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In Vivo and In Vitro Cardiac Preparations Used in Antiarrhythmic Assays
Published in John H. McNeill, Measurement of Cardiovascular Function, 2019
Torsade de pointes is difficult to produce in animals.32 Indeed, polymorphic ventricular arrhythmia induced by different experimental methods of torsade de pointes may not be the same arrhythmia. The following methods have been reported to initiate polymorphic ventricular tachycardia: application of aconitine or electrical stimulation of the epicardium at two distant sites, quinidine intoxication in dogs with a prior infarct, and treatment with class III antiarrhythmics in the presence of alpha adrenergic stimulation (methox-amine) in rabbits.33 We find that high doses of class III antiarrhythmics reliably initiate torsade de pointes in anesthetized primates and that this does not require a “short-long-short” initiation sequence.
The electrocardiogram in ischaemic heart disease
Published in John Edward Boland, David W. M. Muller, Interventional Cardiology and Cardiac Catheterisation, 2019
Geoffrey S. Oldfield, Dennis L. Kuchar
Ventricular tachycardia consists of a series of three or more consecutive ventricular ectopic beats that occur at a rate faster than the underlying sinus rhythm. 3–10 escape beats are common in the first 36 hours after an acute myocardial infarction and are of little prognostic significance. However, rapid polymorphic ventricular tachycardia in the first 36 hours following infarction is of prognostic significance. Patients with a torsades de pointes (TDP) pattern should have attention paid to the pro-arrhythmic effects of existing anti-arrhythmic therapy. TDP is also associated with the use of phenothiazines, tricyclic anti-depressants, erythromycin based anti-histamines, hypokalaemia and hypomagnesaemia. When polymorphic ventricular tachycardia is due solely to the myocardial infarction it usually responds well to anti-arrhythmic therapy.
OCT assessment out of the coronary arteries
Published in Hiram G. Bezerra, Guilherme F. Attizzani, Marco A. Costa, OCT Made Easy, 2017
Jun Li, Daniel Kendrick, Vikram S. Kashyap, Sahil A. Parikh
A 42-year-old woman with a smoking history but otherwise unremarkable prior medical history presents after cardiac arrest while playing golf. Upon evaluation by the emergency medical services, she is found to have polymorphic ventricular tachycardia. Transient anterior stent thrombosis (ST)–segment elevation is present on electrocardiogram soon after her arrival at the hospital. She undergoes emergent coronary angiogram, showing proximal left anterior descending stenosis with near-complete resolution with injection of intracoronary nitroglycerin.
Brugada syndrome
Published in Acta Cardiologica, 2021
Haarika Korlipara, Giridhar Korlipara, Srinivas Pentyala
Patients with BrS have variable clinical phenotypes. Syncope, seizures, chest discomfort and/or nocturnal agonal breathing due to arrhythmias such as polymorphic ventricular tachycardia (PVT) or VF may be the primary manifestation of the disease [2]. If these arrhythmias are sustained, these patients can eventually experience SCD and possibly even endure other arrhythmias such as atrial flutter, atrial fibrillation, Wolff-Parkinson-White (WPW) syndrome and other supraventricular arrhythmias [2,8]. Often, patients are asymptomatic and remain asymptomatic for life, diagnosed incidentally with a Brugada ECG pattern. Sudden unexplained nocturnal death syndrome (SUNDS), which is a disorder associated with the development of critical arrhythmias leading to sudden death in young healthy individuals, has been shown to be genetically, phenotypically and functionally the same as BrS [8,11].
Cardiopulmonary resuscitation–induced consciousness
Published in Baylor University Medical Center Proceedings, 2021
Raman P. Singh, Soumya Adhikari, David Landsberg, Viren Kaul
A 64-year-old woman with ischemic cardiomyopathy presented with worsening dyspnea and lower-extremity swelling. She responded clinically to diuretics for heart failure but was unexpectedly found to be unresponsive and pulseless. CPR was initiated and rhythm check identified polymorphic ventricular tachycardia. She was defibrillated with administration of 1 mg of epinephrine and 2 g of magnesium sulfate. During the following round of compressions, the patient demonstrated purposeful movements and verbalized a desire to halt CPR. Compressions were discontinued and the patient’s movements and interactions ceased. She developed pulseless ventricular tachycardia and was defibrillated with resumption of compressions and administration of 300 mg of amiodarone. The patient again demonstrated purposeful movements. After 21 minutes of CPR, including four defibrillations, 2 mg of epinephrine, 2 mg of magnesium sulfate, and 300 mg of amiodarone, return of spontaneous circulation was obtained. The patient lost pulses again and her surrogate decision maker decided against further resuscitation.
Implantable cardioverter defibrillator for alectinib induced ventricular fibrillation
Published in Clinical Toxicology, 2020
Amit K. J. Mandal, Sarah A. Stokes, Constantinos G. Missouris
Another potential predisposing factor for the development of ventricular arrhythmia, in our patient, was persistent sinus bradycardia, even in the presence of normal QTc interval. Morcas et al. observed that bradycardia was the most common cardiac side effect of alectinib (consistent with other ALK TKIs) seen in 7.9% of patients. Furthermore, an analysis of the ECGs of the 211 patients in this trial revealed that 20% of patients had heart rates <50 bpm at least once. Alectinib associated bradycardia was usually asymptomatic with a mean decrease in heart rate of 11-13 bpm, and rarely requiring interruption of therapy [2]. Polymorphic ventricular tachycardia has an association with bradycardia or frequent electrical pauses, as a result of the inverse relationship between heart rate and repolarisation time. In addition, bradycardia increases the arrhythmogenicity of drugs that inhibit hERCG because of a reverse use-dependent prolongation of action potential [3,4].