特发性QT间期延长一例

患者女性,22岁,主因晕厥5 min来诊.患者晕厥为上班期间突发性晕厥,晕厥前感胸闷、心慌,不伴有抽搐症状,既往无类似病史.无心脏病、高血压、糖尿病病史.家族史中姐姐曾在18岁时有类似发作史.体格检查:患者神清,面色苍白,双肺呼吸音清,心界不大,心脏听诊心率68 次/min,律齐,未闻及杂音,肝脾未触及,双下肢无浮肿,神经系统体检无异常.入院时心电图检查示:Ⅱ、aVF导联ST段斜直性抬高＞0.05 mV;T波宽大波顶切迹,Tu融合;QT/QTc间期为0.56/0.63 s.

QT间期>PP间期引发尖端扭转性室性心动过速一例

长QT综合征(LQTS)中有时可呈现QT间期＞PP间期现象.此时因复极明显延迟,可导致尖端扭转性室性心动过速(TdP).

Objective To investigate therapeutic action of verapamil on QT prolongation induced by arsenic trioxide (As2O3) in guinea pig and to further explore its possible mechanism. Methods Different doses of As2 O3 was infused intravenously to observe the changes of QT interval on the electrocardiogram (ECG) at different times in guinea pig. Patchclamp technique and laser scanning confocal microscopy were utilized to study the action of As2 O3 on action potential duration (APD),L-type calcium current (ICa-L ), rapid delayed rectifier potassium current (IKr) and intracellular calcium concentration ([Ca2+]i) of guinea pig myocytes. At the same time, verapamil was applied preliminarily to evaluate effects of verapamil on changes of the above index induced by As2O3. Results Intravenous administration of As2 O3 at the dose of 1.6mg/kg and 0.8mg/kg prolonged QT interval on ECG obviously in guinea pig hearts dose dependently and time dependently. QTc (corrected QT interval) was progressively prolonged in the 2-hour period of intravenous infusion of 1.6mg/kg As2O3 from (328.5 ± 30.9)ms of control to (388.4 ± 31.3)ms at 2h following As2O3 ( P ＜ 0.01) .When verapamil was pretreated for 5min, then 1.6mg/kg As2 O3 was added, the results showed that QTe was shorter in verapamil-treatment group (357.3±21.4)ms than that in As2O3 group (388.4±31.3)ms (P＜0.05) at 2h. Confocal experiments showed that in normal Tyrode solution, As2 O3 (1μmol/L and 10μmol/L) had no obvious effects on resting [Ca2+]i (P＞0.05) in guinea pig cardiomyocytes, however, 10μmol/L As2 O3 could markedly enhance [Ca2+]i increase induced by KCl 60mmol/L and the peak value increased from 903.4±369.4 to 1674.6±563.2 ( P＜0.05). The action of elevating [Ca2+]icould be blocked by 10μmol/L verapamil incompletely. The patch-clamp studies indicated that As2 O3 at concentration of 10μmol/L prolonged APD50 from (263.6 -±75.2)ms to (523.9±47.8)ms (P＜0.01) and APD90 from (277.5 ± 77.5)ms to (536.3 ±49.6)ms (P ＜0.01) ,and increased ICa-L from (- 6.0±1.5)pA/pF to (-8.7±2.0)pA/pF (P＜0.01) at 0mV and also reduced IKr from (6.7±1.8)pA/pF to (4.5±1.8)pA/pF (P＜0.05). However, 10μmol/L verapamil could modulate prolonging APD50 from (523.9 ± 47.8) ms to (340.4±83.8) ms ( P＜0.01) and APD90 from (536.3 ±49.6)ms to (348.9 ± 85.5)ms (P＜0.01) and correct increasing Ica-L induced by 10μmol/L As2O3 from (-8.7±2.0)pA/pF to ( - 6.6±1.4)pA/pF (P＜0.05) at 0mV. Conclusion As2O3 could induce prolongation of the QT interval on the ECG in guinea pig hearts and the ionic mechanism is associated with increasing Ica-L and inhibiting IKr/HERG. Verapamil may be useful in normalizing QT prolongation during As2 O3 therapy by decreasing Ica-L and [Ca2+]iof ventricular myocytes in guinea pig.

Lesson Twenty-five Prevalence and Prognostic significance of Short QT Interval

Background-Short-QT syndrome is an inherited disorder characterized by a short QT interval and an increased risk of sudden cardiac death.The clinical significance of a short OT interval observed in a randomly recorded ECG is not known.Therefore,we assessed the prevalence and prognostic significance of a short QT interval in a general population.

Although the correlation between long QT interval and sudden death is established today,very little is known about the electrophysiological and prognostic meaning of a short QT interval1.

心脏NOS1AP基因常见遗传变异与QTc间期及心源性猝死

心肌细胞复极化延长与普通人群中心血管疾病发病率与死亡率的增高密切相关[1].长QT综合征易感基因突变能显著增加患者心源性猝死(sudden cardiac death,SCD)的风险:[2].SCD是发达国家常见死因之一[3].体表心电图心率校正的QT间期(corrected QT interval,QTc间期)是心律失常发生与SCD研究中常用的指标之一[1].QTc 间期延长是SCD的危险因素之一[4].大约35％的QT间期变异具有遗传性[5].