Life-threatening cardiac arrhythmias due to drug-induced QT prolongation

2015 ◽  
Vol 111 (4) ◽  
pp. 302-309 ◽  
Author(s):  
G. Michels ◽  
M. Kochanek ◽  
R. Pfister
2020 ◽  
pp. postgradmedj-2020-138661
Author(s):  
Rani Khatib ◽  
Fatima R N Sabir ◽  
Caroline Omari ◽  
Chris Pepper ◽  
Muzahir Hassan Tayebjee

Many drug therapies are associated with prolongation of the QT interval. This may increase the risk of Torsades de Pointes (TdP), a potentially life-threatening cardiac arrhythmia. As the QT interval varies with a change in heart rate, various formulae can adjust for this, producing a ‘corrected QT’ (QTc) value. Normal QTc intervals are typically <450 ms for men and <460 ms for women. For every 10 ms increase, there is a ~5% increase in the risk of arrhythmic events. When prescribing drugs associated with QT prolongation, three key factors should be considered: patient-related risk factors (eg, female sex, age >65 years, uncorrected electrolyte disturbances); the potential risk and degree of QT prolongation associated with the proposed drug; and co-prescribed medicines that could increase the risk of QT prolongation. To support clinicians, who are likely to prescribe such medicines in their daily practice, we developed a simple algorithm to help guide clinical management in patients who are at risk of QT prolongation/TdP, those exposed to QT-prolonging medication or have QT prolongation.


Diseases ◽  
2019 ◽  
Vol 7 (2) ◽  
pp. 38 ◽  
Author(s):  
Prashanth Rawla ◽  
Jeffrey Pradeep Raj ◽  
Sajid Melvin George ◽  
Pavani Nathala ◽  
Anantha R. Vellipuram

Rhabdomyolysis is caused by extensive damage to skeletal muscles resulting in elevated creatine phosphokinase (CPK), Lactate dehydrogenase (LDH), and aspartate aminotransferase (AST), leading to life-threatening consequences like acute renal failure, cardiac arrhythmias, and hyperthermia. A variety of causes for muscle damage are known, and one of the most common is drug-induced. Statins and many other agents are known to induce muscle damage, but here we report Entresto™ (Sacubitril/Valsartan) induced rhabdomyolysis which has not been previously reported as solely responsible in the literature.


2000 ◽  
Vol 11 (6) ◽  
pp. 691-696 ◽  
Author(s):  
CARLO NAPOLITANO ◽  
PETER J. SCHWARTZ ◽  
ARTHUR M. BROWN ◽  
ELENA RONCHETTI ◽  
LAURA BIANCHI ◽  
...  

1992 ◽  
Vol 10 (4) ◽  
pp. 301-316 ◽  
Author(s):  
Bramah N. Singh ◽  
Norman K. Hollenberg ◽  
Philip A. Poole-Wilson ◽  
J Ian S. Robertson

2021 ◽  
Vol 131 ◽  
pp. 104281
Author(s):  
Alaa Alahmadi ◽  
Alan Davies ◽  
Jennifer Royle ◽  
Leanna Goodwin ◽  
Katharine Cresswell ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
Shih Yea Sylvia Wu ◽  
Bridget Faire ◽  
Edward Gane

VIEKIRA PAK (ritonavir-boosted paritaprevir/ombitasvir and dasabuvir) is an approved treatment for compensated patients with genotype 1 (GT1) chronic hepatitis C virus (HCV) infection. This oral regimen has minimal adverse effects and is well tolerated. Cure rates are 97% in patients infected with HCV GT 1a and 99% in those with HCV GT 1b. We report the first case of life-threatening allergic pneumonitis associated with VIEKIRA PAK. This unexpected serious adverse event occurred in a 68-year-old Chinese female with genotype 1b chronic hepatitis C and Child-Pugh A cirrhosis. One week into treatment with VIEKIRA PAK without ribavirin, she was admitted to hospital with respiratory distress and acute kidney injury requiring intensive care input. She was initially diagnosed with community acquired pneumonia and improved promptly with intravenous antibiotics and supported care. No bacterial or viral pathogens were cultured. Following complete recovery, she recommenced VIEKIRA PAK but represented 5 days later with more rapidly progressive respiratory failure, requiring intubation and ventilation, inotropic support, and haemodialysis. The final diagnosis was drug induced pneumonitis.


2005 ◽  
Vol 289 (6) ◽  
pp. H2724-H2732 ◽  
Author(s):  
Xin Zhang ◽  
Indiresha Ramachandra ◽  
Zhongming Liu ◽  
Basharat Muneer ◽  
Steven M. Pogwizd ◽  
...  

Imaging the myocardial activation sequence is critical for improved diagnosis and treatment of life-threatening cardiac arrhythmias. It is desirable to reveal the underlying cardiac electrical activity throughout the three-dimensional (3-D) myocardium (rather than just the endocardial or epicardial surface) from noninvasive body surface potential measurements. A new 3-D electrocardiographic imaging technique (3-DEIT) based on the boundary element method (BEM) and multiobjective nonlinear optimization has been applied to reconstruct the cardiac activation sequences from body surface potential maps. Ultrafast computerized tomography scanning was performed for subsequent construction of the torso and heart models. Experimental studies were then conducted, during left and right ventricular pacing, in which noninvasive assessment of ventricular activation sequence by means of 3-DEIT was performed simultaneously with 3-D intracardiac mapping (up to 200 intramural sites) using specially designed plunge-needle electrodes in closed-chest rabbits. Estimated activation sequences from 3-DEIT were in good agreement with those constructed from simultaneously recorded intracardiac electrograms in the same animals. Averaged over 100 paced beats (from a total of 10 pacing sites), total activation times were comparable (53.3 ± 8.1 vs. 49.8 ± 5.2 ms), the localization error of site of initiation of activation was 5.73 ± 1.77 mm, and the relative error between the estimated and measured activation sequences was 0.32 ± 0.06. The present experimental results demonstrate that the 3-D paced ventricular activation sequence can be reconstructed by using noninvasive multisite body surface electrocardiographic measurements and imaging of heart-torso geometry. This new 3-D electrocardiographic imaging modality has the potential to guide catheter-based ablative interventions for the treatment of life-threatening cardiac arrhythmias.


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