• Journal of Dental Anesthesia and Pain Medicine
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• 제17권4호
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• pp.323-327
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• 2017

QT prolongation is an electrocardiographic change that can lead to lethal arrhythmia. Acquired QT prolongation is known to be caused by drugs and electrolyte abnormalities. We report three cases in which the prolonged QT interval was improved at the time of operation by briefly discontinuing the drugs suspected to have caused the QT prolongation observed on preoperative electrocardiography. The QTc of cases 1, 2, and 3 improved from 518 to 429 ms, 463 to 441 ms, and 473 to 443 ms on discontinuing the use of a gastrointestinal prokinetic agent, a proton pump inhibitor, and a molecular targeted drug, respectively. These cases were considered to have drug-induced QT prolongation. We reaffirmed that even drugs administered for conditions unrelated to cardiac diseases can have adverse side effect of QT prolongation. In conclusion, our cases indicate that dental surgeons should be aware of the dangerous and even potentially lethal side effects of QT prolongation. For safe oral and maxillofacial surgery, cooperation with medical departments in various fields is important.

• 대한임상독성학회지
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• 제3권2호
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• pp.135-138
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• 2005

Amisulpride is a newly developed atypical antipsychotic agent effective in treating the positive and negative symptom of schizophrenia. Over-dose of amisulpride can cause hypocalcemia and thus may lead to QT prolongation. We report a case of hypocalcemia and QT prolongation. The QT prolongation was normalized after calcium supplement.

• Neonatal Medicine
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• 제28권1호
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• pp.59-63
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• 2021

An important, albeit rare, cause of fetal bradycardia is long QT syndrome (LQTS). Congenital LQTS is an ion channelopathy caused by mutations in genes encoding cardiac ion channel proteins. Fetal onset of LQTS imposes high risk of life-threatening tachyarrhythmias and sudden cardiac death. Here, we report the case of a female newborn with fetal onset of bradycardia and a 2:1 atrioventricular (AV) block. After birth, a 12-lead electrocardiogram (ECG) revealed bradycardia with QT prolongation of a corrected QT (QTc) interval of 680 ms and pseudo 2:1 AV block. Genetic testing identified a heterozygous Gly402Ser (c.1204G>A) mutation in CACNA1C, confirming the diagnosis of LQTS type 8 (LQT8). The patient received propranolol at a daily dose of 2 mg/kg. Mexiletine was subsequently administered owing to the sustained prolongation of the QT interval and pseudo 2:1 AV block. One week after mexiletine inception, the ECG still showed QT interval prolongation (QTc, 632 ms), but no AV block was observed. There were no life-threatening tachyarrhythmias in a follow-up period of 13 months.

• 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.

• 대한임상독성학회지
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• 제18권2호
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• pp.66-77
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• 2020

Purpose: The aims of the present study were twofold. First, the research investigated the effect of an individual's risk factors and the prevalence of psychotropic drugs on QTc prolongation, TdP (torsades de pointes), and death. Second, the study compared the risk scoring systems (the Mayo Pro-QT risk score and the Tisadale risk score) on QTc prolongation. Methods: The medical records of intoxicated patients who visited the emergency department between March 2010 and February 2019 were reviewed retrospectively. Among 733 patients, the present study included 426 psychotropic drug-intoxicated patients. The patients were categorized according to the QTc value. The known risk factors of QTc prolongation were examined, and the Mayo Pro-QT risk score and the Tisadale risk score were calculated. The analysis was performed using multiple logistic regression, Spearman correlation, and ROC (receiver operating characteristic). Results: The numbers in the mild to moderate group (male: 470≤QTc<500 ms, female: 480≤QTc<500 ms) and severe group (QTc≥500 ms or increase of QTc at least 60ms from baseline, both sex) were 68 and 95, respectively. TdP did not occur, and the only cause of death was aspiration pneumonia. The statically significant risk factors were multidrug intoxications of TCA (tricyclic antidepressant), atypical antipsychotics, an atypical antidepressant, panic disorder, and hypokalemia. The Tisadale risk score was larger than the Mayo Pro-QT risk score. Conclusion: Multiple psychotropic drugs intoxication (TCA, an atypical antidepressant, and atypical antipsychotics), panic disorder, and hypokalemia have been proven to be the main risk factors of QTc prolongation, which require enhanced attention. The present study showed that the Tisadale score had a stronger correlation and predictive accuracy for QTc prolongation than the Mayo Pro-QT score. As a result, the Tisadale risk score is a crucial assessment tool for psychotropic drug-intoxicated patients in a clinical setting.

• The Korean Journal of Pain
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• 제13권1호
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• pp.115-118
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• 2000

Stellate ganglion block is most commonly used in pain clinic because it is an easy procedure and it has broad indications reported that Angina pectoris, tachyarrhythmia and long QT syndrome (LQTS) are indicated. LQTS is a disorder of the abnormalities of cardiac sympathetic innervation and of myocardial repolarization. LQTS is characterized by marked prolongation of the QT interval, often manifestating as syncope, seizures, or sudden death due to polymorphic ventricular tachyarrhythmia known as torsades de pointes. Treatment of symptomatic patients usually begin with beta blocker. The elective treatment of LQTS patients unresponsive to beta blocker is the left cardiac sympathetic denervation. We report a case of LQTS patient who had received stellate ganglion block.

• Biomolecules & Therapeutics
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• 제17권1호
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• pp.1-11
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• 2009

Since the Committee for Proprietary Medicinal Products (CPMP) of the European Union issued in 1997 a "points to consider" document for the assessment of the potential for QT interval prolongation by non-cardiovascular agents to predict drug-induced torsades de pointes (TdP), the QT liability has become the critical safety issue in the development of pharmaceuticals. As TdP is usually linked to delayed cardiac repolarization, international guideline (ICH S7B) has advocated the standard repolarization assays such as in vitro IKr (hERG current) and in vivo QT interval, or in vitro APD (as a follow up) as the best biomarkers for predicting the TdP risk. However, the recent increasing evidence suggests that the currently used above biomarkers and/or assays are not fully predictive for TdP, but also does not address potential new druginduced TdP due to the selective disruption of hERG protein trafficking to the cell membrane or VT and/or VF with QT shortening. There is, therefore, an urgent need for other surrogate markers or assays that can predict the proarrhythmic potential of drug candidate. In this review, we provide an ideal pre-clinical strategy to predict the potentials of QT liability and lethal arrhythmia of the drug candidates with recent issues in this field in mind, not at the expense of discarding therapeutically innovative drugs.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.77.1-77.1
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• 2003

Prolongation of the QT interval may result in a potentially dangerous arrhythmia. The most commonly proposed mechanism for QT interval prolongation(LQT) by pharmaceuticals is inhibition of the rapid delayed rectifier potassium channel (I$\sub$Kr). The LQT potency of pharmaceuticals can be effectively evaluated by examining the effect on human ether-a go-go-related gene (hERG) channels expressed in CHO cells, known to be equal to I$\sub$kr/. We have transfected JERG into CHO cell lines transiently to express high levels of functional hERG channels. (omitted)

• 생물정신의학
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• 제19권1호
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• pp.38-44
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• 2012

Objectives : QT interval prolongation and dispersion known as indicators of an increased risk for ventricular arrhythmias and sudden death have been reported to be prolonged in patients with anorexia nervosa. The aims of this study were to compare conduction abnormalities in Korean patients with anorexia nervosa and bulimia nervosa, and to examine its relation with clinical and laboratory factors. Methods : We retrospectively examined 45 women with anorexia nervosa and 75 women with bulimia nervosa who were assessed by 12-lead electrocardiogram at baseline. QT interval and corrected QT interval, QT dispersion of the difference between the longest and shortest QT intervals, and abnormal U wave were measured for conduction abnormalities. Results : QT interval was significantly longer in patients with anorexia nervosa compared with those with bulimia nervosa. There were no differences in QTc (Corrected QT), QTd (QT dispersion) and abnormal U wave between patients with anorexia nervosa and those with bulimia nervosa. QTd was significantly correlated with the lowest ever lifetime body mass index ($kg/m^2$) as well as the serum amylase level in patients with anorexia nervosa. Conclusions : These results suggest some conduction abnormalities reported in patients with anorexia nervosa are also found in patients with bulimia nervosa. It appears that severity of weight loss and purging behavior could affect the cardiac arrhythmia in patients with eating disorders. Appropriate attention should be paid to cardiac involvement in patients with eating disorders.

• 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.