Increased expression of myocardial semaphorin 3A in isoproterenol-induced heart failure rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSIONS</b>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.</p>

Reduced left ventricular systolic atrioventricular plane displacement in heart failure patients with preserved ejection fraction / 中华心血管病杂志

<p><b>OBJECTIVE</b>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).</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSION</b>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.</p>

Causes of death analysis in 133 congestive heart failure patients / 中华心血管病杂志

<p><b>OBJECTIVE</b>To analyze the causes of death in patients with heart failure.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>

On angiotensin II receptor distribution after myocardial infarction in dogs / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the effects of valsartan on expression of angiotensin II receptors in different regions of heart after myocardial infarction (MI).</p><p><b>METHODS</b>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.</p><p><b>CONCLUSION</b>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.</p>

Coronary artery and myocardium lesion comparison post atrioventricular ring radiofrequency catheter ablation with different catheters / 中华心血管病杂志

<p><b>OBJECTIVE</b>To analyze the extent of myocardium and coronary artery lesion post atrioventricular ring radiofrequency catheter ablation with different tip catheters.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>

Effects of catheter ablation of ventricular tachycardia and premature ventricular contraction originating from left and right ventricular outflow tracts / 中华心血管病杂志

<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>(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.</p><p><b>CONCLUSIONS</b>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.</p>

Arsenic trioxide eluting stents to prevent restenosis of injured iliac arteries in rabbits / 中华心血管病杂志

<p><b>OBJECTIVE</b>To assess the efficiency of eluting stent coated with arsenic trioxide (As(2)O(3)) suspended in poly-L-lactic acid (PLLA) to prevent in-stent restenosis in rabbits.</p><p><b>METHODS</b>Forty-five male New Zealand white rabbits were assigned to three groups (n = 15 for each group) at random: uncoated stents, stents coated with PLLA or stents coated with As(2)O(3) in PLLA. Animals were euthanized 28 days after stent implantation into the iliac arteries of rabbits. Neointimal thicknesses and apoptosis of vascular smooth muscle cell (VSMC) were measured. Stents coated with As(2)O(3) in PLLA were implanted in another 48 male New Zealand white rabbits, As(2)O(3) concentrations in serum and arterial tissue at implantation site were measured at 2 h and 1, 3, 7, 14, 28 days after As(2)O(3) eluting stent implantation (n = 8 for each time point).</p><p><b>RESULTS</b>Neointimal hyperplasia was significantly reduced 51% and 31% and apoptosis significantly increased (21.0 +/- 3.3; 6.2 +/- 1.9(*); 5.3 +/- 2.1(*), (*)P < 0.01 vs. As(2)O(3) eluting stent) with As(2)O(3) eluting stent, versus PLLA-coated stents and uncoated stents. As(2)O(3) concentrations in arterial tissue at implantation site were 18.6 +/- 9.1 (ng/mg) at 1 day and 0.3 +/- 0.1 (ng/mg) at 28 days after stent implantation.</p><p><b>CONCLUSIONS</b>As(2)O(3) coated stents released As(2)O(3) to local tissue for at least 28 days, suppressed neointimal hyperplasia in rabbit iliac arteries and increased local VSMC apoptosis might be one of the mechanisms for inhibiting restenosis by As(2)O(3) coated stents.</p>