• Journal of Yeungnam Medical Science
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• v.8 no.2
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• pp.52-62
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• 1991

The toxic effect of azalea extract, expecially on cardiovascular system, is relatively unclear. The purpose of this study is to study the possible underlying mechanism and effect of toxic ingredient of azalea on cardiovascular system. The 71 healthy rabbits were divided into 10 groups : In group as preliminary study ; 4cc of normal saline was administered intravenously(N) ; 0.7gm/kg and 1.0gm/kg of azalea extract was administered respectively in the same route, volume(A1, A2) ; atropine was administered intravenously(A) ; after pretreatment with atropine(0.04mg/kg) to block parasympathetic system, azalea extract was injected like the above groups(AA1, AA2) ; normal saline, 0.7gm/kg and 1.0gm/kg of azalea extract were administered respectively with 0.2cc(1 : 1000) epinephrine(E0,E1,E2). We measured the following indices at I minute interval during first 10 minutes and then 10 minute interval during next 30 minutes : RR interval, QTc interval, maximal systolic and diastolic pressure drop with occuring time and presence of significant arrhythmia. The results were as follows : 1. The changes of RR interval, QTc interval were significantly increased in groups by Azalea extract. The blood pressure change was significantly decreased in groups by Azalea extract. There were no significant differences according to dosage of Azalea extract. 2. The changes of RR interval, blood pressure were significant differences between administration of atropine and Azalea extract after pretreatment with atropine, but not in the change of QTc interval. 3. There were no significant differences in the change of RR interval, ATc interval, blood pressure drop according to pretreatment with atropine. 4. The interaction between epineprine and Azalea extract was not noted by the effect of epineprine itself. 5. The ST change by 0.7gm/kg, 1.0gm/kg of Azalea extract was revealed in 1 case(14.0%), 7 case(100%), respectively. 6. Most of all cases with arrhthymia, ventricular tachycardia, ventricular fibrillation, were noted in the group by epineprine, except one case by Azalea extract(1.0gm/kg). It was idioventricular rhythm. In conclusion, azalea extract has negative inotropic and chronotropic effect with arrhythmogenic potential possibly through direct myocardial ischemia or injury but we cann't be absolutely exclusive of actions of autonmic nervous system, especially parasympathetic nervous system.

• Proceedings of the KOSOMBE Conference
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• v.1989 no.05
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• pp.13-14
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• 1989

Prolongation in QT corrected interval (QTc), measured in surface ECG, has been shown in the majority af patients to be marker of bad prognosis in postmyocardial infarction patients (PMIP). Hence it would seem logical that dynamic QTc interval measurement can be a very usefull indicator to stratify prognosis in PMIP. We present a new algorithm for QT as well as for QTP (distance value from Q wave onset to T wave peak) intervals measurement in 24 hour ECG Holter tapes. Validation of the algorithm by hand measurement has been done on first beats of 18 Holter tapes, resulting in a magnitude of deviations between 10 and 15 ms. Application on 24 hour Holter ECG signal has also been done.

• Journal of The Korean Society of Clinical Toxicology
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• v.5 no.1
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• pp.8-14
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• 2007

Purpose: Organophosphorus insecticides tend to be regarded as a homogeneous single entity. We aimed to determine whether organophosphate poisoning differs by subgroups in clinical features and severity. Methods: We retrospectively reviewed medical records of all patients with acute organophophorus poisoning from January 1998 to December 2006. We investigated clinical features, Glasgow coma scale (GCS), laboratory findings, QTc intervals, management, and outcomes. Results: A total of 109 patients were included. The dimethoxy group experienced significantly longer times than the diethoxy group for ventilation duration (0.6 day vs. 0.2 day, p=0.006), ICU duration (2.0 day vs. 0.8 day, p=0.037), and total admission duration (2.8 day vs. 0.9 day, p=0.008), except in cases of dichlorvos poisoning. Also, the GCS of the dimethoxy group (except with dichlorvos) was significantly lower than for the diethoxy group (dimethoxy, $11.2{\pm}5.2$ vs. diethoxy, $13.8{\pm}2.4$, p= 0.021). QTc intervals for the dimethoxy group (except with dichlorvos) tended to be somewhat greater than for the diethoxy group (dimethoxy, $452.9{\pm}16.1\;msec$ vs. diethoxy, $429.6{\pm}40.9\;msec$). There were 65 patients with dichlorvos ingestion, and 2 of these patients (3%) died. Conclusion: When compared to the diethoxy group, the dimethoxy group of organophosphates (with the exception of dichlorvos) were associated with poorer prognostic value for indicators such as GCS, QTc interval, requirement for intubation, ICU duration, and total admission duration. Within the dimethoxy group, patients with dichlorvos poisoning had relatively better prognoses than for the other dimethoxy group organophosphates studied.

• Korean Journal of Veterinary Research
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• v.52 no.3
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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.

• Journal of The Korean Society of Clinical Toxicology
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• v.7 no.2
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• pp.69-76
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• 2009

Purpose: Various electrocardiogram (ECG) changes can occur in patients with acute organophosphate poisoning (OPP) and may be associated with the clinical severity of poisoning. The present study aimed to evaluate the extent and frequency of ECG changes and cardiac manifestations, and their association with acute OPP clinical severity. Methods: Seventy-two adult patients admitted to our emergency department with a diagnosis of acute OPP were studied retrospectively. ECG changes and cardiac manifestations at admission were evaluated. ECG changes between respiratory failure (RF) group and no respiratory failure (no RF) groups were compared. Results: Prolongation of QTc interval (n=40, 55.6%) was the most common ECG change, followed by sinus tachycardia (n=36, 50.0%). ST-T wave changes such as ST segment elevation or depression and T wave change (inversion or non-specific change) were evident in 16 patients (22.2%). Prolongation of QTc interval was significantly higher in the RF group compared with the no RF group (p=0.03), but was not an independent predictor for RF in acute OPP (OR; 4.00, 95% CI; 0.70-23.12, p=0.12). Conclusion: While patients with acute OPP can display ECG changes that include prolongation of QTc interval, sinus tachycardia, and ST-T wave changes at admission, these changes are not predictors of respiratory failure.

• Journal of The Korean Society of Clinical Toxicology
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• v.19 no.2
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• pp.133-138
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• 2021

Glufosinate-containing herbicides is a non-selective herbicide commonly used worldwide. As the use of them increased gradually since paraquat was banned in 2012, the number of suicides by their ingestion is also increasing continuously. Complications of glufosinate-containing herbicide poisoning include various central nervous system (CNS) toxicities such as convulsions, loss of consciousness, memory impairment, and respiratory depression, which may be accompanied by hemodynamic changes such as bradycardia and hypotension. However, it is very rare that arrhythmias other than bradycardia occurred and Takotsubo cardiomyopathy was combined due to cardiotoxicity. A 71-year-old female patient was transferred to our hospital after ingesting 500 mL of glufosinate-containing herbicide and receiving 5 L of gastric lavage at a local hospital. A few hours later, she presented stuporous mentality, respiratory depression, and convulsions, and was accompanied by hypotension and bradycardia. On the second day of admission, electrocardiogram (ECG) showed bradycardia and QTc prolongation with hemodynamic Instability. Accordingly, we conducted the early treatment with continuous renal replacement therapy (CRRT) and the application of temporary cardiac pacemaker. An echocardiogram demonstrated decreased ejection fraction (EF) and Takotsubo cardiomyopathy on the third day of admission. Then, she was discharged safely with conservative treatment. At the follow-up after 1 year, Takotsubo cardiomyopathy, EF and QTc prolongation were recovered on echocardiogram and ECG. Because cardiac toxicity after glufosinate-containing herbicide poisoning may cause life-threatening consequences, caution is required while treating the patient. Therefore, if electrocardiogram changes are seen in the elderly with a large amount of glufosinate herbicide ingestion, additional cardiac function test through echocardiography should be concerned, and early treatment through CRRT or artificial cardiac pacing should be considered.

• Childhood Kidney Diseases
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• v.27 no.2
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• pp.105-110
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• 2023

Purpose: To analyze electrocardiograms (ECGs) of patients with a salt-losing tubulopathy (SLT) and to determine the frequency and risk factors for long QT and arrhythmia. Methods: A total of 203 patients aged <19 years with SLT, specifically Bartter syndrome and Gitelman syndrome, who had a 12-lead ECG were included in this retrospective study. We analyzed the presence of an arrhythmia or prolonged corrected QT (QTc) on ECGs obtained for these patients. Demographic and laboratory data were compared between patients with abnormal and normal ECG findings. Results: Out of the 203 SLT patients, 38 (18.7%) underwent electrocardiography and 10 (40.0%) of 25 patients with inherited SLT had abnormal ECG findings, including prolonged QTc and arrhythmias. The abnormal ECG group had significantly lower serum potassium levels than the normal group (median [interquartile range]: 2.50 mmol/L [2.20-2.83] vs. 2.90 mmol/L [2.70-3.30], P=0.036), whereas other serum chemistry values did not show significant differences. The cutoff level for a significant difference in QTc interval was serum potassium level <2.50 mmol/L. One cardiac event occurred in a 13-year-old boy, who developed paroxysmal supraventricular tachycardia and underwent cardiac ablation. No sudden cardiac deaths occurred in this cohort. Conclusions: The incidence of ECG abnormalities in patients with inherited SLT was 40.0%, whereas the ECG screening rate was relatively low (18.7%). Therefore, we recommend ECG screening in patients with inherited SLT, especially in those with serum potassium level <2.50 mmol/L.

• Journal of Chest Surgery
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• v.42 no.2
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• pp.214-219
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• 2009

Background: Primary focal hyperhidrosis is characterized by overactivity of the sympathetic nervous function, and this has been effectively treated with endoscopic thoracic sympathetic denervation (ESD). The imbalance of sympathetic and parasympathetic nervous system that's created by ESD may affect the heart, lung and other thoracic organs. We analyzed the heart rate and ECG changes after performing ESD at our hospital, and this is the first such study that has been conducted on this. Material and Method: Of the 263 patients who underwent ESD between October 1996 and October 2006, 130 had ECG before and after ESD, and they were classified into 3 groups according to the level of ESD: Group I (n=40) patients underwent ESD at the 2nd rib (T2ESD), Group II (n=80) at the 3rd rib (T3ESD) and Group III (n=10) at the 4th rib (T4ESD). Result: There was no mortality or major morbidity. Heart rate (HR) was significantly decreased from $71.6{\pm}10.6/min\;to\;66.8{\pm}10.2/min$ after ESD (p<0.01); however, the PR (from $148.6{\pm}21.2$ msec to $152.8{\pm}20.5$ msec) and QTc (from $399.2{\pm}15.4$ msec to $404.0{\pm}15.1$ msec) intervals were significantly increased after ESD in the patients who suffered with primary hyperhidrosis (p<0.01). According to the level of ESD, there were significant changes in the HR and QTc interval in group I (T2ESD), the HR and PR interval in group II and the QTc interval in Group III. Conclusion: There were significant changes in the heart rate and ECG findings after ESD. The thoracic sympathetic denervation of T2, T3 and T4 affected the electrical activity of the heart at the resting state.

• Journal of The Korean Society of Clinical Toxicology
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• v.9 no.1
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• pp.20-25
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• 2011

Purpose: This study was designed to analyze the contributing factors, as well as the incidence and nature of the cardiac toxicity, in patients presenting with diphenhydramine overdose. Methods: We retrospectively reviewed the medical records of the intoxicated patients who presented to the ED of Korea University Anam Hospital from January 2008 to December 2010. Those patients who visited due to a diphenhydramine overdose were selected and the following features were recorded for analysis: the general characteristics, vital signs, the amount of ingested diphenhydramine, the time interval from ingestion to presentation, the coingested drugs (if any), the toxicities and the ECG findings. Cardiac toxicity, while defined mainly in terms of the temporary ECG changes such as QTc prolongation, right axis deviation, QRS widening, high degree AV block and ischemic changes, also encompassed cardiogenic shock, which is a clinical finding. Results: A total of eighteen patients were enrolled. Of the eighteen patients, eight had ingested diphenhydramine only, while ten had ingested other drugs in addition to diphenhydramine. The most commonly observed toxicity following diphenhydramine overdose included cardiac toxicity (78%). Cardiac toxicity was observed in all the patients who presented to the emergency department 2 hours after ingestion. The patients with QTc prolongation turned out to have ingested significantly larger amounts of diphenhydramine. Conclusion: QTc prolongation and right axis deviation were common findings for the patients with a diphenhydramine overdose. QTc prolongation was more likely to occur with ingesting larger amounts of diphenhydramine. Close monitoring is mandatory for patients who have ingested large amounts of diphenhydramine to prevent such potentially lethal cardiac toxicity.

• Neonatal Medicine
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• v.28 no.1
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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.