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Clinical management of electrical storm: a current overview.
Guarracini, F, Casella, M, Muser, D, Barbato, G, Notarstefano, P, Sgarito, G, Marini, M, Grandinetti, G, Mariani, MV, Boriani, G, et al
Journal of cardiovascular medicine (Hagerstown, Md.). 2021;(9):669-679
Abstract
The number of patients affected by electrical storm has been continuously increasing in emergency departments. Patients are often affected by multiple comorbidities requiring multidisciplinary interventions to achieve a clinical stability. Careful reprogramming of cardiac devices, correction of electrolyte imbalance, knowledge of underlying heart disease and antiarrhythmic drugs in the acute phase play a crucial role. The aim of this review is to provide a comprehensive overview of pharmacological treatment, latest transcatheter ablation techniques and advanced management of patients with electrical storm.
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Antiarrhythmic drug therapy during cardiopulmonary resuscitation: should we use it?
Soar, J
Current opinion in critical care. 2018;(3):138-142
Abstract
PURPOSE OF REVIEW The optimal antiarrhythmic drug therapy (amiodarone or lidocaine) in the treatment of ventricular fibrillation/pulseless ventricular tachycardia (VF/pVT) cardiac arrest that is refractory to defibrillation is uncertain. This article reviews the evidence for and against these drugs, alternatives treatments for refractory VF/pVT and aims to define the role of antiarrhythmic drugs during cardiopulmonary resuscitation (CPR). RECENT FINDINGS A large randomized controlled trial that compared amiodarone, lidocaine and saline 0.9% sodium chloride for the treatment of refractory VF/pVT out-of-hospital cardiac arrest reported no difference in survival to hospital discharge or neurological outcome. In patients with witnessed arrest, survival was improved with antiarrhythmic drugs compared to saline. SUMMARY The benefit of antiarrhythmic drugs appears to be for those patients in whom initial early CPR and defibrillation attempts fail and the antiarrhythmic drug is given early. There does not appear to be any clear survival benefit for any one particular drug and other factors such as availability and cost should be considered when deciding which drug to use. Furthermore, other interventions (e.g. percutaneous coronary intervention and extra-corporeal CPR) may provide additional survival benefit when defibrillation attempts and antiarrhythmic drugs are not effective.
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Advances in the pharmacologic treatment of ventricular arrhythmias.
Schleifer, JW, Sorajja, D, Shen, WK
Expert opinion on pharmacotherapy. 2015;(17):2637-51
Abstract
INTRODUCTION Despite many advances in nonpharmacologic management of ventricular arrhythmias, antiarrhythmic drugs remain important in both the acute conversion and chronic prevention of ventricular arrhythmias. AREAS COVERED Key trials related to antiarrhythmic drug use are reviewed, emphasizing the impact of recent discoveries. Sodium channel blockers are discussed with an emphasis on recently identified specialized uses. Beta blockers, amiodarone, sotalol, and dofetilide are discussed together in the context of structural heart disease, because they do not increase mortality in this group of patients. Other medications found to reduce ventricular arrhythmia burden are discussed last. EXPERT OPINION Since most patients with ventricular arrhythmias have structural heart disease, pharmacologic treatment is limited to amiodarone, d-,l-sotalol, and dofetilide (off-label indication), in conjunction with defibrillator implantation. While amiodarone has superior reduction in arrhythmias, its long-term extracardiac toxicities can cause significant morbidity. A trial of sotalol is reasonable if there are no contraindications, recognizing that over 20% of patients have to discontinue it because of adverse effects. Beta blockers are first line therapy for most patients. Genetic testing is particularly informative regarding treatment approach in long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic VT. Research should continue to focus on developing more effective antiarrhythmic medications with less long-term toxicity.
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Brugada syndrome and its relevance in the perioperative period.
Sorajja, D, Ramakrishna, H, Poterack, AK, Shen, WK, Mookadam, F
Annals of cardiac anaesthesia. 2015;(3):403-13
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Abstract
Brugada syndrome is an autosomal dominant genetic disorder associated with an increased risk of sudden cardiac death, as well as ventricular tachyarrhythmias.The defective cardiac sodium channels result in usual electrocardiographic findings of a coved-type ST elevation in precordial leads V1 to V3. The majority of patients have uncomplicated courses with anesthesia, surgery, and invasive procedures. However there is risk of worsening ST elevation and ventricular arrhythmias due to perioperative medications, surgical insult, electrolyte abnormalities, fever, autonomic nervous system tone, as well as other perturbations. Given the increasing numbers of patients with inherited conduction disorders presenting for non-cardiac surgery that are at risk of sudden cardiac death, safe anesthetic management depends upon a detailed knowledge of these conditions.
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Prinzmetal angina: ECG changes and clinical considerations: a consensus paper.
de Luna, AB, Cygankiewicz, I, Baranchuk, A, Fiol, M, Birnbaum, Y, Nikus, K, Goldwasser, D, Garcia-Niebla, J, Sclarovsky, S, Wellens, H, et al
Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc. 2014;(5):442-53
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Abstract
BACKGROUND We will focus our attention in this article in the ECG changes of classical Prinzmetal angina that occur during occlusive proximal coronary spasm usually in patients with normal or noncritical coronary stenosis. RESULTS The most important ECG change during a focal proximal coronary spasm is in around 50% of cases the appearance of peaked and symmetrical T wave that is followed, if the spasm persist, by progressive ST-segment elevation that last for a few minutes, and later progressively resolve. The most frequent ECG changes associated with ST-segment elevation are: (a) increased height of the R wave, (b) coincident S-wave diminution, (c) upsloping TQ in many cases, and (d) alternans of the elevated ST-segment and negative T wave deepness in 20% of cases. The presence of arrhythmias is very frequent during Prinzmetal angina crises, especially ventricular arrhythmias. The prevalence and importance of ventricular arrhythmias were related to: (a) duration of episodes, (b) degree of ST-segment elevation, (c) presence of ST-T wave alternans, and (d) the presence of >25% increase of the R wave. CONCLUSIONS The incidence of Prinzmetal angina is much lower then 50 years ago for many reasons including treatment with calcium channel blocks to treat hypertension and ischemia heart disease and the decrease of smoking habits.
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Effect of statins on ventricular tachyarrhythmia, cardiac arrest, and sudden cardiac death: a meta-analysis of published and unpublished evidence from randomized trials.
Rahimi, K, Majoni, W, Merhi, A, Emberson, J
European heart journal. 2012;(13):1571-81
Abstract
AIMS: The effect of statin treatment on ventricular arrhythmic complications is uncertain. We sought to test whether statins reduce the risk of ventricular tachyarrhythmia, cardiac arrest, and sudden cardiac death. METHODS AND RESULTS We searched MEDLINE, EMBASE, and CENTRAL up to October 2010. Randomized controlled trials comparing statin with no statin or comparing intensive vs. standard dose statin, with more than 100 participants and at least 6-month follow-up were considered for inclusion and relevant unpublished data obtained from the investigators. Twenty-nine trials of statin vs. control (113 568 participants) were included in the main analyses. In these trials, statin therapy did not significantly reduce the risk of ventricular tachyarrhythmia [212 vs. 209; odds ratio (OR) = 1.02, 95% confidence interval (CI) 0.84-1.25, P = 0.87] or of cardiac arrest (82 vs. 78; OR = 1.05, 95% CI 0.76-1.45, P = 0.84), but was associated with a significant 10% reduction in sudden cardiac death (1131 vs. 1252; OR = 0.90; 95% CI 0.82-0.97, P = 0.01). This compared with a 22% reduction in the risk of other 'non-sudden' (mostly atherosclerotic) cardiac deaths (1235 vs. 1553; OR = 0.78, 95% CI 0.71-0.87, P < 0.001). Results were not materially altered by inclusion of eight trials (involving 41 452 participants) of intensive vs. standard dose statin regimens. CONCLUSION Statins have a modest beneficial effect on sudden cardiac death. However, previous suggestions of a substantial protective effect on ventricular arrhythmic events could not be supported.
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[Intravenous fat emulsion: lipid therapy as a new antidote].
Fukumoto, M
Chudoku kenkyu : Chudoku Kenkyukai jun kikanshi = The Japanese journal of toxicology. 2012;(3):205-8
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[Amiodarone-induced thyroid gland dysfunctions].
Gassanov, N, Dietlein, M, Caglayan, E, Erdmann, E, Er, F
Deutsche medizinische Wochenschrift (1946). 2010;(16):807-11
Abstract
Amiodarone treatment affects thyroid status in about the half of patients. Amiodarone causes a wide spectrum of effects on the thyroid function including hypothyroidism and thyreotoxicosis. Amiodaron-induced thyroid dysfunction is the most reason for discontinuation of amiodaron therapy. In this report we describe amiodaron-induced thyroid dysfunction and the diagnostic and therapeutic challenges in such patients.
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Fetal ventricular tachycardia secondary to long QT syndrome treated with maternal intravenous magnesium: case report and review of the literature.
Simpson, JM, Maxwell, D, Rosenthal, E, Gill, H
Ultrasound in obstetrics & gynecology : the official journal of the International Society of Ultrasound in Obstetrics and Gynecology. 2009;(4):475-80
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Abstract
Ventricular tachycardia is a very rare fetal arrhythmia accounting for fewer than 2% of fetal tachycardias. We describe a fetus presenting at 30 weeks' gestation with ventricular tachycardia at a rate of 220 beats per min and fetal hydrops. The tachycardia was unresponsive to flecainide but was controlled within 12 h by an intravenous infusion of magnesium to the mother. Despite rapid control of the arrhythmia the fetus developed severe periventricular leukomalacia before birth for which a poor neurological prognosis was given. The baby was delivered preterm at 32 weeks' gestation and died on the sixth day after birth. Long QT syndrome was identified postnatally on the electrocardiogram, and was confirmed by genetic testing which showed a mutation in the KCNH2 gene (p.T613M).
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[Genetic of catecholaminergic polymorphic ventricular tachycardia: basic concepts].
Medeiros-Domingo, A
Archivos de cardiologia de Mexico. 2009;:13-7
Abstract
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a cardiac channelopathy characterized by altered intracellular calcium handling resulting in ventricular arrhythmias and high risk of cardiac sudden death in young cases with normal structural hearts. Patients present with exertional syncope and the trademark dysrhythmia is polymorphic and/or bidirectional ventricular tachycardia during exercise or adrenergic stimulation. Early detection of CPVT is crucial because opportune medical intervention prevents sudden cardiac death. Mutations in the ryanodine receptor RYR2 explain nearly 70% of the CPVT cases and cause the autosomic dominant form of the disease. Mutations in calsequestrin 2 causes a recessive form and explain less than 5% of all cases. Genetic screening in CPVT, besides providing early detection of asymptomatic carriers at risk, has provided important insights in the mechanism underlying the disease. Mutational analysis of RYR2 has been a challenge due to the large size of the gene, 105 exons encoded for 4,967 amino-acids. In this review we analyze general concepts of the disease, differential diagnosis and strategies for genetic screening.