高血压病左室肥厚与QTc离散度关系的研究

目的 探讨高血压病病左室肥厚（ＬＶＨ）与非在室肥厚（ＮＬＶＨ）患者ＱＴｃｄ的关系及临床意义。方法 用分层抽样法测定１０３例原发性高血压病患者住院首次１２导联心电图ＱＴｃ离散度（ＱＴｃｄ）其中合并ＬＶＨ患者５７例，合并ＮＬＶＨ患者４６例，并与２０例健康人作对照，结果 ＱＴｃｄＬＶＨ组分别与ＮＬＶＨ组，对照组比较均有非常显著性差异（Ｐ〈０．０１）ＮＬＶＨ组与对照组比较无显著性差异（Ｐ〉０．０５）。结论     

围绝经期及其前后妇女QTcd离散度的研究

目的探讨绝经后妇女冠心病及心血管事件发生率升高的相关机制.方法分别测量42例围绝经期前健康妇女(Ⅰ组,平均年龄41.40±0.92岁)、43例围绝经期健康妇女(Ⅱ组,平均年龄45.5±4.32岁)、40例绝经后健康妇女(Ⅲ组,平均年龄51.45±7.26岁)的校正QT离散度(QTcd)和性激素(SH)水平,研究其变化规律和相互关系.结果绝经后妇女的QTcd与围绝经期前妇女的QTcd相比略有延长,尚无显著性差异;而围绝经期妇女的QTcd与围绝经期前妇女的QTcd相比延长明显,有显著性差异.结论围绝经期妇女SH紊乱导致心肌电不稳定性增高,是除了脂代谢异常之外的导致冠心病发病率升高及心血管事件发生率升高的机制之一.     

QT and RR intervals in conscious and anesthetized guinea pigs with highly varying RR intervals and given QTc-lengthening test articles.

A facile system for obtaining electrocardiograms from conscious animals was used to conduct studies on 12 animals studied both conscious and anesthetized, on 4 conscious animals given vehicle (0.5% methylcellulose) and QT-lengthening test articles, and on 6 animals given test articles thought to not lengthen QTc. In 12 animals whose ECGs were monitored via a bipolar transthoracic ECG, heart rates were slowed with 1.0 mg/kg zatebradine, while they were conscious in their slings, and after being anesthetized with ketamine/xylazine. The following regression equations were obtained relating QT to RR: QT = 44.7 ln RR - 132.9, r2 = 0.7, for conscious animals; QT = 79.4 ln RR - 287.4, r2 = 0.8 for anesthetized animals, with RR intervals varying between 150 and 550 ms. The anesthetic increases QT at all RR intervals (p < 0.001), but does not change the slope of the relationship between QT and RR when compared with the conscious guinea pig. The Fridericia method was best for correcting QT for RR interval in conscious guinea pigs, but the Bazett method was best for correcting in anesthetized animals. QTc lengthened significantly in all conscious guinea pigs given, orally, cisapride, ketoconazole, and sotalol (positive test articles) and did not change with methylcellulose (the vehicle) or with propranolol, verapamil, or enalapril (negative controls). These techniques and relationships demonstrate that this methodology may be useful in exploring torsadogenic effects of novel pharmacological entities.     

我院住院患者应用胺碘酮对QTc间期的影响

摘 要 目的:评估胺碘酮对住院患者QT/ QTc间期的影响及药品不良反应。方法：纳入2014年1～6月上海浦东新区公利医院心内科使用胺碘酮的住院患者共59例,记录患者一般情况和合并用药等信息,观察应用胺碘酮注射液或胺碘酮片剂后心率、QT间期、QTc间期的变化,以及在用药期间发生药品不良反应。结果：用药后患者的平均心率、QT间期和QTc间期较用药前显著减慢(P<0.01)。59例患者中,12例用药后QTc＞500 ms,5例患者用药后△QTc＞50 ms且 QTc＜500 ms。研究中,共有8例合并使用一种或多种可延长QT间期的药物,包括左氧氟沙星（4例）,阿奇霉素（3例）,氟哌噻吨美利曲辛（1例）,多潘立酮（1例）。32例应用胺碘酮注射液患者中有3例发生注射部位反应,用药中未出现与胺碘酮相关的心律失常[包括尖端扭转性室速(Tdp）]。结论：住院患者应用胺碘酮后QT间期、QTc间期均会不同程度延长,对于用药后QTc＞500 ms、△QTc＞50 ms或合并使用其他可延长QT间期药物的患者,Tdp发生风险增加,应及时调整胺碘酮用药方案并严密监测心电图,避免恶性心律失常事件的发生。     

QT延长与高血压合并心房颤动导管射频消融术后复发的相关性分析

目的 探讨高血压合并阵发性心房颤动患者的QTc是否与心房颤动导管射频消融术后复发相关.方法 回顾性分析201 1年1月至2012年12月在北京安贞医院第1次行导管射频消融术的高血压合并阵发性心房颤动心功能正常患者242例,将纳入患者按疾病复发情况分为复发组（98例）和未复发组（144例）,收集术前心电图和其他临床资料,术后定期随访.结果 随访（17±9）个月,98例患者（40.0％）心房颤动导管消融术后复发.与未复发组相比,复发组QTc明显延长[（429±26） ms比（419 ±23） ms]（P=0.004）.复发组的左心房前后径较未复发组明显增大[（41±6）mm比（38±5）mm]（P=0.003）.QTc与心率存在明显的相关性（r=0.162,P=0.011）.长QTc组（n=53）的导管消融术后心房颤动复发率明显较正常QTc组（n=165）和短QTC组（n=24）高（P =0.001、P=0.069）;左心房直径＜38.3 mm组与左心房直径≥38.3 mm组消融术后心房颤动复发率比较,左心房增大与导管消融术后复发相关（P=0.017）.多因素Cox回归分析表明QTc和左心房前后径是心房颤动复发的独立危险因素（QTc：风险比=2.361,95％置信区间：1.353 ～4.121,P=0.003;左心房前后径：风险比=1.795,95％置信区间：1.041 ～3.094,P=0.035）.长QT患者心房颤动复发的风险比为2.361（95％置信区间：1.353 ～4.121,P=0.003）.与左心房前后径单独预测术后复发相比,左心房前后径和QTc联合能更好地预测心房颤动导管消融术后复发.结论 QT延长是高血压合并心房颤动导管消融复发的独立危险因素.     

心率变异及QTc间期与2型糖尿病慢性并发症的相关分析

目的观测2型糖尿病有、无慢性并发症及其心率变异（HRV）、QTc间期的变化。方法2型糖尿病患者79例,根据临床检查区分各并发症,分为无并发症组（I组17例）、冠心病组（Ⅱ组17例）、糖尿病肾病组（Ⅲ组15例）、糖尿病周围神经病变组（IV组17例）及多种并发症组（V组13例）进行24h动态心电图HRV分析及标准12导联心电图记录QTc间期。结果①2型糖尿病慢性并发症组QTe均〉0．44S,且以冠心病组最为显效,但各组间比较差异无统计学意义（P〉0．05）。②2型糖尿病慢性并发症组其HRV时域及频域指标明显低于无并发症组（P〉0,01）。结论2型糖尿病各种慢性并发症组其QTc间期延长、HRV下降,尤其在冠心病组中更为显著,提示该组存在潜在的高猝死风险。     

Prevalence and Risk Factors of Prolonged QTc Interval in HIV-Infected Patients: Results of the HIV-HEART Study

Abstract

Background: Corrected QT (QTc) prolongation is predictive of cardiovascular mortality in both the general and human immunodeficiency virus (HIV) populations. Objective: As part of the HIV-HEART study, we assessed the prevalence and risk factors of a prolonged QTc interval in patients with HIV infection. Methods: In this cross-sectional cohort study, 802 unselected HIV-infected patients were included. Data were analyzed by the use of gender-specific QTc categories (men abnormal at > 440 ms and women abnormal at >460 ms). Multiple variables related to infection and treatment were collected. Results were analyzed with a multivariable model. Results: The QTc interval was found to be prolonged in 154 patients (19.8%; 95% CI 17–23). The mean (±SD) QTc in men (n = 142) presenting with a prolonged QTc interval was 456 ± 16.3 ms (range 441–548 ms).The mean (±SD) QTc in women (n = 12) presenting with a prolonged QTc interval was 479 ± 9 ms (range 465–498 ms). In the multivariable model, female gender, diabetes mellitus, and arterial hypertension were associated with prolonged QTc. There were no parameters related to HIV independently associated with QT interval prolongation. In particular, no anti-HIV drug was associated with QTc prolongation. Conclusions: Our study demonstrated that in an HIV-infected population, QTc prolongation had a high prevalence of nearly 20% compared to the general population and was possibly influenced by common factors like gender, diabetes, and arterial hypertension.     

Clinical and therapeutic aspects of congenital and acquired long QT syndrome.

The long QT syndrome is characterized by prolongation of the corrected QT (QTc) interval on the surface electrocardiogram. It is associated with precipitation of a polymorphic ventricular tachycardia, torsade de pointes, which may cause sudden death. The syndrome is a disorder of cardiac repolarization caused by the alterations in the transmembrane potassium and sodium currents. Six genetic loci for the congenital forms of the syndrome have been identified; sporadic cases occur because of spontaneous mutations. Acquired causes of the long QT syndrome include drugs, electrolyte imbalance, toxins, marked bradycardia, subarachnoid hemorrhage, stroke, myocardial ischemia, protein-sparing fasting, autonomic neuropathy, and human immunodeficiency virus disease. Clinical symptoms are the result of the precipitation of torsade de pointes and range from such minor symptoms as dizziness to syncope and sudden death. Short-term treatment is aimed at preventing the recurrences of torsade de pointes and includes intravenous magnesium and potassium administration, temporary cardiac pacing, and correction of electrolyte imbalance; rarely, intravenous isoproterenol is indicated. Long-term management includes use of beta-blockers, permanent pacemaker placement, and cardioverter-defibrillator implantation. Asymptomatic patients are treated if under the age of 40 years at the time of diagnosis.