• Journal of Dental Anesthesia and Pain Medicine
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• v.18 no.3
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• pp.189-193
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• 2018

A 57-year-old woman scheduled for cochlear implant removal exhibited preoperative electrocardiographic findings of early repolarization (ER). Four episodes of transient ST segment elevations during surgery raised suspicion for vasospastic angina (VA). In the post-anesthetic care unit, the patient complained of chest discomfort and received sublingual nitroglycerin with uncertain effect. The patient refused to proceed with postoperative invasive coronary angiography, resulting in inconclusive diagnosis. Intraoperative circumstances limit the diagnosis of VA, which emphasizes the need for further testing to confirm the diagnosis. When VA is suspected in patients with underlying ER, it is reasonable to consider invasive examination to establish the diagnosis and prevent recurrence of VA. If ST changes are observed during surgery in patients with preoperative ER, careful monitoring is recommended. Due to general anesthesia, the absence of patient symptoms limits the definitive diagnosis of those with suspected VA. Therefore, additional postoperative surveillance is recommended.

• Journal of Biomedical Engineering Research
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• v.43 no.5
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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.

• Korean Circulation Journal
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• v.52 no.4
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• pp.251-264
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• 2022

Heart failure with preserved ejection fraction (HFpEF) accounts for approximately half of all heart failure (HF) cases. The prevalence of HFpEF is increasing due to an aging population with hypertension, diabetes mellitus, and obesity. HFpEF remains a challenging clinical entity due to a lack of effective treatment options. Traditional HF medications have not been shown to reduce mortality of patients with HFpEF, and an implantable cardioverter-defibrillator is not indicated due to normal ejection fraction. Sudden death is the most common mode of death in patients with HFpEF; however, the underlying mechanisms of sudden death are not fully elucidated. Although ventricular arrhythmias are responsible for the majority of sudden deaths in general, their contribution to sudden deaths in HFpEF patients is likely less significant. The mechanisms of ventricular arrhythmias in HFpEF are 1) reduced conduction velocity due to ventricular hypertrophy, 2) delayed repolarization due to potassium current down-regulation, 3) calcium leakage due to altered excitation-contraction coupling, and 4) increased ventricular fibrosis caused by systemic inflammation. Hypertension and subsequent ventricular hypertrophy reduce the conduction velocity in HFpEF hearts via heterogeneous distribution of connexin 43. Delayed repolarization caused by potassium current down-regulation in HFpEF hearts provides a window for early afterdepolarization to trigger ventricular arrhythmias. Altered excitation-contraction coupling in HFpEF can cause calcium to leak and trigger delayed afterdepolarization. Increased systemic inflammation and subsequent ventricular fibrosis provide substrates for re-entry. Further research is warranted to investigate the detailed mechanisms of ventricular arrhythmias in HFpEF.

• Journal of Yeungnam Medical Science
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• v.31 no.2
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• pp.94-98
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• 2014

Background: We analyzed the changes in QT dispersion (QTd) in children with Kawasaki disease (KD), and determined the presence of repolarization abnormality in these children even in the absence of coronary artery abnormalities. Methods: Ninety-one children with KD and 20 healthy controls were enrolled in this retrospective study. Serial echocardiographic and electrocardiographic (ECG) measurements in the beginning of treatment, 2nd month and 6th month after the diagnosis were compared. Fifty-one of 91 children had at least 2 serial ECG data. The number of patients who had 3 consecutive ECG data was 23. Results: Among the 67 KD patients with no coronary artery changes, the consecutive mean QTd values were 41.86 ms, 37.84 ms, and 25.47 ms, respectively (26 ms for controls). In the analysis of changes among KD patients without coronary artery abnormalities, QTd showed a significant decrease with time (p=0.01). Especially, the 1st month and the 6th month QTd values were significantly different (p=0.028). The mean QTd values in KD patients with coronary artery changes were significantly higher than those in KD patients with no coronary artery changes at each time (1st, 2nd, and 6th month exam). Conclusion: QTd is significantly increased in children during the early stage of KD. Repolarization abnormality may exist during the acute stage of KD, regardless of the echocardiographic changes.

• The Journal of the Korean life insurance medical association
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• v.29 no.2
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• pp.22-28
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• 2010

Medical risk selection or mortality analysis is very important in insurance medicine. Among many kind of source articles there have been several limitations. There are few long-term follow-up studies in rare disease, as Romeo's article. We can do mortality analysis of this type using cause of death within the article and assumption of expected mortality q'. In the case of article which is published in foreign country such as Tikkanen et al, we can use comparative group from the control group within source article. It is another way for mortality analysis of limited article. However Retrospective study even performed in Korea, is unusable for estimation of extra-mortality.

• The Korean Journal of Physiology and Pharmacology
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• v.6 no.1
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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.

• Journal of mucopolysaccharidosis and rare diseases
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• v.4 no.1
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• pp.21-25
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• 2018

Fabry disease is a hereditary lysosomal storage disorder caused by the reduction or absence of lysosomal enzyme alpha-galactosidase A and the accumulation of glycosphingolipids, such as globotriaosylceramide (Gb3), in various organs, including the heart. The prevention of cardiac involvement in Fabry disease can only be achieved by enzyme replacement therapy (ERT), and the method of assessing the efficacy of ERT should be confirmed. Changes in the electrocardiogram, such as the shortening of PQ interval, prolongation of QTc and repolarization abnormalities as well as left ventricular hypertrophy in voltage criteria, can be used to identify Fabry disease patients; however, the usefulness of electrocardiograms for evaluating the efficacy of ERT is limited. The assessment of left ventricular hypertrophy using echocardiography has been established to evaluate the efficacy of ERT during long-term period. A new technique involving speckled tracking method might be useful for detecting early cardiac dysfunction and identifying the effect of ERT for a relatively short period. The estimation of left ventricular hypertrophy using cardiac magnetic resonance (CMR) is also useful for assessing the efficacy of ERT. Identifying late gadolinium enhancement in CMR may affect the effectiveness of ERT, and the new technique of T1 mapping might be useful for monitoring the accumulation of Gb3 during ERT. Histopathology in cardiac biopsy specimens is another potentially useful method for identifying the accumulation of GB3; however, the use of histopathology to evaluate of the efficacy of ERT is limited because of the invasive nature of an endomyocardial biopsy.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.1
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• pp.1-8
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• 2000

To investigate the contributions of intrinsic membrane properties to the spontaneous activity of medial vestibular nucleus (MVN) neurons, we assessed the effects of blocking large and small calcium-activated potassium channels by means of patch clamp recordings. Almost all the MVN neurons recorded in neonatal $(P13{\sim}P17)$ rat were shown to have either a single deep after-hyperpolarization (AHP; type A cells), or an early fast and a delayed slow AHP (type B cells). Among the recorded MVN cells, immature action potential shapes were found. Immature type A cell showed single uniform AHP and immature B cell showed a lack of the early fast AHP, and the delayed AHP was separated from the repolarization phase of the spike by a period of isopotentiality. Application of apamin and charybdotoxin (CTX), which selectively block the small and large calcium-activated potassium channels, respectively, resulted in significant changes in spontaneous firings. In both type A and type B cells, CTX (20 nM) resulted in a significant increase in spike frequency but did not induce bursting activity. By contrast, apamin (300 nM) selectively abolished the delayed slow AHP and induced bursting activity in type B cells. Apamin had no effect on the spike frequency of type A cells. These data suggest that there are differential roles of apamin and CTX sensitive potassium conductances in spontaneous firing patterns of MVN neurons, and these conductances are important in regulating the intrinsic rhythmicity and excitability.