QT离散度对室性心律失常发生的预测价值的再探讨

研究体表心电图QT离散度(QTd)对室性心律失常的发生是否有预测价值。将204例入选心脏病例的QTd按级差5ms分段,计算各时段病例中频发室性早搏(VPB≥30次/小时)以及室性心动过速(VT)+心室颤动(VF)的发生率。以各时段QTd的上限值为变量,对各时段室性心律失常的发生率与QTd上限值进行相关性研究。将上述室性心律失常者分设为VPB组(n=52)和VT+VF组(n=46)。在其余入选病例中选择未发现明显室性心律失常者(VPB<5次/小时)50例设为疾病对照组。另设正常对照组(n=50)。对各组QTd进行组间比较。结果:各时段VPB及VT+VF的发生率与QTd上限值无明显相关性(r1=0.2091,r2=0.1684,P>0.05)。VPB组及VT+VF组的QTd虽明显大于正常对照组(P<0.01),但与疾病对照组比较无显著差异(P>0.05)。结论:QTd对室性心律失常的发生似乎无预测价值。     

高血压伴左心室肥厚与T波顶峰后宽度的关系

目的探讨高血压左心室肥厚(LVH)患者T波顶峰后宽度(TpTe间期)的改变及其临床意义。方法随机抽取2010-10-2011-06桂林医学院附属医院心内科住院的原发性高血压(EH)患者313例,根据超声心动图(UCG)测定的左心室质量指数(LVMI)分为LVH组和非LVH(NLVH)组。比较两组TpTe间期、校正TpTe间期(TpTec)、QT间期、校正QT间期(QTc)、QRS时限、LVMI、左心室舒张末期内径(LVEDD)、室间隔厚度(IVST)、左心室后壁厚度(LVPWT)的改变及其相互关系;比较不同血压水平对TpTe间期的影响;EH患者左心室不同构型TpTe间期改变的特点。结果与NLVH组比较,LVH组TpTe间期[(100.0±23.3)比(85.3±14.1)ms]、TpTec[(108.6±26.7)比(91.4±15.4)ms]、QTc[(435.0±23.6)比(420.0±23.5)ms]、QRS时限[(105.3±22.3)比(95.6±16.1)ms]均延长(均P<0.01),LVMI[(142.8±29.3)比(82.5±19.0)g/m2],LVEDD[(58.9±7.5)比(47.6±6.5)cm],IVST[(9.7±1.0)比(8.8±1.2)cm],LVPWT[(9.4±1.1)比(8.5±1.1)cm]明显增大(均P<0.01),QT间期延长,但差异无统计学意义。TpTe间期在不同左心室构型间的改变为:离心型肥厚>向心性肥厚>左心室游离壁肥厚>正常心室形态。Pearson相关分析表明,TpTe间期、TpTec与LVMI(r=0.43,0.44)、LVEDD(r=0.41,0.43)呈正相关(P<0.05)。多元线性回归分析显示,LVMI、LVEDD是TpTe间期重要的影响因素(β=0.026、0.280)。结论 TpTe间期可作为评价高血压伴左心室肥厚靶器官损害程度的心电学指标之一。     

心脏病室性心律失常患者Tp-e间期、Tp-e/Q-T比值的研究

目的探讨器质性心脏病患者Tp-e间期、Tp-e/Q-T比值与室性心律失常的关系。方法选择器质性心脏病患者85例,分为两组,器质性心脏病室性心律失常组(A组)43例,并进一步按LOWN分级分为两个亚组,A1组(LOWN2-3级)20例,A2组(LOWN3级以上)23例;器质性心脏病无室性心律失常组(B组)42例。另选择健康体检者40例为正常对照组(C组)。采用常规12导联同步心电图及24小时动态心电图分析比较各组的Q-T间期、Q-Tc间期、Tp-e间期、Tp-ec间期和Tp-e/Q-T测值。结果 A组Q-T间期、Q-Tc间期、Tp-e间期、Tp-ec间期、Tp-e/Q-T测值比C组显著升高,差异有统计学意义(P<0.05),而Q-Tc间期、Tp-e间期、Tp-ec间期、Tp-e/Q-T比B组显著升高,差异有统计学意义(P<0.05)。上述各测值A2组比A1组显著升高,差异有统计学意义(P<0.05或P<0.01)。结论 Tp-e间期、Tp-e/Q-T等心电学指标与室性心律失常的发生有关,对室性心律失常的发生具有预测意义。     

扩张性心肌病患者心电图T波峰末间期与室性心律失常关系的探讨

目的探讨扩张性心肌病(DCM)患者心电图T波峰末间期与室性心律失常的关系。方法63例DCM患者依照有无室性心动过速或室颤发生,分为恶性心律失常组与非恶性心律失常组,测定每位患者心电图T波峰末间期即Tp-Te值,以及超声心动图LVEDD和LVEF。结果恶性室性心律失常组的Tp-Te、LVEDD值明显高于非恶性室性心律失常(P<0.05),而LVEF值明显低于非恶性室性心律失常组(P<0.05)。Tp-Te与LVEDD显著正相关(r=0.72,P<0.01,与LVEF显著负相关(r=-0.68,P<0.01)。结论Tp-Te可能反映心室跨壁复极离散度的变化,能预测DCM患者恶性室性心律失常的发生,对评价心功能不全的预后也有一定价值。     

高血压患者TpTe间期的改变及其研究进展

原发性高血压在我国和世界大部分地区都是常见病、多发病,是造成人类死亡的心脑血管疾病之一,长期高血压可引起心肌肥厚,高血压合并心肌肥厚时,心肌缺血、心力衰竭、心律失常甚至心脏猝死(sudden cardiac death,SCD)的发生率增高.心室跨壁复极离散度(transmural dispersion of repolarization,TDR)异常是高血压左心室肥厚(left ventricular hypertrophy,LVH)重要的电生理异常改变之一,TpTe间期(T peak-T end interval)是反映TDR的量化指标.近年研究表明Tp-Te间期对尖端扭转性室性心律失常及Brugada综合征、长短QT间期综合征等所引发的恶性室性心律失常有预测价值[1-3].但关于高血压心脏病与TpTe关系的研究很少.本文就高血压、高血压心脏病患者心电生理学改变、心肌复极离散、TpTe间期的改变及其相关因素综述如下.     

慢性心力衰竭患者QT间期频率依赖性与室性心律失常的关系

目的探索慢性心力衰竭患者QT问期频率依赖性与室性心律失常的关系。方法选31例慢性心力衰竭患者有效病例资料。检测左心室舒张末期内径（LVEDD）、左心室射血分数（LVEF）、QT间期离散度（QTd）、心率变异性（HRV）、QT／RR相关直线的斜率、24h室性早搏（VPB）和非持续性室性心动过速（NSVT）的次数。比较有NSVT和无NSVT患者上述指标的差别,研究上述指标与NSVT的相关性。结果31例心力衰竭患者中,有17例动态心电图记录到NSVT。有NSVT与无NS—VT的患者比较,VPB次数[（5631．2±7218．0）对（285．9±371．7）,P〈0．05],QTe／RR斜率[（0．210±0．049）对（0．161±0．058）,P〈0．05]和QTp／RR斜率[（0．195±0．046）对（0．151±0．041）,P〈0．05]的差异有统计学意义。在全部31例患者中,QTd（r=0．414）、VPB次数（r=0．768）、QTe／RR斜率（r=0．380）、QTp／RR斜率（r=0．433）和NSVT有显著的相关性（P〈0．05）。结论QT间期频率依赖性是反映QT间期动态变化的指标,慢性心力衰竭患者的QT／RR斜率与室性心律失常有较好的相关性,在心脏性猝死的风险评估中有一定价值。     

Tp-e间期与冠心病恶性室性心律失常关系的研究

目的 探讨Tp-e间期与冠心痛恶性室性心律失常的关系.方法 对180例冠心病者分为恶性室性心律失常组(A组,n=42)和非恶性室性心律失常组(B组,n=138),比较两组各导联和12导联平均Tp-e间期、经心率校正的Tp-e(Tp-ec)间期.结果 与B组比较,A组各导联和12导联平均Tp-e间期和Tp-ec间期显著延长,差异有统计学意义(P＜0.05或0.01).结论 Tp-e间期可作为预测冠心病恶性室性心律失常的指标.     

心肌梗塞后诱发室性心动过速(VT)或心室颤动(VF)的电生理特征:心室晚电位与诱发持续性VT所需的配对间期的相关性

本文探讨心梗后心室晚电位与诱发持续性室速或室颤所必需的配对间期的相关性。 对象为83例既往心肌梗塞患者,56例被证实有持续性VT发作史,15例有VF发作史,12例为不明原因晕厥。心室分级程序刺激诱发持续性单形性室速(SMVT)71例(作为VT组),诱发室颤12例(为VF组)。SMVT和VF均在SR-S_2-S_3或S_1-S_2-S-3刺激时诱发。VT组诱发VT和VF所需配对间期之和(SCI)显著长于VF组(485±59对387±36ms,P<0.001),有效不应期与第二配对间期之差小于VF组(-3±40对24±29ms,     

心率变异性及QT间期变异性与急性心肌梗死患者病情严重程度、预后及室性心律失常的关系研究

目的探究心率变异性(HRV)及QT间期变异性(QTV)与急性心肌梗死(AMI)患者病情严重程度、预后及室性心律失常的关系。方法选取2013年1月—2014年9月在首都医科大学附属北京潞河医院心内科住院治疗的AMI患者86例作为AMI组,根据梗死部位分为前壁心肌梗死组45例和非前壁心肌梗死组41例;根据预后分为死亡组39例和存活组47例;根据室性心律失常分级量表分为室性心律失常组42例和非室性心律失常组44例。另选择同期体检正常者73例作为对照组。比较AMI组和对照组受试者、不同亚组AMI患者HRV指标〔时域分析指标:24 h内正常RR间期的标准差(SDNN)、24 h内相邻RR间期差值的均方根(RMSSD)、24 h连续5 min正常RR间期标准差的均值(SDNNIndex),频域分析指标:总频谱成分(TF)、低频成分(LF)、高频成分(HF)、LF/HF比值〕和QTV。结果 AMI组患者SDNN、RMSSD、SDNNIndex、TF、LF、HF及QTV均小于对照组(P<0.05);两组患者LF/HF比值比较,差异无统计学意义(P>0.05)。前壁心肌梗死组患者SDNN、RMSSD、SDNNIndex、TF、LF、HF及QTV小于非前壁心肌梗死组,LF/HF比值大于非前壁心肌梗死组(P<0.05)。死亡组患者SDNN、RMSSD、SDNNIndex、TF、LF、HF及QTV均小于存活组,LF/HF比值大于存活组(P<0.05)。室性心律失常组患者SDNN、RMSSD、SDNNIndex、TF、LF、HF及QTV小于非室性心律失常组,LF/HF比值大于非室性心律失常组(P<0.05)。结论 HRV及QTV与AMI患者病情严重程度、预后及室性心律失常的发生有关,其对病情严重程度、预后及室性心律失常的发生有一定的预测价值。     

犬急性心肌梗塞及再灌注时QTc间期的改变

本文分析了犬急性心肌梗塞前后及再灌注后QTc间期及血浆丙二醛含量的改变。结果表明心肌梗塞后多数犬出现QTc延长及室性心律失常,再灌注后QTc延长更加明显,室性心律失常发生率也明显高于对照组(p<0.05)。血浆丙二醛浓度心肌梗塞前为1.40±0.38n mol/ml,梗塞后为 2.96±0.53n mol/ml,再灌注时达5.07±0.40n mol/ml。相关分析表明血浆丙二醛浓度与QTc间期呈良好正相关(r=0.761,p<0.05)。     

Exploring QT interval changes as a precursor to the onset of ventricular fibrillation/tachycardia

In the present study, we have retrospectively analyzed the corrected QT (QTc) interval before spontaneous episodes of sudden cardiac arrest in patients with a wearable cardioverter defibrillator. Corrected QT interval was measured for all normal beats from 32 recordings of baseline rhythm and compared to normal rhythm before a paired spontaneous cardiac arrhythmia. Before arrhythmia, the QTc (505 ± 73 ms) was not significantly longer than the baseline rhythm (497 ± 73 ms) (P = .23). Considering ventricular tachycardia (VT) events only (12 patients), event QTc (526 ± 75 ms) was not significantly longer than baseline QTc (520 ± 74 ms) (P = .41). Considering fast VT/ventricular fibrillation (VF) events only (20 patients), event QTc (494 ± 70 ms) was not significantly longer than baseline QTc (483 ± 71 ms) (P = .26). The influence of QTc as a measure to indicate an impending VT event in a variety of VT/VF patients remains unclear.     

室性早搏与心室颤动的导管消融治疗的病例选择

室早、室速/室颤常有共同的起源和病理基质,是相互联系与动态演变的统一体。消融与否,不取决于其发病形式,而取决于其病因、症状和预后的严重性。消融方法无固定的模式,应根据病人的具体情况灵活多变,以追求简单、安全、高效和对正常组织损伤最小为原则。目前消融的有效性主要取决于室早/室颤的基础疾病和起源部位。特发与病变局限的室早/室颤,消融效果好,病变广泛或进行性发展的室早/室颤,消融效果有待提高。起源靠近心内膜,尤其是起源于希氏-蒲肯野系统的室早/室颤,容易消融;起源靠近心外膜或心脏的重要结构,如左主干开口,希氏束旁者,消融的难度或风险大。     

Induction of ventricular fibrillation versus monomorphic ventricular tachycardia during programmed stimulation. Role of premature beat conduction delay.

BACKGROUND. Premature stimuli can cause ventricular fibrillation (VF) during electrophysiological testing. The electrophysiological correlations associated with the onset of VF were evaluated in 40 patients who had this rhythm induced during programmed ventricular stimulation. These parameters were compared with those observed in 51 patients who had inducible sustained monomorphic ventricular tachycardia (VT) and 45 patients who had no inducible sustained ventricular tachyarrhythmias. METHODS AND RESULTS. Shortest premature coupling intervals for S2, S3, and S4 at induction of tachycardia or before achieving refractoriness, corresponding conduction latencies (defined as the time from the premature stimulus to the upstroke of the depolarization wave front recorded 35 mm away from the stimulation site), and ventricular activation times (defined as the time from the premature stimulus to the end of the depolarization wave) were compared. The mean coupling intervals were longest in the inducible VT patients: 300 +/- 30, 254 +/- 57, and 228 +/- 32 msec for S2, S3, and S4, respectively. In the inducible VF group, the coupling intervals were 260 +/- 37, 208 +/- 20, and 213 +/- 30 msec. In the group with no inducible VT or VF, these coupling intervals were 251 +/- 24 (p less than 0.01 versus inducible VT group), 209 +/- 27 (p less than 0.001 versus inducible VT group), and 194 +/- 21 msec (p less than 0.05 versus inducible VT and VF groups). The coupling interval of the last premature extrastimulus was above 200 msec in 70% of the patients in whom VF was induced. The largest increases in latency and activation times were recorded in patients in whom VF was induced. The cumulative increase in latency, defined as increased conduction time from baseline, summed for all the premature stimuli was also the greatest at initiation of VF. In contrast, the smallest increases in these parameters were noted in the patients with no inducible VT or VF. Measurements of total activation time yielded similar results as those recorded for latencies. The most important parameters distinguishing the VT patient population from the other two groups were the low ejection fractions and the longer coupling intervals at which VT was induced, whereas in the VF group, the most important discriminating factor was cumulative activation time. Sixty-three percent of the inducible VF patients presented with abnormal hearts (myocardial infarction or cardiomyopathy), whereas 88% of the inducible VT patients had abnormal hearts. In contrast, only 25% of the patients in whom no arrhythmia was induced presented with abnormal hearts. Mean ejection fraction was 32 +/- 15% for the inducible VT group, 45 +/- 13%* for the inducible VF group, and 51 +/- 17%* for patients with no inducible VT/VF (*p less than 0.001 versus VT). CONCLUSIONS. The results suggest that 1) initiation of ventricular tachycardia during programmed ventricular stimulation occurs with minimal conduction latency; 2) because of the large overlap in coupling intervals where VF or VT were induced, a single coupling interval cannot be recommended to adequately separate these groups; and 3) induction of VF was preceded by increased latency and prolongation of the local activation time. These parameters should not be allowed to prolong if VF is to be avoided during programmed stimulation. In addition, 4) the initiation of VF during electrophysiological studies is often associated with the presence of structural heart disease; such structural disease may promote conduction latency and the development of VF.     

Identification of patients at high risk for recurrence of sustained ventricular tachycardia after healing of acute myocardial infarction.

A prognostic index for nonfatal recurrences of ventricular tachycardia (VT) was developed using a retrospective analysis of a group of 206 patients with sustained monomorphic VT or ventricular fibrillation (VF) after healing of acute myocardial infarction. 74 patients (36%) (64 with VT and 10 with VF) had recurrences of sustained monomorphic VT during 3.4 +/- 9 years of follow-up. Three clinical variables were selected and weighted by stepwise logistic discriminant analysis of the study group. They were coded as follows: interval of myocardial infarction to arrhythmia (less than 2 months = 1; 2 to 6 months = 2; greater than 6 months = 3), drug therapy with or without sotalol (with = 1, without = 2), and VT or VF as the presenting arrhythmia (VT = 1, VF = 2). The prognostic index was: 3.41 - (0.56 x interval) - (1.94 x therapy) + (0.86 x arrhythmia). This index was validated prospectively in a test group of 158 consecutive patients with VT or VF after healing of acute myocardial infarction. Patients were allocated into different classes with decreasing prognostic index values associated with increasing risk for recurrences of VT. In the test group, 27 of 158 (17%) patients (22 with VT and 5 with VF) had recurrences of VT (follow-up of 2 +/- 2 years). Two risk classes of patients were identified: high risk for recurrences of VT (61%) corresponding to patients with a negative index; and low risk (4%) consisting of those with a positive index. Thus, using O as the cutoff point, the sensitivity, specificity, and positive and negative predictive values were 81, 89, 62 and 96%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Spatial dispersion of action potential duration restitution kinetics is associated with induction of ventricular tachycardia/fibrillation in humans

INTRODUCTION: Action potential duration restitution (APDR) plays a role in initiation and maintenance of ventricular tachycardia (VT)/ventricular fibrillation (VF). We hypothesized that the steeply sloped APDR and its spatial heterogeneity contribute to VT/VF inducibility in patients with ventricular arrhythmia. METHOD AND RESULTS: After programmed ventricular stimulation (PVS) for evaluation of clinically documented VT, patients (n = 20, 15 male, age 52.5 +/- 9.5 years) were divided into two groups: inducible sustained VT/VF (IVT, n = 10) and noninducible VT/VF (NVT, n = 10). Data were compared with the corresponding results obtained from normal controls (C, n = 10). Right ventricular (RV) monophasic action potential duration at 90% repolarization (APD90) and ventricular effective refractory period (VERP) in the right ventricular apex (RVA) and right ventricular outflow tract (RVOT) were determined. APDR was acquired by scanning diastole with premature ventricular beats during a pacing cycle length of 600 msec (S1-S2) in all patients and by rapid pacing at the cycle lengths that induced APD alternans in three patients. Maximal slopes (Smax) of the APDR curves and DeltaAPD90 (APD90 at S2 400 ms - APD90 at the shortest S2) were measured. VERP and APD90 at each RV site did not differ among the three groups. Smax obtained by S1-S2 (1.6 +/- 0.6) did not differ from Smax obtained by rapid pacing (1.2 +/- 0.7), with a significant correlation noted between these values (r = 0.92, P < 0.01). The IVT group had a higher spatial dispersion of Smax (Smax at RVOT - Smax at RVA) compared to the C group (P < 0.05), with no difference between the NVT group and the IVT or C groups. The IVT group had a higher spatial dispersion of DeltaAPD90 compared to the NVT and C groups (P < 0.01, respectively). Smax at the RVOT (2.7 +/- 1.9) was steeper than that at the RVA (1.9 +/- 1.2, P < 0.05). Inducibility of sustained VT/VF was greater at the RVOT (83.3%) than at the RVA (50.0%, P < 0.05). CONCLUSION: In patients with ventricular arrhythmia, VT/VF is highly inducible under conditions of greater spatial dispersion of ventricular refractoriness and APDR.     

Postextrasystolic Repolarization Abnormalities in ST‐U Segment in Patients with Ventricular Arrhythmias

Background: Changes in U‐wave amplitude after premature ventricular contractions (PVC) are known as prognostic markers in the long QT syndrome dependent on bradycardia. The purpose of the study was to find correlation between postextrasystolic ST‐U segment changes and a history of sustained ventricular tachycardia or ventricular fibrillation (VT/VF). Methods: The ST‐U segment configurations were taken from the 24‐hour ambulatory ECG. The comparison of the morphology of these segments was performed between sinus beats preceding PVC's and first postextrasystolic beats. Population: Two groups of patients were evaluated: 1) 32 patients with VT/VF history (VT/VF group), and 2) 36 patients with potentially malignant arrhythmia (structural heart disease with frequent PVCs and/or nonsustained VT‐nsVT) tnon‐VT/VF group). Results: We found T‐wave changes in 8 patients (25%) from the VT/VF group and in 12 patients (33.3%) from the nonVT/VF group (P = NS) and U‐wave changes in 13 patients (40.6%) and 3 patients (8.3%), respectively (P < 0.05). Other ECG indexes related to PVC's were also considered: RR interval, coupling interval (Cl), prematurity index (Pl), and postextrasystolic pause (PP). The analysis of these ECG indices revealed, when compared with patients without T‐U‐wave changes, that the occurrence of U‐wave changes was significantly related to longer RR interval of the sinus rhythm preceding PVC: 1025 ± 211 vs 918 ± 200 ms (P < 0.05). The prematurity index was lowest in patients with U‐wave changes: 0.54 ± 0.12 vs 0.65 ± 0.16 (P < 0.01) while postextrasystolic pauses leading to the postextrasystolic U‐wave changes were significantly longer: 1383 ± 223 vs 1130 ± 247 ms (P < 0.001). Cl did not differentiate patients: 556 ± 108 vs 584 ± 117 ms (P = NS). Conclusions: Postextrasystolic changes in ST‐U segment configuration are dependent on bradycardia, low prematurity index of the PVC, and the lengthening of the postextrasystolic pause. U‐wave changes more frequently appeared in patients with malignant arrhythmias. Follow‐up study is needed to assess if they might be predictive for the occurrence or reoccurrence of arrhythmic episodes. A.N.E. 2002;7(1):17–21     

Electrophysiologic and antiarrhythmic effects of sotalol in patients with life-threatening ventricular tachyarrhythmias

Sotalol is a unique beta-blocker that lengthens cardiac repolarization and effective refractory period (ERP). Its efficacy after intravenous (1.5 mg/kg) and oral (160 to 480 mg bid) administration was therefore evaluated in 37 patients with refractory recurrent ventricular tachycardia/fibrillation (VT/VF). Thirty-five patients, 33 with inducible VT/VF, underwent electrophysiologic testing. Intravenous sotalol lengthened the ERP in the atrium (+24.6%, p less than .01), atrioventricular node (+24.9%, p less than .01), and ventricle (+14.9%, p less than .01). It also significantly lengthened sinus node recovery time, corrected QT interval (QTc), and the AH interval, but not the HV interval. Sotalol prevented reinduction of VT/VF in 15 patients (45.5%). Twenty-five of the 33 patients (15 with positive results of electrophysiologic tests; 10 with negative results) were given oral sotalol. The drug was ineffective in seven (26.9%) and aggravated arrhythmia in one (3.8%). In four patients sotalol was withdrawn because of side effects; arrhythmias recurred late in two (7.7%). Eleven patients (42.3%) have continued on oral sotalol over a mean follow-up period of 9.2 +/- 8.6 months. Sotalol reduced (n = 21) total premature ventricular complex (PVC) count on the Holter electrocardiogram by 73% (p less than .01), paired PVCs by 89% (p less than .01), and beats of ventricular tachycardia by 95% (p less than .01). In 52% (n = 11), total reduction in PVCs was at least 85%, and incidence of paired and tachycardiac beats was reduced at least 90% (group A). In the remainder (n = 10), PVC suppression was not significant (group B). Group A included nine patients with nonreinducible VT/VF and two in whom it was reinducible; in group B, eight of 10 patients had reinducible VT/VF. The difference between the two groups (Fisher exact test) was significant (p less than .01). The prevention of reinduction of VT/VF by intravenous sotalol and suppression of spontaneously occurring arrhythmias by the oral drug were both predictive of long-term drug efficacy. Sotalol is a significant advance in the short- and long-term management of life-threatening ventricular tachyarrhythmias.