双腔起搏器不同房室延迟时心功能及QT间期的变化

观察DDD起搏不同房室延迟 (AVD)时心功能与体表心电图QT间期的变化 ,探讨根据心电图QT间期优化AVD的可行性。选择 19例完全性房室阻滞置入DDD永久人工心脏起搏器患者 ,男 10例 ,女 9例 ,年龄 6 6 .79±15 .5 2岁 ,采用彩色多普勒超声心动图测量不同AVD起搏时每搏输出量 (SV)、心排量 (CO)、左室收缩末期内径和舒张末期内径 (LVESd/LVEDd)、左室射血分数 (LVEF)等 ,同时单盲测量不同AVD起搏时 12导联心电图QT间期。心房起搏频率预设为 75次 /分 ,AVD自 90ms起以 30ms步长依次递增至 2 4 0ms。结果 :随着AVD的递增 ,心功能和QT间期随之改善和延长 ,达峰值后又逐渐下降。超声心功能最佳时所对应的AVD与QT间期最长时所对应的AVD无显著差异 (15 8.80± 13.6 4msvs 16 3.30± 30 .4 1ms;P >0 .0 5 ) ;QT间期最长时所对应的心功能各参数与最佳超声心功能各参数相似 (CO :6 .2 9± 1.75L/minvs 6 .5 0± 1.5 4L/min ;SV :87.37± 17.0 9ml/bpmvs91.4 7± 16 .2 5ml/bpm ;LVEF :0 .6 6± 0 .11vs0 .6 7± 0 .11;P均 >0 .0 5 ) ;QT与CO、SV呈显著正相关 (相关系数分别为0 .70 ,0 .6 7,P <0 .0 5 ,0 .0 0 1)。结论 :AVD对心功能有明显影响 ;QT间期随不同AVD时心功能变化而发生变化 ;通过测量体表心电图QT间期可优化     

冠心病心肌缺血QT间期与T波相关性的诊断价值

本研究旨在探讨心电图对冠心病心肌缺血 QT间期与T波的相关性 ,提高对冠心病心肌缺血诊断率。 1993- 0 2～1999- 0 6我院经冠状动脉造影 (CAG)连续的 2 35例患者 ,其中冠状动脉狭窄≥ 75 % :12 8例 ;冠状动脉狭窄 <75 % :10 7例。男 2 10例 ,女 2 5例。平均年龄 5 3.4± 17.0。病程 2 .0±3.6年。剔除了束支与房室传导阻滞、预激综合征、心肌炎、β-受体阻滞剂、胺碘酮及电解质紊乱等影响检测 QT间期结果的病例。双盲法测量 QT间期、T波。除外额面边缘 a VL, 导联及负性 a VR,V1 导联。根据 Bazett公式计算 QTc(ms)=QT/ R- R。根…     

短QT间期的心电图诊断标准探讨

目的用2种已报道的诊断标准研究一组心电图短QT间期者所占比例,并比较2种方法的异同。方法随机选取547例健康人,做常规12导联心电图,准确测量QT间期,根据RR间期(RR)和心率(HR)计算QT间期校正值(QTc)和QT间期预计值(QTp),以QT相似文献   

多普勒超声心动图在双腔心脏起搏最佳房室间期设置中的应用价值

目的 :探讨多普勒超声心动图在双腔心脏起搏最佳房室间期设置中的应用价值。方法 :19例患有完全性房室传导阻滞并植入永久性双腔心脏起搏器的患者 ,程控房室间期从 90ms逐渐递增至 2 5 0ms ,每次递增量 2 0ms ,脉冲多普勒测量不同房室间期时每搏量和二尖瓣血流频谱的变化。结果 :每搏量最大时的最佳房室间期为 (16 8.9± 15 .6 )ms ,二尖瓣血流频谱的A波终末与二尖瓣叶完全关闭信号同步时的房室间期为 (178.4±2 3.4 )ms ,两者之间存在良好的线性回归关系 (Y =86 .2± 0 .5X ,r =0 .70 ,SEE =11.5 ,P <0 .0 1)。结论 :多普勒超声可以对双腔心脏起搏时的最佳房室间期作出准确地选择 ,并且具有无创、可重复和简便易行的特点。     

依那普利对高血压病左心室肥厚患者QT离散度的影响

目的　研究长期使用依那普利治疗高血压病合并左心室肥厚时对QT离散度的影响。方法　 2 4例高血压病 (EH)合并左心室肥厚 (LVH)者 ,服用依那普利 (10mg 1次 /d) 3年 ,用标准 12导联心电图测量QT间期、校正的QT间期 (QTc)、QT间期离散度 (QTd)及校正的QT间期离散度 (QTcd) ;用二维及M型超声心动测定有关心血管参数。结果　依那普利不仅能迅速降压 ,而且能逐渐降低左心室重量指数 (LVMI)达 3 9% (P <0 .0 0 1) ,显著提高左心室泵血功能 ;同时明显缩短QTd[从 (61± 2 1)到 (41± 15 )ms、QTcd从 (67± 2 7)到 (46± 18)ms] ,QT及QTc也同样明显缩短。结论　长期用依那普利治疗EH合并LVH ,能明显使患者左心室肥厚回缩 ,提高其左心室收缩功能 ,并通过降低QTd及QTcd ,进一步降低室性心律失常发生率 ,从而改善预后。     

典型心房扑动消融术后峡部时间间期的变化预测双向阻滞的价值

通过比较心房扑动 (简称房扑 )成功消融前后右心房峡部时间间期 ,分析峡部时间间期的延长程度对峡部完全性双向阻滞的预测价值。选择 1996～ 2 0 0 2年在我院行射频消融治疗的典型房扑患者 30例 ,男 2 3例、女 7例 ,年龄 4 7.85± 9.35岁 ,采用解剖和影像定位法 ,在冠状静脉窦口持续起搏下消融峡部。结果 :2 9例消融成功 ,达到双向传导阻滞的标准 ,成功率 96 .6 7%。消融后起搏信号至右房下侧壁的时间间期 (SAH1 2 )和起搏信号至冠状窦口CS3 4的时间间期明显延长 (14 0 .4 7± 2 0 .4 8msvs73.82± 13.0 1ms ;138.17± 15 .5 5msvs77.6 3± 8.36ms ,P <0 .0 0 0 1)。 2 9例中有 17例在完全性传导阻滞前可以记录到不完全性传导阻滞 ,峡部不完全性传导阻滞时SAH1 2 比术前增加 4 5 .4 9%± 8.7%。消融前后右心房峡部传导时间间期增加≥ 5 0 % ,预测峡部完全性双向传导阻滞的灵敏度 10 0 % ,特异度 83.3%。结论 :右心房峡部传导时间间期的定量分析是判断峡部完全性双向传导阻滞的有价值的方法。     

心房颤动患者体表心电图QT间期的变化

探讨心房颤动(简称房颤)患者体表心电图QT间期的变化。入选81例房颤患者和71例对照者,测量Ⅰ导联和V2导联QT间期,根据Bazett公式计算QTc。结果:窦性心律时V2导联QT间期可测量性略高于Ⅰ导联,而房颤时相反。V2导联测得的QTc比Ⅰ导联长。房颤组与对照组比较,窦性心律时Ⅰ导联和V2导联的QTc两组间均无明显差异;房颤发作时Ⅰ导联QTc较对照组延长(429.01±43.08msvs408.50±31.93ms,P<0.05);V2导联QTc较对照组也延长(444.45±33.16msvs414.82±25.57ms,P<0.05)。房颤组房颤发作时与窦性心律时的自身对照比较,V2导联的QTc也延长(448.63±31.59msvs426.22±29.08ms,P<0.05)。结论:房颤患者在房颤发作时QTc延长,而房颤患者窦性心律时QTc与对照组无差异。     

长QT综合征伴尖端扭转性室性心动过速一例

患者女性 ,2 9岁。 1991年起曾多次发作晕厥、头痛、恶心、呕吐症状。曾误诊为“癫痫、病毒性脑炎”。 1998年症状发作时心电图证实为长QT综合征。发作时血钾偏低 ,服用心得安可预防症状发生。其祖父、父亲QT间期分别为 5 2 0 ,5 40ms ,均有周期性双下肢瘫痪病史。其弟、姐QTc间期分别为 470 ,42 0ms,其姐有头晕病史 (发作时QTc 460ms)。     

Tp-e/QT比值、低钾对扩张型心肌病患者室性心律失常的影响陈小贞 闫继锋 于运福 闫瑞 杨鹏伟作者单位:450008 河南省胸科医院心六科,郑州市纬五路1号通讯作者:陈小贞, 主治医师, 硕士, 心脏电生理的研究 E-mail:meilidechenxz@163.com 电话13525515104

目的：通过观察扩张型心脏病的临床特点并且寻找室性心律失常发生的相关因素。 方法：将扩张型心肌病患者162 分为室性心律失常组(VA组)和非室性心律失常组(NVA 组),低钾组及血钾正常组,分析其临床特点并观察超声指标及心电图V3 和V4 导联的Tp-e 间期和Tp-e/QT比值的差异,分析其临床意义。结果：VA组左室舒张末期内径(LVEDD)较NVA组大(72.88±6.81mm vs 62.67±4.91mm,P<0．05)；左室射血分数(LVEF)VA组较NVA组低(0.24±0.04 vs 0.32±0.05,P<0．05)；NA组Ｖ3 和Ｖ4 导联 Ｔp-e /QT比值均值(0.268±0.050 vs 0.216±0.016, P<0．05)均比NVA组大；低钾组Ｖ3 和Ｖ4 导联 Ｔp-e /QT比值的均值(0.291±0.047 vs 0.260±0.048, P<0．05)均比血钾正常组大；随着Ｔp-e /QT比值的增加多形性室速更易发生。结论：跨膜复极离散度增大是室性心律失常发生的重要原因,Ｔp-e /QT可以反应复极离散度,有望通过Ｔp-e /QT比值预测扩张型心肌病患者室速发生的风险,扩张型心肌病患者通过心脏彩超、心电图、电解质等指标可进行危险分层。     

先天性长QT综合征20个家系187例的调查与研究

目的调查与研究先天性长QT综合征(longQTsyndrome,LQTS)的遗传特点及家系图谱分析,LQTS的心电图分型、诊断以及治疗.方法应用惠普12导联心电图机对先证者及其家庭成员分别记录6导联及12导联常规体表心电图,对先证者行24h动态心电图检查,分别测量Ⅱ、V2导联的QT、QTc以及QTd.先证者及家族中有症状的患者给予普萘洛尔2～3mg/kg,每日3次治疗.结果187个家庭成员中有31例为LQTS患者,男性11例,女性20例.其中LQT118例,LQT212例,LQT31例.QT间期为(0.57±0.08)s,QTc为(0.58±0.08)s,QTd为(0.16±0.03)s.除1例应用阿托品治疗有效,6例猝死外,其余24例(77.4%)患者应用普萘洛尔治疗有效.无症状的QTc延长者56例,男性23例,女性33例,LQT122例,LQT234例.QT间期为(0.47±0.09)s,QTc为(0.52±0.07)s,QTd为(0.08±0.03)s,有症状组与无症状组相比有统计学意义.家系图谱分析符合常染色体显性遗传规律.结论12导联体表心电图是LQTS常用的最简单的检查方法,心电图对LQTS的临床分型基本准确可靠.普萘洛尔是预防LQTS患者猝死的有效药物.     

“Torsades de pointes” and atrioventricular block

In order to elucidate the trigger factor of the production of torsades de pointes (TdP), electrophysiological study was conducted in 15 patients with atrioventricular (AV) block; 6 with TdP (TdP group) and 9 without TdP (control group). In the TdP group, all had an episode of syncope and frequent ventricular premature beats (VPBs) on routine ECG, while four (44%) had syncope and three (33%) had VPBs in the control group. Aging, QRS width, ventricular cycle length, QT interval, and block site from His bundle electrogram were similar in both groups, however the QT_c interval was significantly (p<0.01) longer in the TdP group than in the control group (580±112 vs. 459±37, respectively). Furthermore, four patients (67%) in the TdP group showed advanced AV block in which a slow ventricular rate and an irregular rhythm were characteristic, whereas only one control (11%) showed advanced AV block and all other control patients (89%) had complete AV block. These data indicate that patients with advanced atrioventricular block associated with prolonged QT_c interval and frequent ventricular premature beats might induce torsades de pointes.     

Acquired long QT interval: a case series of multifactorial QT prolongation

Background:

Acquired long QT (LQT) interval is thought to be a consequence of drug therapy and electrolyte disturbances.

Hypothesis:

We characterize the potential effects of polypharmacy in a case series of acquired LQT and torsades de pointes (TdP) in order to determine whether multiple risk factors play a role in the development of LQT.

Methods:

The case series consisted of 11 patients presenting to 4 tertiary care hospitals with LQT and ≥2 risk factors for developing LQT. Clinical characteristics, medications, electrolyte disturbances, and course in hospital were analyzed.

Results:

Mean age was 49.1 ± 5.8 years. Eight patients were female. Four had hypertension, 1 had a history of dilated cardiomyopathy, and 1 patient demonstrated complete atrioventricular block. Average QTc interval at presentation was 633.8 ± 29.2 ms. Nine patients developed TdP. In 3, LQT was not initially detected and amiodarone was administered, followed by development of TdP. Patients were taking an average of 2.8 ± 0.3 QT‐prolonging medications—an antidepressant in 6 cases and a diuretic in 8 cases. All patients had an electrolyte abnormality; 8 patients presented with severe hypokalemia (<3.0 mmol/L). Average serum potassium and magnesium were 2.82 ± 0.10 mmol/L and 0.75 ± 0.03 mmol/L, respectively. There were no deaths.

Conclusions:

This case series highlights the risks of polypharmacy in the development of LQT and TdP. It illustrates the importance of early detection of LQT in patients with multiple risk factors in ensuring appropriate treatment. © 2011 Wiley Periodicals, Inc. The authors have no funding, financial relationships, or conflicts of interest to disclose.     

Bradycardia-induced abnormal QT prolongation in patients with complete atrioventricular block with torsades de pointes.

Fourteen patients with complete atrioventricular block with or without torsades de pointes (TdP) were included in this study. They were divided into 2 groups, 6 patients with TdP (TdP[+] group) and 8 patients without TdP (TdP[-] group). The patients were evaluated at 2 different periods, before (acute period) and after (chronic period) pacemaker implantation. In the acute period, the QRS and heart rate during the escape rhythm were not significantly different between the 2 groups; however, the QT and QTc intervals were significantly longer in the TdP(+) group than in the TdP(-) group: 753 +/- 57.5 vs 635 +/- 78.4 ms (p less than 0.01) and 585 +/- 44.8 vs 476 +/- 58.3 ms (p less than 0.01). In the chronic period (greater than 2 months after pacemaker implantation), we changed the pacemaker rate from 90 or 100 beats/min to 50 beats/min and examined the QT interval changes in relation to the heart rate. The QT interval in the TdP(+) group was significantly prolonged compared with the TdP(-) group when the pacing rate was decreased less than or equal to 60 beats/min: 551 +/- 40 vs 503 +/- 36 ms at 60 beats/min (p less than 0.05), and 700 +/- 46 vs 529 +/- 43 ms at 50 beats/min (p less than 0.001). Patients with complete atrioventricular block with TdP had a bradycardia-sensitive repolarization abnormality and this characteristic remained after pacemaker implantation. The critical heart rate that induced abnormal QT prolongation in the TdP(+) group was less than or equal to 60 beats/min.     

The morphology of the QT interval predicts torsade de pointes during acquired bradyarrhythmias.

OBJECTIVES: The purpose of this study was to define the electrocardiographic (ECG) predictors of torsade de pointes (TdP) during acquired bradyarrhythmias. BACKGROUND: Complete atrioventricular block (CAVB) might lead to downregulation of potassium channels, QT interval prolongation, and TdP. Because potassium-channel malfunction causes characteristic T-wave abnormalities in the congenital long QT syndrome (LQTS), we reasoned that T-wave abnormalities like those described in the congenital LQTS would identify patients at risk for TdP during acquired bradyarrhythmias. METHODS: In a case-control study, we compared 30 cases of bradyarrhythmias complicated by TdP with 113 cases of uncomplicated bradyarrhythmias. On the basis of the criteria used for the congenital LQTS, T waves were defined as LQT1-like (long QT interval with broad T waves), LQT2-like (notched T waves), and LQT3-like (small and late) T waves. RESULTS: Neither the ventricular rate nor the QRS width at the time of worst bradyarrhythmia predicted the risk of TdP. However, the QT, corrected QT (QTc), and T(peak)-T(end) intervals correlated with the risk of TdP. The best single discriminator was a T(peak)-T(end) of 117 ms. LQT1-like and LQT3-like morphologies were rare during bradyarrhythmias. In contrast, LQT2-like "notched T waves" were observed in 55% of patients with TdP but in only 3% of patients with uncomplicated bradyarrhythmias (p < 0.001). A 2-step model based on QT duration and the presence of LQT2-like T waves identified patients at risk for TdP with a positive predictive value of 84%. CONCLUSIONS: Prolonged QT interval, QTc interval, and T(peak)-T(end) correlate with increased risk for TdP during acquired bradyarrhythmias, particularly when accompanied by LQT2-like notched T waves.     

Increased Propensity of Women to Develop Torsades de Pointes During Complete Heart Block

TdP and Complete Heart Block. Introduction : To determine whether an increased female gender susceptibility to torsades de pointes (TdP) may exist in a clinical model of bradycardia- induced long QT syndrome, we investigated reported cases of TdP associated with acquired complete heart block.
Methods and Results : Seventy-two cases reported in the medical literature dating from 1941 through 1993 were identified, all describing TdP or "transient ventricular tachycardia/fibrillation" (to include those cases reported prior to the use of TdP terminology) in the setting of acquired complete heart block unassociated with QT prolonging drugs. Expected female prevalence in complete heart block was estimated at 52%, based on projections derived from 206,016 hospital discharges in the National Inpatient Profile (Commission on Professional and Hospital Activities, Ann Arbor, MI), over the years 1985 through 1992. During complete heart block, mean heart rate was 37 beats/min in both sexes (combined n = 43), and absolute QT interval ranged from 0.52 to 0.88 seconds, with a mean of 0.68 seconds (n = 25). Female prevalence among patients with TdP during complete heart block was greater than expected: 72% for all studied cases (P < 0.001); 70% (P < 0.04) and 74% (P < 0.02) among those reported prior to (n = 35) and during or alter (n = 37) 1980, respectively; 73% (P < 0.03) among those with documented normokalemia (n = 26); and 68% (P = 0.2) among those with a prolonged QT interval and known polymorphic VT (i.e., unequivocal TdP; n = 25).
Conclusion : Despite inherent limitations of this retrospective study, the data are consistent in suggesting a greater than expected female prevalence among patients with TdP related to complete heart block. This finding lends support to a broadening concept of increased susceptibility of women to the development of TdP in various settings of QT prolongation.     

Beta-blocker decreases the increase in QT dispersion and transmural dispersion of repolarization induced by bepridil.

Bepridil is effective for intractable cardiac arrhythmia, but in rare cases will induce torsades de pointes (TdP) associated with QT interval prolongation. Beta-blockers will effectively prevent TdP in some clinical settings, so the effect of beta-blocker on the change in QT interval, QT dispersion and transmural dispersion of repolarization (TDR) induced by bepridil was investigated in 10 patients (7 male, 3 female; 62+/-6 years old) with intractable paroxysmal atrial fibrillation. The QTc interval, QTc dispersion and TDR were measured before and after 1 month of administration of bepridil, and then a beta-blocker was added and the QTc interval, QTc dispersion and TDR re-measured 1 month later. Bepridil significantly prolonged the QTc interval (0.42+/-0.05 to 0.50+/-0.08; p<0.01), and increased both the QT dispersion (0.07+/-0.05 to 0.14+/-0.08; p<0.01) and TDR (0.10+/-0.04 to 0.16+/-0.05; p<0.01). The addition of a beta-blocker decreased the QTc interval (0.50+/-0.08 to 0.47+/-0.04; p=0.09) and significantly decreased both the QTc dispersion (0.14 +/-0.08 to 0.06+/-0.02; p<0.01) and TDR (0.16+/-0.05 to 0.11+/-0.04; p<0.001). Compared with the control, the combination therapy significantly prolonged the QTc interval, but did not increase either QTc dispersion or TDR, and so was effective in all patients with intractable AF. The findings suggest that beta-blocker reduces the increase in QT dispersion and TDR induced by bepridil, and combined therapy with bepridil and beta-blocker might thus be useful for intractable atrial fibrillation.     

Beat-to-beat variability of QT intervals is increased in patients with drug-induced long-QT syndrome: a case control pilot study.

AIMS: Torsades de pointes arrhythmias (TdP) occur by definition in the setting of prolonged QT intervals. Animal models of drug induced Long-QT syndrome (dLQTS) have shown higher predictive value for proarrhythmia with beat-to-beat variability of repolarization duration (BVR) when compared with QT intervals. Here, we evaluate variability of QT intervals in patients with a history of drug-induced long QT syndrome (dLQTS) and TdP in absence of a mutation in any of the major LQTS genes. METHODS AND RESULTS: Twenty patients with documented TdP under drugs with QT-prolonging potential were compared with 20 matched control individuals. An observer blinded to diagnosis manually measured lead-II, RR, and QT intervals from 30 consecutive beats. BVR was determined from Poincaré plots of QT intervals as short-term variability (STV(QT) = Sigma|QT(n)(+1) - QT(n)|/[30 x radical2]). QRS interval and cycle length was comparable between study groups and controls. No difference was found in QTc between dLQTS and controls (428 +/- 25 vs. 421 +/- 34 ms, P = 0.26), whereas STV(QT) was significantly higher in dLQTS when compared with controls (8.1 +/- 3.7 vs. 3.6 +/- 1.3 ms, P = 0.001). Proarrhythmic predictive power of STV(QT) was superior to that of the QTc interval (AUC: 0.89 vs. 0.57, 95% CI: 0.79-0.99 vs. 0.39-0.75). CONCLUSION: In the absence of QTc prolongation, baseline STV(QT) characterized patients with documented drug-induced proarrhythmia. STV(QT) could prove to be a useful non-invasive, easily obtainable parameter aiding the identification of the patient at risk for potentially life threatening arrhythmia in the context of drugs with QT prolonging potential.     

Takotsubo cardiomyopathy and QT interval prolongation: who are the patients at risk for torsades de pointes?

Objectives

QT interval prolongation is prevalent among patients with Takotsubo cardiomyopathy (TC), whereas torsades de pointes (TdP) has rarely been reported in these patients. We studied all peer-reviewed reports on TC-associated QT interval prolongation and all peer-reviewed reports on TC-associated TdP to characterize the clinical circumstances leading to TdP in patients with TC.

Methods

The literature search yielded 14 reports on TC-associated TdP and 26 reports on TC-associated QT interval prolongation. Overall, 15 patients with TC-associated TdP and 86 patients with TC-associated QT interval prolongation were reported. We systematically reviewed each report and recorded the risk factors for TdP as well as the clinical circumstances of TC.

Results

The prevalence of the male sex was higher among patients with TC-associated TdP relative to patients with TC-associated QT interval prolongation (26.7% vs 5.8%; P = .01). There was a trend in the mean maximal corrected QT interval being longer among patients with TC-associated TdP relative to patients with TC-associated QT interval prolongation (679.9 ± 230.6 vs 555.9 ± 63.8 milliseconds; P = .06). There were no differences between patients with TC-associated TdP and patients with TC-associated QT interval prolongation in mean age, maximal troponin levels, and lowest ejection fraction. Overall, 12 (80.0%) patients with TC-associated TdP had risk factors for TdP other than the female sex and systolic dysfunction, including suspicion of congenital long QT syndrome, bradycardia, hypokalemia, recent conversion from atrial fibrillation to sinus rhythm, and using QT prolonging agents.

Conclusions

Men with TC-associated QT interval prolongation are at risk for TdP. Most patients with TC-associated TdP have risk factors for TdP other than the female sex and systolic dysfunction.