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Genetically Determined Ventricular Arrhythmias
Published in Andrea Natale, Oussama M. Wazni, Kalyanam Shivkumar, Francis E. Marchlinski, Handbook of Cardiac Electrophysiology, 2020
Houman Khakpour, Jason S. Bradfield
Congenital long QT syndrome (LQTS) is a heterogeneous channelopathy that is characterized by ECG alterations—with prolongation of the QT interval as its hallmark—and risk of arrhythmic events. Clinical manifestations of LQTS include syncope due to torsade de pointes (TdP), cardiac arrest, and SCD. The estimated prevalence of LQTS is 1:2000 persons among caucasians, though this does not take into account mutation-positive patients with normal QTc.1 This discussion excludes secondary causes of QT prolongation that can occur with drugs, electrolyte imbalance, and acquired cardiac conditions.
Pharmacological Management of Huntington’s Disease
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Sonia Sharma, Sushant Sharma, Shallina Gupta
Girotti et al. (1984) examined the effect of haloperidol on 18 HD patients and observed that this drug reduced abnormal involuntary movement. In another study, Koller and Trimble (1985) investigated effect of haloperidol drugs on 13 HD patients. At a dose of 2–80 mg of haloperidol, chorea decreased in all patients. The main caution is advised to a patient when prescribed with QT-prolongation condition. The increased concentration of the drug has been reported when it was given with other drugs used as inhibitors or substrate of CYP2D6 or CYP3A4 isoenzymes. Intake of haloperidol with carbamazepine or rifampin has been associated with a reduction of haloperidol level in plasma.
The QT interval
Published in Andrew R Houghton, Making Sense of the ECG, 2019
Drug-induced QT interval prolongation is associated with an increased risk of torsades de pointes (Chapter 8), which can lead to ventricular fibrillation and sudden cardiac death. Awareness of the risk of drug-induced QT prolongation is therefore important, particularly when managing individuals with increased susceptibility to such effects. This includes those with: Simultaneous treatment with more than one QT-prolonging drugOverdose with a QT-prolonging drugPre-existing QT interval prolongationElectrolyte abnormalitiesUnderlying cardiovascular disease
Characterization and management of adverse events observed with mobocertinib (TAK-788) treatment for EGFR exon 20 insertion–positive non–small cell lung cancer
Published in Expert Review of Anticancer Therapy, 2023
James Chih-Hsin Yang, Caicun Zhou, Pasi A. Jänne, Suresh S. Ramalingam, Tae Min Kim, Gregory J Riely, Alexander I Spira, Zofia Piotrowska, Tarek Mekhail, Maria Rosario Garcia Campelo, Enriqueta Felip, Lyudmila Bazhenova, Shu Jin, Manmit Kaur, Paul M. Diderichsen, Neeraj Gupta, Veronica Bunn, Jianchang Lin, Eric N. Churchill, Minal Mehta, Danny Nguyen
Treatment-related cardiac disorders, which include cardiac failure and QTc interval prolongation, were observed in 12% of the patients; Grade ≥3 treatment-emergent cardiac disorders were observed in 13% of the patients, 11% with SAEs, and 2% discontinuing. Cardiac failure (including congestive cardiac failure, decreased ejection fraction, and cardiomyopathy) occurred in 2.3% of the patients. Grade 3 cardiac failure occurred in 0.8% of the patients. Grade 4 and fatal cardiac failure occurred in one patient each (0.4%). QTc interval prolongation (including electrocardiogram QT prolongation and ventricular arrhythmia) occurred in 8% of the patients. Grade 3 QTc interval prolongation occurred in 1.6% of the patients and Grade 4 QTc interval prolongation occurred in 1 patient (0.4%).
Prolongation of QTc interval due to increased parity and great grand multiparity
Published in Journal of Obstetrics and Gynaecology, 2022
Mehmet Ozgeyik, Ozge Turgay Yildirim
Electrocardiography is one of the most widely using diagnostic tool to detect predisposition factors for ventricular arrhythmias and sudden cardiac death (Stern 2012). Previous studies showed that QT prolongation is associated with life-threatening arrhythmias and sudden cardiac death (Goldenberg et al. 2006). Women start to have slower cardiac repolarisation along with the puberty (Cheng 2006) (QTc) intervals and more prone to develop ventricular arrhythmias than men. In addition, drugs that prolong the cardiac repolarisation increase this risk far more beyond (Makkar et al. 1993; Drici et al. 1998; Gowda et al. 2004; Cheng 2006). Sex hormones alter the function of the ion channels and these changes are the most probable cause of gender differences for arrhythmia (Drici et al. 1996; Waldegger et al. 1996; Hara et al. 1998; Liu et al. 1998).
Magnesium and COVID-19 – Some Further Comments – A Commentary on Wallace TC. Combating COVID-19 and Building Immune Resilience: A Potential Role for Magnesium Nutrition? J Am Coll Nutr. 2020;1–9. doi:10.1080/07315724.2020.1785971. Cited in: PMID: 32649272
Published in Journal of the American College of Nutrition, 2021
Oliver Micke, Jürgen Vormann, Klaus Kisters
Possible drugs for the treatment of COVID-19 increase the risk of QT interval prolongation and, subsequently, the risk of life-threatening torsade-de-pointes arrhythmias (TdP) and sudden cardiac death, e.g., chloroquine, hydroxychloroquine, azithromycin, lopinavir, ritonavir (17, 18). QT prolongation is also caused by a lack of Mg and/or potassium (17). Therefore, it is necessary to avoid and correct Mg and/or potassium deficiency before using QT prolonging drugs (18–20). In a single-centre study (n = 524) with COVID-19 patients and COVID-19 related medication a high proportion of patients with QT prolongation was identified (n = 103, corresponding to 19.7%) (20). In the event of hemodynamically stable TdP intravenous Mg sulfate is the therapy of choice, regardless of whether the patient is hypomagnesemic or normomagnesemic (17).