Association of AGTR1 and ACE2 gene polymorphisms with structural atrial fibrillation in a Chinese Han population.

The renin-angiotensin system (RAS) is thought to play an important role in atrial fibrillation (AF). The RAS contains the ACE/AngII/AGTR1 axis and the ACE2/Ang(1-7)/MAS axis, which restrict each other via mutual antagonism and regulate myocardial hypertrophy, fibrosis and remodelling. The aim of our study was to investigate the association between single nucleotide polymorphisms (SNPs) in angiotensin-II type-1 receptor (AGTR1) and angiotensin-converting enzyme 2 (ACE2) and structural AF in a Chinese Han population. The SNPs (rs1492100, rs1492099, rs1492097, rs3772616) in AGTR1 and the SNP rs6632677 in ACE2 were compared in 300 structural AF patients (67.61±12.56 years) and 300 controls (66.08±12.47 years). The genotype frequencies of SNP rs1492099 in AGTR1 in the structural AF cohort vs controls were as follows: GG, 72.7 vs 83.0%; AG 26.0 vs 16.3%; AA 1.3 vs 0.7% (P=0.009). The frequency of the minor allele of SNP rs1492099 in AGTR1 was 14.2% in the structural AF group compared with 8.8% in the controls (t=0.004; odds ratio [OR], 1.727; 95% confidence interval [CI]: 1.154-2.487). In addition, the genotype frequencies of SNP rs6632677 in ACE2 in the structural AF male patients vs male controls were as follows: GG, 70.5 vs 83.1%; CG 26.3 vs 15.6%; and CC 3.2 vs 1.3% (P=0.029). The frequency of the minor allele of SNP rs6632677 in ACE2 was 16.3% in structural AF male patients compared with 9.1% in male controls (P=0.008; OR, 1.954; 95%CI: 1.196-3.192). Furthermore, we found an interaction between the SNP rs6632677 in ACE2 and the SNPs (rs1492100/rs1492099/rs3772616) in AGTR1 in structural AF patients by the multifactor dimensionality reduction (MDR) method. The results indicate that polymorphism rs1492099 in the AGTR1 gene is associated with structural AF in a Chinese Han population. It was hypothesized that the ACE2 gene, which maps to the X chromosome, may be correlated with the risk of structural AF in a Chinese Han male population. Furthermore, we found an interaction between ACE2 and AGTR1 in structural AF patients in a Chinese Han population.

Atrial fibrillation increases sympathetic and parasympathetic neurons in the intrinsic cardiac nervous system.

BACKGROUND: Chronic atrial fibrillation (AF) leads to heterogeneous autonomic nerve innervation termed neural remodeling. The quantitative changes in neural density as a function of autonomic remodeling and its association with sustained AF has not been previously determined. METHOD AND RESULTS: Seven dogs (paced group) were chronically paced with electrodes sutured to the epicardium of left atrial appendages. Seven dogs (control animals) were not paced. All paced dogs developed sustained AF by 5 weeks of pacing. The fat pads on the atrial epicardium containing ganglionated plexuses (GP) were separated along with underlying myocardial tissue. Immunocytochemical techniques were used to identify the neurons immunoreactive to anti-tyrosine hydroxylase (TH) and anti-acetylcholine antibodies. After chronic AF, sympathetic and parasympathetic neurons in the atrial intrinsic cardiac ganglia increased significantly. In paced dogs, the density of sympathetic neurons was 3,022 ± 507 µm(2) /mm(2) in the right atrial GP (vs control P < 0.01), 8,571 ± 476 µm(2) /mm(2) in the ventral left atrial GP (vs control P < 0.0001)， 6,422 ± 464 µm(2) /mm(2) in the dorsal atrial GP (vs control P < 0.0001) and 5,392 ± 595 µm(2) /mm(2) in the inferior vena cava-inferior atrial GP (vs control P <0.0001), respectively. The density of parasympathetic neurons was 4,396 ± 877 µm(2) /mm(2) in the right atrial GP, 7,769 ± 465 µm(2) /mm(2) in the ventral left atrial GP， 7,016.47 ± 687 µm(2) /mm(2) in the dorsal atrial GP and 5,485 ± 554 µm(2) /mm(2) in the inferior vena cava-inferior atrial GP, respectively, which was higher than control cohorts in corresponding GP (P < 0.05). CONCLUSIONS: This study provides evidence for the remodeling in atrial intrinsic cardiac ganglia in the dogs with pacing induced AF. A significant increase of sympathetic and parasympathetic neurons was present in atrial intrinsic cardiac ganglia.

Usefulness of the heart-rate variability complex for predicting cardiac mortality after acute myocardial infarction.

BACKGROUND: Previous studies indicate that decreased heart-rate variability (HRV) is related to the risk of death in patients after acute myocardial infarction (AMI). However, the conventional indices of HRV have poor predictive value for mortality. Our aim was to develop novel predictive models based on support vector machine (SVM) to study the integrated features of HRV for improving risk stratification after AMI. METHODS: A series of heart-rate dynamic parameters from 208 patients were analyzed after a mean follow-up time of 28 months. Patient electrocardiographic data were classified as either survivals or cardiac deaths. SVM models were established based on different combinations of heart-rate dynamic variables and compared to left ventricular ejection fraction (LVEF), standard deviation of normal-to-normal intervals (SDNN) and deceleration capacity (DC) of heart rate. We tested the accuracy of predictors by assessing the area under the receiver-operator characteristics curve (AUC). RESULTS: We evaluated a SVM algorithm that integrated various electrocardiographic features based on three models: (A) HRV complex; (B) 6 dimension vector; and (C) 8 dimension vector. Mean AUC of HRV complex was 0.8902, 0.8880 for 6 dimension vector and 0.8579 for 8 dimension vector, compared with 0.7424 for LVEF, 0.7932 for SDNN and 0.7399 for DC. CONCLUSIONS: HRV complex yielded the largest AUC and is the best classifier for predicting cardiac death after AMI.

Relationship between c-reactive protein and the asymmetric dimethylarginine-induced endothelial dysfunction pathway in vasospastic angina.

Vasospastic angina (VSA) is a special form of atherosclerotic disease. There is some evidence suggesting a relationship between inflammation and VSA. We sought to demonstrate the relationship between high-sensitivity c-reactive protein (hs-CRP), a sensitive marker of inflammation, and the asymmetric dimethylarginine (ADMA)-induced endothelial dysfunction pathway in patients with VSA. We studied 68 patients who were diagnosed with VSA with typical symptoms and had a positive hyperventilation test. We determined plasma levels of hs-CRP, ADMA, brachial flow-mediated dilation (FMD), and other biochemical parameters in these 68 VSA patients and 68 age-matched non-VSA subjects. Multivariate logistic regression indicated that hs-CRP (OR, 3.81 P < 0.001) and a history of smoking (OR, 3.06 P = 0.008) were independently associated with the incidence of VSA. Moreover, we found that CRP was directly related to ADMA (r = 0.69, P < 0.001) but inversely related to brachial FMD (r = -0.66, P < 0.001) in patients with VSA. Additionally, ADMA was inversely related to brachial FMD (r = -0.75, P < 0.001) in patients with VSA. These results indicate that there is a relationship between CRP and the ADMA-induced endothelial dysfunction pathway in patients with VSA. Anti-inflammatory agents may be a potential strategy for the treatment of endothelial dysfunction in VSA.

Prognostic significance of heart rate turbulence parameters in patients with chronic heart failure.

BACKGROUND: This study is aimed to evaluate the clinical significance of heart rate turbulence (HRT) parameters in predicting the prognosis in patients with chronic heart failure (CHF). METHODS: From June 2011 to December 2012, a total of 104 CHF patients and 30 healthy controls were enrolled in this study. We obtained a 24-hour Holter ECG recording to assess the HRT parameters, included turbulence onset (TO), turbulence slope (TS), standard deviation of N-N intervals (SDNN), and resting heart rate (RHR). The relationships between HRT parameters and the prognosis of CHF patients were determined. RESULTS: The assessment follow-up period lasted until January 31, 2013. The overall mortality of CHF patients was 9.6% (10/104). Our results revealed that CHF patients had higher levels of TO than those of healthy subjects, but the TS levels of CHF patients were lower than that of the control group. CHF patients with NYHA grade IV had higher HRT1/2 rate than those with NYHA grade II/III. There were statistical differences in TS, LVEF, SDNN and RHR between the non-deteriorating group and the non-survivor group. Significant differences in TS among the three groups were also found. Furthermore, CHF patients in the non-survivor group had lower levels of TS than those in the deteriorating group. Correlation analyses indicated that TO negatively correlate with SDNN, while TS positively correlated with SDNN and left ventricular ejection fraction (LVEF). We also observed negative correlations between TS and left ventricular end-diastolic cavity dimension (LVEDD), RHR, homocysteine (Hcy) and C-reactive protein (CRP). Multivariate Cox regression analysis further confirmed that LVEF (≤30%), HRT2, SDNN and RHR were independent risk factors which can indicate poor prognosis in CHF patients. CONCLUSIONS: Our findings indicate that HRT may have good clinical predictive value in patients with CHF. Thus, quantifying HRT parameters could be a useful tool for predicting mortality in CHF patients.

A computer-aided diagnostic algorithm improves the accuracy of transesophageal echocardiography for left atrial thrombi: a single-center prospective study.

OBJECTIVES: We investigated whether transesophageal echocardiography (TEE) assisted with a computer-aided diagnostic (CAD) algorithm was superior to TEE in diagnosing left atrial (LA)/left atrial appendage (LAA) thrombi in patients with atrial fibrillation (AF) in a single prospective study. METHODS: Transesophageal echocardiography was performed in patients with AF, and images were reconstructed. Gray level co-occurrence matrix-based features were calculated and then classified using an artificial neural network. The original data and processed images by the CAD system were studied by 5 radiologists independently in a blind manner. The diagnostic performance of each radiologist was evaluated. RESULTS: One hundred thirty patients with AF were investigated. Thirty-one patients (23.9%) had a diagnosis of LA/LAA thrombi. The mean sensitivity ± SD of TEE for LA/LAA thrombi was 0.933 ± 0.027, which was noticeably improved by CAD (0.955 ± 0.021; P < .05). The specificity of TEE was 0.811 ± 0.055, which was markedly lower than that by TEE plus CAD (0.970 ± 0.009; P < .05). The positive predictive value of TEE was low (0.613 ± 0.073) compared to that of TEE plus CAD (0.908 ± 0.027; P < .001), whereas the negative predictive values were comparable for TEE, CAD, and TEE plus CAD. Diagnosis of an LA/LAA thrombus by TEE plus CAD had a higher accuracy rate (0.966 ± 0.011) than that by TEE (0.840 ± 0.047; P < .01). The mean area under the receiver operating characteristic curve (Az) for TEE was 0.834 ± 0.009 (95% confidence interval [CI], 0.815-0.852), which was markedly lower than the Az for TEE plus CAD (0.932 ± 0.005; 95% CI, 0.921-0.943). The use of CAD significantly improved the Az values for all 5 radiologists (P < .001). CONCLUSIONS: The CAD algorithm significantly improves the diagnostic accuracy of TEE for LA/LAA thrombi in patients with AF.

Parasympathetic and substance P-immunoreactive nerve denervation in atrial fibrillation models.

BACKGROUND: Recent studies demonstrated that atrial fibrillation (AF) induced heterogeneous sympathetic hyperinnervation and baroreflex impartation, but the changes of vagal and afferent nerve are not clear. METHODS: Six dogs underwent atrial pacing at 600 beats/min (AF group). All paced dogs developed sustained AF by 5 weeks of pacing. Tissues from six healthy dogs were used as controls. Immunohistochemistry staining of cardiac nerves was performed using anti-growth-associated protein 43 (anti-GAP43), anti-tyrosine hydroxylase, antiacetylcholine (anti-ACh), and anti-substance P (anti-SP) antibodies. RESULTS: In AF group, the density of GAP43-positive in the right atrium (RA), atrial septum (AS), and left atrium (LA) was 5590.24±1417.51, 8083.22±1271.39, and 10854.56±1877.56 µm(2)/mm(2), respectively, which was significantly (P<.01) higher than the control group. Most of the newly sprouting nerves are sympathetic nerve. Sympathetic nerve density in AF group was significantly higher than that of control group (P<.001). Whereas denervation of parasympathetic and SP-immunoreactive nerve occurred in AF group. In the dogs with AF, the density of ACh-positive nerve in the RA, AS, and LA was 506.04±104.44, 317.72±84.10, and 114.9±29. 62 µm(2)/mm(2), respectively, which was lower than the control group (P<.01). At the same time, the density of SP-positive nerve in the atria of AF dogs was also significantly lower than the control tissues (P<.01). CONCLUSION: AF led to significant nerve sprouting and sympathetic hyperinnervation in the canine models, but the newly sprouting nerve did not include parasympathetic and SP-immunoreactive nerve. Heterogeneous parasympathetic and SP-immunoreactive nerve denervation occurred in the AF dogs.

Increased expression of myocardial semaphorin 3A in isoproterenol-induced heart failure rats.

BACKGROUND: Maintenance of normal cardiac function is controlled by the autonomic nervous system. In congestive heart failure (CHF), sympathetic nerve denervation is increasingly recognized. The sympathetic fiber density depends on the balance between neurotrophins and neural guidance molecules. Semaphorin 3A (sema3a), a secreted neural guidance factor, is a well characterized member of the newly found semaphorin family. It can induce sympathetic growth cone collapse and axon repulsion. We conducted this study to investigate cell sources of sema3a in the heart, the expression level of sema3a in CHF and discuss the possible role of sema3a in CHF. METHODS: Rats were divided into four groups: 30 days control group rats, 30 days CHF rats, 60 days control group rats, 60 days CHF rats. The heart failure model was induced by injection of isoproterenol (ISO) 340 mg/kg continuously two days. All animals underwent echocardiography and haemodynamics measurements. Cardiac expression of sema3a was determined by real time polymerase chain reaction (RT-PCR) and Western blotting analysis. Immunohistochemical analysis was used to determine the cell source of sema3a in the heart. RESULTS: Isoproterenol induced 30 days and 60 days CHF rats displayed left ventricular dilation, systolic and diastolic function decrease. Sema3a was secreted by the cardiocytes and increased significantly in 30 days and 60 days CHF rats compared with the controls (RT-PCR: 30 days group: 0.32 ± 0.05 vs. 0.58 ± 0.06, P < 0.01; 60 days group: 0.34 ± 0.08 vs. 0.71 ± 0.07, P < 0.01. Western blotting: 30 days group: 0.25 ± 0.10 vs. 0.46 ± 0.10, P < 0.05; 60 days group: 0.29 ± 0.10 vs. 0.55 ± 0.16, P < 0.01. Immunohistochemical analysis: 30 days group: 2.91 ± 0.20 vs. 5.31 ± 0.30, P < 0.01; 60 days group: 2.94 ± 0.30 vs. 5.80 ± 0.30, P < 0.01). CONCLUSIONS: Sema3a was expressed in the heart by cardiocytes. Increased expression of sema3a may partly account for sympathetic denervation in CHF; modulation of this pathway may prove beneficial in heart failure sympathetic remodeling.

[Coronary artery and myocardium lesion comparison post atrioventricular ring radiofrequency catheter ablation with different catheters].

OBJECTIVE: To analyze the extent of myocardium and coronary artery lesion post atrioventricular ring radiofrequency catheter ablation with different tip catheters. METHODS: Twenty-one healthy dogs were randomly divided into 64 degrees C/50 W/100 s, 64 degrees C/100 W/100 s, 45 degrees C/45 W/100 s groups and ablated by 4 mm tip catheter, 8 mm tip catheter and irrigated tip catheter respectively. Left atrioventricular ring and right atrioventricular ring ablation were performed in all dogs. After ablation, myocardium lesion volume was calculated as 1/6pi x length x width x depth. Histological examinations were performed at the myocardium tissue at ablation sites. RESULTS: The lesion depths post 8 mm tip catheter ablation (7.18 +/- 1.72) mm and irrigated tip catheter ablation (7.99 +/- 1.77) mm were similar and significantly deeper than that post 4 mm tip catheter ablation (4.54 +/- 1.38) mm, P < 0.01. Similar results were found in terms of lesion volume [(356.76 +/- 94.44) mm(3) post 8 mm tip catheter ablation, (391.69 +/- 109.54) mm(3) post irrigated tip catheter ablation and (191.34 +/- 74.52) mm(3) post 4 mm tip catheter ablation]. Five (5/42, 11.9%) transmural myocardium necrosis and 8 (8/42, 19%) coronary artery lesions were observed post ablations. CONCLUSION: The extents of post ablation myocardium and coronary artery lesion were significantly higher induced by 8 mm tip catheter and irrigate tip catheter compared those by 4 mm tip catheter.

[On angiotensin II receptor distribution after myocardial infarction in dogs].

OBJECTIVE: To investigate the effects of valsartan on expression of angiotensin II receptors in different regions of heart after myocardial infarction (MI). METHODS: Canines were divided into sham-operated control group (n=7), infarction group (n=7) and Valsartan group (10 mg x kg(-1) x day(-1) for 4 weeks after MI operation, n=7). Four weeks after operation, Doppler tissue imaging (DTI) was used to evaluate regional ventricular function in the noninfarcted myocardium (apical and basal near to the infarction region). The mRNA and protein expressions of angiotensin II type 1 receptor (AT1-R) and angiotensin II type 2 receptor (AT2-R) on the corresponding regions were detected by competitive reverse-transcriptase polymerase chain reaction technique and immunohistochemical technique respectively. Results The protein and mRNA expressions of AT1-R were significantly increased in both apical and basal regions near to the infarction in dogs with MI compared with those in control group (P < 0.05) which could be downregulated by valsartan (P < 0.05). AT2-R expressions were significantly upregulated in infarction group in both apical and basal regions compared with those in control group and valsartan further increased AT2-R expressions in both areas (P < 0.05). Myocardial peak systolic velocity (Sm), myocardial peak early diastolic velocity (Em) and myocardial peak late diastolic velocity (Am) at both apical and basal regions near to the infarction regions were significantly lower in MI group than those in the control group which could be significantly improved by valsartan. CONCLUSION: Both mRNA and protein expressions of AT1-R and AT2-R are upregulated in noninfarcted regions near MI, valsartan improved myocardial function via inhibiting AT1-R upregulation and enhancing AT2-R upregulation.

[Effect of benazepril on atrial cytoskeleton remodeling in the canine atrial fibrillation models].

OBJECTIVE: To investigate the effect of benazepril on atrial cytoskeleton remodeling in atrial fibrillation (AF) canines induced by chronic rapid atrial pacing (RAP). METHODS: Twenty canines were randomly divided into 3 groups: (1) Sham-operated group without RAP; (2) AF group: AF established by RAP at 600 beats per minute for 6 weeks; (3) Benazepril group: benazepril was dosed from 1 week pre-pacing to 6 weeks post-pacing. The diameter of atrial cardiomyocyte was measured, collagen volume fraction (CVF) analyzed by Masson staining and the expression and distribution of desmin were assayed by immunohistochemistry. RT-PCR method was used to semi-quantify the mRNA expression of beta-tubulin and desmin. RESULTS: The diameter of atrial cardiomyocyte increased in AF group [LA:(27.9 +/- 3.8) microm; RA: (26.8 +/- 3.2) microm] and benazepril group[LA: (25.1 +/- 3.4) microm; RA: (25.2 +/- 3.5) microm] than sham-operated group [LA: (19.6 +/- 2.9) microm; RA: (18.7 +/- 2.6) microm] (P < 0.01). CVF increased in AF group than sham-operated group [LA: (16.9 +/- 1.1)% vs (9.2 +/- 0.9)%, RA: (15.7 +/- 2.3)% vs (9.3 +/- 0.8)%, P < 0.01] and it decreased in benazepril group than AF group [LA: (11.3 +/- 0.8)% vs (16.9 +/- 1.1)%, RA: (10.9 +/- 0.8)% vs (15.7 +/- 2.3)%, P < 0.01]. Normal desmin cross-striations were lost in atrial cardiomyocyte and the desmin organization became irregular in AF group. The A values analyzed by immunohistochemistry of desmin increased in AF group than sham-operated group and they decreased in benazepril group than AF group (P < 0.01). The expression of mRNA level of desmin and beta-tubulin were up-regulated in AF group than sham-operated group, (LA:1.0 +/- 0.3 vs 0.6 +/- 0.3, 0.9 +/- 0.4 vs 0.6 +/- 0.3; RA: 1.0 +/- 0.6 vs 0.6 +/- 0.2, 1.1 +/- 0.3 vs 0.7 +/- 0.4, P < 0.01) and they were down-regulated in benazepril group than AF group (LA:0.8 +/- 0.4 vs 1.0 +/- 0.3, 0.7 +/- 0.3 vs 0.9 +/- 0.4; RA:0.7 +/- 0.3 vs 1.0 +/- 0.6, 0.7 +/- 0.3 vs 1.1 +/- 0.3, P < 0.01). CONCLUSION: Benazepril can favorably improve atrial cytoskeleton remodeling in the canine atrial fibrillation model.

[Causes of death analysis in 133 congestive heart failure patients].

OBJECTIVE: To analyze the causes of death in patients with heart failure. METHODS: A total of 133 heart failure patients died during hospitalization in our hospital between January 2005 and December 2008 were enrolled in this study. Patients were divided to two groups: sudden death (group A, n = 73, 54.9%), chronic end-stage pump failure (group B, n = 55, 41.4%). The remaining 5 cases died of other causes were excluded from the final analysis. Clinical data (medical history, blood pressure, clinical manifestation, NYHA cardiac function class, left ventricular diameter of diastole, left ventricular ejection fraction, ventricular arrhythmias, drug therapy) of group A and B were analyzed. RESULTS: There were no significant differences in terms of medical history (including hypertension and diabetes), blood pressure, heart rate and the incidence of ventricular arrhythmia between the two groups. In group A, the NYHA functional class was mostly II or III grade, and LVEF value was significantly higher than that of group B. The incidence of angina pectoris was significantly higher in group A compared to group B. beta-blocker and angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker use was also significantly higher in group A than in group B, however, the treatment dose was significantly lower and therapy duration was significantly shorter in group A than in group B. There were significantly less patients received statins and anti-platelet aggregation drugs in group A compared to group B. CONCLUSION: In our patient cohort, sudden cardiac death often occurred in heart failure patients with NYHA cardiac function II to III grade, angina pectoris, probably due to the unstable coronary plaque and less statins and anti-platelet drug use in these patients.

[Sympathetic nerve in rat with pressure overload left ventricular hypertrophy].

OBJECTIVE: To explore the remodeling mechanism of myocardium and sympathetic nerve in pressure overload left ventricular hypertrophy and elucidate the protective effect of statins. METHODS: Pressure-overload left ventricular hypertrophy (LVH) of rats was induced by partial coarctation of abdominal aorta; a sham-operated group served as the control (SHAM, n = 22). At 8 weeks post-operation, the animals were divided into two groups and a 12-week treatment period was investigated. At the end of treatment period, echocardiographic evaluations and hemodynamic measurements were performed. Sympathetic innervation was investigated by analyzing nerve growth factor (NGF), growth associated protein-43 (GAP43) and tyrosine hydroxylase (TH). RESULTS: In LVH rats, a significant increase of left ventricular weight, left ventricular weight/body weight, echocardiographic left ventricular end-diastolic diameter, interventricular septum thickness, posterior left ventricular wall thickness, left ventricular systolic pressure and dP/dt was observed. The expressions of NGF and GAP43 protein were significantly down-regulated (0.82 +/- 0.06 vs 1.53 +/- 0.10, 0.68 +/- 0.06 vs 0.81 +/- 0.10) and TH level was up-regulated (0.44 +/- 0.10 vs 0.62 +/- 0.06) by RSV treatment. CONCLUSION: A HMG CoA inhibitor reverses the development of left ventricular hypertrophy and inhibits sympathetic innervation in abdominal aortic-clamped animals.

[Reduced left ventricular systolic atrioventricular plane displacement in heart failure patients with preserved ejection fraction].

OBJECTIVE: To determine whether patients with suspected heart failure but preserved left ventricular ejection fraction (LVEF) have systolic dysfunction in left ventricular long axis detected by left ventricular systolic atrioventricular plane displacement (AVPD). METHODS: The data of 96 patients with heart failure who admitted to our hospital between August 2007 and October 2008 were collected. Heart failure with preserved LVEF was diagnosed in 48 patients and heart failure with reduced LVEF was diagnosed in another 48 patients. Fifty age-matched healthy subjects served as the control group. The NYHA classification, etiology of heart failure, AVPD and plasma NT-proBNP concentration were compared among the 3 groups. RESULTS: There was no difference in terms of NYHA classification between patients with preserved LVEF and reduced LVEF. Hypertension and coronary heart disease were often diagnosed in heart failure patients with preserved LVEF. The degree of AVPD decrease was more significant in heart failure patients with reduced LVEF than those with preserved LVEF. In all subjects, the AVPD was negatively correlated with the NT-proBNP concentration (r = -0.35, P < 0.05). CONCLUSION: Left ventricular systolic atrioventricular plane displacement was decreased in heart failure patients with preserved LVEF, therefore, besides "diastolic heart failure", systolic dysfunction was also impaired in these patients.

[Effects of catheter ablation of ventricular tachycardia and premature ventricular contraction originating from left and right ventricular outflow tracts].

OBJECTIVE: To observe the ECG and electrophysiological characteristic of patients with idiopathic ventricular tachycardia (VT) and premature ventricular contraction (PVC) originating from left (LVOT) and right (RVOT) ventricular outflow tracts and assess the clinical effect of radio frequency catheter ablation (RFCA) on these patients. METHODS: RFCA was performed in 58 patients (10 with VT and 48 with PVC, 5 patients with VT from RVOT under the guidance of non-contact mapping system Ensite3000). VT or PVC originated from LVOT in 15 patients (12 out of 15 from left sinus of Valsalva) and RVOT in 43 patients. RESULTS: (1) R wave in II, III, aVF leads was the common characteristics of VT or PVC originated from LVOT and RVOT and difference in wave duration index and R/S-wave amplitude ratio in V(1) or V(2) could be used to define VT and PVC originated from LVOT or RVOT. (2) Ablation was successful in 55 out of 58 patients (9 patients with the 2nd ablation, evaluated as arrhythmia-free at 3 months post ablation without medication) and failed in 3 patients. One patient developed pericardial tamponade during ablation and recovered without complication after related treatments. CONCLUSIONS: RFCA is an effective, safe and curative therapy for VT or PVC originated from LVOT and RVOT. Non-contact mapping system (Ensite3000) is a safe and reliable tool to guide mapping and ablation in patients with complex VT and unstable hemodynamics.

[The tone of sympathetic and expression of beta1 receptor in the dogs with sustained atrial fibrillation].

OBJECTIVE: To detect the influence of sustained atrial fibrillation on autonomic nerve. METHODS: 7 healthy mongrel dogs were paced at 600/min. ter sustained reversing into sinus rhythm. HRV was obtained by Holter. Noradrenaline in left atrial appendage, left atrial, atrial septal, right atrial appendage and right atrial was detected. Nerve growth factor was determined and beta1 receptor in atrial myocardium was evaluated. All the indexes were compared with control animals. RESULTS: ter sustained, the tone of sympathetic increased. LF in dogs with long term (1682 +/- 362) ms2 and short term (1247 +/- 219) ms2 were higher than control dogs (798 +/- 154) ms2 (P < 0.01). The HF in dogs with long term (232 +/- 75) ms2 and short term (310 +/- 165) ms2 was lower than control dogs (1041 +/- 195) ms2 (P < 0.01). The SDNN [long term (32 +/- 7) ms, short term (51 +/- 7) ms] and HRV indexes (long term 16 +/- 4, short term 24 +/- 8) in group were inferior to corresponding indexes in control group [(103 +/- 14) ms and 38 +/- 5 respectively, P < 0.01]. The content of noradrenaline in myocardium was higher in group (P < 0.01). Furthermore, the increase of noradrenaline in the atrium was heterogeneous (P < 0.01), which was not observed in control group. The expression of NGF increased in group. beta1 receptor down regulated in group. CONCLUSION: Sustained caused increased tone of sympathetic, heterogeneous accumulation of noradrenaline and down regulation of beta1 receptor, which was mediated by NGF.

[Relationship between plasma asymmetrical dimethylarginine and coronary artery disease].

OBJECTIVE: To investigate whether the plasma asymmetrical dimethylarginine (ADMA) level correlates with the extent and severity of coronary atherosclerosis. METHODS: 110 consecutive patients undergoing coronary angiography were divided into five groups according to the result thereof: control group (n = 22, with normal coronary artery), mild coronary artery disease (CAD) group (n = 21, with stenosis < 50% of the major coronary arteries), single branch CAD group III (n = 22, with stenosis >/= 50% of one major coronary artery); double branch CAD group IV (n = 23, with stenosis >/= 50% of two major coronary arteries); and multi-branch CAD group (n = 22, with significant stenosis >/= 50% of more than two major coronary arteries or companies with stenosis of left major coronary). ELISA was used to detect the plasma ADMA. Nitric acid reductase method and colorimetry were used to measure the levels of plasma nitric oxide (NO) and nitrogen oxide synthase (NOS). The relationship between the plasma ADMA and severity of CAD was analyzed. RESULTS: The plasma ADMA levels of in last three a groups were 1.52 micromol/L +/- 0.61 micromol/L, 1.67 micromol/L +/- 0.80 micromol/L, and 2.60 micromol/L +/- 0.62 micromol/L all significantly higher than that of the control group (0.79 micromol/L +/- 0.54 micromol/L, P < 0.01). The plasma NO and NOS levels of the multi-branch CAD group were significantly lower than those of the other groups (all P < 0.01), and there were not significant differences in Plasma NO and NOS levels among the other groups. Multivariate stepwise logistic regression analysis showed that the plasma ADMA level was significantly positively correlated with the severity of coronary atherosclerosis (r = 0.684, P = 0.007) and total cholesterol and triglyceride (r = 0.623 and 0.536 respectively), and significantly negatively correlated with the NO and NOS levels (r = -0.709 and -0.701 respectively). CONCLUSION: Correlated significantly with the severity of coronary atherosclerosis, the plasma ADMA level may become a novel marker of CAD.

[Clinical evaluation of catheter ablation for idiopathic ventricular arrhythmia originating from ventricular outflow tract].

OBJECTIVE: To study the ECG and electrophysiological characteristic of idiopathic ventricular tachycardia (VT) and premature ventricular contraction (PVC) originating from ventricular outflow tract and assess the clinical effect of radiofrequency catheter ablation (RFCA) for treatment. METHODS: 105 patients aged from 12 to 73 years old were treated with RFCA. Activation mapping, pace mapping and non-contact mapping system of Ensite 3000 were used during the procedure. RESULTS: (1) VT and PVC were successfully ablated in 97 out of the 105 patients (93.3%), 15 were recurrent but succeed in the second time. (2) 84 patients originated from right ventricle outflow tract (RVOT) and the remaining 21 patients from left ventricle outflow tract (LVOT). (3) 3 patients have the pericardial tamponade during ablation. CONCLUSION: RFCA is an effective and curative therapy for ventricular arrhythmia originating from ventricular outflow tract.

[Effect of chronic myocardial infarction on the distribution of beta-adrenoceptors in heart: experiment with dogs].

OBJECTIVE: To investigate the distribution of beta-adrenoceptors at different sites of heart after myocardial infarction (MI). METHODS: 14 dogs were randomly divided into 2 equal groups: MI group, undergoing ligation of the left anterior descending coronary artery, and control group undergoing sham-operation. Four weeks later metoprolol, a beta 1-adrenergic receptor antagonist, was injected intravenously. Doppler tissue imaging (DTI) was used to evaluate the peak systolic myocardial velocity (Sm) of the regions apical and basal to the infarction region before and after the injection. Then the dogs were killed with their hearts taken out. Reverse-transcriptase polymerase chain reaction was used to examine the mRNA expression of beta 1-receptor and beta 2-receptor in the non-infracted myocardial tissues apical and basal to the infarction region. RESULTS: The Sm values at the regions apical and basal to the infarction region of the MI group were 3.93 +/- 0.47 and 0.81 +/- 0.19 cm/s respectively, both significantly lower than those of the control group (10.84 +/- 1.97 and 5.85 +/- 1.15 cm/s respectively, both P < 0.05). After injection of metoprolol, the Sm values at the regions apical and basal to the infarction region of the MI group were 3.43 +/- 0.37 and 0.73 +/- 0.14 cm/s respectively, not significantly different from those before the injection; however, the corresponding Sm values of the control group were 8.69 +/- 1.14 and 4.33 +/- 0.29 cm/s respectively, both significantly lower than those before the injection (both P < 0.05). The mRNA expression levels of beta 1-receptor decreased in both apical and basal regions in the MI group compared with those in the control group, and the degree of expression decrease at the apical region was significantly greater than that at the basal region. However, there was no significant difference in the expression level of beta 1-receptor mRNA between the apical and basal regions in the control group. There was no significant difference in the mRNA expression of beta 2-receptor in different regions of the heart in both groups. CONCLUSION: After MI regional variation occurs for the beta 1-receptor mRNA expression, but not to the beta 2-receptor.