Amiodarone‐Induced Giant T Wave Alternans Hastens Proarrhythmic Response

Tomcsányi, János; Somlói, Miklós; Horváth, L

doi:10.1046/j.1540-8167.2002.00629.x

Cited by 12 publications

(7 citation statements)

References 2 publications

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“…[56][57][58][59]62,63 QT interval prolongation sets the stage for increased spatial heterogeneity of repolarization across the ventricular wall, 64 leading to increased intracellular calcium levels and predisposing to afterdepolarizations. [56][57][58][59]62,63 QT interval prolongation sets the stage for increased spatial heterogeneity of repolarization across the ventricular wall, 64 leading to increased intracellular calcium levels and predisposing to afterdepolarizations.…”

Section: Proarrhythmia and Twa With Noncardiac Medicationsmentioning

confidence: 99%

Usefulness of T‐Wave Alternans in Sudden Death Risk Stratification and Guiding Medical Therapy

Nieminen¹,

Verrier²

2010

Noninvasive Electrocardiol

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Visible T-wave alternans (TWA), a beat-to-beat alternation in the morphology and amplitude of the ST segment or T wave, has been observed for over a century to occur in association with life-threatening arrhythmias in patients with acute coronary syndrome, heart failure, and cardiac channelopathies. This compelling linkage prompted development of quantitative techniques leading to FDA-cleared commercial methodologies for measuring nonvisible levels of TWA in the frequency and time domains. The first aim of this review is to summarize evidence from more than a hundred studies enrolling a total of >12,000 patients that support the predictivity of TWA for cardiovascular mortality and sudden cardiac death. The second focus is on the usefulness of TWA in guiding therapy. Until recently, TWA has been used primarily in decision making for cardioverter-defibrillator implantation. Its potential utility in guiding pharmacologic therapy has been underappreciated. We review clinical literature supporting the usefulness of TWA as an index of antiarrhythmic effects and proarrhythmia for different drug classes. Beta-adrenergic and sodium channel-blocking agents are the most widely studied drugs in clinical TWA investigations, with both reducing TWA magnitude; the exception is patients in whom sodium channel blockade discloses the Brugada syndrome and provokes macroscopic TWA. An intriguing possibility is that TWA may help to detect beneficial effects of nonantiarrhythmic agents such as the angiotensin II receptor blocker valsartan, which indirectly protects from arrhythmia through improving myocardial remodeling. We conclude that quantitative analysis of TWA has considerable potential to guide pharmacologic intervention and thereby serve as a therapeutic target.

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Section: Proarrhythmia and Twa With Noncardiac Medicationsmentioning

confidence: 99%

Usefulness of T‐Wave Alternans in Sudden Death Risk Stratification and Guiding Medical Therapy

Nieminen¹,

Verrier²

2010

Noninvasive Electrocardiol

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“…Moreover, treatment with d-sotalol or verapamil has also been shown to suppress TWA. However, there are published case reports documenting macroscopic TWA following administration of either sotalol or amiodarone19; 44; 46. Whether this was an indication of toxic levels of either drug needs further investigation.…”

Section: How Do Commonly Used Medications Affect Twa?mentioning

confidence: 99%

Explaining the clinical manifestations of T wave alternans in patients at risk for sudden cardiac death

Cutler

Rosenbaum

2009

Heart Rhythm

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The mechanisms underlying sudden cardiac death (SCD) are complex and diverse. Therefore, correct application of any marker to risk stratify patients for appropriate therapy requires knowledge regarding how the marker is reflective of a particular electro-anatomical substrate for arrhythmias. Non-invasive measurement of beat-to-beat alternation of the electrocardiographic T-wave, referred to as T-wave alternans (TWA), is an important marker of risk for sudden cardiac death (SCD). Is this relationship a mere association or is TWA mechanistically linked to SCD? Recent experimental evidence strongly supports a mechanistic relationship between TWA and SCD. This review will consider the underlying mechanisms of TWA derived from experimental studies, as they relate to clinical observations of TWA in humans, addressing the following questions derived from common clinical observations: 1) Where does TWA on the surface ECG come from? 2) Why is controlled heart rate elevation required to elicit TWA? 3) Why is TWA associated with risk for SCD? 4) Why is TWA associated with a broad range of ventricular arrhythmias? and 5) How do commonly used medications affect TWA?

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“…It has been established clinically that administration of β‐adrenergic blockade 34,35 or other antiarrhythmic agents 36,37 suppresses TWA magnitude, but this effect does not interfere with its predictive capacity, presumably because the parameter accurately reflects suppression of ventricular arrhythmias. Visible TWA has also been reported in cases of drug‐induced torsade de pointes or ventricular fibrillation 11,28,38–41 . New technology for TWA monitoring of ambulatory ECGs permits quantitation of TWA magnitude during daily life even in nonvisible ranges 7,42,43 …”

Section: Editorial Commentmentioning

confidence: 99%

“…Visible TWA has also been reported in cases of drug-induced torsade de pointes or ventricular fibrillation. 11,28,[38][39][40][41] New technology for TWA monitoring of ambulatory ECGs permits quantitation of TWA magnitude during daily life even in nonvisible ranges. 7,42,43 It is also important to recognize that depending on the pathophysiology, alternation may be more marked in the first half of the T wave, 4,5 whereas in channelopathies such as the long QT 27 and Brugada syndromes, 28,29 the entire T wave alternates.…”

Section: Editorial Commentmentioning

confidence: 99%