Biomedical subjects

Ying-Tsung Chen

Publications and source records attributed to Ying-Tsung Chen.

At least 19 recordsLinked to original sources

PubMed2007

Positive associations of bone mineral density with body mass index, physical activity, and blood triglyceride level in men over 70 years old: a TCVGHAGE study.

It is known that osteoporosis decreases physical function in older males. However, the role of metabolic parameters and physical activity influencing older men's bone status remains unclear. Thus, this study was designed to evaluate calcaneus bone mass by ultrasonic screening and the associated physical and metabolic functions in older men. This was a cross-sectional study. Three hundred sixty-eight older men (average age, 78.8 years) living in a veterans' home were enrolled. We measured body height and weight, waist and hip circumference, body fat, lean body mass, blood pressure, 6-min walking distance, complete blood count, and blood biochemical profile. Broadband ultrasound attenuation (BUA) and T-score were recorded using Soundscan quantitative ultrasound over the right calcaneus. The range of calcaneus BUA was 27.3-134.0; T-score was from -4.78 to 3.43. Of the total participants, 36.4% were osteopenic (-2.5 < T-score < -1.0) and 16.3% were osteoporotic (T-score <or= -2.5). BUA correlated with weight, body mass index (BMI), waist circumference, hip circumference, body fat, lean body mass, serum triglycerides, high-density lipoprotein-cholesterol, albumin, prealbumin, fasting and PC-2h blood insulin, red blood cell count, hemoglobin concentration, and 6-min walking distance. Multiple regression stepwise analysis revealed that only BMI, distance of 6-min walking, and blood triglyceride level were independently and positively associated with the values of BUA. Calcaneus bone mass is significantly and positively associated with BMI, blood triglycerides, and 6-min walking distance in older men.

Aged↗

PubMed2006

Intra-cardiac echocardiography guided trans-septal puncture in patients with dilated left atrium undergoing percutaneous transvenous mitral commissurotomy.

Percutaneous transvenous mitral commissurotomy (PTMC) is an effective treatment for mitral stenosis, but trans-septal puncture carries a certain risk of complications. There have been few reports on phase-array intra-cardiac echocardiography (ICE) guidance in trans-septal puncture for PTMC, especially in patients with dilated left atrium or distorted anatomy. Herein, we report our preliminary experience with ICE-guided trans-septal puncture in patients with dilated left atrium (>or=5.5 cm) who underwent PTMC. From June 2005 to March 2006, there were nine consecutive patients with symptomatic mitral stenosis and left atrium size larger than 5.5 cm who underwent trans-septal puncture for PTMC with the ICE guidance in this institution by a same operator. The procedural and catheterization results were analyzed. Using ICE guidance, the success rate for trans-septal puncture was 100% for all patients with dilated left atrium (>or=5.5 cm). The trans-septal procedures were free of major and minor complications and the patients were not exposed to contrast medium. Mitral valve area increased significantly from 1.0+/-0.2 cm(2) to 1.9+/-0.2 cm(2). Our preliminary result showed that ICE safely and effectively guided trans-septal puncture for PTMC in patients with dilated left atrium (>or=5.5 cm), thus eliminating contrast medium usage and avoiding unnecessary longer X-ray exposure.

Cardiac Surgical Procedures↗

PubMed2006

Iso-osmolar contrast medium better preserves short- and long-term renal function after cardiovascular catheterizations in patients with severe baseline renal insufficiency.

BACKGROUND: Iso-osmolar iodixanol was shown to least affect very-short-term renal function. However, its short- and long-term renal effects after cardiovascular catheterizations in severe renal insufficiency remain unknown. METHODS: Patients undergoing elective cardiovascular catheterizations and having pre-procedural serum creatinine (Scr) > or =2.5 mg/dl were prospectively studied. The results were compared to those of historical controls who received iopromide. RESULTS: The iodixanol group included 27 patients, aged 73+/-1 years, and the case-matched control group consisted of another 27 patients, aged 71+/-1 years. The baseline Scr were 3.0+/-0.3 and 3.0+/-0.2 mg/dl respectively. Although the Scr at 3 months was similar, the Scr at 6 months was lower in the iodixanol group (2.7+/-0.3 vs 4.2+/-0.5 mg/dl, p = 0.017). The absolute and percentage increments in Scr at 3 months (0.0+/-0.2 vs 0.6+/-0.2 mg/dl, p = 0.014, and 1+/-4% vs 24+/-6%, p = 0.003, respectively) and 6 months (-0.3+/-0.2 vs 1.3+/-0.4 mg/dl, p = 0.001, and -10+/-5% vs 47+/-12%, p < 0.001, respectively) were lower in the iodixanol group. CONCLUSIONS: Iodixanol better preserves short- and long-term renal outcomes in patients with severe baseline renal insufficiency.

Cardiac Catheterization↗

PubMed2006

Caveolin-1 expression is associated with plaque formation in hypercholesterolemic rabbits.

Caveolin-1, the major structural protein of caveolae, is present in several cell types known to play a role in the development of atherosclerosis. In this study, the distribution and expression of caveolin-1 in the arterial walls were studied in hypercholesterolemic rabbits. Immunohistochemical results indicated that the staining intensity of caveolin-1 reached a high level in the arterial intima at 5 weeks after high-cholesterol-diet treatment and decreased to a very low level at 8 weeks when atheromatous plaques appeared. Western blot analysis showed that in rabbits fed a high-cholesterol diet for 5 weeks, the expression of caveolin-1 reached its highest level and then decreased from 8 to 12 weeks. The proliferative activity of smooth muscle cells (SMCs) decreased to the lowest level at 5 weeks and then increased at 8 and 12 weeks. Nitric oxide synthase activity gradually decreased in animals fed a high-cholesterol diet throughout the experiment. These studies demonstrate that the change in abundance of caveolin-1 is associated with SMC proliferation in the formation of atheromatous plaque after hypercholesterolemia insult.

Animals↗

PubMed2006

Berberine suppresses MEK/ERK-dependent Egr-1 signaling pathway and inhibits vascular smooth muscle cell regrowth after in vitro mechanical injury.

Vascular smooth muscle cell (SMC) proliferation plays an important role in the pathogenesis of atherosclerosis and post-angioplasty restenosis. Berberine is a well-known component of the Chinese herb medicine Huanglian (Coptis chinensis), and is capable of inhibiting SMC contraction and proliferation, yet the exact mechanism is unknown. We therefore investigated the effect of berberine on SMC growth after mechanic injury in vitro. DNA synthesis and cell proliferation assay were performed to show that berberine inhibited serum-stimulated rat aortic SMC growth in a concentration-dependent manner. Mechanical injury with sterile pipette tip stimulated the regrowth of SMCs. Treatment with berberine prevented the regrowth and migration of SMCs into the denuded trauma zone. Western blot analysis showed that activation of the MEK1/2 (mitogen-activated protein kinase kinase 1/2), extracellular signal-regulated kinase (ERK), and up-regulation of early growth response gene (Egr-1), c-Fos and Cyclin D1 were observed sequentially after mechanic injury in vitro. Semi-quantitative reverse-transcription PCR assay further confirmed the increase of Egr-1, c-Fos, platelet-derived growth factor (PDGF) and Cyclin D1 expression in a transcriptional level. However, berberine significantly attenuated MEK/ERK activation and downstream target (Egr-1, c-Fos, Cyclin D1 and PDGF-A) expression after mechanic injury in vitro. Our study showed that berberine blocked injury-induced SMC regrowth by inactivation of ERK/Egr-1 signaling pathway thereby preventing early signaling induced by injury in vitro. The anti-proliferative properties of berberine may be useful in treating disorders due to inappropriate SMC growth.

Animals↗

PubMed2006

The presence of metabolic syndrome is independently associated with elevated serum CD40 ligand and disease severity in patients with symptomatic coronary artery disease.

Nontraditional atherosclerotic risk factors have become the focus of attention in recent years. In addition, metabolic syndrome is gaining recognition as another multiplex cardiovascular risk factor. However, to date, no studies have investigated the effect of metabolic syndrome on circulating soluble CD40 ligand (sCD40L), monocyte chemoattractant protein 1, cellular adhesion molecules, and disease severity in patients with symptomatic coronary artery diseases. This study was conducted to address this issue. Patients with stable angina who received percutaneous coronary interventions for significant (> or = 70% diameter stenosis) de novo lesions between January 1999 and January 2004 and had preprocedural serum samples were enrolled. Metabolic syndrome was defined by the National Cholesterol Education Program criteria with waist criterion modified into body mass index of more than 25 kg/m2. The serum samples were thawed and analyzed for circulating sCD40L, monocyte chemoattractant protein 1, adhesion molecules, and high sensitivity C-reactive protein (hs-CRP). Coronary severity was assessed by a modified version of Gensini scoring system. A total of 313 patients, 248 males and 65 females, were studied. Among them, 222 (70.9%, 170 males and 52 females) had metabolic syndrome. Patients with metabolic syndrome had higher serum creatinine level and lower low-density lipoprotein cholesterol despite higher triglyceride concentration. In multivariate analysis, patients with metabolic syndrome had higher sCD40L (6057 +/- 275 vs. 5051 +/- 423 pg/mL, P = .037) and more hs-CRP in higher tertiles (P = .005) than patients without, but similar levels of intercellular adhesion molecule 1, vascular cell adhesion molecule 1, and P selectin. Metabolic syndrome was also significantly associated with multiple coronary vessel involvements with 70% or higher diameter stenosis (36.5% double-vessel and 14% triple-vessel diseases vs 30.8% double-vessel and 5.5% triple-vessel diseases, P = .026) and multiple coronary segment involvements with 50% or higher diameter stenosis (P = .014) in multivariate analysis. In conclusion, the presence of metabolic syndrome is independently associated with elevated sCD40L, hs-CRP, and coronary disease severity in patients with coronary artery disease requiring interventional treatment of stable angina.

Aged↗

PubMed2006

Coronary artery disease progression is associated with C-reactive protein and conventional risk factors but not soluble CD40 ligand.

BACKGROUND: Coronary artery disease (CAD) is a major cause of death worldwide. Epidemiological studies have documented conventional risk factors; however, no studies to date have addressed the roles of soluble CD40 ligand (sCD40L) and monocyte chemoattractant protein-1 (MCP-1), and there have been few reports on other novel risk factors in CAD progression. The aim of the present study was to explore the roles of novel and conventional risk factors in CAD progression. METHODS: Patients with stable angina pectoris who underwent repeat coronary angiograms and had serum samples at the time of their first catheterization between March 1999 and January 2004 were enrolled. Those who had progression of coronary atherosclerosis were classified into the progression group (n = 66). Those who did not have CAD progression were classified into the nonprogression group (n = 124). RESULTS: There were more cases of diabetes mellitus (36% versus 20%; P = 0.024) and more men (92% versus 81%; P = 0.040) in the CAD progression group than in the nonprogression group, respectively. The progression group also had poorer lipid profiles than the nonprogression group, including higher total cholesterol (188+/-42 mg/dL versus 173+/-39 mg/dL, respectively; P = 0.014) and low density lipoprotein cholesterol (122+/-38 mg/dL versus 112+/-36 mg/dL, respectively; P = 0.025). In terms of inflammatory markers, progression patients had higher baseline high-sensitivity C-reactive protein (hs-CRP) concentrations (P = 0.018), which was also related to the subsequent angiographic severity score changes; however, sCD40L (6182+/-4352 pg/mL versus 6244+/-4602 pg/mL; P = 0.961), MCP-1 (427+/-540 pg/mL versus 341+/-128 pg/mL; P = 0.580) and adhesion molecules concentrations were indifferent between the progression group and the nonprogression group, respectively. Using a multivariate logistical regression model, the ORs for predicting progression were 2.19 for diabetes mellitus, 2.04 for hypercholesterolemia and 1.52 for hs-CRP (P < 0.05). CONCLUSION: In the present study, only conventional risk factors, and particularly hs-CRP, were markers for predicting CAD progression. Novel risk factors, such as concentrations of sCD40L, MCP-1 and adhesion molecules, did not play significant roles.

Aged↗

PubMed2006

High-dose norepinephrine induces disruption of myocardial extracellular matrix and left ventricular dilatation and dysfunction in a novel feline model.

BACKGROUND: Intravenous norepinephrine (NE) at a dose of 1-6 microg/kg/minute can induce increased extracellular matrix (ECM) and hypertrophic cardiomyopathy. This study aimed to investigate the effects of a higher dose of NE on cardiac remodeling. METHODS: After intraperitoneal urethane-chloralose anesthesia, 7 cats (3.03 +/- 0.58 kg) received intravenous infusion of NE 30 microg/kg/minute for 3 hours. Aortic blood pressure and heart rate (HR) were measured by polygraphy at 0, 5, 15, 30, 60, 90, 120, and 180 minutes. Left ventricular size and ejection fraction (EF) were measured by M-mode echocardiography before and after NE administration. Histopathology was performed by hematoxylin-eosin, silver impregnation, and Sirius red staining. Activity of matrix metalloproteinases (MMP) in the left ventricle was measured by zymography. RESULTS: Mean blood pressure (mmHg) increased from 139 +/- 20 to 198 +/- 19, 187 +/- 23, and 166 +/- 16 at 15, 30, and 60 minutes, respectively, during NE infusion. HR (beats/minute) decreased from 214 +/- 10 to 158 +/- 28 at 15 minutes and then recovered gradually. The left ventricles showed significant dilatation (end-diastolic diameter: from 1.20 +/- 0.18 to 1.58 +/- 0.23cm, p=0.003; end-systolic diameter: from 0.62 +/- 0.23 to 1.35 +/- 0.29cm, p=0.002) and hypokinesia (EF: from 86.2 +/- 5.2 to 33.1 +/- 16.5%, p < 0.001). Histopathology revealed that left ventricular myocytes were elongated, wavy, and fragmented, while collagen fibers were overstretched, straightened, and disrupted. MMP-9 activity was significantly elevated (p = 0.003 vs. control), while MMP-2 activity was unchanged. CONCLUSION: High-dose NE increases MMP-9 activity and causes ECM disruption, left ventricular dilatation and dysfunction.

Animals↗

PubMed2006

The mechanisms of an increased dominant frequency in the left atrial posterior wall during atrial fibrillation in acute atrial dilatation.

BACKGROUND: Previous studies have shown that the highest dominant frequency (DF) is located in the left atrium (LA) during atrial fibrillation (AF) in pacing-induced AF. However, there have been few studies on the mechanisms of the increased DF of AF during acute atrial dilatation. The purpose of this study was to investigate the mechanisms of the increased maximal DF (max DF) in pacing-induced AF during acute atrial dilatation. METHODS: In eight Langendorff-perfused canine hearts (26 +/- 2 kg), noncontact balloon catheters were placed into the right atrium (RA) and LA, respectively. AF was induced by extrastimulation pre- and postdilatation in the atrium (0 and 15 cm H(2)O, respectively). Fast Fourier transformation analysis was performed to analyze the max DF and harmonic index (HI) from the bi-atrial unipolar virtual electrograms during AF. The fibrillation cycle lengths were obtained from different atrial sites. The number of wavefronts was analyzed during AF. The frequency of regional splitting was defined as the number of wavefront splits per second in different atrial regions during AF. The percentage of the low-voltage zones (<0.5 mV) was defined as the ratio of the area of the low-voltage zones to the total atrial surface area. RESULTS: The DF was measured during AF. The shortest fibrillation cycle length was located in the LA posterior wall and became shorter during acute atrial dilatation. The max DF was located in the LA posterior wall and increased during acute atrial dilatation (7.1 +/- 0.8 vs 8.8 +/- 2.1, P = 0.02). The max DF of the LA correlated with the wavefront number (r = 0.797, P < 0.001 predilatation; r = 0.860, P < 0.001 postdilatation). The splitting of wavefronts facilitated the formation of new wavefronts. During acute atrial dilatation, the frequency of regional splitting was closely correlated with the percentage of the low-voltage zones (r = 0.876, P < 0.001). Furthermore, the LA posterior wall had a higher percentage of the low-voltage zones than the other sites. CONCLUSION: In acute atrial dilatation, the percentage of the low-voltage zones increased, especially in the LA posterior wall, which correlated with the regional splitting of the AF wavefronts. The increase in the splitting facilitated the formation of new wavefronts and resulted in a higher max DF during acute atrial dilatation.

Animals↗

PubMed2005

Circulating CD40 ligand is elevated only in patients with more advanced symptomatic peripheral arterial diseases.

INTRODUCTION: CD40 and its ligand participate in atherosclerosis formation, progression and destabilization. Increased soluble CD40 ligand (sCD40L) was observed in hypercholesterolemia, unstable angina and conditions with platelet activation. To date, there is no report on the association of sCD40L with angiographic peripheral artery disease (PAD) disease severity. MATERIALS AND METHODS: From March 1999 to April 2004, consecutive patients having angiographically documented PAD and given consents for pre-procedural serum sample use were recruited into this study. The key PAD lesions should be > or = 70% diameter stenotic at the lower limbs and patients were dichotomized into two groups depending on total PAD lengths. Peer angiographic control subjects were those free of coronary disease, PAD and major medical diseases. The serum samples were thawed and analyzed for sCD40L, monocyte chemotactic protein 1 (MCP-1) and hs-CRP in a single batch. RESULTS: A total of 63 well-defined lower-limb PAD patients and 30 control subjects were studied. Patients with PAD lengths >5 cm (N=38) presented higher sCD40L than those with lesions < or = 5 cm (N=25) (5430+/-459 vs. 3889+/-507 pg/ml, p=0.037) and control subjects (5430+/-459 vs. 3973+/-551 pg/ml, p=0.037). However, there was no significant difference in circulating MCP-1 (375+/-49 vs. 310+/-49 pg/ml and 297+/-24 pg/ml, respectively, p=0.371) or hs-CRP (0.64+/-0.16 vs. 0.51+/-0.15 mg/ml and 0.46+/-0.15 mg/dl, respectively, p=0.682) across three groups. PAD patients with associated coronary lesions did not differ in circulating CD40L, MCP-1 or hs-CRP from without and control subjects. CONCLUSIONS: Soluble CD40L was significantly elevated in patients with more advanced symptomatic PAD and might be an indicator for disease extent stratification. The distribution of sCD40L in PAD was not affected by coronary involvement or not.

Aged↗

PubMed2005

Intravenous aminophylline provides no additional renal protection in patient with severe atherosclerotic renal artery stenosis treated by delicate percutaneous renal intervention.

BACKGROUND: Clinical trials on contrast-induced nephropathy (CIN) prevention with different approaches generated various results. In this study, we investigated whether intravenous aminophylline preceding percutaneous transluminal renal artery stenting (PTRS) might provide better renal protection. METHODS: Patients with severe atherosclerotic renal artery stenosis and undergoing PTRS were prospectively studied. Intravenous aminophylline 250 mg was administered 30 min before PTRS. RESULTS: The aminophylline group included 15 patients (mean age, 68+/-4 years) and the case-matched control group consisted of another 15 patients (mean age, 71+/-2 years). After a mean follow-up of 5-6 months, both groups showed similar serum creatinine (1.7+/-0.2 vs. 1.6+/-0.1 mg/dl, P=NS), BUN (20.0+/-3.0 vs. 24.0+/-3.0 mg/dl, P=NS), fall in systolic (-15+/-13 vs. -11+/-3 mm Hg, P=NS) and diastolic BP (-2+/-4 vs. -6+/-5 mm Hg, P=NS). The incidence of post-operative renal deterioration was 6.7% in the study group and none in the control group. CONCLUSION: Pre-treatment intravenous aminophylline provides no additional renal protective effect in delicately practiced PTRS.

Aged↗

PubMed2005

Short- and long-term renal outcomes of immediate prophylactic hemodialysis after cardiovascular catheterizations in patients with severe renal insufficiency.

BACKGROUND: The short- and long-term effects of prophylactic hemodialysis (HD) immediately after cardiovascular catheterizations on renal function in patients with severe baseline renal insufficiency remain unknown though previous studies reported non-beneficial very-short-term effect in less severe patients. METHODS AND RESULTS: Patients who had pre-procedural serum creatinine (Scr) between 2.5 and 5.5 mg/dl were retrospectively studied. Twenty of them (14 M/6 F, aged 69 +/- 2 years) had received prophylactic HD after radiocontrast exposure and constituted the HD group. Another 20 patients were case-matched to the baseline demographics of the HD group and served as the non-HD group. The baseline Scr were 3.9 +/- 0.2 and 3.5 +/-0.2 mg/dl, respectively (p = NS). Although the Scr at 3 months was significantly higher in the HD group (4.3 +/- 0.3 vs. 3.4 +/- 0.2 mg/dl, p = 0.02), the absolute and percentage increments from baseline to 3 months (0.4 +/- 0.2 vs. 0.0 +/- 0.2 mg/dl, p = NS, and 11 +/- 5% vs. 1 +/- 7%, p = NS, respectively) and 6 months (0.6 +/- 0.3 vs. 0.4 +/- 0.4 mg/dl, p = NS, and 18 +/- 8% vs. 8 +/- 10%, p = NS, respectively) were not statistically different. Patients who developed end-stage renal disease requiring permanent HD at 1 year were also similar in both groups (four vs. three, respectively, p = NS). CONCLUSIONS: Our study confirmed that prophylactic HD immediately after contrast media administration in catheterizations failed to affect the short- and long-term renal and clinical outcomes even in patients with severe baseline renal insufficiency.

Acute Kidney Injury↗

PubMed2005

Sympathetic activity and myocardial damage after stimulation of dorsal medulla and vagotomy in a novel animal model.

Many kinds of brain lesions cause sympathetic hyperexcitation and myocardial damage. A novel animal model was developed for the correlation of sympathetic excitation with ventricular dysfunction and myocardial damage. Six cats (3.23+/-0.26 kg) under intraperitoneal urethane-chloralose anesthesia were artificially ventilated and bilaterally vagotomized. They underwent an electrical stimulation of unilateral dorsal medulla for 180 min (monopolar square-wave pulses, 10 Hz, 10 V, 0.5 ms). Mean blood pressure, heart rate plasma concentration of norepinephrine and left ventricular size and ejection fraction were measured at 0, 5, 15, 30, 60, 90, 120 and 180 min. Mean blood pressure (mm Hg), heart rate (beats/min) and norepinephrine (pg/ml) increased abruptly from 128+/-15, 203+/-22 and 353+/-123 to 234+/-26, 240+/-13 and 4727+/-2159 at 5 min after electrical stimulation (all p<0.01). The left ventricles showed significant dilatation (end-diastolic diameter: from 1.35+/-0.13 to 1.84+/-0.21 cm, p=0.006; end-systolic diameter: from 0.65+/-0.20 to 1.54+/-0.24 cm, p=0.002) and hypokinesia (ejection fraction: from 88.9+/-6.4% to 37.3+/-8.7%, p<0.001). Cardiac pathology revealed myocardial hemorrhage, cardiomyocyte apoptosis and coagulative myocytolysis (contraction band necrosis), characterized by sarcoplasmic coagulation, granulation and disruption. In conclusions, the present experiment develops a novel animal model in which stimulation of the pressor area in the dorsal medulla in vagotomized cats produces sympathetic hyperexcitation accompanied with myocardial dysfunction and damage. This model may be applicable for studying protective effect of drugs on myocardial dysfunction and damage caused by sympathetic hyperexcitation occurring in brain diseases.

Animals↗

PubMed2005

Comparison of critical closing pressures extracted from carotid tonometry and finger plethysmography.

BACKGROUND: The reliability of critical closing pressure (CrCP) estimates derived from peripheral blood pressure (BP) measurements is unclear. We attempted to evaluate the influences of peripheral circulation on determining CrCP. METHODS: Twenty-five young healthy volunteers were studied. BP waves were obtained with plethysmography (Portapres) and carotid applanatory tonometry, respectively, for analysis. Transcranial Doppler was used to monitor cerebral flow velocity. Using linear regression analysis, beat-to-beat CrCP was calculated at rest, during voluntary hyperventilation and during 5% CO2 inhalation. RESULTS: Twenty of 25 participants demonstrating satisfactory tonometric tracings for both tests were included in the analysis. The systolic BP measured using plethysmography was higher than that derived from tonometry (139.4 +/- 24.7 vs. 105.5 +/- 29.6, p < 0.001). CrCP values derived from tonometry were all positive and higher than CrCP values derived from plethysmography (62.9 +/- 19.9 vs. 11.1 +/- 17.8, p < 0.001). The changes in CrCP induced by 5% CO2 inhalation and hyperventilation had a correlation between two BP monitoring methods (r = 0.52, p = 0.001). CONCLUSIONS: Pressure waveform is an important determinant in calculating CrCP by linear regression analysis. The relative changes in CrCP induced by hemodynamic challenges remained a relevant indicator of cerebrovascular regulation regardless of the methods used for non-invasive BP recording.

Adolescent↗

PubMed2005

Changes in flow-mediated dilatation, cytokines and carotid arterial stenosis during aggressive atorvastatin treatment in normocholesterolemic patients.

BACKGROUND: Aggressive statin therapy to reduce low-density lipoprotein (LDL) cholesterol in patients with normal LDL-cholesterol levels reduces the incidence of future cardiovascular events and enhances atherosclerotic regression in the common carotid artery. We tried to quantify changes in flow-mediated dilatation (FMD), inflammatory cytokines, and the severity of carotid arterial stenosis, after aggressive statin administration to patients with normal LDL-cholesterol levels, and stroke or transient ischemic attack ipsilateral to carotid arterial stenosis. METHODS: Twenty patients with at least a 50% reduction in the diameter of the carotid artery were studied. Atorvastatin 10 mg daily was prescribed for 4 months. Serial changes in the severity of carotid arterial stenosis, and brachial-artery FMD were evaluated by high-resolution ultrasound. Tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), vascular cell adhesion molecule (VCAM), intracellular adhesion molecule (ICAM), soluble endothelin-1 (ET-1), and high-sensitivity C-reactive protein (hs-CRP), were measured before, and after 2 and 4 months of, atorvastatin treatment. RESULTS: Atorvastatin significantly decreased plasma levels of total cholesterol and LDL-cholesterol after 1, 2 and 4 months of treatment (p < 0.01). FMD showed significant improvement after only 4 months (10.0% vs 6.8% at baseline; p = 0.019). The overall severity of carotid arterial lesions was not significantly reduced by atorvastatin. Changes in TNF-alpha, IL-1beta, IL-6 and ET-1 showed trends towards a progressive decline after atorvastatin, but none of the cytokines was reduced significantly. FMD did not correlate with the severity of carotid arterial stenosis, lipid profile, or cytokine levels. CONCLUSION: Atorvastatin effectively reduced plasma concentrations of total cholesterol and LDL-cholesterol, and had beneficial effects on endothelial function, in Chinese patients with carotid arterial stenosis and normal LDL-cholesterol levels.

Aged↗

PubMed2005

Increased extracellular collagen matrix in myocardial sleeves of pulmonary veins: an additional mechanism facilitating repetitive rapid activities in chronic pacing-induced sustained atrial fibrillation.

UNLABELLED: Increased ECM in canine PVs. INTRODUCTION: Cell uncoupling due to fibrosis or increased extracellular collagen matrix (ECM) affects the formation of ectopic focal activity. Whether or not the increase of ECM also exists in the pulmonary veins (PVs) with rapid atrial pacing is unknown. We sought to test the hypothesis that in chronic atrial pacing dogs with sustained atrial fibrillation (AF), the amount of ECM was increased in both atria and the PVs. METHODS AND RESULTS: We induced sustained AF in dogs by rapid atrial pacing. Computerized mapping techniques were used to map both atria and the PVs. We also used histological assessment to quantify the amount of ECM. After 118+/-24 days of rapid atrial pacing, sustained AF was induced in 7 dogs. Repetitive rapid activities (RRAs) either continuously or intermittently arose from the PVs during sustained AF. Histological study shows that there was no fibrosis in both atrial free walls and the PVs. However, the amount of ECM was increased in these regions. The mean ECM surface area fraction at each region in the dogs with sustained AF was all significantly higher compared to the corresponding region in normal dogs. Similarly, the heterogeneity of the ECM surface area fraction at each region in the dogs with sustained AF was also all significantly higher compared to normal dogs. CONCLUSIONS: In chronic atrial pacing-induced sustained AF, structural remodeling (i.e., inhomogeneous increase of ECM) also involves the PVs. Reduced coupling of the myocytes in the PV due to histological changes may provide an additional mechanism facilitating RRAs.

Animals↗

PubMed2005

Delicate percutaneous renal artery stenting minimizes postoperative renal injury and protects kidney in patients with severe atherosclerotic renal artery stenosis and impaired renal function.

Percutaneous transluminal renal artery stenting (PTRAS) is associated with declining renal function in a non-negligible portion of patients and is inflicted by different mechanisms, including atheroembolism. This study investigated whether delicate PTRAS to reduce atheroembolism might minimize postoperative renal injury and better preserve renal function. Patients undergoing PTRAS performed by experienced interventional cardiologists, applying coronary intervention concepts, techniques, devices and delicacy principles whenever possible, were prospectively studied. A total of 34 patients (29 M/5 F) with impaired renal function (group A, creatinine 2.4 +/- 0.1 mg/dL) and another 20 patients (16 M/4 F) with normal serum creatinine (group B, baseline creatinine 1.2 +/- 0.0 mg/dL) were studied. PTRAS was successfully performed in all but one group A patient. During a 6-month follow-up, systolic and diastolic blood pressure (130 +/- 2 versus 148 +/- 4 mmHg, P = 0.001 and 70 +/- 2 versus 78 +/- 3 mmHg, P = 0.006) and serum creatinine (2.1 +/- 0.1 versus 2.4 +/- 0.1 mg/dL, P < 0.001) were all significantly lowered in group A patients. Using a 20% change cut-off value, renal function improved in eight (24%), remained unchanged in 24 patients (73%), and deteriorated in only one patient (3%). The corresponding alterations in blood pressure and renal function were insignificant in group B patients. Patients with bilateral involvement (eleven patients) also had significantly lowered serum creatinine on follow-up. In conclusion, delicately practiced PTRAS can reduce the rate of postprocedural renal deterioration in patients with impaired renal function, and should be adopted in every renal intervention.

Aged↗

PubMed2005

An autosomal genome-wide scan for loci linked to pre-diabetic phenotypes in nondiabetic Chinese subjects from the Stanford Asia-Pacific Program of Hypertension and Insulin Resistance Family Study.

Type 2 diabetes is a complex disease involving both genetic and environmental components. Abnormalities in insulin secretion and insulin action usually precede the development of type 2 diabetes and can serve as good quantitative measures for genetic mapping. We therefore undertook an autosomal genomic search to locate the quantitative trait locus (QTL) linked to these traits in 1,365 nondiabetic Chinese subjects from 411 nuclear families. Residuals of these log-transformed quantitative traits were analyzed in multipoint linkage analysis using a variance-components approach. The most significant QTL for fasting insulin, which coincides with the QTL for homeostasis model assessment of insulin resistance, was located at 37 cM on chromosome 20, with a maximum empirical logarithm of odds (LOD) score of 3.01 (empirical P = 0.00006) when adjusted for age, sex, BMI, antihypertensive medications, recruitment centers, and environmental factors. In the same region, a QTL for fasting glucose was identified at 51 cM, with an empirical LOD score of 2.03 (empirical P = 0.0012). There were other loci with maximum empirical LOD scores >or=1.29 located on chromosomes 1q, 2p, 5q, 7p, 9q, 10p, 14q, 18q, and 19q for different diabetes-related traits. These loci may harbor genes that regulate glucose homeostasis either independently or via interactions of the genes within these regions.

Asian People↗