• Journal of Chest Surgery
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• 제25권2호
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• pp.188-193
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• 1992

Life-threatening cardiac arrhythmia is a frequent complication of open heart surgery. There are many causes of postoperative cardiac arrhythmias. Electrolyte imbalance such as hypokalemia and acidemia are major causes of ventricular arrhythmias. Infrequently, however, antiarrhythmic agents and /or hypomagnesemia induce[s] a ventricular arrhythmia such as "torsade de pointes" by increasing the repolarization time of myocardium, Recently, we have experienced two cases of "Torsade de pointes" associated with hyp-omagnesemia after replacement of mitral valve and one of whom after use of procainamide. Intravenous infusion of magnesium immediately and successfully abolished the torsade de pointes in both cases.intes in both cases.

• 생물정신의학
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• 제1권1호
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• pp.124-128
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• 1994

항정신병약물 perphenazine 20mg/day, chlorpromazine 100mg/day. trifluoperazine 15mg/day 등을 투여중인 정신분열증 42세 여자 환자에서 심실성 빈맥의 하나인 torsade de pointes이 나타난 사례를 보고한다. 본 환자는 항정신병약물을 복용하여 오던 중 여러차례 실신과 호흡곤란을 경험하였으며, 심전도상에 QT 간격의 연장과 함께 다양한 모양의 QRS 파를 동반한 심실성 빈맥의 소견이 있어 torsade de pointes을 의심할 수 있었다. 심혈관계에 영향이 적은 항정신병약물인 haloperidol로 바꾼 후 부정맥의 소견이 없다가 퇴원 후 haloperidol을 증량하는 과정에 흉부 불편감, 실신의 증상과 함께 QT 간격의 연장이 다시 발생하여 torsade de pointes이 나타난 원인이 항정신병약물 때문이라는 것을 확인할 수 있었다. 항정신병약물을 사용중인 환자에서 발생하는 급사의 원인으로 심실성 빈맥이 가장 흔하게 제기되고 있다. 따라서 항정신병약물을 처방하는 임상의들은 이에 대한 충분한 지식과 주위가 필요할 것으로 생각된다.

• Journal of Yeungnam Medical Science
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• 제28권1호
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• pp.90-93
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• 2011

Although amiodarone is generally regarded as safe with a low incidence of associated arrhythmias, torsade de pointes (TdP) has been observed usually in the presence of predisposing factors. We report a case of amiodarone-induced TdP after long-term administration of alow dose of oral amiodarone in the absence of predisposing factors.

• The Korean Journal of Physiology and Pharmacology
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• 제6권1호
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• pp.1-7
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• 2002

Congenital Long QT syndrome (LQTs) is a relatively rare pathologic disorder but results frequently in sudden cardiac death. Of the six LQTs that have been clinically described, five have been worked out for their genetic and biophysical profile. Most are generated by mutations which cause a loss of function in two delayed $K^+$ currents, $i_{Ks}\;and\;i_{Kr}.$ One syndrome is generated by mutations in the $Na^+$ channel which causes essentially a gain of function in the channel. Clinically the syndromes are characterized by slowed repolarization of the cardiac ventricular action potential and the occurrence of typical arrhythmias with undulating peaks in the electrocardiogram, called Torsade de Pointes. Arrhythmias are initiated by early or delayed afterdepolarizations and continue as reentry. Triggers for cardiac events are exercise (swimming; LQT1), emotion (arousal; LQT2) and rest/sleep (LQT3). ${\beta}-blockers$ have a high efficacy in the treatment of LQT1 and LQT2. In LQT3 their use is questionable. The study of congenital LQTsyndromes is a remarkable example of how basic and clinical science converge and take profit of each other's contribution.

• The Korean Journal of Pain
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• 제31권1호
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• pp.3-9
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• 2018

Long QT syndrome is a cardiac repolarization disorder and is associated with an increased risk of torsades de pointes. The acquired form is most often attributable to administration of specific medications and/or electrolyte imbalance. This review provides insights into the risk for QT prolongation associated with drugs frequently used in the treatment of chronic pain. In the field of pain medicine all the major drug classes (i.e. NSAIDs, opioids, anticonvulsive and antidepressant drugs, cannabinoids, muscle relaxants) contain agents that increase the risk of QT prolongation. Other substances, not used in the treatment of pain, such as proton pump inhibitors, antiemetics, and diuretics are also associated with long QT syndrome. When the possible benefits of therapy outweigh the associated risks, slow dose titration and electrocardiography monitoring are recommended.

• 대한의용생체공학회:의공학회지
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• 제43권5호
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• pp.331-340
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• 2022

Early afterdepolarization (EAD), a significant cause of fatal ventricular arrhythmias including Torsade de Pointes (TdP) in long QT syndromes, is a depolarizing afterpotential at the plateau or repolarization phase in action potential (AP) profile early before completing one pace. AP duration prolongation is related to EAD but is not necessarily accounted for EAD. Several computational studies suggested EAD can form from an abnormality in the late plateau and/or repolarization phase of AP shape. In this sense, we hypothesized the slope during repolarization has the characteristics to predict TdP risk, mainly focusing on the maximum slope during repolarization (dVm/dt_{max_repol}). This study aimed to predict the sensitivity of dVm/dt_{max_repol} to ion channel conductances as a TdP risk metric through a population simulation considering multiple effects of simultaneous reduction in six ion channel conductances of g_NaL, g_Kr, g_Ks, g_to, g_K1, and g_CaL. Additionally, we verified the availability of dVm/dt_{max_repol} for TdP risk prediction through the correlation analysis with qNet, the representative TdP metric. We performed the population simulations based on the methodology of Gemmel et al. using the human ventricular myocyte model of Dutta et al. Among the sixion channel conductances, dVm/dt_{max_repol} and qNet responded most sensitively to the change in g_Kr, followed by g_NaL. Furthermore, dVm/dt_{max_repol} showed a statistically significant high negative correlation with qNet. The dVm/dt_{max_repol} values were significantly different according to three TdP risk levels of high, intermediate, and low by qNet (p<0.001). In conclusion, we suggested dVm/dt_{max_repol} as a new biomarker metric for TdP risk assessment.

• 한국임상수의학회지
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• 제23권3호
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• pp.329-333
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• 2006

9살령 수컷 져먼 세퍼드종 개가 주기적인 실신 증상으로 내원하였다. 신체 검사, 혈액 생화학 검사 및 진단영상학 검사에서 특별한 이상 소견은 관찰되지 않았다. 실신 직후 실시한 12-lead심전도에서 환견은 심실조기박동을 동반한 악성 심실성 빈맥(torsade depointes)소견이 관찰되었다. Lidocaine정맥주사 후 심실성 부정맥의 빈도수는 감소되었다. 병력과 심전도 검사(event recordings)를 토대로 본 증례를 져먼 세퍼드종의 유전성 심실성 부정맥증으로 진단하였다. 환견은 초기에 sotalol 구강투여로 증상이 개선되었지만 한달 후 특별한 증상 없이 급사하였다. 본 증례는 국내에서 최초로 보고된 유전성 악성 심실성 부정맥증이다.

• 대한의생명과학회지
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• 제16권4호
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• pp.299-305
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• 2010

KCNE1 is the causal gene of long QT syndrome. KCNE1 gene is located in chromosome 21. In compliance with this KCNE1 gene the proteins come out. KCNE1 is responsible for $K^+$ channel which maintains the normal function of the heart muscle for contraction. Affected individuals manifest prolongation of the QT interval on electrocardiongrams, a sign of abnormal cardiac repolarization. The clinical features of LQT result from episodic cardiac arrhythmias, such as torsade de pointes and ventricular fibrllation. Blood DNA was isolated and kept in $4^{\circ}C$ refrigerator. The KCNE1 gene was amplified by PCR method and about 414 bp band was identified by agarose gel electrophoresis. PCR products were inserted into pGEX-4T-1 vector in order to express KCNE1 protein after treatment with IPTG SDS-PAGE was carried out and the protein band which was about 47 kDa was clearly odserved. Results of this study would contribute to the detailed understanding of KCNE1 protein function and to designing better treatment of Long QT symdrome.

• 대한수의학회지
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• 제52권3호
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• pp.163-167
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• 2012

Mosapride stimulated dietary motility was introduced because of the arrhythmogenic effect of cisapride. Cisapride, 5-HT receptor agonist, induces prolongation of QT interval. Additionally, this condition can raise the possibility of acute, "malignant" arrhythmias such as torsade de pointes. It is hard to find any reports about effects of mosapride on cardiac parameters in dogs. By confirming electrocardiogram (ECG) parameters, the surface extremity leads ECG that was obtained from the four-limb electrodes and which was recorded by an ECG recorder after administration of mosapride 3 mg/kg PO b.i.d, and mosapride 3 mg/kg with itraconazole 5 mg/kg PO b.i.d, respectively. QT interval was shortened on the days of 3, 5, and post-day 1 in both mosapride 3 mg/kg administrated group and mosapride with itraconazole group. Heart rate increased significantly. QTc was slightly prolonged in mosapride administration group and mosapride with itraconazole group. However, all dogs of QTc were in normal variation (150~250 msec). Besides, the dogs showed no side effects reported in human medicine during the administration with these drugs. Although mosapride can increase the heart rate, this study suggest that mosapride may be useful for the dogs with disorders of gastrointestinal motility because of no fatal arrhythmogenic effect inspite of administration with itraconazole in dogs.

• 대한의용생체공학회:의공학회지
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• 제42권6호
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• pp.287-294
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• 2021

Cardiotoxicity assessment of all drugs has been performed according to the ICH guidelines since 2005. Non-clinical evaluation S7B has focused on the hERG assay, which has a low specificity problem. The comprehensive in vitro proarrhythmia assay (CiPA) project was initiated to correct this problem, which presented a model for classifying the Torsade de pointes (TdP)-induced risk of drugs as biomarkers calculated through an in silico ventricular model. In this study, we propose a TdP-induced risk group classifier of artificial neural network (ANN)-based. The model was trained with 12 drugs and tested with 16 drugs. The ANN model was performed according to nine features, seven features, five features as an individual ANN model input, and the model with the highest performance was selected and compared with the classification performance of the qNet input logistic regression model. When the five features model was used, the results were AUC 0.93 in the high-risk group, AUC 0.73 in the intermediate-risk group, and 0.92 in the low-risk group. The model's performance using qNet was lower than the ANN model in the high-risk group by 17.6% and in the low-risk group by 29.5%. This study was able to express performance in the three risk groups, and it is a model that solved the problem of low specificity, which is the problem of hERG assay.