Biomedical subjects

Chih-Tai Ting

Publications and source records attributed to Chih-Tai Ting.

At least 19 recordsLinked to original sources

PubMed2007

Bidirectional regulation of upstream IGF-I/insulin receptor signaling and downstream FOXO1 in cardiomyocytes.

Signaling pathways of IGF-I and insulin receptors play important roles in the regulation of myocardial function. FOXO1 is a member of the forkhead transcriptional factor family, but how insulin and IGF-I receptor signaling regulate FOXO1 in cardiomyocytes is not well understood. This study was carried out to elucidate how IGF-I and insulin receptor signaling modulate FOXO1 in cardiomyocytes. In cardiomyocytes, activation of IGF-I receptor and insulin receptor lead to rapid phosphorylation of FOXO1. Inhibition of phosphatidylinositol 3-kinase/Akt pathway suppressed the effect of insulin and IGF-I on FOXO1 phosphorylation. Prolonged incubation with IGF-I increased ubiquitination of FOXO1 and down-regulated the abundance of FOXO1 proteins, which suggested that IGF-I might modulate FOXO1 degradation. To explore whether FOXO1 could modulate IGF-I and insulin signaling, a constitutively active FOXO1 was overexpressed in cardiomyocytes. The abundance of insulin receptor and IGF-I receptor was significantly upregulated in the cells overexpressing active FOXO1, accompanied by increased receptor phosphorylation upon insulin/IGF-I stimulation. Interestingly, overexpression of constitutively active FOXO1 also led to activation of MEK and Akt phosphorylation. IGF-I-stimulated MEK and Akt phosphorylation were augmented byoverexpression of constitutively active FOXO1. These findings indicate bidirectional regulation of insulin/IGF-I receptor signaling and FOXO1 in cardiomyocytes. FOXO1 may provide feedback control through upregulation of insulin and IGF-I receptor signaling.

Adenoviridae↗

PubMed2006

Regulation of IGF-I receptor signaling in diabetic cardiac muscle: dysregulation of cytosolic and mitochondria HSP60.

Insulin deficiency downregulates HSP60 and IGF-I receptor signaling and disrupts intracellular signaling homeostasis in diabetic cardiac muscle. Our previous studies had shown that IGF-I receptor signaling can be modulated by the abundance of HSP60. Since HSP60 localizes to the cytoplasmic compartment and mitochondria, this study was carried out to determine the distribution of cytosolic and mitochondria HSP60 in diabetic myocardium and to explore whether cytosolic HSP60 can modulate IGF-I receptor signaling in cardiac muscle cells. In streptozotocin-induced diabetes, both the cytosolic and mitochondrial fractions of HSP60 were decreased in the myocardium. Incubating primary cardiomyocytes with insulin leads to increased abundance of HSP60 in the cytosolic and mitochondria compartments. To determine whether cytosolic HSP60 can modulate IGF-I receptor signaling, we used rhodamine 6G to deplete functional mitochondria in cardiomyocytes. In the mitochondria-depleted cells, overexpression of HSP60 with adenoviral vector increased the abundance of IGF-I receptor, enhanced IGF-I-activated receptor phosphorylation, and augmented IGF-I activation of Akt and ERK. Thus overexpressing HSP60 in the cytosolic compartment enhanced IGF-I receptor signaling through upregulation of IGF-I receptor protein. However, IGF-I receptor signaling was significantly reduced in the mitochondria-depleted cells, which suggested that maintaining normal IGF-I receptor signaling in cardiomyocytes required functioning mitochondria. The effect of cytosolic HSP60 involved suppression of ubiquitin conjugation to IGF-I receptor in cardiomyocytes. These data suggest two different mechanisms that can regulate IGF-I signaling, one via cytosolic HSP60 suppression of IGF-I receptor ubiquitination and the other via mitochondria modulation. These findings provide new insight into the regulation of IGF-I signaling in diabetic cardiomyopathy.

Animals↗

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

Ventricular fibrillation during no-flow global ischemia in isolated rabbit hearts.

INTRODUCTION: The dominant frequency (DF) during ventricular fibrillation (VF) in Langendorff-perfused guinea pig hearts is higher in left ventricle (LV) than in right ventricle (RV). However, the onset of VF invariably leads to global ischemia. Whether or not a high DF source exists in LV during global ischemia is unknown. METHODS AND RESULTS: By using a two-camera optical mapping system, epicardial activation patterns of VF were studied in 12 isolated rabbit hearts during baseline, no-flow global ischemia, and reperfusion. Simultaneous endocardial electrode recording was performed in 4 of the 12 hearts. Optical mapping showed type 1 VF at baseline, with multiple wandering and short-lived wavelets. After the onset of global ischemia, VF showed progressively increased spatiotemporal periodicity. The majority (65%) of VF recorded after 7 minutes of global ischemia showed type 2 VF, containing a single epicardial site with stable (> or = 3.85 seconds in duration) repetitive activities. Among the 33 sites with these activities, 24 were located near the interventricular septum, and 27 showed an epicardial breakthrough pattern with centrifugal propagation and wavebreaks distant from the focal site. After 10 minutes of global ischemia, the DF was lower on LV epicardium (5.0 +/- 1.4 Hz) than on RV epicardium (8.6 +/- 2.5 Hz, P < 0.001). However, there was no DF gradient between RV and LV endocardium (9.7 +/- 1.0 vs 9.6 +/- 0.9 Hz). CONCLUSIONS: VF during prolonged global ischemia is consistent with type 2 VF with a single subepicardial source of rapid activation, mostly near the interventricular septum. The DF in LV is not higher than in RV.

Action Potentials↗

PubMed2006

Substrate mapping to detect abnormal atrial endocardium with slow conduction in patients with atypical right atrial flutter.

OBJECTIVES: The purpose of this study was to investigate the relationship between the abnormal substrate and peak negative voltage (PNV) in the right atrium (RA) with atypical flutter. BACKGROUND: The impact of a local abnormally low voltage electrogram on the local activation pattern and velocity of atrial flutter (AFL) remains unclear. METHODS: Twelve patients with clinically documented AFL were included to undergo noncontact mapping of the RA. The atrial substrate was characterized by the: 1) activation mapping; 2) high-density voltage mapping; and 3) conduction velocity along the flutter re-entrant circuit. The normalized PNV (i.e., the relative ratio to the maximal PNV) in each virtual electrode recording was used to produce the voltage maps of the entire chamber. The protected isthmus was bordered by low voltage zones. RESULTS: Atypical AFL of the RA was induced by atrial pacing in 12 patients, including 10 upper loop re-entry and 2 RA free wall re-entry flutter. These protected isthmuses were located near the crista terminalis. The mean width of the protected isthmus was 1.7 +/- 0.3 cm and mean voltage at the isthmus was -0.91 +/- 0.39 mV. The conduction velocities within these paths were significantly slower than outside the path (0.30 +/- 0.18 m/s vs. 1.14 +/- 0.41 m/s, respectively; p = 0.004). The ratiometric PNV of 37.6% of the maximal PNV had the best cut-off value to predict slow conduction, with a high sensitivity (92.3%) and specificity (85.7%). CONCLUSIONS: Characterization of the RA substrate in terms of the unipolar PNV is an effective predictor of the slow conduction path within the critical isthmus of the re-entrant circuit.

Adult↗

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

Sustained elevation of circulating vascular endothelial growth factor after percutaneous angioplasty for peripheral arterial diseases.

Whether percutaneous transluminal angioplasty (PTA) for peripheral arterial diseases (PAD) can modify circulating vasogenic factors remains unclear. The present study consisted of 27 patients with symptomatic peripheral arterial diseases undergoing percutaneous angioplasty for 33 culprit vessels. Levels of four vasogenic growth factors, including vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), hepatocyte growth factor (HGF), and insulin-like growth factor-I (IGF-I), were measured at baseline and after interventions. As a result, circulating levels of vascular endothelial growth factor but not other factors were elevated at 2 weeks and at least for 3 months post procedure. Thus, percutaneous angioplasty may extend its role from local revascularization to systemic angiogenesis through upregulating circulating vascular endothelial growth factor levels. However, whether this phenomenon translates into clinical benefits awaits further investigation.

Aged↗

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

Immediate and late outcomes of patients undergoing transseptal left-sided heart catheterization for symptomatic valvular and arrhythmic diseases.

BACKGROUND: The transseptal technique has been widely used for diagnostic and therapeutic left-sided heart catheterization. However, its differential immediate and late outcomes among patients with various valvular and arrhythmic diseases are not yet determined. METHODS: Beginning from 1993, all patients undergoing transseptal procedures were screened and categorized into diagnosis, arrhythmia, and valvuloplasty groups according to the purposes of the catheterization. Incidences of transseptum-related acute major events (cardiac perforation, embolic stroke, and bradyarrhythmia during the procedure) and late complications (residual atrial septal defect [ASD], embolic stroke, bradyarrhythmia, and death up to 18 months) were analyzed and compared between groups. RESULTS: From January 1993 to May 2003, a total of 176 patients underwent 184 transseptal procedures for diagnosis of valvular heart diseases (n = 8), catheter ablation of arrhythmogenic foci (n = 29), and mitral valvuloplasty (n = 147). The immediate outcome was similar among the 3 groups, with an overall acute complication incidence of 3.8%. At follow-up, the incidences of bradyarrhythmia, embolic stroke, and death were not different among the 3 groups. Patients undergoing valvuloplasty had a significantly higher prevalence of residual ASD, especially for those with more severe mitral stenosis and less valvuloplasty success. However, presence of ASD did not impose disadvantage over the 1.5-year prognosis. CONCLUSION: Transseptal left-sided heart catheterization can be safely applied to patients with different categories of cardiac diseases with comparably good immediate and late outcomes. Although patients undergoing percutaneous valvuloplasty have a higher chance of permanent ASD creation, their prognosis is not influenced.

Adolescent↗

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

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↗

PubMed2006

High-resolution mapping around the eustachian ridge during typical atrial flutter.

BACKGROUND: Although the reentrant circuit of typical atrial flutter (AFL) has been well recognized, the activation around the Eustachian ridge (ER) has not been fully characterized. The aim of this study was to delineate the activation patterns around the ER during typical AFL using high-resolution noncontact mapping. METHODS: Fifty-three patients (M/F = 43/10, 62 +/- 14 years) with typical AFL were included. The high-resolution mapping of the right atrium using a noncontact mapping system during AFL and pacing from the coronary sinus (CS) was performed to evaluate the conduction through the ER. RESULTS: Three types of activation patterns around the ER could be classified according to the ER conduction during AFL and CS pacing. Type I (n = 21, M/F = 16/5, 61 +/- 13 years) exhibited conduction block at the ER during AFL and CS pacing. The local unipolar electrograms at the ER exhibited long double potentials (DPs) (109 +/- 12 ms, range 77-153 ms) during AFL and CS pacing (84 +/- 18 ms, range 48-129 ms). Type II (n = 8, M/F = 7/1, 61 +/- 15 years) exhibited conduction block at the ER during AFL, but conduction through the ER during CS pacing. The unipolar electrograms exhibited long DPs (119 +/- 12 ms, range 97-141 ms) at the ER during the tachycardia and an rS pattern during CS pacing. Type III (n = 24, M/F = 20/4, 61 +/- 16 years) exhibited an activation wavefront that passed along the ER, with the sinus venosa as the posterior barrier during AFL. During CS pacing, all cases exhibited conduction through the ER with an rS pattern. CONCLUSIONS: This study is the first to demonstrate the three patterns of activation along the ER during AFL and CS pacing. This finding suggested that the ER is an anatomic and functional barrier during typical AFL.

Aged↗

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

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

Atropine-induced HRV alteration is not amended by electroacupuncture on Zusanli.

Acupuncture is known to influence autonomic nervous activity. Acupuncture on Zusanli points has been shown to enhance the regularity of gastric myoelectrical activity and accelerate gastric emptying, partly through the vagal pathway, in dogs. The aim of this study was to evaluate whether atropine-induced autonomic nervous alteration, measured by heart rate variability (HRV), could be amended by electroacupuncture on Zusanli points. HRV measurements were recorded in 15 healthy volunteers before, during and after electroacupuncture. Each subject was studied for three sessions in a randomized sequence, which included electroacupuncture on the Zusanli (St 36) points with or without premedication of atropine and placebo stimulation on a non-acupoint. The analysis of low frequency (LF), high frequency (HF) and LF/HF ratios were compared between different sessions. Serum levels of gastrin, motilin and pancreatic polypeptide (PP) levels were also measured. There was an increase in the LF/HF ratio (indicating increased sympathetic activity) during the post-acupuncture period with 2 Hz of electrical stimulation on the Zusanli acupoints. When IV atropine was used immediately before the electroacupuncture, there was a decrease in the LF power and HF power during the acupuncture and post-acupuncture periods. In addition, there was a significant increase in the LF/HF ratio during the acupuncture and post-acupuncture periods. There was a significant decrease in serum PP in the post-acupuncture period after premedication with IV atropine. In conclusion, atropine-induced HRV change might be mediated via the vagal pathway. However, atropine-induced HRV alteration is not amended by electroacupuncture on Zusanli points.

Adult↗