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International journal of cardiology 04/2013; · 7.08 Impact Factor
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ABSTRACT: To investigate the effect of temperature on hospital admission among patients with chronic systolic heart failure (CSHF).
Data regarding in-hospital patients with CSHF were gathered from 12 hospitals in Hubei province, between 2000 and 2010. Patients with a history of congenital heart disease and the history of cancer from this series, were excluded. Chi-square (χ(2)) tests and t tests were used for descriptive analysis. Univariate and multivariate logistic regression methods were performed to determinate the risk of hospital admission of every month to compare with the previous one. We used 2-tailed 95% confidence interval (CI), and tests with P < 0.01 to consider the significant levels, statistically. We also used the SPSS 13.0 for Windows, release 15, 2006 (SPSS Inc, Chicago, Ill) for data analyses.
(1) 48 964 patients were enrolled in the present study. The numbers of admission increased 18.71%, 13.84%, -21.90%, -34.62%, -21.97%, -3.81%, -2.04%, 10.13%, -17.13%, -0.85%, 21.54% and 42.70% from January to December when compared to the average number of admission. (2) The odds ratios (ORs) (95% CI, P values) of hospital admission in January, February and December were 1.09 (0.96 - 1.23, 0.54), 0.98 (0.84 - 1.10, 0.46) and 0.96 (0.84 - 1.08, 0.59), respectively in females which did not show any significant differences when compared to the number in August. However the ratios were 0.61 (0.54 - 0.69, < 0.01), 0.80 (0.68 - 0.92, < 0.01) and 0.73 (0.64 - 0.83, < 0.01), respectively, in males that showed significant differences when, compared to the figures in August. (3) The OR of admission increased more when temperature got lower for patients with coronary artery disease, hypertension heart disease or rheumatic heart disease, but not with dilated cardiomyopathy. (4) The OR of admission showed a different impact on patients with different occupation, along with the change of temperature. Low or high temperature did not seem to have different effects on the OR of admission in patients who were free-lanced or unemployed.
Temperature seemed to have significant effects on the risk of admission, which related to gender, etiology or occupation.
Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi 01/2013; 34(1):67-70.
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ABSTRACT: We have previously demonstrated that catheter-based renal sympathetic denervation (RSD) could suppress atrial fibrillation (AF) in canines with short-time rapid right atrial pacing (RAP). However, the role of renal denervation on atrial remodeling is unclear. The aim of the present study was to explore the long-term effect of RSD on the atrial remodeling during prolonged RAP. Twenty mongrel dogs were implanted with a high-frequency cardiac pacemaker with a transvenous lead inserted into the right atrial appendage. The dogs were divided into three groups: a sham-operated group (n = 6), the chronic RAP (CRAP) group (n = 7), and the CRAP+RSD group (n = 7). In the CRAP+RSD group, a pacemaker was implanted 6 weeks after RSD was performed bilaterally for recovery. RAP was maintained for 5 weeks in CRAP group and CRAP+RSD group. The plasma levels of Angiotensin II and aldosterone were significantly increased in CRAP group compared with sham-operated group, but the increasing trend was inhibited in CRAP+RSD group compared with CRAP group (P<0.05). Similarly, RSD suppressed the increasing trend that prolonged RAP produced in the left atrial levels of ANP, TNF-α and IL-6. Compared with the sham-operated group, the CRAP group had significantly increased levels of caspase-3, bax and Cx40 whereas the level of Bcl-2 decreased (P<0.05). RSD markedly reduced the upregulation of caspase-3, bax and Cx40 and the downregulation of Bcl-2 expression compared with the CRAP group (P<0.05). Picric acid-sirius red staining study suggested that RSD could markedly alleviate the lesion degree of cardic fibrosis induced by CRAP (P<0.05). Immunohistochemistry results showed that the densities of TH- and GAP43- positive nerves were significantly elevated in the CRAP group compared with the sham-operated group, while RSD operation signicantly inhibited the these changes produced by CRAP. These findings suggest that renal denervation could suppress the atrial remodeling after prolonged RAP in ambulatory canines.
PLoS ONE 01/2013; 8(5):e64611. · 4.09 Impact Factor
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ABSTRACT: The effects of anxiety and depression on the recurrence of persistent atrial fibrillation (AF) after circumferential pulmonary vein ablation (CPVA) are not clear. Whether CPVA can alleviate the anxiety and depression symptoms of persistent AF patients is unknown.
One hundred and sixty-four patients with persistent AF, of which 43 treated with CPVA (CPVA group) and 103 treated with anti-arrhythmics drugs (medicine group), were enrolled. The Zung Self-Rating Anxiety Scale (SAS), and Zung Self-Rating Depression Scale (SDS) were assessed before and 12 months after treatment in all patients.
The scores of SAS (40.33 ± 7.90 vs. 49.76 ± 9.52, P < 0.01) and SDS (42.33 ± 8.73 vs. 48.17 ± 8.77, P < 0.01) decreased 12 months after CPVA. Over 12 months follow-up, AF relapsed in 17 patients in CPVA group. Compared with the data in the recurrent group (17 patients), the scores of SAS and SDS were significantly lower in the non-recurrent group (26 patients) at baseline. The results of multivariate Logistic regression analysis showed normal scores of SAS and SDS were the independent risk factors of AF recurrence after CPVA.
Anxiety and depression increase the recurrence risk of persistent AF after CPVA. CPVA can ameliorate the anxiety and depression symptoms in patients with persistent AF.
Chinese medical journal 12/2012; 125(24):4368-72. · 0.86 Impact Factor
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ABSTRACT: The aim of this study was to elucidate the effects of regulator of G-protein signaling 5 (Rgs5), a negative regulator of G-protein-mediated signaling, on cardiac repolarization and arrhythmia in mice. Wild-type and Rgs5(-/-) mice were subjected to in vivo, in vitro, and cellular electrophysiological experiments. Rgs5(-/-) mouse hearts showed significantly prolonged cardiac repolarization, including prolonged QT interval and action potential duration (APD). Consistent with these findings, measurement of K(+) currents in ventricular myocytes of Rgs5(-/-) mice revealed significant reduction of the outward voltage-dependent K(+) currents, including I(peak), I(to,)I(Kur), and I(ss), compared to that in wild-type mice. Transcript and protein expression levels of Kv4.2, Kv4.3, Kv1.5, and Kv2.1 were downregulated in Rgs5(-/-) mouse ventricles compared with those in wild-type mice (P<0.05). In addition, electrically induced ventricular tachyarrhythmias were facilitated by Rgs5(-/-) in isolated hearts. Importantly, the increased incidence and duration of electrically induced ventricular tachyarrhythmias were associated with enhanced dispersion of APD and spatial heterogeneity of I(peak), I(to) and I(Kur) between the epicardium and endocardium in the Rgs5(-/-) heart. This study showed the relationship between the absence of Rgs5 and cardiac electrophysiological abnormality. The results strongly indicate that Rgs5(-/-) induced prolonged repolarization and ventricular tachyarrhythmia, which were closely related to the remodeling of voltage-dependent K(+) currents.
Journal of Molecular and Cellular Cardiology 10/2012; · 5.17 Impact Factor
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ABSTRACT: Ghrelin has a protective role in a rat model of myocardial infarction (MI), but the underlying mechanism is not clear. Here, we investigated the effects of ghrelin treatment on angiogenesis in an experimental rat MI model. Adult male Sprague-Dawley rats were subjected to MI by ligating the anterior descending coronary artery. The rats were then treated with a subcutaneous injection of ghrelin (100μg/kg) or saline (control group) for 4weeks. Sham animals underwent thoracotomy and pericardiotomy, but not LAD ligation. At 28days after ligation, the ghrelin treatment group showed a higher density of α-SMA positive vessels than the saline treatment MI group in myocardial infarct (6±2.1/mm(2) vs 4±1.8/mm(2), P<0.05) and peri-infarct zones (25±9.5/mm(2) vs 15±5.7/mm(2), P<0.05). RT-PCR and western-blot analyses showed that ghrelin significantly increased vascular endothelial growth factor (VEGF) expression in the peri-infarct zone compared with the control group. Moreover, there was a two-fold increase of Bcl-2 and a 3.5-fold reduction of the Bax protein in the ghrelin-treated MI group compared to the saline treatment MI group. Taken together, ghrelin could induce angiogenesis in rats after MI, the process that may be associated with the enhancement of VEGF and an anti-apoptosis effect.
Regulatory Peptides 09/2012; 179(1-3):39-42. · 2.11 Impact Factor
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ABSTRACT: To investigate the alterations of cardiac electrophysiological properties and substantial mechanism and find the stable arrhythmia mouse model in Kunming (KM) and C57BL6/J (C57) mice.
Electrocardiogram recordings were used to analyze the QT interval in vivo, and mono- phasic action potential of right and left ventricular epicardium was recorded to elicit changes of action potential duration (APD) in conventional and programmed electrical stimulation (PES). Transient outward potassium current (Ito) was recorded via whole-cell patch-clamp technique in single right and left epicardial myocytes.
QT interval was prolonged in KM mice relative to C57 mice (62.51±4.47 ms vs. 52.59±4.85 ms, P<0.05) The APD at 50% repolarization of the left ventricular epicardium (18.60±0.91 ms vs. 12.90±0.35 ms), and APDs at 50% (17.31±6.05 ms vs. 12.00±3.24 ms) and 70% repolarization (36.13±5.32 ms vs. 21.95±8.06 ms) of the right ventricular epicardium in KM mice were more sensitive to PES-induced ventricular tachycardia (25%, 3 of 12 hearts), and especially to Burst-induced ventricular tachycardia (50%, 6 of 12 hearts)compared with C57 mice, which were 20% (2 of 10 hearts) and 30% (3 of 10 hearts) respectively. Ito densities both in the left and right ventricular epicardial myocytes from KM mice were significantly decreased compared with C57 mice, respectively (all P<0.01).
Our data showed that KM mice with the prolonged QT interval and APD are vulnerabilities to ventricular arrhythmia, which are attributed to lower Ito densities in ventricular myocytes obtained from KM mice than that from C57 mice.
Chinese Medical Sciences Journal 07/2012; 27(2):80-7.
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ABSTRACT: Sudden cardiac death (SCD) is a major cause of morbidity and mortality in patients with coronary artery diseases and myocardial infarction (MI). Sympathetic stimulation and sympathetic neural remodeling are important in the generation of SCD in diseased heart. The balance of nerve growth factor (NGF) and semaphoring 3A determines the sympathetic innervation patterning. Recently studies showed that P75 neurotrophin receptor (P75 NTR) is the main receptor for NGF mediates sympathetic hyperinnervation in the heart, and also interacts with semaphoring 3A. Sympathetic axons lacking P75 NTR are more sensitive to semaphoring 3A in vitro than control neurons, resulting in decreased sympathetic innervation in the left ventricular subendocardium. P75 NTR(-/-) mice had increased sympathetic heterogeneity and more spontaneous ventricular arrhythmias. Based on current studies, we present a hypothesis that P75 NTR plays an important regulatory role in sudden cardiac after myocardial infarction and hope to find new therapeutic target for SCD.
Medical Hypotheses 06/2012; 79(3):361-2. · 1.39 Impact Factor
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ABSTRACT: Studies have shown that increased levels of serum uric acid (SUA) are associated with atrial fibrillation (AF). However, less is known about the prognostic value of SUA levels for AF in patients with chronic heart failure (CHF). The aim of the study was to examine the prognostic value of SUA levels for AF in patients with CHF.
Sixteen thousand six hundred and eighty-one patients diagnosed with CHF from 12 hospitals were analyzed. Patients were categorized into AF group and non-AF group, death group, and survival group according to the results of the patients' medical records and follow-up. Univariate and multivariate Cox proportional hazards analyses were performed to examine the risk of AF. The sensitivity and specificity of SUA level in predicting the prognosis were examined by multivariate Cox models and receiver operating characteristic (ROC) curves.
The results of univariate predictors in overall patients showed that the higher SUA level was associated with AF. SUA level (HR, 1.084; 95%CI, 1.017 - 1.144; P < 0.001), diuretics (HR, 1.549; 95%CI, 1.246 - 1.854; P < 0.001), and New York Heart Association (NYHA) (HR, 1.237; 95%CI, 1.168 - 1.306; P < 0.001) function class were the independent risk factors for AF. The sensitivity and specificity of the models were 29.6% and 83.8% respectively for predicting AF. When SUA level was added to these models, it remained significant (Wald c(2), 1494.88; P < 0.001 for AF); 58.8% (95%CI, 57.7% - 60.0%) of the observed results were concordant with the separate model.
Higher SUA level is associated strongly with AF in patients with CHF. SUA level can increase the sensitivity and specificity in predicting AF.
Chinese medical journal 05/2012; 125(10):1708-12. · 0.86 Impact Factor
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ABSTRACT: To determinate the prognostic value of red cell distribution width (RDW) and the relationships between RDW and clinical characteristics in patients with chronic heart failure (CHF).
A total of 16 681 in-hospital patients with chronic systolic HF and LVEF < 50% from 12 hospitals in Hubei province, China were enrolled. All patients were followed up with telephone call. Patients were divided into RDW ≤ 13.2% (n = 3981), 13.3% - 14.1% (n = 3996), 14.2% - 14.8% (n = 4319) and ≥ 14.9% (n = 4385) groups. Multivariate Cox regression analysis was performed to determine whether RDW is an independent risk factor of all-cause mortality in overall patients, patients with various etiologies. Multivariate Cox proportional hazard analysis was performed to determine the risk of all-cause mortality among various RDW groups.
(1) Compared with RDW ≤ 13.2% group, adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) of all-cause mortality for RDW 13.3% - 14.1%, 14.2% - 14.8% and ≥ 14.9% were 0.892 (95%CI 0.818 - 0.973, P = 0.01), 0.859 (95%CI 0.793 - 0.931, P < 0.01) and 1.034 (95%CI 0.961 - 1.111, P = 0.373) respectively. (2) Compared with MCV normal group, the adjusted HRs of MCV elevation and MCV decline groups were 1.351 (95%CI 1.063 - 1.718, P < 0.01) and 1.316 (95%CI 1.034 - 1.675, P < 0.01), respectively. (3) Compared to patients with rheumatic heart diseases, the adjusted HR for all-cause mortality in patients with coronary heart disease, dilated cardiomyopathy and hypertensive heart disease with RDW > 16% were 1.437 (95%CI 1.141 - 1.810, P < 0.01), 1.651 (95%CI 1.276 - 2.138, P < 0.01) and 1.276 (95%CI 1.004 - 1.621, P < 0.01), respectively. (4) The RDW is independently correlated with BMI (r = -0.345, P < 0.01), diastolic blood pressure (r = -0.321, P < 0.01), albumin (r = -0.411, P < 0.01), blood urine nitrogen (r = 0.476, P < 0.01), right ventricular end-diastolic diameter (r = 0.383, P < 0.01), LVEF (r = -0.463, P < 0.01) and heart rate (r = 0.379, P < 0.01).
There is a J shape relationship between all-cause mortality and RDW. The elevation or decline of MCV with increased RDW is linked with increased all-cause mortality in CHF patients.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 03/2012; 40(3):237-42.
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ABSTRACT: Researchers still do not reach the consensus on the incidence, characters and the prognostic value of pericardial effusion (PE) in patients with chronic heart failure (CHF). This study is to investigate the incidence, characters and the prognostic value of pericardial effusion (PE) in patients with CHF.
One thousand one hundred and eighty-nine patients, with a diagnosis of CHF consecutively admitted to three centers, were enrolled. M-mode echocardiography was used to determine the presence or absence of PE and to semi-quantify it. The 118 patients with PE and 472 without PE were followed up. The relationship between the PE and other parameters and the prognostic value of PE for CHF were analyzed by univariate and multivariate analyses.
After following up, 550 patients were analyzed, of which 226 were dead. The incidence of PE was 9.92%. Moderate PE was the most common which account 90.68% (107/118). The 6.78% of the patients (8/118) had small while only 2.54% (3/118) had large one. The systolic blood pressure (OR=1.04, 95%CI (1.01-1.07), P=0.08), left ventricular ejection fraction (LVEF) (OR=1.09, 95%CI (1.02-1.15), P=0.06), and main pulmonary artery diameter (MPAD) (OR=1.51, 95%CI (1.24-1.85), P<0.001) were the independent predictors of PE. The glomerular filtration rate (GFR) (OR=1.013, 95%CI (1.005-1.026), P=0.02), systolic blood pressure (OR=1.02, 95%CI (1.00-1.03), P=0.015), LVEF (OR=1.08, 95%CI (1.04-1.12), P<0.001) and diabetes mellitus (OR=3.53, 95%CI (1.99-6.44), P<0.001) were determined as the independent predictors of CHF prognosis.
The PE is not uncommon in CHF patients and most PE are small to moderate. PE is not related to the etiology of CHF while is strongly connected with higher systolic blood pressure, low LVEF and large MPAD. PE dose not increase the risk of death in patients with CHF.
Chinese medical journal 03/2012; 125(5):882-7. · 0.86 Impact Factor
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ABSTRACT: To investigate the prevalence and related factors of medicinal therapy in patients with chronic systolic heart failure (CSHF).
Data on in-hospital patients with CSHF were studied from 12 hospitals in Hubei province, in 2000 and 2010. Differences on gender and age were calculated and Multivariate Cox regression analysis was performed to determinate the independent risk factors of all-cause mortality.
(1) 16 681 patients were enrolled in this study. Among which, 6453 died during the 5.82 ± 1.63 years of follow-up. The annual medical expenditure was larger in the survival group than in the dead ones (3.19 ± 0.65 vs. 3.32 ± 0.57, P < 0.01). (2) The prevalence of Angiotensin II receptor blocker increased along with age which accounted as 7.73%, 7.35%, 12.26%, 14.29%, 17.19%, 19.87% and 20.49%, respectively, in the < 30, 30 - 39, 40 - 49, 50 - 59, 60 - 69, 70 - 79 and ≥ 80-year groups. The distribution of digitalis, diuretics, β-receptor blocker, Angiorensin-converting enzyke inhibitors showed inversed U shape. (3) The annual medical expenditure increased as patients got older, with age groups < 30, 30 - 39, 40 - 49, 50 - 59, 60 - 69 and 70 - 79 years old as 2.96 ± 0.70, 3.09 ± 0.62, 3.15 ± 0.58, 3.30 ± 0.59 and 3.25 ± 0.58, respectively (P < 0.01). It reduced to the same level as in the 50 - 59 year-old group. The distribution of annual medical expenditure showed similar pattern in males. However, the trends were only found in patients at 50 - 59, 60 - 69, 70 - 79 and ≥ 80 years-old groups in female.
More attention should be paid to medicinal therapy in patients with CSHF. Medicinal therapy shifted with age and gender, of which females had more adverse trend than in males.
Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi 02/2012; 33(2):229-33.
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ABSTRACT: AIMS: The aim of this study was to elucidate the effects of regulator of G-protein signaling 5 (Rgs5), a negative regulator of G protein-mediated signaling, on atrial repolarization and tachyarrhythmia (ATA) in mice. METHODS AND RESULTS: In present study, the incidence of ATA were increased in Rgs5(-/-) Langendorff-perfused mouse hearts during program electrical stimulation (PES) (46.7%, 7 of 15) and burst pacing (26.7%, 4 of 15) compared with wild-type (WT) mice (PES: 7.1%,1 of 14; burst:7.1%,1 of 14) (P<0.05). And the duration of ATA also shown longer in Rgs5(-/-) heart than that in WT, 2 out of 15 hearts exhibited sustained ATA (>30 s) but none of them observed in WT mice. Atrial prolonged repolarization was observed in Rgs5(-/-) hearts including widened P wave in surface ECG recording, increased action potential duration (APD) and atrial effective refractory periods (AERP), all of them showed significant difference with WT mice (P<0.05). At the cellular level, whole-cell patch clamp recorded markedly decreased densities of repolarizing K(+) currents including I(Kur) (at +60 mV: 14.0±2.2 pF/pA) and I(to) (at +60 mV: 16.7±1.3 pA/pF) in Rgs5(-/-) atrial cardiomyocytes, compared to those of WT mice (at +60 mV I(to): 20.4±2.0 pA/pF; I(kur): 17.9±2.0 pF/pA) (P<0.05). CONCLUSION: These results suggest that Rgs5 is an important regulator of arrhythmogenesis in the mouse atrium and that the enhanced susceptibility to atrial tachyarrhythmias in Rgs5(-/-) mice may contribute to abnormalities of atrial repolarization.
PLoS ONE 01/2012; 7(11):e46856. · 4.09 Impact Factor
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ABSTRACT: Backgroud Previous randomized studies have reported conflicting results on the efficacy of omega-3 fatty acids in preventing atrial fibrillation (AF) recurrences after cardioversion. Objective A systematic review and meta-analysis of the role of omega-3 fatty acids in the prevention of atrial fibrillation recurrences after cardioversion was conducted. Methods PubMed, Cochrane Library, Elsevier, Science Online database were searched up to the end of January 2012 to identify all of the studies in human subjects that reported the effects of omega-3 fatty acids on the prevention of atrial fibrillation recurrences after cardioversion. Results Overall, omega-3 fatty acids had no significant effect on the prevention of AF recurrences after cardioversion (OR: 0.63,95% CI 0.35-1.13; p=0.12). The heterogeneity among the studies was significant (p=0.01, I(2)=66%). Subgroup analysis showed that by administering omega-3 fatty acids at least 4 weeks prior to cardioversion and continuing thereafter, the recurrence rate of AF is significantly low (OR: 0.39, 95% CI 0.25-0.61; p<0.0001). Conclusion In the subgroup administered omega-3 fatty acids at least 4 weeks prior to cardioversion and continued thereafter, the recurrence rate of AF was significantly low. More double-blind, randomized, placebo-controlled, multicenter studies with high quality and longer follow-up periods are needed to affirm our conclusion.
Internal Medicine 01/2012; 51(18):2503-8. · 0.94 Impact Factor
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ABSTRACT: Ghrelin is a novel growth hormone-releasing peptide, which has been shown to exert beneficial effects on ventricular remodeling. In this study, we investigated whether ghrelin could decrease vulnerability to ventricular arrhythmias in rats with myocardial infarction and the possible mechanism. Twenty-four hours after ligation of the anterior descending artery, adult male Sprague-Dawley rats were randomized to ghrelin (100 μg/kg) and saline (control group) for 4 weeks. Sham animals underwent thoracotomy and pericardiotomy, but not LAD ligation. Myocardial endothelin-1 (ET-1) levels were significantly elevated in saline-treated rats at the border zone compared with sham-operated rats. Myocardial connexin43 (Cx43) expression at the border zone was significantly decreased in saline-treated infarcted rats compared with sham-operated rats. Ghrelin significantly decreased the inducibility of ventricular tachyarrhythmias compared with control group. Arrhythmias sores during programmed stimulation in saline-treated rats were significantly higher than scores in those treated with ghrelin. The electrophysiological improvement of fatal ventricular tachyarrhythmias was accompanied with increased immunofluorescence-stained Cx43, myocardial Cx43 protein and mRNA levels in ghrelin treated rats. We also shown that ghrelin significantly decreased tissue ET-1 levels at the infarcted border zone. Thus, ghrelin showed the protective effect on ventricular arrhythmias after myocardial infarction. Although the precise mechanism by which ghrelin modulates the dephosphorylation of Cx43 remains unknown, it is most likely that the ghrelin increased expression of Cx43 through the inhibition of ET-1.
Peptides 11/2011; 32(11):2357-61. · 2.43 Impact Factor
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International journal of cardiology 08/2011; 152(2):266-7. · 7.08 Impact Factor
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ABSTRACT: To evaluate the current status of chronic heart failure (CHF) in Hubei province and analyze the epidemiology of CHF including the general condition, etiology and pharmacological therapy.
Data of in-hospital patients with CHF were investigated between 2000 and 2010 from 12 hospitals in Hubei Province. Inclusion criteria: over 18 years of age, organic heart disease and with the symptom of HF including dyspnea and fatigue. Patients with a history of myocardial infarction in the prior 12 months, congenital heart disease, pericardial disease and the history of cancer were excluded.
(1) A total of 12 450 patients were enrolled (7166 male, 57.56%). The average age was (62.0 ± 14.5) years. Patients in the scale of age ≥ 80, 70 - 79, 60 - 69, 50 - 59, 40 - 49 and < 40 was 9.53% (1187/12 450), 30.80% (3835/12 450), 23.45% (2920/12 450), 18.81% (2342/12 450), 10.73% (1336/12 450) and 6.67% (830/12 450), respectively (P < 0.01). The NYHA class I, II, III and IV was 0.60%, 23.20%, 50.31% and 26.50%, respectively. (2) The age of patients was significant reduced from 2000 - 2003, 2004 - 2006 to 2007 - 2010 [(66.4 ± 14.1) years, (64.9 ± 14.4) years and (64.2 ± 14.8) years, P < 0.01]. (3) The major causes of CHF were hypertension (31.54%), coronary heart disease (28.24%), dilated cardiomyopathy (26.57%) and rheumatic valvular heart disease (17.49%). The most frequent etiology for CHF was rheumatic valvular heart disease in patients aged less than 40 years old, dilated cardiomyopathy in patients aged 40 - 49 and 50 - 59 years and hypertension in patients aged 60-69, 70-79 and ≥ 80 years. (4) Drug use was as follows: Digitalis (47.49%), diuretics (68.75%), ACEI (50.66%), β-blocker (44.06%) and aldosterone antagonist (53.08%). Use of digitalis (Wald χ(2) = 903.41, P < 0.01;r = 0.271, P < 0.01), diuretics (Wald χ(2) = 818.05, P < 0.01; r = 0.249, P < 0.01), aldosterone antagonists (Wald χ(2) = 76.92, P < 0.01; r = 0.091, P < 0.01) increased while the β-blocker (Wald χ(2) = 160.65, P < 0.01; r = -0.117, P < 0.01) declined in proportion to NYHA class increase.
The age of in-hospital patients with CHF declined in the previous 10 years. The primary etiology was hypertension for aged CHF in-hospital patients with CHF. There was big gap between guideline recommended standard therapy and current drug use for in-hospital patients with CHF in Hubei province.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 06/2011; 39(6):549-52.
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ABSTRACT: Epicardial ganglionated plexi (GP) ablation can prevent atrial fibrillation inducibility. However, the long-term effects of GP ablation on atrial fibrillation have not been elucidated.
Thirteen adult dogs of either sex, weighing 13-17kg, were randomly assigned to a sham-operated group (n=6) or a GP ablation group (n=7). After right thoracotomy, the atrial effective refractory period (AERP) was measured and atrial fibrillation was induced by right atrial rapid burst pacing. Atrial fibrillation and AERP were remeasured after anterior right and inferior right GP ablation in the GP ablation group. The animals were allowed to recover for 8 weeks, after which atrial fibrillation and AERP were measured again. Concentrations of C-reactive protein, tumour necrosis factor-alpha (TNF-α) and interleukin-6 were measured in the blood and atrial tissues.
After 8 weeks, atrial fibrillation was induced in all animals in the GP ablation group. AERP and dispersion of AERP (dAERP; maximum AERP minus minimum AERP) were increased after GP ablation but AERP recovered after 8 weeks. There were no significant differences in the concentrations of C-reactive protein, TNF-α or interleukin-6 in venous blood between the two groups and the concentration of C-reactive protein in the atrium did not change before and after GP ablation. However, the concentrations of TNF-α and interleukin-6 in the atrium increased significantly 8 weeks after GP ablation (P<0.05).
Increased concentrations of TNF-α and interleukin-6 in the atrium after GP ablation provide a new causative factor in terms of atrial fibrillation vulnerability.
Archives of cardiovascular diseases 04/2011; 104(4):227-33. · 0.66 Impact Factor
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Bo He,
Hong Jiang,
Zhibing Lu,
Meichun Zhang,
Xiaorong Hu,
Bo Yang, He Huang,
Gang Wu,
Jun Wan,
Huafen Liu,
Xiaohong Wang,
Congxin Huang
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ABSTRACT: The feasibility and safety of the transradial approach for catheter ablation of idiopathic left ventricular tachycardia (ILVT) have not been evaluated. The aim of this study was to investigate the feasibility and safety of transradial approach for catheter ablation in ILVT patients.
Thirty consecutive ILVT patients with negative Allen's test undergoing catheter ablation via transradial approach were enrolled to compare the safety and efficacy with 30 other ILVT patients who previously underwent catheter ablation via transfemoral approach.
Ablation was successfully performed in all patients. In the transradial group, the total procedural and the fluoroscopy time (42.8 ± 6.9 min and 9.7 ± 1.9 min, respectively) were significantly shorter when compared with transfemoral group (52.8 ± 8.4 min and 11.5 ± 2.1 min, respectively) (both P < 0.05). The two groups were similar in the number of current applications (4.1 ± 0.8 vs. 4.4 ± 1.1, P > 0.05), the power energy (47.3 ± 7.3 vs. 49.7 ± 6.9 W, P > 0.05), and the total duration of current application (110.3 ± 15.6 vs. 112.3 ± 16.5 s, P > 0.05), respectively. The duration of hospitalization in transradial group was shorter than that in transfemoral group (4.1 ± 0.9 vs. 5.8 ± 1.1 days, P < 0.05). During follow-up, there was no recurrence of tachycardia in all patients. One patient in transfemoral group developed access site complications while none occurred in the transradial group.
The transradial approach is feasible and safe for catheter ablation of ILVT.
Clinical Research in Cardiology 01/2011; 100(1):37-43. · 2.95 Impact Factor
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ABSTRACT: To investigate the effects and mechanism of verapamil preventing ischemia/reperfusion (I/R) injury by cardiac performance intracellular free [Ca(2+)](i) and L-type calcium current (I(Ca-L)) in cardiomyocytes of diabetes mellitus rats.
Diabetic rats were streptozotocin-induced and received verapamil (8 mg×kg(-1)×d(-1)) from 6 - 14 weeks old. The in vitro heart models of I/R rats were randomly divided into normal control group diabetes group, verapamil control group. the changes of heart functions were observed through a Langendorff-perfusion system. The fluorescence intensity of intracellular Ca(2+) was detected with Fluo-3/AM loading by laser scanning confocal microscope. I(Ca-L) was recorded by the whole-cell technique of patch clamp in enzymatically dissociated single rat ventricular myocytes.
(1) In verapamil diabetes group, the values of left ventricular developed pressure [(91.3 ± 4.6) mm Hg], diastolic end pressure [(1535 ± 280) mm Hg], the maximum rising rates of left ventricular pressure [(5833 ± 256) mm Hg/s] and coronary arterial flow [(13.7 ± 0.9) ml/min] were all significantly increased, and the maximum dropping rates of left ventricular pressure [(3504 ± 319) mm Hg/s] was obviously decreased (compared with diabetes group, P < 0.01, respectively). (2) The fluorescence intensities of intracellular free Ca(2+)[(155.6 ± 10.9) nmol/L] in verapamil diabetes group were significantly reduced compared with diabetes group (245.2 ± 17.5 nmol/L, P < 0.01). (3) When clamp voltage was -20mV, I(Ca-L) was (-6.81 ± 0.76) pA/pF in verapamil diabetes group (compared with normal group (-8.17 ± 2.07) pA/pF, P < 0.05, and with diabetes group (-3.21 ± 0.54) pA/pF, P < 0.01, and with verapamil control group (-7.14 ± 2.17) pA/pF, P > 0.05). The current-voltage curve was changed to the lower position with -20mV of peak clamp potential in verapamil diabetes group compared with diabetes group.
A poor heart function is closely correlated with a rising [Ca(2+)]i and a declining I(Ca-L) associated with I/R injury in diabetic rats hearts. Along-term verapamil therapy may significantly improve the severe cardiac impairment. The mechanism is probably attributed to the fact that verapamil can adjust I(Ca-L) influx, normalize the balance of intercellular [Ca(2+)]i, and block the Ca(2+) overload trigger by the effects of Ca(2+)-induced Ca(2+) release in diabetic cardiomyocytes.
Zhonghua yi xue za zhi 11/2010; 90(42):3003-7.
