Role of implantable cardioverter defibrillator therapy in patients with acquired long QT syndrome: A long-term follow-up

Mönnig, Gerold; Köbe, Julia; Löher, Andreas; Wasmer, Kristina; Milberg, Peter; Zellerhoff, Stephan; Pott, Christian; Zumhagen, Sven; Radu, Razvan I; Scheld, Hans H.; Haverkamp, Wilhelm; Schulze‐Bahr, Eric; Eckardt, Lars

doi:10.1093/europace/eur316

Cited by 33 publications

(24 citation statements)

References 23 publications

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“…It should be highlighted, however, that an unknown percentage of supposedly high risk drug induced long QT patients have congenital LQTS and would therefore be entitled to an ICD implantation according to current recommendations. Moreover, the study by Mönnig et al supported the need for a more aggressive preventive strategy in ALQTS patients surviving cardiac arrest 26. This study suggested the proarrhythmic risk in this study population is not due solely to a transient trigger but an underlying persistent predisposition or exposure to other as yet unrecognised factors that cause QT prolongation.…”

Section: Clinical Managementsupporting

confidence: 57%

“…Their study was the first to use a continuous multi-lead QT/QTc monitoring system to examine QT prolongation in an acutely ill hospitalised population, and the authors suggested it could be prudent to provide QT monitoring to all acutely ill patients with multiple risk factors for QT prolongation. A study by Mönnig et al brought invaluable data to our current understanding of the real risk underlying ALQTS 26. The authors evaluated the long term follow-up of patients with ALQTS who had received an ICD for secondary prevention of sudden cardiac arrest and reported that appropriate shocks occurred in 44% of patients during a mean follow-up of 84±55 months—128 shocks in 19 of 43 patients, secondary to polymorphic VT and ventricular fibrillation.…”

Section: Clinical Managementmentioning

confidence: 99%

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Post-acute management of the acquired long QT syndrome

Barra

Agarwal

Begley

et al. 2014

Postgraduate Medical Journal

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The mechanisms underlying drug induced QT prolongation and the immediate treatment of torsade de pointes have been extensively studied but the post-acute management of the Acquired Long QT Syndrome (ALQTS) remains to be addressed. We aimed to review the state of the art data regarding risk stratification, arrhythmic prevention and treatment of patients with ALQTS. A comprehensive review of the scientific data collectable from MEDLINE, EMBASE and COCHRANE (from inception to April 2013) was performed, and descriptive and qualitative information was extracted from the most relevant manuscripts. QT prolonging drugs are widely used in hospital clinical practice, and several studies have shown a high prevalence of QT interval prolongation in patients admitted to hospital and a high rate of prescription of QT interval prolonging drugs to patients presenting with QT interval prolongation. Therefore, the acute and post-acute management of ALQTS is of the utmost importance. Avoidance of offending triggers, electrocardiographic screening, pacing at a relatively fast lower rate limit and using pause prevention programming (preferably with concomitant β blocker treatment), implantable defibrillators in the highest risk patients, genetic testing and counselling in selected cases, and family screening are among the potentially applicable strategies. The latter is justifiable by the fact that some studies unveiled a surprisingly similar positive mutation rate in drug induced LQTS compared with congenital LQTS, supporting the hypothesis that the former can be regarded as a latent form of the latter. Drug challenge with D,L-sotalol in suspected LQTS and treatment with a carvedilol analogue, verapamil or an Ikr activating drug are still in need of further investigation. The post-acute management of patients with ALQTS has received scarce attention in the past, probably due to the fact that it is considered a reversible phenomenon in most cases. Considering the relatively high risk of arrhythmic recurrence in the highest risk ALQTS patients, effective preventive and treatment strategies are warranted, and further research is needed.

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Section: Clinical Managementsupporting

confidence: 57%

Section: Clinical Managementmentioning

confidence: 99%

Post-acute management of the acquired long QT syndrome

Barra

Agarwal

Begley

et al. 2014

Postgraduate Medical Journal

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“…1, 2 Occasionally, the condition is congenital, caused by mutation(s) in one of the genes encoding cardiac ion channel subunits or auxiliary proteins. 3–7 More commonly, it is acquired, 8–10 caused by exposure to certain medications, electrolyte abnormalities or coronary ischemia. The mechanism linking action potential (AP) prolongation to ventricular arrhythmias remains incompletely understood.…”

Section: Introductionmentioning

confidence: 99%

Synchronous Systolic Subcellular Ca ²⁺ -Elevations Underlie Ventricular Arrhythmia in Drug-Induced Long QT Type 2

Kim

Němec

et al. 2015

Circ: Arrhythmia and Electrophysiology

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Background Repolarization-delay is a common clinical problem which can promote ventricular arrhythmias. In myocytes, abnormal sarcoplasmic reticulum Ca2+-release is proposed as the mechanism that causes early afterdepolarizations, the cellular equivalent of ectopic-activity in drug-induced long QT syndrome. A crucial missing link is how such a stochastic process can overcome the source-sink mismatch to depolarize sufficient ventricular tissue to initiate arrhythmias. Methods and Results Optical maps of action potentials (APs) and Ca2+-transients (CaT) from Langendorff rabbit hearts were measured at low (150×150 μm2/pixel) and high (1.5×1.5 μm2/pixel) resolution before and during arrhythmias. Drug-induced long QT type 2, elicited with dofetilide inhibition, produced spontaneous Ca2+-elevations during diastole and systole, before the onset of arrhythmias. Diastolic Ca2+− waves appeared randomly, propagated within individual myocytes, were out-of-phase with adjacent myocytes and often died-out. Systolic secondary Ca2+− elevations were synchronous within individual myocytes, appeared 188±30ms after the AP-upstroke, occurred during high cytosolic-Ca2+ (40–60% of peak-CaT), appeared first in small islands (0.5×0.5 mm2) that enlarged and spread throughout the epicardium. Synchronous systolic Ca2+-elevations preceded voltage-depolarizations (9.2±5ms, n=5) and produced pronounced Spatial Heterogeneities of CaT-durations and AP-durations. Early afterdepolarizations originating from sites with the steepest gradients of membrane-potential propagated and initiated arrhythmias. Interestingly, more complex subcellular Ca2+-dynamics (multiple chaotic Ca2+-waves) occurred during arrhythmias. K201, a ryanodine receptor stabilizer, eliminated Ca2+-elevations and arrhythmias. Conclusions The results indicate that systolic and diastolic Ca2+-elevations emanate from sarcoplasmic reticulum Ca2+-release and systolic Ca2+-elevations are synchronous because of high cytosolic and luminal-sarcoplasmic reticulum Ca2+ which overcomes source-sink mismatch to trigger arrhythmias in intact hearts.

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“…Patients that progress to TdP should receive intravenous magnesium sulphate and trans-venous cardiac pacing [41,42]. In patients that develop VF the use of an ICD should also be considered [43].…”

Section: Discussionmentioning

confidence: 99%

Torsades de pointesfollowing clarithromycin treatment

Gysel

Vieweg

Hasnain

et al. 2013

Expert Review of Cardiovascular Therapy

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A 75-year-old woman presenting with pre-syncope, shortness of breath and nausea was admitted to the emergency department following treatment with clarithromycin. Shortly after admission she developed a prolonged QT interval leading to torsades de pointes (TdP) and cardiac arrest. She was successfully cardioverted and clarithromycin was discontinued resulting in restoration of her usual QT interval. This case is an example of acquired long QT syndrome; a disorder that can be precipitated by macrolide antibiotics such as clarithromycin. Additional risk factors present in this case include: female gender, old age, heart disease, hypokalemia and hypomagnesemia. In this manuscript we comprehensively review past cases of clarithromycin-induced long QT syndrome (LQTS) and discuss them within the context of this case.

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Role of implantable cardioverter defibrillator therapy in patients with acquired long QT syndrome: A long-term follow-up

Abstract: Appropriate ICD shocks are a common finding in patients with aLQTS and SCA irrespective of the underlying cause or structural heart disease. Thus, even in the presence of relevant acquired proarrhythmia ICD may be beneficial.

Cited by 33 publications

References 23 publications

Post-acute management of the acquired long QT syndrome

Post-acute management of the acquired long QT syndrome

Synchronous Systolic Subcellular Ca ²⁺ -Elevations Underlie Ventricular Arrhythmia in Drug-Induced Long QT Type 2

Torsades de pointesfollowing clarithromycin treatment

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Role of implantable cardioverter defibrillator therapy in patients with acquired long QT syndrome: A long-term follow-up

Abstract: Appropriate ICD shocks are a common finding in patients with aLQTS and SCA irrespective of the underlying cause or structural heart disease. Thus, even in the presence of relevant acquired proarrhythmia ICD may be beneficial.

Cited by 33 publications

References 23 publications

Post-acute management of the acquired long QT syndrome

Post-acute management of the acquired long QT syndrome

Synchronous Systolic Subcellular Ca 2+ -Elevations Underlie Ventricular Arrhythmia in Drug-Induced Long QT Type 2

Torsades de pointesfollowing clarithromycin treatment

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Product

Resources

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Synchronous Systolic Subcellular Ca ²⁺ -Elevations Underlie Ventricular Arrhythmia in Drug-Induced Long QT Type 2