结合QRS检测和小波阈值的膈肌肌电信号降噪方法

为了消去夹杂在膈肌肌电(EMGdi)信号中的心电干扰,在比例阈值算法的基础上,提出一种结合QRS检测和小波阈值的降噪方法.首先,根据小波系数的相关性构造QRS波群的检测方法,分析确定干扰的位置和范围;其次,将小波系数分为受干扰和未受干扰两部分,并构造相应的阈值算法,针对性地处理受干扰系数,以未受干扰部分系数作为阈值算法构造的依据;最后,重构处理后的小波系数,得到降噪后的EMGdi信号.对临床采集信号的处理对比表明,该方法能够更为有效地去除心电干扰,并更好地保留EMGdi的有用信号.     

急性心肌梗死患者碎裂QRS波的临床分析

目的 探讨心电图碎裂QRS波(fQRS)在诊断急性心肌梗死(AMI)中的临床应用.方法 比较fQRS在AMI患者和冠脉造影阴性者中的发生率.比较fQRS与病理性Q波在ST段抬高型AMI(STEMI)与非ST段抬高型AMI(NSTEMI)者中的发生率.比较有fQRS者与无fQRS者住院期间心律失常、再发心绞痛、左室射血分数(LVEF)降低(≤40%)、心源性休克和心源性死亡的发生率.结果 162例AMI者中有fQRS者36例(22.22%),对照组有fQRS者仅8例(4.94%).观察组与对照组fQRS的发生率比较,差异有统计学意义(χ2=20.618,P＜0.05).NSTEMI者中fQRS的发生率高于病理性Q波(P＜0.05).有fQRS者住院期间心律失常、再发心绞痛、LVEF降低、心源性死亡的发生率明显高于无fQRS者(P＜0.05).结论 fQRS可作为心电图诊断AMI的一个新指标,尤其是对非Q波型急性心肌梗死、NSTEMI者,可减少漏诊;并可作为早期识别AMI高危人群的指标之一.     

Filtered QRS duration on signal-averaged electrocardiography correlates with ventricular dyssynchrony assessed by tissue Doppler imaging in patients with reduced ventricular ejection fraction

Objectives

The relationships between filtered QRS duration and ventricular dyssynchrony were studied.

Methods

We measured filtered QRS duration on signal-averaged electrocardiography and analyzed tissue Doppler imaging in chronic heart failure patients with ejection fraction less than 50%.

Results

In 64 patients, interventricular and intraventricular dyssynchronies were observed in 25 and 38 patients, respectively. All patients with interventricular dyssynchrony were associated with intraventricular dyssynchrony. Filtered QRS showed 0.82 and 0.78 of the area under the curve (AUC) in the receiver operating characteristic curve (ROC) for the detection of interventricular and intraventricular dyssynchrony, respectively, with 89.7% and 96.2% specificity and 52.0% and 52.6% sensitivity, with cutoff values of 174 and 153 milliseconds. Specificity and sensitivity as well as AUC were lower in the ROC of QRS duration than filtered QRS duration.

Conclusion

Filtered QRS duration provided more reliable information to estimate ventricular dyssynchrony in patients with reduced ventricular ejection fraction than QRS duration did.     

Effect of changes in left ventricular anatomy and conduction velocity on the QRS voltage and morphology in left ventricular hypertrophy: a model study

The increased QRS voltage is considered to be a specific electrocardiogram (ECG) sign of left ventricular hypertrophy (LVH), and it is expected that the QRS voltage reflects the increase in left ventricular mass (LVM). However, the increased QRS voltage is only one of QRS patterns observed in patients with LVH. According to the solid angle theory, the resultant QRS voltage is influenced not only by spatial (anatomic) but also by nonspatial (electrophysiologic) determinants. In this study, we used a computer model to evaluate the effect of changes in anatomy and conduction velocity of the left ventricle on QRS complex characteristics.

Material and Methods

The model defines the geometry of cardiac ventricles analytically as parts of ellipsoids and allows to change dimensions of the ventricles, as well as the conduction velocity in the individual layers of myocardium. Three types of anatomic changes were simulated: concentric hypertrophy, eccentric hypertrophy, and dilatation. The conduction velocity was slowed in the inner layer of the left ventricle representing the Purkinje fiber mesh and in the layers representing the working myocardium. The outcomes of the model are presented as the time course of the spatial QRS vector magnitude, the vectorcardiographic QRS loops (VCGs) in horizontal, left sagittal, and frontal planes, as well as derived 12-lead ECGs. The following indicators of the 12-lead ECG were evaluated: the left axis deviation, the intrinsicoid deflection in V6, Cornell voltage, Cornell voltage-duration product, and Sokolow-Lyon index.

Results

The increase in LVM did not affect the QRS voltage proportionally, and the LVM and type of hypertrophy were not the only determinants of the QRS patterns. The conduction velocity slowing resulted in a spectrum of QRS patterns including increased QRS voltage and duration, left axis deviation, prolonged intrinsicoid deflection, VCG patterns of left bundle branch block, as well as pseudo-normal VCG/ECG patterns. The anatomic changes and conduction velocity slowing affected differently Sokolow-Lyon index and Cornell criteria.

Conclusion

We showed that the LVM is not the only determinant of the QRS complex changes in LVH, but it is rather a combination of anatomic and electric remodeling that creates the whole spectrum of the QRS complex changes seen in LVH patients. The slowed conduction velocity in the model heart produced QRS patterns consistent with changes described in LVH, even if the LVM was not changed.     

Ventricular arrhythmia is predicted by sum absolute QRST integralbut not by QRS width

Background

There is a controversy regarding the association between QRS width and ventricular arrhythmias (VAs). We hypothesized that predictive value of the QRS width could be improved if QRS width were considered in the context of the sum magnitude of the absolute QRST integral in 3 orthogonal leads sum absolute QRST integral (SAI QRST). We explored correlations between QRS width, SAI QRST, and VA in primary prevention implantable cardioverter-defibrillator (ICD) patients with structural heart disease.

Methods

Baseline orthogonal electrocardiograms were recorded at rest in 355 patients with implanted primary prevention ICDs (mean age, 59.5 ± 12.4 years; 279 male [79%]). Patients were observed prospectively at least 6 months; appropriate ICD therapies because of sustained VA served as end points. The sum magnitude of the absolute QRST integral in 3 orthogonal leads (SAI QRST) was calculated.

Results

During a mean follow-up of 18 months, 48 patients had sustained VA and received appropriate ICD therapies. There was no difference in baseline QRS width between patients with and those without arrhythmia (114.9 ± 32.8 vs 108.9 ± 24.7 milliseconds; P = .230). SAI QRST was significantly lower in patients with VA at follow-up than in patients without VA (102.6 ± 27.6 vs 112.0 ± 31.9 mV·ms; P = 0.034). Patients with SAI QRST (≤145 mV·ms) had a 3-fold higher risk of ventricular tachycardia (VT)/ventricular fibrillation (VF) (hazard ratio [HR], 3.25; 95% confidence interval [CI], 1.59-6.75; P = .001). In the univariate analysis, QRS width did not predict VT/VF. In the bivariate Cox regression model, every 1 millisecond of incremental QRS widening with a simultaneous 1 mV·ms SAI QRST decrease raised the risk of VT/VF by 2% (HR, 1.02; 95% CI, 1.01-1.03; P = .005).

Conclusion

QRS widening is associated with ventricular tachyarrhythmia only if accompanied by low SAI QRST.     

丹红注射液对兔离体左心室心电图及致心律失常作用

目的 观察丹红注射液(抗凝中药)对兔心脏电活动除极和复极过程的影响.方法 选用冠状动脉灌注兔左心室楔形组织块标本,对标本施加刺激周长(BCL)1000 ms基础刺激,1 h后进行实验;实验组给予丹红注射液;同时,分别以卡托普利和司帕沙星作为阴性对照组和阳性对照组,观察对跨壁心电图QRs复合波时程、QT间期、T波峰值至终点的时程(Tp-e)的影响,以及是否引早期后除极(EAD)和尖端扭转型室速(TdP).结果 丹红注射液对QRS波宽度无明显影响;当给予20、60 mL·L~(-1)时,较阴性对照组QT间期轻度延长(P<0.05),并与相关浓度的卡托普利作用一致;但对Tp-e间期及Tp-e/QT比值均无明显影响(P>0.05),且未诱发EAD或Tdp.结论 丹红注射液在本实验浓度范围内,仍无明显诱发尖端扭转型室速和其他室性心律失常的危险性.     

Does adenosine A1 receptor stimulation causes QRS prolongation by blocking beta adrenergic receptors in amitriptyline poisoning?

Aims

To investigate the role of beta receptor blockade via adenosine A₁ receptor stimulation on amitriptyline-induced QRS prolongation.

Methods

Isolated rat hearts were randomized into three groups (n = 8 for each group). After pretreatment with 5% dextrose (control) or DPCPX (8-cyclopentyl-1,3-dipropylxanthine), or propranolol + DPCPX, amitriptyline infusion was given to all groups. Intact beta adrenergic receptor response was verified with a bolus dose of isoproteranol (3 × 10⁻⁵ M).

Results

Amitriptyline (5.5 × 10⁻⁵ M) infusion following pretreatment with 5% dextrose or 10⁻⁴ M DPCPX prolonged QRS by 40–110% and 30–75%, respectively. After the beta receptor blockade with 10⁻² M propranolol bolus, amitriptyline infusion following pretreatment with DPCPX prolonged QRS by 40–130%. Amitriptyline infusion following pretreatment with DPCPX (10⁻⁴ M) shortened the QRS at 40, 50 and 60  min significantly when compared to propranolol + DPCPX group (168.8 ± 4.9%, p < 0.05; 170.8 ± 6.9%, p < 0.01; 174.0 ± 6.9%, p < 0.01, respectively). Amitriptyline infusion following pretreatment with 5% dextrose prolonged QRS duration significantly at 50th minutes (209.5 ± 6.1%, p < 0.05) compared to DPCPX pretreatment group.

Conclusion

DPCPX pretreatment shortened amitriptyline-induced QRS prolongation. Beta adrenergic receptor blockade enhanced QRS prolongation shortened by DPCPX pretreatment. Adenosine A₁ receptor stimulation related to beta adrenergic receptor blockade may play a role in amitriptyline-induced QRS prolongation in isolated rat hearts.     

平板运动试验诱发宽QRS心动过速的鉴别诊断

目的 了解Vereckei法新四步流程图对宽QRS心动过速(WQRST)的鉴别诊断价值.方法 选择在心电图平板运动试验(ETT)过程中诱发WQRST的受检者27例,应用Vereckei法新四步流程图鉴别诊断WQRST.结果 Vereckei法新四步流程图诊断WQRST的符合率为92.6%,误诊率为7.4%.受检者ETT诱发的WQRST均自行终止,未致严重后果.4例ETT阳性的缺血性室性心动过速(VT)患者和1例ETT阳性的缺血性室上性心动过速(SVT)伴束支传导阻滞者,经积极救治均痊愈出院.结论 Vereckei法新四步流程图对ETT诱发的WQRST有鉴别诊断的价值,有助于及时正确识别VT和SVT,对疾病的治疗和预后有积极的作用.     

胺碘酮治疗58例宽QRS波心动过速临床体会

目的观察胺碘酮对宽QRS波心动过速的复律效果及使用过程中低血压、心动过缓的发生率。方法应用体表心电图进行宽QRS波心动过速的诊断和鉴别诊断。对58例血流动力学稳定的宽QRS波心动过速患者予以胺碘酮静脉注射,并监测血压、心率的变化。结果用胺碘酮后,在全部患者、室上速患者、室速患者以及不能鉴别者中分别有47、8、35和4例成功转复窦性心律,其样本阳性率分别为81．0％、88．9％、81．4％和66．7％,总体阳性率95％可信区间分别为70．9％～91．1％、52％～100％、67％～92％和22％～96％。用药后有5例患者发生低血压,有3例患者发生较严重的心动过缓（〈50次／min）,其样本阳性率分别为8．6％和5．2％,相应总体阳性率95％可信区间分别为1．4％～15．8％和0％～10．7％。结论胺碘酮对宽QRS波心动过速具有较好的复律作用,且应用安全性较高。     

Narrow QRS Tachycardia in a Patient with Tachycardiomyopathy: What Is the Mechanism?

A 50‐year‐old female presented with incessant palpitation of 2 weeks duration. She was hemodynamically stable and there was no evidence of heart failure. A transthoracic echocardiogram showed mild left ventricular (LV) dysfunction with LV ejection fraction of 45%. Electrocardiogram (12 lead and rhythm strip) was taken during the palpitation. What is the mechanism?