scholarly journals TORSADE DE POINTES

2013 ◽  
Vol 4 (2) ◽  
Author(s):  
Shinta M Latulola ◽  
Reginald L Lefrandt
Keyword(s):  
Heart Failure ◽  
Ventricular Tachycardia ◽  
Long Qt Syndrome ◽  
Heart Diseases ◽  
Torsade De Pointes ◽  
Electrolyte Imbalance ◽  
Long Qt ◽  
Polymorphic Type ◽  
Qt Syndrome ◽  
Digoxin Therapy

Abstract: Torsade de pointes (TdP) is a disturbance of heart rhythme, a ventricular tachycardia polymorphic type, with irregular ventricle contractions more than 200-250 per minute, and the QRS axis shows a twisting of points.We reported a 63-year-old female with torsade de pointes and a long QT syndrome. The causes of this TdP were multifactorial, such as electrolyte imbalance (hypokalemia and hypomagnesemia), medicine (amiodarone and digoxin), and chronic heart diseases. The management of this patient was defibrillation, magnesium supply, cease of amiodarone and digoxin therapy, correction of electrolyte imbalance, supression of EADs, and heart failure treatment.Key words: torsade de pointes, arrythmia, multifactorialAbstrak: Torsade de pointes (TdP) adalah gangguan irama jantung berupa takikardi ventrikuler tipe polimorfik, dimana ventrikel berkontraksi lebih dari 200 sampai 250 kali per menit secara tidak beraturan dengan sumbu axis QRS yang bervariasi, membentuk gambaran seperti kumparan (twisting of points). Kami melaporkan kasus seorang perempuan dengan torsade de pointes dan long QT syndrome yang didapat. Faktor penyebab multifaktorial berupa gangguan elektrolit (hipokalemia dan hipomagnesemia), obat-obatan (amiodaron dan digoksin), serta adanya penyakit jantung kronik. Penanganan pada kasus ini terdiri dari defibrilasi, pemberian magnesium, penghentian pemberian amiodaron dan digoksin, koreksi ketidakseimbangan elektrolit, supresi EADs, serta penanganan gagal jantung.Kata kunci: torsade de pointes, aritmia, multifaktorial

scholarly journals Balance Between Rapid Delayed Rectifier K + Current and Late Na + Current on Ventricular Repolarization

2020 ◽  
Vol 13 (4) ◽  
Author(s):  
Bence Hegyi ◽  
Ye Chen-Izu ◽  
Leighton T. Izu ◽  
Sridharan Rajamani ◽  
Luiz Belardinelli ◽  
...  
Keyword(s):  
Heart Failure ◽  
Long Qt Syndrome ◽  
Therapeutic Potential ◽  
Heart Diseases ◽  
Ionic Currents ◽  
Close Correlation ◽  
Delayed Rectifier ◽  
Long Qt ◽  
Comparable Amount ◽  
Qt Syndrome

Background: Rapid delayed rectifier K + current (I Kr ) and late Na + current (I NaL ) significantly shape the cardiac action potential (AP). Changes in their magnitudes can cause either long or short QT syndromes associated with malignant ventricular arrhythmias and sudden cardiac death. Methods: Physiological self AP-clamp was used to measure I NaL and I Kr during the AP in rabbit and porcine ventricular cardiomyocytes to test our hypothesis that the balance between I Kr and I NaL affects repolarization stability in health and disease conditions. Results: We found comparable amount of net charge carried by I Kr and I NaL during the physiological AP, suggesting that outward K + current via I Kr and inward Na + current via I NaL are in balance during physiological repolarization. Remarkably, I Kr and I NaL integrals in each control myocyte were highly correlated in both healthy rabbit and pig myocytes, despite high overall cell-to-cell variability. This close correlation was lost in heart failure myocytes from both species. Pretreatment with E-4031 to block I Kr (mimicking long QT syndrome 2) or with sea anemone toxin II to impair Na + channel inactivation (mimicking long QT syndrome 3) prolonged AP duration (APD); however, using GS-967 to inhibit I NaL sufficiently restored APD to control in both cases. Importantly, I NaL inhibition significantly reduced the beat-to-beat and short-term variabilities of APD. Moreover, I NaL inhibition also restored APD and repolarization stability in heart failure. Conversely, pretreatment with GS-967 shortened APD (mimicking short QT syndrome), and E-4031 reverted APD shortening. Furthermore, the amplitude of AP alternans occurring at high pacing frequency was decreased by I NaL inhibition, increased by I Kr inhibition, and restored by combined I NaL and I Kr inhibitions. Conclusions: Our data demonstrate that I Kr and I NaL are counterbalancing currents during the physiological ventricular AP and their integrals covary in individual myocytes. Targeting these ionic currents to normalize their balance may have significant therapeutic potential in heart diseases with repolarization abnormalities. Visual Overview: A visual overview is available for this article.

Video-Assisted Modified Left Sympathectomy for Long-QT Syndrome

2000 ◽  
Vol 8 (1) ◽  
pp. 52-53 ◽  
Author(s):  
Guo Xing Weng ◽  
Hang Ding ◽  
Juan Qi ◽  
Chun Xuan Xu
Keyword(s):  
Ventricular Tachycardia ◽  
Long Qt Syndrome ◽  
Qt Interval ◽  
Torsade De Pointes ◽  
Horner’S Syndrome ◽  
Horner's Syndrome ◽  
Long Qt ◽  
Video Assisted ◽  
Qt Syndrome

A 22-year-old female suffering from idiopathic long-QT syndrome complicated by frequent syncope, torsade-de-pointes-type ventricular tachycardia, and asthma, was successfully treated by video-assisted extensive left second and third thoracic sympathetic ganglionectomy, instead of left stellate and first thoracic ganglio-nectomy, to avoid postoperative Horner's syndrome. The QT interval was significantly shortened from 0.6 to 0.43 seconds four days after the surgery. It remained at 0.43 seconds during a 3-month follow-up with no recurrence of tachycardia or syncope.

scholarly journals Paediatric/young versus adult patients with long QT syndrome or catecholaminergic polymorphic ventricular tachycardia

2021 ◽  
Author(s):  
Sharen Lee ◽  
Jiandong Zhou ◽  
Kamalan Jeevaratnam ◽  
Wing Tak Wong ◽  
Ian Chi Kei Wong ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Long Qt Syndrome ◽  
Primary Outcome ◽  
Public Hospitals ◽  
Adult Patients ◽  
Polymorphic Ventricular Tachycardia ◽  
Qtc Interval ◽  
Long Qt ◽  
Old Patients ◽  
Qt Syndrome

AbstractIntroductionLong QT syndrome (LQTS) and catecholaminergic ventricular tachycardia (CPVT) are less prevalent cardiac ion channelopathies than Brugada syndrome in Asia. The present study compared paediatric/young and adult patients with these conditions.MethodsThis was a territory-wide retrospective cohort study of consecutive patients diagnosed with LQTS and CPVT attending public hospitals in Hong Kong. The primary outcome was spontaneous ventricular tachycardia/ventricular fibrillation (VT/VF).ResultsA total of 142 LQTS (mean onset age= 27±23 years old) and 16 CPVT (mean presentation age=11±4 years old) patients were included. For LQTS, arrhythmias other than VT/VF (HR=4.67, 95% confidence interval=[1.53-14.3], p=0.007), initial VT/VF (HR=3.25 [1.29-8.16], p=0.012) and Schwartz score (HR=1.90 [1.11-3.26], p=0.020) were predictive of the primary outcome for the overall cohort, whilst arrhythmias other than VT/VF (HR=5.41 [1.36-21.4], p=0.016) and Schwartz score (HR=4.67 [1.48-14.7], p=0.009) were predictive for the adult subgroup (>25 years old; n=58). All CPVT patients presented before the age of 25 but no significant predictors of VT/VF were identified. A random survival forest model identified initial VT/VF, Schwartz score, initial QTc interval, family history of LQTS, initially asymptomatic, and arrhythmias other than VT/VF as the most important variables for risk prediction in LQTS, and initial VT/VF/sudden cardiac death, palpitations, QTc, initially symptomatic and heart rate in CPVT.ConclusionClinical and ECG presentation vary between the pediatric/young and adult LQTS population. All CPVT patients presented before the age of 25. Machine learning models achieved more accurate VT/VF prediction.

Acquired long QT syndrome and torsade de pointes

2018 ◽  
Vol 41 (4) ◽  
pp. 414-421 ◽  
Author(s):  
Nabil El-Sherif ◽  
Gioia Turitto ◽  
Mohamed Boutjdir
Keyword(s):  
Long Qt Syndrome ◽  
Torsade De Pointes ◽  
Long Qt ◽  
Acquired Long Qt Syndrome ◽  
Qt Syndrome

scholarly journals Complex and Novel Arrhythmias Precede Stillbirth in Fetuses With De Novo Long QT Syndrome

2020 ◽  
Vol 13 (5) ◽  
Author(s):  
Sarah Strand ◽  
Janette F. Strasburger ◽  
Bettina F. Cuneo ◽  
Ronald T. Wakai
Keyword(s):  
Atrioventricular Block ◽  
Long Qt Syndrome ◽  
De Novo ◽  
Perinatal Death ◽  
Torsade De Pointes ◽  
Fetal Loss ◽  
Long Qt ◽  
Premature Ventricular Contractions ◽  
Fetal Magnetocardiography ◽  
Qt Syndrome

Background: Long QT syndrome (LQTS) is a leading cause of sudden cardiac death in early life and has been implicated in ≈10% of sudden infant deaths and unexplained stillbirths. The purpose of our study was to use fetal magnetocardiography to characterize the electrophysiology and rhythm phenotypes of fetuses with de novo and inherited LQTS variants and identify risk factors for sudden death before birth. Methods: We reviewed the fetal magnetocardiography database from the University of Wisconsin Biomagnetism Laboratory for fetuses with confirmed LQTS. We assessed waveform intervals, heart rate, and rhythm, including the signature LQTS rhythms: functional 2° atrioventricular block, T-wave alternans, and torsade de pointes (TdP). Results: Thirty-nine fetuses had pathogenic variants in LQTS genes: 27 carried the family variant, 11 had de novo variants, and 1 was indeterminate. De novo variants, especially de novo SCN5A variants, were strongly associated with a severe rhythm phenotype and perinatal death: 9 (82%) showed signature LQTS rhythms, 6 (55%) showed TdP, 5 (45%) were stillborn, and 1 (9%) died in infancy. Those that died exhibited novel fetal rhythms, including atrioventricular block with 3:1 conduction ratio, QRS alternans in 2:1 atrioventricular block, long-cycle length TdP, and slow monomorphic ventricular tachycardia. Premature ventricular contractions were also strongly associated with TdP and perinatal death. Fetuses with familial variants showed a lower incidence of signature LQTS rhythm (6/27=22%), including TdP (3/27=11%). All were live born. Conclusions: The malignancy of de novo LQTS variants was remarkably high and demonstrate that these mutations are a significant cause of stillbirth. Their ability to manifest rhythms not known to be associated with LQTS increases the difficulty of echocardiographic diagnosis and decreases the likelihood that a resultant fetal loss is attributed to LQTS. Registration: URL: http://www.clinicaltrials.gov . Unique identifier: NCT03047161.

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