2010 Vol. 7, No. 1
Display Method:
2010, 7(1): 3-6.
Abstract:
Objective Carotid angioplasty and stenting (CAS) has been suggested to be the procedure of choice in patients with high risk cardiovascular profile. Unfortunately, such patients are often aged with several comorbidities, such as a high prevalence of coronary artery disease, peripheral artery disease and hostile anatomy that complicate the CAS performance. We sought to evaluate the results of CAS in elderly patients, outlining the encountered challenges and the eventual proposed global cardiovascular management. Methods We retrospectively searched the database for patients > 65-year-old who were referred to Cardiovascular Diagnosis and Endoluminal Interventions, Rovigo General Hospital, over a 24-month period (December 2007–November 2009) for CAS. Coronary angiography and peripheral screening were performed in all patients. All eventual challenges and related solutions were analyzed. Results Totally, 160 patients were enrolled. Among which, 50 patients (31.2%, mean age 80 ± 6.4 years) underwent CAS over a 24-month period: 24 patients (48%) had concurrent coronary artery disease (three-vessel in 7 patients, bivessel in 8 patients, single vessel in 5 patients and left main in 4 patients); 13 patients (26%) and peripheral artery disease at the site of arterial access; 15 patients and type Ⅲaortic arch (30%), 7 patients severe tortuosity of the common carotid artery (14%), and 8 angulated takeoff of carotid or internal artery (16%). Concurrent percutaneous coronary intervention was performed in 14 patients, including 3 patients with left main disease. Concurrent peripheral intervention was performed in 7 patients ( all with bilateral common or external critical disease) due to the impossibility to gain another access. Successful carotid cannulation was achieved in all patients with hostile neck. Two-wire technique has been used in 17 patients, three-wire technique in 9 patients, and four-wire technique in 4 patients. Conclusion Elderly patients submitted to CAS represent a complex and challenging subgroup in which often cardiac and peripheral technical expertise is required to gain success of the procedure: interventional cardiologists are probably the preferred performers in such complex patients.
Objective Carotid angioplasty and stenting (CAS) has been suggested to be the procedure of choice in patients with high risk cardiovascular profile. Unfortunately, such patients are often aged with several comorbidities, such as a high prevalence of coronary artery disease, peripheral artery disease and hostile anatomy that complicate the CAS performance. We sought to evaluate the results of CAS in elderly patients, outlining the encountered challenges and the eventual proposed global cardiovascular management. Methods We retrospectively searched the database for patients > 65-year-old who were referred to Cardiovascular Diagnosis and Endoluminal Interventions, Rovigo General Hospital, over a 24-month period (December 2007–November 2009) for CAS. Coronary angiography and peripheral screening were performed in all patients. All eventual challenges and related solutions were analyzed. Results Totally, 160 patients were enrolled. Among which, 50 patients (31.2%, mean age 80 ± 6.4 years) underwent CAS over a 24-month period: 24 patients (48%) had concurrent coronary artery disease (three-vessel in 7 patients, bivessel in 8 patients, single vessel in 5 patients and left main in 4 patients); 13 patients (26%) and peripheral artery disease at the site of arterial access; 15 patients and type Ⅲaortic arch (30%), 7 patients severe tortuosity of the common carotid artery (14%), and 8 angulated takeoff of carotid or internal artery (16%). Concurrent percutaneous coronary intervention was performed in 14 patients, including 3 patients with left main disease. Concurrent peripheral intervention was performed in 7 patients ( all with bilateral common or external critical disease) due to the impossibility to gain another access. Successful carotid cannulation was achieved in all patients with hostile neck. Two-wire technique has been used in 17 patients, three-wire technique in 9 patients, and four-wire technique in 4 patients. Conclusion Elderly patients submitted to CAS represent a complex and challenging subgroup in which often cardiac and peripheral technical expertise is required to gain success of the procedure: interventional cardiologists are probably the preferred performers in such complex patients.
2010, 7(1): 7-10.
Abstract:
Objective To assess the association between 1-year risk of all-cause and cardiovascular disease (CVD) mortality and ankle-brachial index (ABI) in Chinese patients who were at high CVD risk. Methods Totally 3733 patients with high CV risk had bilateral ABI measurements at baseline and were followed up for 1-1.5 years. Patients were divided to four groups: 1) coronary heart disease (CHD); 2) ischemic stroke (IS); 3) diabetes mellitus (DM); 4) very high risk group(VHR), low ABI was defined as <0.9. Results A total of 3179 patients were analyzed. The prevalence of low ABI was 28.1%. At 1 year, all-cause mortality was 8.7%, and 27.6% was attributable to CVD; mortality due to CV events was 4.8% and 1.5%.After adjusting other risk factors the hazard ratio of low ABI was 1.623 for all-cause mortalityand 2.304 for CVD mortality. Similar in patient with and without low ABI, respectively were found in four groups.Conclusion ABI is a strong and independent predictor of mortality. Patients with a low ABI have a substantially increased risk of all-cause mortality and CVD mortality.
Objective To assess the association between 1-year risk of all-cause and cardiovascular disease (CVD) mortality and ankle-brachial index (ABI) in Chinese patients who were at high CVD risk. Methods Totally 3733 patients with high CV risk had bilateral ABI measurements at baseline and were followed up for 1-1.5 years. Patients were divided to four groups: 1) coronary heart disease (CHD); 2) ischemic stroke (IS); 3) diabetes mellitus (DM); 4) very high risk group(VHR), low ABI was defined as <0.9. Results A total of 3179 patients were analyzed. The prevalence of low ABI was 28.1%. At 1 year, all-cause mortality was 8.7%, and 27.6% was attributable to CVD; mortality due to CV events was 4.8% and 1.5%.After adjusting other risk factors the hazard ratio of low ABI was 1.623 for all-cause mortalityand 2.304 for CVD mortality. Similar in patient with and without low ABI, respectively were found in four groups.Conclusion ABI is a strong and independent predictor of mortality. Patients with a low ABI have a substantially increased risk of all-cause mortality and CVD mortality.
2010, 7(1): 11-13.
Abstract:
Objective The purpose of this study was to compare remote magnetic catheter navigation with manual navigation for the ablation of atrioventricular nodal reentry tachycardia (AVNRT). Methods From November 2007 to November 2009, 30 consecutive patients with AVNRT received radiofrequency ablation in the Institute of Geriatric Cardiology. Of them, 14 were treated with remote magnetic navigation (RMN) and 16 with manual catheter navigation (MCN). Total fluoroscopic time,procedure time, procedural success rate, and complication rate were compared between the two groups. Results Total fluoroscopy time and precise orientation time were reduced in RMN group compared to MCN group (7.5±0.3 min vs 13.9±5.3 min, and 1.0±0.3 min vs 3.2±0.6 min, respectively, both P0.05) was similar between the 2 groups. No procedural complications occurred in both groups. Conclusions RMN for mapping and ablation of AVNRT significantly reduce precise orientation time, total fluoroscopy time and number of lesions delivered compared to the conventional technique of manual steering of deflectable catheters. Remote magnetic control mapping and ablation of AVNRT is more safe and feasible
Objective The purpose of this study was to compare remote magnetic catheter navigation with manual navigation for the ablation of atrioventricular nodal reentry tachycardia (AVNRT). Methods From November 2007 to November 2009, 30 consecutive patients with AVNRT received radiofrequency ablation in the Institute of Geriatric Cardiology. Of them, 14 were treated with remote magnetic navigation (RMN) and 16 with manual catheter navigation (MCN). Total fluoroscopic time,procedure time, procedural success rate, and complication rate were compared between the two groups. Results Total fluoroscopy time and precise orientation time were reduced in RMN group compared to MCN group (7.5±0.3 min vs 13.9±5.3 min, and 1.0±0.3 min vs 3.2±0.6 min, respectively, both P0.05) was similar between the 2 groups. No procedural complications occurred in both groups. Conclusions RMN for mapping and ablation of AVNRT significantly reduce precise orientation time, total fluoroscopy time and number of lesions delivered compared to the conventional technique of manual steering of deflectable catheters. Remote magnetic control mapping and ablation of AVNRT is more safe and feasible
2010, 7(1): 21-24.
Abstract:
Objective To evaluate the factors influencing the outcome of patients who suffered in-hospital ventricular fibrillation (IHVF). Methods Data of patients with IHVF in a single center were collected. Clinical characteristics of patients were compared between those survived (n=112) and those died (n=94), and those with IHVF occurred in inpatient ward and in emergency center. Multiple logistic regression analysis was used to identify factors associated with survival. Results There were 206 events in the analysis. The most common underlying disease was coronary artery disease (CAD), especially acute myocardial infarction (AMI). On multiple logistic regression analysis, independent predictors for failure to survive were higher NYHA class (odds ratio 1.7, 95% CI, 1.3-2.2, P 1s) before the occurrence of IHVF, while those with left anterior descending artery as IRAoften showed tachycardia (R-R interval < 0.6s) (8/12, 66.7%). Conclusion The most common disease causing IHVF isCAD. Keeping [K+] above 4.5mmol/l could prevent on-setting IHVF, especially toAMI patients. The worse heart function is associated with higher rate of IHVF and worse prognosis.
Objective To evaluate the factors influencing the outcome of patients who suffered in-hospital ventricular fibrillation (IHVF). Methods Data of patients with IHVF in a single center were collected. Clinical characteristics of patients were compared between those survived (n=112) and those died (n=94), and those with IHVF occurred in inpatient ward and in emergency center. Multiple logistic regression analysis was used to identify factors associated with survival. Results There were 206 events in the analysis. The most common underlying disease was coronary artery disease (CAD), especially acute myocardial infarction (AMI). On multiple logistic regression analysis, independent predictors for failure to survive were higher NYHA class (odds ratio 1.7, 95% CI, 1.3-2.2, P 1s) before the occurrence of IHVF, while those with left anterior descending artery as IRAoften showed tachycardia (R-R interval < 0.6s) (8/12, 66.7%). Conclusion The most common disease causing IHVF isCAD. Keeping [K+] above 4.5mmol/l could prevent on-setting IHVF, especially toAMI patients. The worse heart function is associated with higher rate of IHVF and worse prognosis.
2010, 7(1): 30-35.
Abstract:
Objective The underlying mechanisms responsible for both electrical and mechanical remodeling of the atrium after cardioversion of atrial tachyarrhythmias may be similar, but they are still incompletely understood, and whether the changes in atrial myocardium structure after short-term rapid atrial activation is the basis for this remodeling is unknown. We aimed to investigate atrial mechanical function and atrial ultrastructural change before and after short-term rapid atrial activation, and the possible relation between lest atrial contractile and anatomical remodeling. Methods Seventeen anesthetized mongrel dogs were divided into experimental (n=12) and control (n=5) groups. The experimental group underwent insertion of a transvenous lead at the right atrial appendage and 5-hour of atrial pacing at 450bpm. Effective refractory period (ERP) and P-wave duration were measured before and after 5-hour pacing. Acoustic quantification (AQ) of left atrial waveforms was recorded before and after 5-hour pacing. All measurements were made in sinus rhythm. Dogs were killed and the myocardium in left atrial trabeculae and appendages was examined by light and electron microscopy. Control dogs did not undergo pacing, but the examinations were performed at the times corresponding to that for the experimental group. Results Despite the absence of changes in heart rate and left ventricular pressure after 5-hour rapid atrial pacing in the experimental group, left atrial reservoir and conduit function did not change, whereas atrial size increased and atrial booster function decreased. Marked changes were seen in cellular substructures, such as loss of myofibrils, accumulation of glycogen, and changes in mitochondrial shape and size. No changes were found in the control group. Conclusions Short-term rapid atrial activation can cause electrophysiological remodeling and left atrial contractile and anatomical remodeling, and anatomical remodeling may contribute to the development of atrial electrical and contractile remodeling.
Objective The underlying mechanisms responsible for both electrical and mechanical remodeling of the atrium after cardioversion of atrial tachyarrhythmias may be similar, but they are still incompletely understood, and whether the changes in atrial myocardium structure after short-term rapid atrial activation is the basis for this remodeling is unknown. We aimed to investigate atrial mechanical function and atrial ultrastructural change before and after short-term rapid atrial activation, and the possible relation between lest atrial contractile and anatomical remodeling. Methods Seventeen anesthetized mongrel dogs were divided into experimental (n=12) and control (n=5) groups. The experimental group underwent insertion of a transvenous lead at the right atrial appendage and 5-hour of atrial pacing at 450bpm. Effective refractory period (ERP) and P-wave duration were measured before and after 5-hour pacing. Acoustic quantification (AQ) of left atrial waveforms was recorded before and after 5-hour pacing. All measurements were made in sinus rhythm. Dogs were killed and the myocardium in left atrial trabeculae and appendages was examined by light and electron microscopy. Control dogs did not undergo pacing, but the examinations were performed at the times corresponding to that for the experimental group. Results Despite the absence of changes in heart rate and left ventricular pressure after 5-hour rapid atrial pacing in the experimental group, left atrial reservoir and conduit function did not change, whereas atrial size increased and atrial booster function decreased. Marked changes were seen in cellular substructures, such as loss of myofibrils, accumulation of glycogen, and changes in mitochondrial shape and size. No changes were found in the control group. Conclusions Short-term rapid atrial activation can cause electrophysiological remodeling and left atrial contractile and anatomical remodeling, and anatomical remodeling may contribute to the development of atrial electrical and contractile remodeling.
2010, 7(1): 25-29.
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Objective Abnormal QT prolongation associated with arrhythmias is considered the major cardiac electrical disorder and a significant predictor of mortality in diabetic patients. The precise ionic mechanisms for diabetic QT prolongation remained unclear. The present study was designed to analyze the changes of ventricular repolarization and the underlying ionic mechanisms in diabetic rabbit hearts. Methods Diabetes was induced by a single injection of alloxan (145mg/kg, i.v. ). After the development of diabetes (10 weeks), ECG was measured. Whole-cell patch-clamp technique was applied to record the action potential duration (APD50, APD90), slowly activating outward rectifying potassium current (IKs), L-type calcium current (ICa-L) and inward rectifying potassium current (IK1). Results The action potential duration (APD50 and APD90) of ventricular myocytes was obviously prolonged from 271.5±32.3 ms and 347.8±36.3 ms to 556.6±72.5 ms and 647.9±72.2 ms respectively (P< 0.05). Meanwhile the normalized peak current densities of IKs in ventricular myocytes investigated by whole-cell patch clamp was smaller in diabetic rabbits than that in control group at test potential of +50mV (1.27±0.20 pA/pF vs 3.08±0.67 pA/pF, P<0.05). And the density of the ICa-L was increased apparently at the test potential of 10 mV (-2.67±0.41 pA/pF vs -5.40±1.08 pA/pF, P<0.05). Conclusion Ventricular repolarization was prolonged in diabetic rabbits, it may be partly due to the increased L-type calcium current and reduced slow delayed rectifier K+ current (IKs).
Objective Abnormal QT prolongation associated with arrhythmias is considered the major cardiac electrical disorder and a significant predictor of mortality in diabetic patients. The precise ionic mechanisms for diabetic QT prolongation remained unclear. The present study was designed to analyze the changes of ventricular repolarization and the underlying ionic mechanisms in diabetic rabbit hearts. Methods Diabetes was induced by a single injection of alloxan (145mg/kg, i.v. ). After the development of diabetes (10 weeks), ECG was measured. Whole-cell patch-clamp technique was applied to record the action potential duration (APD50, APD90), slowly activating outward rectifying potassium current (IKs), L-type calcium current (ICa-L) and inward rectifying potassium current (IK1). Results The action potential duration (APD50 and APD90) of ventricular myocytes was obviously prolonged from 271.5±32.3 ms and 347.8±36.3 ms to 556.6±72.5 ms and 647.9±72.2 ms respectively (P< 0.05). Meanwhile the normalized peak current densities of IKs in ventricular myocytes investigated by whole-cell patch clamp was smaller in diabetic rabbits than that in control group at test potential of +50mV (1.27±0.20 pA/pF vs 3.08±0.67 pA/pF, P<0.05). And the density of the ICa-L was increased apparently at the test potential of 10 mV (-2.67±0.41 pA/pF vs -5.40±1.08 pA/pF, P<0.05). Conclusion Ventricular repolarization was prolonged in diabetic rabbits, it may be partly due to the increased L-type calcium current and reduced slow delayed rectifier K+ current (IKs).
2010, 7(1): 36-39.
Abstract:
Objective To investigate the effects of glucose and aldosterone on the proliferation of rat cardiac fibroblasts. Methods The neonatal SD rat cardiac fibroblasts (Cfs) were separated by the differential attachment technique. Cfs were incubated in different Dglucose concentrations for 24 hours, with or without aldosterone. DNA synthesis and metabolic activity of the Cfs were measured simultaneously with Brdu incorporation and WST-1 ELISA, respectively. Results Glucose at high concentrations (15 and 25 mmol/L) significantly increased the proliferation of Cfs, compared with glucose at low concentration (5.6 mmol/L, P0.05). Further analysis suggested that aldosterone have significant interaction on Cfs DNA synthesis (P=0.012). Conclusions Both glucose and aldosterone could stimulate the proliferation of cultured Cfs. In high glucose concentration, the stimulatory effect for Cfs proliferation may be masked.
Objective To investigate the effects of glucose and aldosterone on the proliferation of rat cardiac fibroblasts. Methods The neonatal SD rat cardiac fibroblasts (Cfs) were separated by the differential attachment technique. Cfs were incubated in different Dglucose concentrations for 24 hours, with or without aldosterone. DNA synthesis and metabolic activity of the Cfs were measured simultaneously with Brdu incorporation and WST-1 ELISA, respectively. Results Glucose at high concentrations (15 and 25 mmol/L) significantly increased the proliferation of Cfs, compared with glucose at low concentration (5.6 mmol/L, P0.05). Further analysis suggested that aldosterone have significant interaction on Cfs DNA synthesis (P=0.012). Conclusions Both glucose and aldosterone could stimulate the proliferation of cultured Cfs. In high glucose concentration, the stimulatory effect for Cfs proliferation may be masked.
2010, 7(1): 40-46.
Abstract:
Objective The purpose of our study is to observe the voltage-gated potassium channel Kv1.3 expressed on CD4+CD28null T cells from the peripheral blood of acute coronary syndrome (ACS) patients by the patch clamp technique. Methods Kv1.3 potassium channels expression from 17 patients with ACS and 11 healthy age-match controls was detected in single cell(CD4+CD28null T cells and CD4+CD28+T cells) by fluorescence microscopy and patch clamp. Results The percentage of CD4+CD28null T cells was higher in the ACS patients [(6.97±2.05)%] than that in the controls [(1.38±0.84)%, P<0.05]. The concentration of hsCRP was directly correlated with the number of the CD4+CD28null T cells in the ACS patients (r=0.52, P<0.05). The conductance (6.89±1.17ns vs 3.36±0.66ns), dens (1.95±0.80μm2 vs 1.13±0.57μm2) and numbers (574.5±97.6 n/cell vs. 280.3±55.3 n/cell) of the Kv1.3 channels on the CD4+CD28null T cells were significantly higher than those on the CD4+CD28+ T cells (all P<0.01) in ACS patients, but were similar on CD4+CD28+T between ACS patients and controls. Conclusion The CD4+CD28null T cells and the numbers of Kv1.3 channels on the CD4+CD28null T cells from patients with ACS are significantly upregulated and might contribute to the pathogenesis of ACS.
Objective The purpose of our study is to observe the voltage-gated potassium channel Kv1.3 expressed on CD4+CD28null T cells from the peripheral blood of acute coronary syndrome (ACS) patients by the patch clamp technique. Methods Kv1.3 potassium channels expression from 17 patients with ACS and 11 healthy age-match controls was detected in single cell(CD4+CD28null T cells and CD4+CD28+T cells) by fluorescence microscopy and patch clamp. Results The percentage of CD4+CD28null T cells was higher in the ACS patients [(6.97±2.05)%] than that in the controls [(1.38±0.84)%, P<0.05]. The concentration of hsCRP was directly correlated with the number of the CD4+CD28null T cells in the ACS patients (r=0.52, P<0.05). The conductance (6.89±1.17ns vs 3.36±0.66ns), dens (1.95±0.80μm2 vs 1.13±0.57μm2) and numbers (574.5±97.6 n/cell vs. 280.3±55.3 n/cell) of the Kv1.3 channels on the CD4+CD28null T cells were significantly higher than those on the CD4+CD28+ T cells (all P<0.01) in ACS patients, but were similar on CD4+CD28+T between ACS patients and controls. Conclusion The CD4+CD28null T cells and the numbers of Kv1.3 channels on the CD4+CD28null T cells from patients with ACS are significantly upregulated and might contribute to the pathogenesis of ACS.
2010, 7(1): 47-51.
Abstract:
Objective To study the effects of simvastatin on the hypertrophy of cultured rat cardiac myocytes induced by serum and the role of phosphatase and tensin homolog deleted on chromosome ten (PTEN) in the signal pathway. Methods Cultured neonatal Sprague-Dawley (SD) rat cardiac myocytes were treated with 15% fetal bovine serum, or without serum, or different consentrations of simvastatin. Image analysis system was used to measure the cardiac myocytes surface area. Protein synthesis of myocytes was measured via [3H]-leucine incorporation method. The expression level of atrial natriuretic peptide (ANP) mRNA in myocytes was determined with reverse transcription polymerase chain reaction (RT-PCR). The mRNA and protein expression levels of PTEN in cardiac myocytes were investigated with RT-PCR and Western blot respectively. Results At 24 hours, cardiac myocytes surface area was significantly higher in 15% serum group (1611.16±160.75 μm2) than in serum-free group (538.04±118.60 μm2, P<0.01). Simvastatin decreased the cell surface area in a concentration dependent manner. The cell surface area in 10-5 and 10-6 mol/L simvastatin groups were 799.84±167.70 μm2 and 1076.88±199.28 μm2 respectively, which were both significantly lower than that in 15% fetal bovine serum group (P<0.01). Incorporation rate of [3H]-leucine was significantly higher in 15% fetal bovine serum group (2360±106cpm/well) than that in serum-free group (1305±92 cpm/well, P<0.01). Incorporation rate of [3H]-leucine in 10-5 and 10-6 mol/L simvastatin groups were 1707±101 cpm /well and 1962±125 cpm/well respectively, which were both lower than that in serum group (P<0.01). With the increase of simvastatin concentration, the expression level of ANP mRNA in cardiac myocytes was decreased gradually, which were 0.29±0.03 and 0.40±0.03 respectively in 10-5 and 10-6 mol/L simvastatin groups, and significantly lower than that in serum group(0.60±0.03, P<0.01). Simvastatin increased the expressions of PTEN mRNA and protein in cardiac myocytes in a concentration dependent manner. PTEN mRNA expression level in 10-7, 10-6 and 10-5 mol/L simvastatin groups were 0.38±0.03, 0.83±0.04 and 0.85±0.05, respectively, which were all higher than that in 15% fetal bovine serum group (0.29±0.04, P<0.05). Similarly, PTEN protein level in 10-7, 10-6 and 10-5 mol/L simvastatin groups (39.25±3.41, 46.35±1.78 and 47.22±2.39 respectively) were also significantly higher than that in 15% fetal bovine serum group (32.21±4.06, P<0.05). Conclusion Simvastatin can inhibit the hypertrophy of cultured rat cardiac myocytes induced by serum, and the increase of expression level of PTEN might be involved in the mechanism.
Objective To study the effects of simvastatin on the hypertrophy of cultured rat cardiac myocytes induced by serum and the role of phosphatase and tensin homolog deleted on chromosome ten (PTEN) in the signal pathway. Methods Cultured neonatal Sprague-Dawley (SD) rat cardiac myocytes were treated with 15% fetal bovine serum, or without serum, or different consentrations of simvastatin. Image analysis system was used to measure the cardiac myocytes surface area. Protein synthesis of myocytes was measured via [3H]-leucine incorporation method. The expression level of atrial natriuretic peptide (ANP) mRNA in myocytes was determined with reverse transcription polymerase chain reaction (RT-PCR). The mRNA and protein expression levels of PTEN in cardiac myocytes were investigated with RT-PCR and Western blot respectively. Results At 24 hours, cardiac myocytes surface area was significantly higher in 15% serum group (1611.16±160.75 μm2) than in serum-free group (538.04±118.60 μm2, P<0.01). Simvastatin decreased the cell surface area in a concentration dependent manner. The cell surface area in 10-5 and 10-6 mol/L simvastatin groups were 799.84±167.70 μm2 and 1076.88±199.28 μm2 respectively, which were both significantly lower than that in 15% fetal bovine serum group (P<0.01). Incorporation rate of [3H]-leucine was significantly higher in 15% fetal bovine serum group (2360±106cpm/well) than that in serum-free group (1305±92 cpm/well, P<0.01). Incorporation rate of [3H]-leucine in 10-5 and 10-6 mol/L simvastatin groups were 1707±101 cpm /well and 1962±125 cpm/well respectively, which were both lower than that in serum group (P<0.01). With the increase of simvastatin concentration, the expression level of ANP mRNA in cardiac myocytes was decreased gradually, which were 0.29±0.03 and 0.40±0.03 respectively in 10-5 and 10-6 mol/L simvastatin groups, and significantly lower than that in serum group(0.60±0.03, P<0.01). Simvastatin increased the expressions of PTEN mRNA and protein in cardiac myocytes in a concentration dependent manner. PTEN mRNA expression level in 10-7, 10-6 and 10-5 mol/L simvastatin groups were 0.38±0.03, 0.83±0.04 and 0.85±0.05, respectively, which were all higher than that in 15% fetal bovine serum group (0.29±0.04, P<0.05). Similarly, PTEN protein level in 10-7, 10-6 and 10-5 mol/L simvastatin groups (39.25±3.41, 46.35±1.78 and 47.22±2.39 respectively) were also significantly higher than that in 15% fetal bovine serum group (32.21±4.06, P<0.05). Conclusion Simvastatin can inhibit the hypertrophy of cultured rat cardiac myocytes induced by serum, and the increase of expression level of PTEN might be involved in the mechanism.
2010, 7(1): 52-57.
Abstract:
Objective The aims of the present study were to investigate the associations of 46 A>G, 79 C>G, 491 C>T and 659 C>G genetic variants of the human beta 2-adrenergic receptor (b2-AR), ADRB2, gene with essential hypertension (EH) in Xinjiang Kazakans population.Methods A gender-matched case-control (271 hypertensive cases and 267 normotensive controls) study was used to investigate the associations of the four variations in the coding region of ADRB2 with EH. The genotypes of the variants were identified by the polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) methods. Results 46 A>G, 79 C>G and 659 C>G polymorphisms were common in the Kazakan population, but 491 C>T was a mutation (frequency of T allele was only 0.003) and only found in EH group. The frequency distributions of genotypes and alleles for 659 C>G between the EH and control groups was significantly different (PG and 79 C>G polymorphisms were not statistically different. Logistic regression analysis suggested that the G allele of 659 C>G polymorphism was a risk factor for hypertension (minor allele vs common homo; odds ratio, 13.240, 95% CI, 4.052-43.274; PG were significantly higher than those in the CC group, but no significant difference of blood pressure were found between common homo and minor allele for 46 A>G and 79C>G polymorphisms. Haplotype analysis showed that two hyplotypes, H1: 46A79C491C523C(48%)and H5:46A79C491C659G, were associated with EH.Conclusion ADRB2 genetic variants may play independent roles in the molecular genetic mechanism of EH in Xinjiang Kazakans population.
Objective The aims of the present study were to investigate the associations of 46 A>G, 79 C>G, 491 C>T and 659 C>G genetic variants of the human beta 2-adrenergic receptor (b2-AR), ADRB2, gene with essential hypertension (EH) in Xinjiang Kazakans population.Methods A gender-matched case-control (271 hypertensive cases and 267 normotensive controls) study was used to investigate the associations of the four variations in the coding region of ADRB2 with EH. The genotypes of the variants were identified by the polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) methods. Results 46 A>G, 79 C>G and 659 C>G polymorphisms were common in the Kazakan population, but 491 C>T was a mutation (frequency of T allele was only 0.003) and only found in EH group. The frequency distributions of genotypes and alleles for 659 C>G between the EH and control groups was significantly different (PG and 79 C>G polymorphisms were not statistically different. Logistic regression analysis suggested that the G allele of 659 C>G polymorphism was a risk factor for hypertension (minor allele vs common homo; odds ratio, 13.240, 95% CI, 4.052-43.274; PG were significantly higher than those in the CC group, but no significant difference of blood pressure were found between common homo and minor allele for 46 A>G and 79C>G polymorphisms. Haplotype analysis showed that two hyplotypes, H1: 46A79C491C523C(48%)and H5:46A79C491C659G, were associated with EH.Conclusion ADRB2 genetic variants may play independent roles in the molecular genetic mechanism of EH in Xinjiang Kazakans population.
2010, 7(1): 58-60.
Abstract:
Implantation of implantable cardioverter defibrillators (ICD) has widely been accepted for secondary prevention of sudden cardiac death (SCD) in cardiac arrest survivors.1 Currently there are increasing interests in primary prevention of SCD in selected high risk patients who have not experienced cardiac arrest.1 Despite extensive investigation for risk stratification, our current ability to accurately identify patients at high risk for SCD remains very poor. The primary reason is probably due to our limited understanding of the mechanisms underlying the pathogenesis of ventricular tachy-arrhythmias and sudden cardiac death (Fig.1). Although ventricular tachycardia (VT) or fibrillation (VF) is still considered the most common mechanism of SCD in patients with advanced heart failure, many causes other than VT/VF (such as bradycardia) may account for up to 50% of SCD, particularly in non-ischemic dilated cardiomyopathy (DCM).
Implantation of implantable cardioverter defibrillators (ICD) has widely been accepted for secondary prevention of sudden cardiac death (SCD) in cardiac arrest survivors.1 Currently there are increasing interests in primary prevention of SCD in selected high risk patients who have not experienced cardiac arrest.1 Despite extensive investigation for risk stratification, our current ability to accurately identify patients at high risk for SCD remains very poor. The primary reason is probably due to our limited understanding of the mechanisms underlying the pathogenesis of ventricular tachy-arrhythmias and sudden cardiac death (Fig.1). Although ventricular tachycardia (VT) or fibrillation (VF) is still considered the most common mechanism of SCD in patients with advanced heart failure, many causes other than VT/VF (such as bradycardia) may account for up to 50% of SCD, particularly in non-ischemic dilated cardiomyopathy (DCM).
