measured in various extracellular calcium concentrations and at different pacing rates. The whole-cell calcium current recording, and mRNA and protein levels of cellular calcium-handling proteins were also analyzed. With 2 mM Ca2+ and stimulation at 3 Hz, the contractile force of HC strips was less than that of the controls (3.63 +/- 0.20 vs. 4.61 +/- 0.50 mN, p < 0.05). The time to peak tension was longer for HC strips (93.3 +/- 2.16 vs. 82.2 +/- 2.81 ms, p < 0.05). The peak L-type calcium inward current density was slightly higher in HC myocytes but did not reach statistical significance (-14.90 +/- 0.94 vs. -12.44 +/- 0.84 pA/pF, p = 0.15). The mRNA level of sarcoplasmic reticulum Ca2+-ATPase (SERCA), normalized to GAPDH, was significantly lower in the HC than that in the control group (2.85 +/- 0.14 vs. 7.67 +/- 0.67, p < 0.05), as was the ryanodine receptor (RyR; 0.42 +/- 0.06 vs. 0.71 +/- 0.13, p < 0.05). The mRNA of the Na+/Ca2+ exchanger (NCX) was statistically higher in the HC group (0.90 +/- 0.12 vs. 0.48 +/- 0.05, p < 0.05). Western blot experiments revealed that protein expression of SERCA in the HC strips decreased, but that of the NCX increased. The protein expression of the dihydropyridine receptor was similar between these two groups. We concluded that hypercholesterolemia results in suppression of the maximal contractile function and in a longer systolic contractile time course. These changes may partially be mediated through a decrease in SERCA and RyR but an increase in NCX expression.

Animals↗

Dietary cholesterol affects sympathetic nerve function in rabbit hearts.

In order to assess the effect of hypercholesterolemia on cardiac sympathetic nerve function, New Zealand white rabbits were fed a normal diet (the control group) or one enriched with 0.5% cholesterol [the hypercholesterol (HC) group] for 3 months. Before and after the 3-month diet treatment, we performed serial imaging examinations and analyzed the uptake and washout ratio of (123)I-meta-iodobenzylguanidine ((123)I-MIBG) from the myocardium by administration of (123)I-MIBG through an ear vein. At the end of the experiments, the rabbits were sacrificed, and right ventricular strips were taken from their hearts. The inotropic response of the right ventricular strips to isoproterenol (ISO) and norepinephrine (NE) were evaluated. The cardiac MIBG uptake of the HC group, which was evaluated using the heart to mediastinum ratio, was higher than that of the age-matched control group. However, the washout ratios of (123)I-MIBG did not differ statistically between the two groups. On pretreatment with cocaine, NE-enhanced contractility was greater in papillary muscles isolated from the HC group. The concentration-response curve to ISO was shifted to the right in the HC group, compared with that in the control group. In conclusion, hypercholesterolemia in rabbits resulted in an increase in sympathetic nerve density in the myocardium, a decrease in the inotropic response to ISO and an increase in the inotropic response to NE in cocaine-treated myocardium. Both the in vivo and in vitro studies demonstrated the functional significance of neural remodeling induced by hypercholesterolemia.

3-Iodobenzylguanidine↗

Optical mapping of myocardial reactive oxygen species production throughout the reperfusion of global ischemia.

Reactive oxygen species (ROS) are short-lived, highly reactive chemical entities that play significant roles in all levels of biology. However, their measurement requires destructive preparation, thereby limiting the continuous measurement of ROS in a living tissue. We develop an optical mapping system to visualize ROS production in an isolated and perfused rat heart. By staining the heart with dihydroethidium (DHE), a 532-nm laser beam is directed to the epicardial surface, where we collect the red fluorescence (>600 nm) for semiquantitative analysis. With this system, ROS production as well as ventricular pressure and ECG in isolated perfused rat hearts are monitored throughout the reperfusion of global ischemia. Ischemia would decrease myocardial ROS production, while reperfusion would immediately result in sustained ROS overproduction. Optical mapping would provide information regarding the spatial distribution and temporal evolution of myocardial ROS production, which would enhance knowledge of the role of free radicals in cardiovascular biology.

Animals↗

Myocardial tissue characterization based on a polarization-sensitive optical coherence tomography system with an ultrashort pulsed laser.

A polarization-sensitive optical coherence tomography (PSOCT) system using a femtosecond-laser as the broadband light source is implemented with the axial resolution of 5 microm in free space. Through the design of path-length difference between the two polarization inputs and the modulation of one of the polarization inputs, the PSOCT images of various input and output polarization combinations can be distinguished and simultaneously collected. The PSOCT system is then used for in vitro scanning of the myocardium tissues of normal and infarcted rat hearts. The destruction of the birefringence nature of the fiber muscle in the infarcted heart can be clearly observed.

Animals↗