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Yuan-Teh Lee

Publications and source records attributed to Yuan-Teh Lee.

At least 19 recordsLinked to original sources

Metabolic syndrome as a risk factor for coronary heart disease and stroke: an 11-year prospective cohort in Taiwan community.

OBJECTIVE: Patterns of metabolic syndrome among populations in the Asia-Pacific region remain unknown. This study sought to establish the prevalence of metabolic syndrome in Taiwan and the risk of cardiovascular disease imparted by this syndrome. METHODS AND RESULTS: A cohort of 3602 individuals aged 35 years and above from one Taiwan community in 1990-1991 was followed up for a median of 9.0 years (inter-quartile range: 7.9-10.0 years). Women had a higher prevalence rates of age-standardized metabolic syndrome than men (28.9% versus 16.6%) by original NCEP-ATP III criteria, and the rates increased progressively. As numbers of metabolic syndrome increased, the hazard risk (HR) increased significantly, up to 5.5 (95% confidence interval [CI], 2.2-13.7) for coronary heart disease and 3.5 (95% CI, 1.9-6.5) for stroke. We found that low HDL cholesterol and high BMI had the highest risk for coronary heart disease (HR, 2.3), followed by metabolic syndrome (HR, 1.8). For stroke events, high blood pressure had the highest risk (HR, 3.0), also followed by metabolic syndrome (HR, 2.1). The highest attributable risk for the general population was low HDL cholesterol for coronary heart disease event and high blood pressure for stroke. CONCLUSIONS: Metabolic syndrome was highly prevalent among the adult population and associated with an increased risk for coronary heart disease and stroke.

Adult↗

Heritability and major gene effects on left ventricular mass in the Chinese population: a family study.

BACKGROUND: Genetic components controlling for echocardiographically determined left ventricular (LV) mass are still unclear in the Chinese population. METHODS: We conducted a family study from the Chin-San community, Taiwan, and a total of 368 families, 1145 subjects, were recruited to undergo echocardiography to measure LV mass. Commingling analysis, familial correlation, and complex segregation analysis were applied to detect component distributions and the mode of inheritance. RESULTS: The two-component distribution model was the best-fitting model to describe the distribution of LV mass. The highest familial correlation coefficients were mother-son (0.379, P < .0001) and father-son (0.356, P < .0001). Genetic heritability (h2) of LV mass was estimated as 0.268 +/- 0.061 (P < .0001); it decreased to 0.153 +/- 0.052 (P = .0009) after systolic blood pressure adjustment. Major gene effects with polygenic components were the best-fitting model to explain the inheritance mode of LV mass. The estimated allele frequency of the gene was 0.089. CONCLUSION: There were significant familial correlations, heritability and a major gene effect on LV mass in the population-based families.

Adolescent↗

Interaction of obesity, metabolic syndrome and Framingham risk on steatohepatitis among healthy Taiwanese: population-based nested case-control study.

BACKGROUND: There have been scant reports on the cumulative effects of atherosclerotic risk factors on steatohepatitis. METHODS: We defined cases of steatohepatitis (n = 124) from one health examination center at National Taiwan University Hospital from January to December 2002. We selected controls, matched by age, gender and drinking status. Metabolic syndrome was defined by the modified ATP-III guidelines. High-dimensional interactions of risk factors for steatohepatitis were evaluated. RESULTS: Steatohepatitis cases had the highest C-reactive protein, lymphocytes, Framingham scores and predicted coronary risks. The odds ratio (OR) of metabolic syndrome for steatohepatitis was the highest (OR = 9.9), followed by high glucose status (OR = 4.5) and obesity (OR = 3.6). The highest area under the ROC curve was metabolic syndrome (area = 0.80), followed by obesity (0.75) and high glucose level (0.73). Metabolic syndrome was the highest population-attributable risk factor (0.59). Significant interaction was found with a three-factor model, including obesity, metabolic syndrome and Framingham risk status, with lesser average prediction error (22.6%), higher average cross-validation consistency (6.3) and lower average prediction error (24.3%). Compared with persons with no risk factors, OR increased as the number of risk factors increased (OR = 3.0 with one risk factor, 17.5 with two risk factors, 10.8 with three risk factors, respectively). CONCLUSION: Metabolic syndrome, inflammation markers and atherosclerotic risk scores are significantly related to steatohepatitis status among the healthy examinee population in Taiwan.

Adult↗

Enhanced external counterpulsation reduces lung/heart ratio at stress in patients with coronary artery disease.

Enhanced external counterpulsation (EECP) is a recently approved treatment modality for patients with angina and heart failure. However, the efficacy of EECP on left ventricular (LV) function has not been well established. The study was aimed to determine whether EECP leads to an improvement in objective parameters of LV function. Patients with coronary artery disease (n = 10) who showed evidence of stress-induced myocardial ischemia despite conventional medical or surgical therapies were enrolled and received EECP therapy for a total of 35 h. The therapeutic effects of EECP were examined by thallium-201 single-photon emission computed tomography (201Tl-SPECT). Compared with baseline, the lung/heart ratio at stress decreased significantly from 0.40 +/- 0.08 to 0.35 +/- 0.08 (p = 0.001) at 1 month and 0.33 +/- 0.10 (p = 0.03) at 6 months following EECP treatment. LV ejection fraction marginally improved from 56.7 +/- 7.7% to 57.6 +/- 5.9% (p = 0.382) at 1 month and to 60.1 +/- 8.6% (p = 0.062) at 6 months after EECP therapy, although not statistically significant. We concluded that EECP improved LV function, shown as the reduction of lung/heart ratio at stress, in patients with coronary artery disease, up to 6 months after EECP treatment.

Coronary Artery Disease↗

Segregation analysis of apolipoprotein A1 levels in families of adolescents: a community-based study in Taiwan.

BACKGROUND: Apolipoprotein (Apo) A1 is a protective factor for cardiovascular events. This study aimed to perform complex segregation analyses of Apo A1 levels in families of adolescents systematically ascertained from the junior high school students in a rural community. Both siblings and parents of the adolescent probands were recruited for the study. Apo A1 concentrations were measured by turbidimetric immunoassay methods. After adjustment for gender, age, body mass index, smoking and drinking status, residual values of Apo A1 were subjected to subsequent analyses. RESULTS: Significant mother-father and parent-offspring correlations were found. Commingling analyses indicated that a four-component distribution model was needed to account for the Apo A1 variation. Segregation analysis using regressive models revealed that the best-fit model of Apo A1 was a model of environmental effect plus familial correlation (heritability = 23.9%), in which a significant mother-father correlation existed. Models containing major gene effect could be rejected. CONCLUSION: These results suggest that variations of Apo A1 levels in the normal range, especially during adolescence, are likely to be influenced by multiple factors without significant contribution from major genes.

Adolescent↗

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↗

Major gene effects on apolipoprotein B concentrations in families of adolescents--results from a community-based study in Taiwan.

BACKGROUND: Apolipoprotein (Apo) B is considered as a risk factor for atherosclerosis. Previous reports of segregation analyses on the mode of inheritance of Apo B were inconsistent because of heterogeneity in study population or elderly adult diseased probands. We performed complex segregation analysis of Apo B levels in the families of adolescents, systematically ascertained from junior high school students in a rural community in Taiwan. RESULTS: There is a sex-specific influence in the variation of apo B levels. The mother-daughter (0.216), sister-sister (0.181), sister-brother (0.179) correlations were higher than father-son (0.206), brother-brother (0.002) or cross-sex correlations for the variation in Apo B levels. By the variance component model, the heritability estimate was 26.3+/-6.7% (P<.0001) in Apo B levels. Commingling analysis indicated that a 2-component distribution was needed to account for Apo B variation. Segregation analysis using regressive models revealed that the best-fit model of Apo B was the model of major gene effect plus familial correlation. The gene frequency controlling high Apo B was 0.17, and 3 means of genotypes were 56.3, 54,2, and 117.2 mg/dl. CONCLUSION: Variations of Apo B levels in the normal range among adolescent families are controlled by major gene, and further identification of this gene locus will be mandatory.

Adolescent↗

Hyperuricemia as a risk factor on cardiovascular events in Taiwan: The Chin-Shan Community Cardiovascular Cohort Study.

Little is known about uric acid role for cardiovascular events in the Asian-Pacific countries with relatively low coronary heart disease (CHD) but high stroke events. Also, there is scanty evidence for repeated measures of uric acid levels among population. We examined associations of basic and repeated measures of uric acid level with CHD and stroke events in one Taiwanese adult community prospectively. Cox proportional hazards models, treating uric acid as baseline and time-dependent covariates, were used to assess the 11-year risk of CHD and stroke events. Among 3602 adult subjects older than 35 years, 86 incident CHD and 155 incident stroke cases were identified. The rate ratios of hyperuricemia ranged between 2.00 and 3.96, with higher risk ratios in women than in men. The rate differences and population attributable fractions were also higher in women than in men, implying that women had high risk of uric acid on cardiovascular events. After adjustment for age effect, time-dependent uric acid was associated with significant CHD risk in both genders (hazard risk [HR] 1.43, 95% CI: 1.10-1.87 in men and HR 1.22, 95% CI: 1.03-1.44 in women). But the magnitude of hazard risks decreased after adjusting more atherosclerotic risk factors for CHD. For stroke event, the age-adjusted hazard risk of time-dependent continuous uric acid level was 1.23 (95% CI: 1.00-1.54) in men and 1.36 (95% CI: 1.05-1.75) in women. Multiple adjustment by risk factors demonstrated that uric acid was still a significant predictor for stroke in women (HR 1.32, 95% CI: 1.00-1.73). The similar hazard risk patterns existed for binary categories of hyperuricemia. Subgroup analyses demonstrated uric acid had significant risk only in hypertension and metabolic syndrome subgroups, not in their counterparts. We concluded that uric acid, in the baseline and time-dependent variables, could predict cardiovascular events in the community of relatively low CHD but high stroke risk in Taiwan.

Adult↗

High-density lipoprotein antagonizes oxidized low-density lipoprotein by suppressing oxygen free-radical formation and preserving nitric oxide bioactivity.

The antiatherogenic role of high-density lipoprotein (HDL) has been related to its ability to increase the activity of endothelial nitric oxide synthase (eNOS) and to protect low-density lipoprotein (LDL) against oxidative modification. The present study was aimed to determine whether and how HDL antagonizes oxidized LDL (oxLDL) that has been formed and accumulated in circulation. Pre-infusion of rats with HDL effectively prevented oxLDL-induced renal vascular constriction. Consistently, pre-incubation of human saphenous vein endothelial cells with HDL (100 microg/ml) reversed the oxLDL-induced suppression of endothelium-dependent cyclic-GMP production in co-cultured smooth muscle cells. However, the changes of Akt phosphorylation and eNOS activity in endothelial cells in response to lipoprotein treatments under our assay condition were not significant. Intriguingly, pretreatment of human umbilical vein endothelial cells with HDL (50 microg/ml) for only 30s effectively reduced the level of free radicals generated by oxLDL or H(2)O(2). In kidneys of living rats, renal arterial infusion of oxLDL greatly enhanced ischemia/reperfusion-induced free radicals, which could be attenuated by HDL pretreatment. We conclude that HDL may antagonize oxLDL on endothelial function through an Akt-independent pathway in which HDL preserves nitric oxide bioactivity by attenuating oxLDL-triggered free radical generation.

Animals↗

Twenty-four-hour ambulatory blood pressure and duration of hypertension as major determinants for intima-media thickness and atherosclerosis of carotid arteries.

The relationship between time factors of elevated blood pressure (BP) and carotid atherosclerosis (CA) is still unclear. The associations between time-weighted average 24 h ambulatory systolic BP (TWA-SBP), duration of hypertension in years (hypertension-year), and CA were investigated in a petrochemical company sample of 95 executives and 91 gender- and age-matched non-executives employees. Intima-media thickness (IMT) and plaque scores of extracranial carotid artery (ECCA) were determined bilaterally by high-resolution B-mode ultrasound. The determinants of segment-specific carotid IMT and odds ratios for CA, in terms of thicker IMT (IMT > or = 75th percentile) and ECCA score > or = 3, were evaluated by multivariate regression analysis. Results revealed TWA-SBP and hypertension-year were two major determinants of IMT at common carotid artery (CCA) and carotid bulb by using mixed regression models. However, TWA-DBP was a negative determinant of IMT at CCA and carotid bulb. Meanwhile, the executives were found to be a negative association with IMT at carotid bulb. Measurements at both internal carotid artery and bulb identified duration of diabetes mellitus as significant determinant of IMT. After controlling covariates, multivariate logistic regression analysis identified TWA-SBP and hypertension-year as the important determinants for thicker IMT and ECCA > or = 3. And, TWA-DBP was found as a negative determinant for CA. In conclusion, both TWA-SBP and hypertension-year were two major determinants for carotid IMT and CA, which seem to imply that both short-term and long-term durations of elevated BP are probably crucial in the pathogenesis of CA.

Blood Pressure↗

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↗

Treatment of fibrate-induced rhabdomyolysis with plasma exchange in ESRD.

Hypertriglyceridemia is a common metabolic disorder in patients with chronic renal failure. Fibrate derivatives are often used for lipid lowering in this population with adjusted dosage. However, fibrate-related adverse reaction still occasionally occurs. The authors report a case of end-stage renal disease in a patient who underwent hemodialysis regularly, taking a reduced dosage of bezafibrate (200 mg/d) for refractory hypertriglyceridemia. She did not take any statins, cyclosporine, monoamine oxidase inhibitors, or warfarin concurrently. Rhabdomyolysis was complicated along with an increased serum bezafibrate level. Plasma exchange was performed, which dramatically decreased the level of bezafibrate, and rhabdomyolysis resolved rapidly thereafter. A lower dose of bezafibrate, 200 mg every third day, was prescribed with cautious monitoring of symptoms and laboratory parameters, and better triglyceride control was achieved uneventfully. This is the first report using plasma exchange to remove excessive bezafibrate, a highly protein-bound molecule that is unlikely to be cleared by hemodialysis in an end-stage renal disease patient with serious adverse reaction caused by accumulation of bezafibrate. In contrast to a traditional wait-and-see strategy, plasma exchange seems to be a safe and effective treatment in addition to supportive care for rhabdomyolysis in such clinical scenarios.

Bezafibrate↗

Relative importance of atherosclerotic risk factors for coronary heart disease in Taiwan.

BACKGROUND: The relative importance of atherosclerotic risk factors, such as hypertension, dyslipidemia, diabetes and smoking, was associated with cardiovascular events and varied among different ethnic groups. For a population with relatively low coronary heart disease (CHD) such as Asian-Pacific countries, it is crucial to differentiate the roles of these risk factors. METHODS: We examined the relative importance of various risk factors for CHD in a community-based cohort in Taiwan, consisting of 3602 adults aged 35 and older with a median follow-up time of 9.0 years since 1990. Regular death certificate verification and medical record reviews were performed in the follow-up activities. RESULTS: There were 85 cases defined as CHD. In the Cox proportional hazard analysis, men were at higher risk than women [hazard risk (HR)=2.22, 95% confidence interval (CI)=1.39-3.56]. Hypertension was the most common risk factor for CHD. Dyslipidemia, especially lowered high-density lipoprotein cholesterol, also played an important role (HR=2.09, 95% CI=1.33-3.29) in CHD events. Hypertension had a greater influence in males (HR=6.08, P<0.001) than in females (HR=2.80, P<0.001). No independent association was found for smoking or body mass index in cardiovascular events. CONCLUSION: This study found that in a community-based cohort, hypertension, and dyslipidemia attribute an important role to cardiovascular events.

Adult↗

Gene expression profiles in hypoxic preconditioning using cDNA microarray analysis: altered expression of an angiogenic factor, carcinoembryonic antigen-related cell adhesion molecule 1.

Hypoxic preconditioning has been shown to exhibit cardioprotective effects on myocardium from ischemic or reperfusion injury. The specific regulated gene involved in the hypoxia-induced cardioprotective effects is profiled in this study. Young male Wistar rats and ICR mice were exposed to sea level (as normal control) or simulated high altitude for 15 h/day for 2, 4, or 8 weeks, or for 4 weeks at high altitude after 2 weeks at sea level. The left ventricles of the animals were isolated for mRNA isolation and cDNA microarray analysis. Our data demonstrated that hypoxic preconditioning significantly ameliorated cardiac ischemic injury by minimizing the infarct size. After cluster analysis of expression profiles after different courses of hypoxic preconditioning (0, 2, 4, and 8 weeks), 386 genes showed an ascending pattern, whereas 301 genes showed a descending pattern. The ascending genes include several angiogenic factors: FGF receptor 4, vascular endothelial growth factor (vEGF), and carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM-1). The microvessel density was also significantly increased in hypoxic hearts. Using Western blotting and immunohistochemical analysis, the protein expression level and localization of CEACAM-1 were observed in hypoxic myocardium. The results also indicated that CEACAM-1 was upregulated as with other hypoxic angiogenic factors, heme oxygenase 1 (HO-1) and hypoxia inducible factor-1alpha (HIF-1alpha), in in vitro cultured cardiomyocytes (H9c2) after hypoxia treatment and in vivo hypoxic preconditioning. Furthermore, incubation with recombinant vEGF could also increase the expression level of CEACAM-1 in H9c2 cells. These results demonstrated that hypoxic preconditioning resulted in transcriptional changes, and some of these genes have been correlated with angiogenesis. The HIF-1/vEGF/CEACAM-1 pathway might be important for hypoxia-induced angiogenesis in the heart during hypoxic preconditioning.

Animals↗

Lipoprotein-X reduces LDL atherogenicity in primary biliary cirrhosis by preventing LDL oxidation.

Hypercholesterolemic human LDL contains oxidized subfractions that have atherogenic properties. Paradoxically, atherosclerosis incidence is low in patients with primary biliary cirrhosis (PBC), a disease characterized by marked increases in plasma LDL, including the LDL subfraction lipoprotein-X (Lp-X). To investigate the mechanisms underlying this paradox, we first examined the propensity to oxidation of unfractionated LDL isolated from PBC patients. After prolonged incubation with copper, PBC-LDL failed to increase the oxidation index or electrophoretic mobility noted in control LDL. An admixture of PBC-LDL or Lp-X with control LDL prevented oxidation of the latter in a dose-dependent manner. PBC-LDL was also noncompetitive against copper-oxidized LDL (oxLDL) for binding with a murine monoclonal anti-oxLDL antibody in a competitive ELISA. OxLDL exerts its proapoptotic and antiangiogenic effects in part by inhibiting fibroblast growth factor 2 (FGF2) expression. Preincubation of oxLDL with PBC-LDL, but not control LDL, attenuated the inhibitory effects of oxLDL on FGF2 expression in cultured bovine aortic endothelial cells (ECs). The antioxidant and prosurvival properties of PBC-LDL diminished after the patients underwent orthotopic liver transplantation. These results suggest that Lp-X reduces LDL atherogenicity by preventing LDL oxidation to protect EC integrity in the presence of hypercholesterolemia. They also suggest that altering LDL composition may be as important as reducing LDL concentration in preventing or treating atherosclerosis.

Animals↗

Ascorbate supplement reduces oxidative stress in dyslipidemic patients undergoing apheresis.

OBJECTIVE: The effect of ascorbate treatment on apheresis-induced oxidative stress in uremic and dyslipidemic patients was evaluated. METHODS AND RESULTS: We developed a chemiluminescence-emission spectrum and high-performance liquid chromatography analysis to assess the effect of ascorbate supplement on plasma reactive oxygen species (ROS) scavenging activity and oxidized lipid/protein production in hyperlipidemic and uremic patients undergoing apheresis. Apheresis was efficient in reduction of atherogenic lipoproteins, complement, fibrinogen, soluble intercellular adhesion molecule-1, and oxidative parameters including phosphatidylcholine hydroperoxide (PCOOH), malonaldehyde, methylguanidine, and diotyrosine. Apheresis itself, however, activated leukocytes to increase ROS activity and reduced the plasma ROS scavenging activity. Ascorbate administration selectively diminished apheresis-enhanced H2O2 and inflammatory mediators such as tumor necrosis factor alpha (TNF-alpha) and monocyte chemoattractant protein-1. Chronically dyslipidemic and uremic patients undergoing biweekly apheresis plus ascorbate treatment had lower levels of C-reactive protein and PCOOH than did those without ascorbate treatment during a 6-month follow-up study period. CONCLUSIONS: We demonstrate that apheresis with ascorbate treatment provides a therapeutic potential in reducing atherosclerotic risk via inhibition of H2O2-induced oxidative stress in patients with uremia or dyslipidemia.

Adult↗