Safety of the novel atrial-selective K+-channel blocker AVE0118 in experimental heart failure

Congestive heart failure (CHF) is often associated with atrial fibrillation. The safety of many antiarrhythmic drugs in CHF is limited by proarrhythmic effects. We aimed to assess the safety of a novel atrial-selective K⁺-channel blocker AVE0118 in CHF compared to a selective (dofetilide) and a non-selective IKr blocker (terfenadine). For the induction of CHF, rabbits (n = 12) underwent rapid right ventricular pacing (330–380 bpm for 30 days). AVE0118 (1 mg/kg) dofetilide (0.02 mg/kg) and terfenadine (2 mg/kg) were administered in baseline (BL) and CHF. A six-lead ECG was continuously recorded digitally for 30 min after each drug administration. At BL, dofetilide and terfenadine significantly prolonged QTc interval (218 ± 30 ms vs 155 ± 8 ms, p = 0.001 and 178 ± 23 ms vs. 153 ± 12 ms, p =  0.01, respectively) while QTc intervals were constant after administration of AVE0118 (p = n.s.). In CHF, dofetilide and terfenadine caused torsades de pointes and symptomatic bradycardia, respectively, and prolonged QTc interval (178 ± 30 ms vs. 153 ± 14 ms, p = 0.02 and 157 ± 7 ms vs. 147 ± 10 ms, p = 0.02, respectively) even at reduced dosages, whereas no QTc-prolongation or arrhythmia was observed after full-dose administration of AVE0118. In conclusion, atrial-selective K⁺-channel blockade by AVE0118 appears safe in experimental CHF. H.-J. Schneider and O. Husser contributed equally.     

The effect of continuous positive airway pressure on heart rate variability during the night in patients with chronic heart failure and central sleep apnoea

Continuous positive airway pressure (CPAP) improves autonomic activity in patients with chronic heart failure (CHF) and central sleep apnoea (CSA), but its effect on heart rate variability (HRV) during therapy has not been reported. We hypothesized that CPAP may decrease HRV, despite its beneficial effects on sympathetic overactivation, due to the expected stabilization of breathing. Sixty‐seven CHF patients underwent polysomnography (PSG). Ten of them presented with CSA (age 66.1±8.5 years, apnoea‐hypopnea index [AHI]=57.6±23.3, central AHI [cAHI]=41.6±24.6 [mean±SD]) and were subjected to a second PSG with manual CPAP titration. Beat‐to‐beat heart intervals for a 6‐hour period of sleep were extracted from each recording and HRV was analysed. CPAP significantly reduced AHI (AHI=23.1±18.3 P=.004). Standard deviation of normal‐normal interbeat interval (SDNN) (61.5±29.0 vs 49.5±19.3 ms, P=.021), root mean square of successive differences (RMSSD) (21.8±9.2 vs 16.4±7.1 ms, P=.042), total power (lnTP=7.8±1.1 vs 7.4±0.8 ms², P=.037), low frequency power (lnLF=5.5±1.5 vs 5.0±1.4 ms², P=.003) and high frequency power (lnHF=4.6±1.0 vs 4.0±1.0 ms², P=.024) were decreased. There was a strong correlation between the decrease in AHI and the decrease in lnHF (Spearman's ρ=.782). CPAP leads to a decrease in spectral and time domain parameters of HRV during therapy in CHF patients with CSA. These changes are best explained by the effect which CPAP‐influenced breathing pattern and lowered AHI exert on HRV.     

Heart rate variability in patients after cardiac valve surgery

The aim of study was to analyze heart rate variability (HRV) after different cardiac valve surgery procedures and the prognostic values of these findings. This study included 101 consecutive patients who underwent surgical implantation for an artificial valve. The mean age of the patients was 62 ± 10 years. An aortic valve was implanted in 65 patients. A mitral valve was implanted in 36 patients. HRV was analyzed from 24 hours Holter electrocardiographic (ECG) records. The time from the operation to the recording of Holter ECG and measuring HRV was 3.8 ± 1.4 months. After discharged from stationary cardiac rehabilitation, all involved patients were contacted to provide data on their health in the follow-up period (33 ± 21 months). A total of 46 patients with an implanted artificial valve had decreased overall HRV or standard deviation of all normal R-R intervals (SDNN) < 93 ms. Patients with an implanted artificial mitral valve had a shorter RR interval (817 ± 122 vs. 863 ± 122ms, p=0.03) and lower values of total power (1166 ± 1888 vs. 2802 ± 3601 ms², p<0.001) compared to patients with an implanted artificial aortic valve. The results of study show that several months after cardiac surgery, almost half of the patients with an implanted artificial valve have decreased HRV. However, postoperative decreased HRV in those patients have no importance in long-term prediction of mortality rate.     

Nitric oxide inhibits isoprenaline-induced positive inotropic effects in normal, but not in hypertrophied rat heart

Evidence has accumulated that, in the rat heart, nitric oxide (NO) inhibits β-adrenoceptor-mediated positive inotropic effects. The aim of this study was to investigate whether this effect of NO may be altered in cardiac hypertrophy. For this purpose we studied the effects of the NO-donor SNAP (S-nitroso-N-acetyl-D,L-penicillamine) on isoprenaline-induced positive inotropic effects in left ventricular strips from three models of cardiac hypertrophy: a) 12–16 weeks old male spontaneously hypertensive rats (SHR) vs. age-matched normotensive Wistar-Kyoto (WKY) rats, b) six weeks old male Wistar WKY-rats subtotally nephrectomized (SNX) 7 weeks after SNX vs. sham-operated rats (SOP) and c) four weeks old male Wistar WKY-rats supra-renal aortic-banded (AOB, band diameter 1.0 mm) 8 weeks after AOB vs. SOP. In all three models of cardiac hypertrophy the heart weight/body weight ratio was significantly higher than in their respective controls. On isolated electrically driven ventricular strips isoprenaline (10^–10–10^–5 M) caused concentration-dependent increases in force of contraction. Maximal increases (E_max) were similar in SHR vs. WKY-rats, but reduced in SNX- (2.9±0.29 vs. 5.1±0.34 mN, p<0.01) and AOB-rats (2.3±0.37 vs. 4.2±0.33 mN, p<0.01). In control rats (WKY and the respective SOP) the NO-donor SNAP (10^–5 M) caused a significant rightward-shift of the concentration-response curve for isoprenaline; this rightward-shift could be inhibited by methylene blue (10^–5 M). In ventricular strips of SHR, SNX- and AOB-rats, however, 10^–5 M SNAP failed to significantly affect isoprenaline-induced positive inotropic effect. We conclude that in cardiac hypertrophy effects of NO are attenuated. Such an impairement of the NO-system could contribute to the development and/or maintenance of cardiac hypertrophy. Received: 16 February 1998 / Accepted: 11 March 1998     

坎地沙坦对慢性心力衰竭患者脑钠肽水平及心功能的影响

目的探讨坎地沙坦对慢性心力衰竭(CHF)患者脑钠肽(BNP)水平和心功能的影响。方法已接受常规治疗,按照纽约心脏病协会(NYHA)分级标准,心功能3～4级的CHF患者80例,随机分为2组:治疗组40例,对照组40例。治疗组在常规治疗基础上加用坎地沙坦8mg治疗12周。对比分析治疗前后两组患者的血浆BNP水平、NYHA分级、血压、超声心动图等指标。结果治疗组较对照组左室舒张末期内径(LVEDd)[(61±6)mmvs.(57±5)mm]、左室收缩末期内径(LVESd)[(51±7)mmvs.(45±4)mm]显著下降(P均<0.05),左室射血分数(LVEF)显著升高[(40±10)%vs.(48±7)%](P<0.05),血浆BNP[(131±52)ng/Lvs.(71±8)ng/L]显著降低(P<0.05);此外,坎地沙坦治疗前后,患者血浆BNP降低值与左室舒张末期内径(r=0.80)、左室收缩末期内径(r=0.79)减少呈正相关(P均<0.01),而与LVEF的增加呈负相关(r=-0.86,P<0.01)。结论坎地沙坦治疗充血性心力衰竭(CHF)的总有效率达92%以上,坎地沙坦能阻断CHF的发展进程,改善心功能及降低血清BNP水平,血浆BNP可作为评价血管紧张素Ⅱ受体拮抗剂治疗CHF的监测指标之一。     

血压及心率变异性对急性心肌梗死后患者预后价值的研究

目的　研究急性心肌梗死后患者心率变异性 (HRV)、血压变异性 (BPV)的改变 ,评价 HRV及BPV对患者远期恶性心律失常及心脏性猝死的预测价值 ,探讨 BPV预测价值的临床意义。方法　 6 8例急性心肌梗死后行 2 4 h动态心电血压监测检查的患者 ,根据动态心电图检查结果分为非心律失常组及心律失常组 ,记录非心律失常组 HRV、BPV各值及心律失常组的 BPV各值 ,并与 19名正常对照组的 HRV、BPV值相比较。全部患者平均随访 12个月。比较两组发生恶性心脏事件及猝死者与未发生者 HRV、BPV改变情况 ,分别评价心律失常组 BPV,非心律失常组 BPV、H RV各自及两者结合的预测敏感度、特异度。结果　与正常对照组比较 ,急性心肌梗死后患者 HRV各值减小 ,BPV各值增大。在随访期内非心律失常组发生心脏事件 4例 ,心律失常组发生 3例。以 SDNN<5 0 ms及 DSD夜 >8m m Hg为指标 ,非心律失常组 HRV预测的敏感度为 75 % ,特异度为 87% ,BPV预测的敏感度为 5 0 % ,特异度 77% ,两者结合预测的敏感度、特异度分别为 5 0 % ,97%。心律失常组以 DSD夜>8mm Hg为指标预测的敏感度、特异度分别为 6 7% ,74 %。结论　与 HRV相比 BPV也是一个较好的心肌梗死预后指标 ,BPV与 H RV两者结合可以显著提高预测价值。 BPV对心肌梗死后合并心律失?     

Differential expression of potassium channels and abnormal conduction in experimental tachycardia-induced heart failure

Heart failure causes electrophysiological changes in the heart. Downregulation of repolarizing K+-currents leads to a prolongation of the cardiac action potential. Nevertheless, little is known about the differential expression of atrial and ventricular K+-channels in the failing heart. Ten rabbits underwent progressive rapid right ventricular pacing for 30 days. Digitized ECGs and echocardiograms were obtained. Left ventricular and left atrial tissue was harvested and mRNA levels of BNP, Kv4.3, rERG, Kv1.5, and KvLQT1 were measured by real time PCR. Experimental heart failure was characterized by left ventricular dilatation (13 ± 1 mm vs. 9 ± 1, p < .001), depressed fractional shortening (25 ± 5% vs. 40 ± 4, p < .001), and left atrial remodeling with increased diameter (16 mm ± 2 vs. 12 ± 1, p = .002) and weight (1.3 g ± 0.2 vs. 0.5 ± 0.1, p = .01). A prolongation of P-wave (44 ± 5 ms vs. 40 ± 4, p = .001) and PQ-interval (73 ± 10 ms vs. 66 ± 9, p = .009) occurred. In heart failure, BNP mRNA levels showed a significant upregulation in the left ventricle and atrium (1.83 AU ±1.31 vs. 0.67 ± 0.65, p < .05 and 7.16 AU ±1.76 vs. 0.77 ± 0.48, p < .05). Left ventricular Kv1.5 mRNA was reduced by 50% (p < .001) and KvLQT1 was reduced by 70% (p < .001). rERG and Kv4.3 mRNA were unchanged (n = ns). In contrast, left atrial Kv4.3 and KvLQT1 were reduced by 70% (p < .001), whereas rERG and Kv1.5 were unchanged (p = ns). Significant correlations were present between BNP and K+-channel expressions. Heart failure is characterized by significant changes in the gene expression of repolarizing K+-currents with a differential atrial and ventricular pattern. These molecular changes occur together with changes in cardiac function, geometry, conduction, and BNP expression and provide a functional basis for electrical vulnerability in heart failure.     

稳心颗粒治疗右室流出道室性早搏的疗效评价

目的观察稳心颗粒治疗右室流出道室性早搏的疗效。方法:对35例右室流出道性早搏患者,给予稳心颗粒口服治疗,剂量为每次9g,每日3次,4周为一疗程。疗效及不良反应采用动态心电图结果及临床症状评定。结果:稳心颗粒治疗后,总有效率为86.7%,治疗前QTd:59.44±17.32ms.治疗后QTd:30.52±18.41ms(P<0.01),无心功能恶化,不良反就轻微。结论:稳心颗粒能改善心室肌复极的不稳定状态,治疗右心室流出道室性早搏疗效确切。     

Cardiomyopathy confers susceptibility to particulate matter-induced oxidative stress,vagal dominance,arrhythmia and pulmonary inflammation in heart failure-prone rats

Abstract

Acute exposure to ambient fine particulate matter (PM_2.5) is tied to cardiovascular morbidity and mortality, especially among those with prior cardiac injury. The mechanisms and pathophysiological events precipitating these outcomes remain poorly understood but may involve inflammation, oxidative stress, arrhythmia and autonomic nervous system imbalance. Cardiomyopathy results from cardiac injury, is the leading cause of heart failure, and can be induced in heart failure-prone rats through sub-chronic infusion of isoproterenol (ISO). To test whether cardiomyopathy confers susceptibility to inhaled PM_2.5 and can elucidate potential mechanisms, we investigated the cardiophysiologic, ventilatory, inflammatory and oxidative effects of a single nose-only inhalation of a metal-rich PM_2.5 (580?µg/m³, 4?h) in ISO-pretreated (35 days?×?1.0?mg/kg/day sc) rats. During the 5 days post-treatment, ISO-treated rats had decreased HR and BP and increased pre-ejection period (PEP, an inverse correlate of contractility) relative to saline-treated rats. Before inhalation exposure, ISO-pretreated rats had increased PR and ventricular repolarization time (QT) and heterogeneity (Tp-Te). Relative to clean air, PM_2.5 further prolonged PR-interval and decreased systolic BP during inhalation exposure; increased tidal volume, expiratory time, heart rate variability (HRV) parameters of parasympathetic tone and atrioventricular block arrhythmias over the hours post-exposure; increased pulmonary neutrophils, macrophages and total antioxidant status one day post-exposure; and decreased pulmonary glutathione peroxidase 8 weeks after exposure, with all effects occurring exclusively in ISO-pretreated rats but not saline-pretreated rats. Ultimately, our findings indicate that cardiomyopathy confers susceptibility to the oxidative, inflammatory, ventilatory, autonomic and arrhythmogenic effects of acute PM_2.5 inhalation.     

美托洛尔对充血性心力衰竭患者QT离散度的影响及临床意义

目的:探讨美托洛尔对充血性心力衰竭患者QT离散度的影响及临床意义。方法:将54例CHF患者随机分为治疗组(26例)和对照组(28例),治疗组加用美托洛尔,对照组常规治疗,并作治疗前后的QTd测量及比较。结果:QTd与心功能受损的程度呈正相关;CHF伴室性心律失常者QTd大于不伴室性心律失常者(P<0.05);给予美托洛尔治疗后CHF患者QTd明显缩短(P<0.05)。结论:CHF患者QTd明显增大。美托洛尔可使QTd缩小,对防治室性心律失常和猝死有重要意义。     

无症状先天性心脏病患者心率变异性的动态变化

目的　研究无症状先天性心脏病患者不同运动状态下的心率变异性。方法　应用心肺运动功能仪 ,采用连续递增运动 (ramp- pattern)方案测定 2 0例无症状先天性心脏病患者 (研究组 )和 2 0名正常人 (对照组 )的心肺功能和心率变异指标进行比较。结果　研究组运动达到 5 0 %最大摄氧量 (VO2 max)和最大摄氧量时与运动前比较 ,5 min高频成分 [(6 2 0± 5 11) ms2 / Hz,(392± 2 88) ms2 / Hz,(10 4 2± 96 7) ms2 / Hz,P<0 .0 0 1) ]和低频成分[(6 0 3± 4 93) m s2 / Hz,(4 90± 4 0 2 ) ms2 / Hz,(989± 87) m s2 / Hz,P<0 .0 0 1) ]均低于运动前安静状态 ,并低于正常对照组 (P<0 .0 5 )。结论　无症状先天性心脏病患者的心率变异性比正常人减低 ,运动后心率变异减低更明显     

Decreased vancomycin clearance in patients with congestive heart failure

Purpose

Congestive heart failure (CHF) alters the pharmacokinetics of various drugs, including cardiovascular agents, due to decreased cardiac output and decreased renal blood flow. The purpose of this study was to evaluate the influence of CHF on the clearance of vancomycin, a glycopeptide antibacterial agent.

Methods

After reviewing more than 1,500 clinical charts of patients who received vancomycin therapy and whose serum vancomycin level was monitored, we identified 101 patients who also had the left ventricular ejection fraction (LVEF) assessed at that time. The fluorescence polarization immunoassay method was used to measure vancomycin serum concentrations in these patients 1 h after the end of vancomycin infusion and just before the next administration. Using these two measurements, we calculated the pharmacokinetic parameters using the Bayesian estimator.

Results

Patients with an LVEF of?<40 % (16 patients) or those with an LVEF of ≥ 40 %? and <60 % (40 %?≤?LVEF?<?60 % ; 32 patients) had a significantly lower vancomycin clearance than patients with LVEF of?≥60 % (53 patients) (2.29?±?0.95 or 2.79?±?0.99 vs. 3.50?±?1.04 L/h; p?<?0.001 or p?<?0.01, respectively). Vancomycin clearance was strongly correlated not only with estimated creatinine clearance (CLcr) in patients with an LVEF of?<40 % (r?=?0.828) and 40 %?≤?LVEF?<?60 % (r?=?0.773), but also with an LVEF in patients with a CLcr of?<60 mL/min (r?=?0.646). Consistent with these findings, multiple regression analysis revealed that CLcr, LVEF and body weight were important independent variables for vancomycin clearance (r ²?=?0.649).

Conclusions

Vancomycin clearance decreased with decreasing cardiac function (LVEF) and decreasing CLcr. This finding suggests that vancomycin clearance is affected by cardiac function and would be predicted not only CLcr but also by LVEF.     

Electrocardiographic changes during exposure to residual oil fly ash (ROFA) particles in a rat model of myocardial infarction.

Epidemiological studies have reported a positive association of short-term increases in ambient particulate matter (PM) with daily mortality and hospital admissions for cardiovascular disease. Although patients with cardiopulmonary disease appear to be most at risk, particulate-related cardiac effects following myocardial infarction (MI) have not been examined. To improve understanding of mechanisms, we developed and tested a model for investigating the effects of inhaled PM on arrhythmias and heart rate variability (HRV), a measure of autonomic nervous system activity, in rats with acute MI. Left-ventricular MI was induced in 31 Sprague-Dawley rats by thermocoagulation of the left coronary artery; 32 additional rats served as sham-operated controls. Diazepam-sedated rats were exposed (1 h) to residual oil fly ash (ROFA), carbon black, or room air at 12-18 h after surgery. Each exposure was immediately preceded and followed by a 1-h exposure to room air (baseline and recovery periods, respectively). Lead-II electrocardiograms were recorded. In the MI group, 41% of rats exhibited one or more premature ventricular complexes (PVCs) during the baseline period. Exposure to ROFA, but not to carbon black or room air, increased arrhythmia frequency in animals with preexisting PVCs. Furthermore, MI rats exposed to ROFA, but not to carbon black or room air, decreased HRV. There was no difference in arrhythmia frequency or HRV among sham-operated animals. These results underscore the usefulness of this model for elucidating the physiologic mechanisms of pollution-induced cardiovascular arrhythmias and contribute to defining the specific constituents of ambient particles responsible for arrhythmias.     

Fetal and offspring arrhythmia following exposure to nicotine during pregnancy

Although recent studies have demonstrated prenatal nicotine can increase cardiovascular risk in the offspring, it is unknown whether exposure to nicotine during pregnancy also may be a risk for development of arrhythmia in the offspring. In addition, in previous studies of fetal arrhythmia affected by smoking, only two patterns, bradycardia and tachycardia, were observed. The present study examined acute effects of maternal nicotine on the fetal arrhythmia in utero, and chronic influence on offspring arrhythmia at adult stage following prenatal exposure to nicotine. Nicotine was administered to pregnant ewes and rats. In the fetal sheep, intravenous nicotine not only induced changes of fetal heart rate, but also caused cardiac cycle irregularity, single and multiple dropped cardiac cycles. Although maternal nicotine had no influence on fetal blood pH, lactic acid, hemocrit, Na⁺, K⁺ levels and plasma osmolality, fetal blood PO₂ levels were significantly decreased following maternal nicotine in ewes. In offspring rats at 4–5 months after birth, prenatal exposure to nicotine significantly increased heart rate and premature ventricular contraction in restraint stress. In addition, arrhythmias induced by injection of nicotine were higher in the offspring prenatal exposure to nicotine in utero. The results provide new evidence that exposure to nicotine in pregnancy can cause fetal arrhythmia in various patterns besides tachycardia and bradycardia, the possible mechanisms for nicotine‐induced fetal arrhythmia included in utero hypoxia. Importantly, following exposure to nicotine significantly increased risk of arrhythmia in the adult offspring. The finding offers new insight for development of cardiac rhythm problems in fetal origins. Copyright © 2009 John Wiley & Sons, Ltd.     

The In-vivo Cardiovascular Effects of a Putative Class III Anti-arrhythmic Drug,AM 92016

AM 92016(1-(4-methanesulphonamidophenoxy)-3-(N-methyl-3–4-dichlorophenethylamino)-2-propanol benzoic acid salt), an oxypropanolamine analogue of sotalol, has been shown to possess Class III antiarrhythmic properties in-vitro at concentrations showing 1000 times more potency than sotalol. The aim of this study was to characterize the effects of AM 92016 in-vivo. When administered to anaesthetized guinea-pigs, AM 92016 (10 μg kg^?1-5 mg kg^?1) significantly increased heart rate, systolic arterial blood pressure, left ventricular systolic pressure and the contractile index dp/dt_max. AM 92016 also significantly decreased the QT interval of the electrocardiogram from 135 ± 10 to 105 ± 4 ms (5 mg kg^?1). The time to onset of the first arrhythmia and ventricular fibrillation, induced by intravenous infusion of ouabain, was shortened in the presence of AM 92016. Ouabain-induced ventricular fibrillation occurred at 18 ± 5 and 12 ± 3 min (P < 005) in control and AM 92016-(1 mg kg^?1) treated guinea-pigs, respectively. An infusion of AM 92016 (2.5 μg kg^?1 min^?1) to anaesthetized pigs significantly increased the total number of arrhythmias occurring following coronary artery occlusion from 266 ·26 in control pigs to 535 ± 148 (P < 005) in those receiving AM 92016. The time to onset of ventricular fibrillation was also significantly reduced in anaesthetized pigs from 24 ± 1 to 18 ± 3 min in the presence of AM 92016. The drug did not change haemodynamics in the anaesthetized pig. We conclude that AM 92016 exhibited proarrhythmic rather than antiarrhythmic activity when administered in-vivo to either guinea-pigs or pigs.     

Association between heart rate variability indices and features of spontaneous ventricular tachyarrhythmias in mice

Direct evidence is limited for the association between heart rate variability (HRV) indices and ventricular tachyarrhythmias (VTAs). While galectin-3 (Gal-3) is regarded as a causal factor for cardiac remodelling and a biomarker for arrhythmias, its regulation on VTAs and HVR is unknown. Using aged transgenic (TG) mice with cardiac overexpression of β₂-adrenoceptors and spontaneous VTAs, we studied whether changes in HRV indices correlated with the severity of VTAs, and whether Gal-3 gene knockout (KO) in TG mice might limit VTA. Body-surface ECG was recorded (10-minute period) in 9- to 10-month-old mice of non-transgenic (nTG), TG and TG × Gal-3 knockout (TG/KO). Time-domain, frequency-domain and nonlinear-domain HRV indices were calculated using the R-R intervals extracted from ECG signals and compared with frequency of VTAs. TG and TG/KO mice developed frequent VTAs and showed significant changes in certain time-domain and nonlinear-domain HRV indices relative to nTG mice. The severity of VTAs in TG and TG/KO mice in combination, estimated by VTA counts and arrhythmia score, was significantly correlated with certain time-domain and nonlinear-domain HRV indices. In conclusion, significant changes in HRV indices were evident and correlated with the severity of spontaneous VTAs in TG mice. The frequency of VTA and HRV indices were largely comparable between TG and TG/KO mice. Deletion of Gal-3 in TG mice altered certain HRV indices implying influence by neuronally localized Gal-3 on autonomic nervous activity.     

美托洛尔与依那普利治疗充血性心力衰竭效果比较

目的观察并比较美托洛尔和依那普利对冠心病充血性心力衰竭并室性心律失常的疗效。方法2004-04～2005-04选择我院心内科门诊或病房的冠心病充血性心力衰竭(NYHAⅢ-Ⅳ)伴有室性心律失常患者42例,在强心、利尿、硝酸酯治疗的基础上,随机给予美托洛尔(12.5～100mg/d)或依那普利(2.5～20mg/d),治疗16周。分别于治疗前、后进行24h动态心电图监测与临床心功能评估。结果治疗后24h室性心律失常总检出率美托洛尔组下降了41.1%,依那普利组下降了17.1%。二者差异显著(P<0.01)。复杂室性心律失常及室性心动过速检出率美托洛尔组分别下降了64.4%、66.7%,依那普利组下降了15.3%、12.5%,两组差异显著(均P<0.01)。两组患者心功能均获明显提高,但组间无显著性差异(P>0.05)。结论美托洛尔和依那普利均较好改善冠心病心衰患者心功能,美托洛尔同时具有干预高级别室性心律失常发生的特殊效应。笔者认为在冠心病心力衰竭治疗中先于血管紧张素转换酶抑制剂使用更好。     

Overnight heart rate variability in patients with obstructive sleep apnoea: A time and frequency domain study

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心肌梗死患者QT间期变异性和心率变异的分析

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美西律抑制频发室性早搏的疗效及其对心率变异的影响

目的：评价美西律治疗频发室性早搏（ 简称室早） 的疗效及其对心率变异（ＨＲＶ） 的影响。方法：２４ ｈ 动态心电图记录室早＞ ５ 次／ｍｉｎ 的病人３１例,男性１４ 例,女性１７ 例,年龄（４２ ±ｓ １６） ａ,用美西律０ ．１ ～０ ．２ ｇ , ｐｏ,ｔｉｄ, 疗程２ ｗｋ 以上。治疗后复查动态心电图,观察室早和ＨＲＶ 的变化。结果：治疗前后２４ ｈ 室早的自然对数分别为（８ ．９ ±０ ．９）次和（６ ±３） 次,下降（２ ．５ ±２ ．９） 次（ Ｐ＜ ０ ．０１） , 成对室早对数由（２ ．１ ±２ ．３） 次下降至（１ ．０ ±１ ．９） 次（ Ｐ＜ ０ ．０１） ,２４ ｈ 室性心动过速的对数由（ ０ ．９ ±１ ．６） 次降至（０ ．４ ±１ ．１） 次（ Ｐ＜ ０ ．０１） 。但５ 个ＨＲＶ 时域指标在治疗前后无明显变化。结论：美西律对室性早搏有显著的抑制作用,未发现其对心率变异时域指标有明显影响。