Survival with oral d-Sotalol in patients with left ventricular dysfunction after myocardial infarction: Rationale, design, and methods (the SWORD trial)

Waldo, Albert L.; Camm, A. John; deRuyter, Hans; Friedman, Peter L.; MacNeil, Daniel J.; Pitt, Bertram; Pratt, Craig M.; Rodda, Bruce E.; Schwartz, Peter J.; Investigators, The SWORD

doi:10.1016/s0002-9149(99)80717-6

Cited by 106 publications

(44 citation statements)

References 25 publications

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“…However, the results of trials of antiarrhythmic drugs have mostly been adverse: 4,5,19,20 antiarrhythmic drug therapy was associated with increased deaths, in most cases sudden and presumably arrhythmic, that were attributed to a proarrhythmic effect. Yusuf and colleagues' meta-analysis 21 of trials of antiarrhythmic drugs after myocardial infarction showed that sodium-channel blockers were harmful and that calcium-channel antagonists had no beneficial effects; by contrast, a favourable effect was observed with the use of amiodarone in a small population.…”

Section: Discussionmentioning

confidence: 99%

Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT

Julian¹,

et al. 1997

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Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT Julian, D.G.; Camm, A.J.; Frangin, G.; Janse, M.J.; Munoz, A.; Schwartz, P.J.; Simon, P. General rightsIt is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Download date: 22 Mar 2019Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT D G Julian, A J Camm, G Frangin, M J Janse, A Munoz, P J Schwartz, P Simon, for the European Myocardial Infarct Amiodarone Trial Investigators* THE LANCET SummaryBackground Ventricular arrhythmias are a major cause of death after myocardial infarction, especially in patients w it h poor left -vent ric ular func t ion. P revious at t empt s t o ident ify and suppress arrhy t hmias w it h v arious antiarrhythmic drugs failed to reduce or actually increase mortality. Amiodarone is a powerful antiarrhythmic drug with several potentially beneficial actions, and has shown benefit in several small-scale studies. We postulated that this drug might reduce mortality in patients at high risk of death after myocardial infarction because of impaired vent ric ular func t ion, irrespective of w hether they had ventricular arrhythmias.

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Section: Discussionmentioning

confidence: 99%

Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT

Julian¹,

et al. 1997

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“…While challenging, finding a reasonably specific, sensitive and cost-effective risk stratification tool to identify high risk patients for SCD has become a much needed end-point to reduce premature mortality. Pharmacological therapy targeting ion channels for preventing SCD failed to provide effective and reliable protection (7)(8)(9)(10). Alternative approaches with more upstream strategies targeted against the substrate of the VT and VF rather than downstream strategies targeting specific ion channels may eventually prove to be more effective and useful strategy.…”

Section: Resultsmentioning

confidence: 99%

“…The ventricles of patients with HCM have an 8-fold increase in matrix collagen (6) and increased collagen turnover rate (7). The DCM variant of heart failure also manifests increased collagen content (8) and increased collagen turnover rate (9,10). Furthermore, patients with aortic stenosis (AS) manifest increased interstitial fibrosis and collagen deposition that positively correlates with increased left ventricular end-diastolic pressure and decreased left ventricular ejection fraction (LVEF) (11) a marker of SCD (12).…”

Section: Myocardial Fibrosis; a New Target For Scd Preventionmentioning

confidence: 99%

Serum transforming growth factor-ß1 as a risk stratifier of sudden cardiac death

Sovari¹,

Morita

Weiss

et al. 2008

Medical Hypotheses

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Sudden cardiac death prematurely claims the lives of some 7 million each year worldwide. It occurs primarily in patients with an underlying structural cardiac abnormality, and regardless of the type of the underlying pathology (heart failure, dilated and hypertrophic cardiomyopathies, myocardial infarction and aging), death is almost always caused by ventricular tachycardia (VT) which rapidly degenerates to ventricular fibrillation (VF). Implantable cardioverter defibrillator is an effective but expensive therapy for preventing SCD, and finding a reasonably specific, sensitive and cost-effective risk stratification tool for patients at high risk of sudden cardiac death will have great clinical utility in preventing premature sudden cardiac death. Increased myocardial fibrosis has been shown to develop in a wide range of cardiac diseases all manifesting increased risk of VT and VF. Clinical and experimental studies attribute a major role for fibrosis in the initiation of VT, VF and sudden cardiac death. Transforming growth factor-beta1 (TGF-beta1) has been shown to promote myocardial tissue fibrosis and perhaps more importantly in cardiac conditions associated with increased myocardial fibrosis are shown to be positively correlated with increased serum levels of TGF-beta1. In the present hypothesis we suggest that monitoring the serum levels of TGF-beta1 may be a cost-effective risk stratifier to identify patients at high risk of sudden cardiac death caused by VT and VF. BACK GROUND AND THE SCOPE OF THE PROBLEMSudden cardiac death (SCD) prematurely claims each year the lives of more than 300,000 Americans (1) and some 7 million worldwide, and is almost always caused by ventricular tachycardia (VT) that rapidly degenerates to ventricular fibrillation (VF) (1).Myocardial tissue electrical heterogeneity and myocardial structural remodeling such as interstitial fibrosis have been traditionally considered to play a major role in promoting activation wave front instabilities (wavebreaks) that degenerate to VF (2-4). Experimental studies have shown that atrial (5) and ventricular (6) fibrosis considerably increase the incidence of atrial fibrillation and VF initiated by triggered activity. At the present there is no reliable pharmacological approach to effectively prevent VT and VF and as such the placement of implantable cardioverter defibrillator (ICD) remains the only effective approach against SCD (4). Identification of non-invasive markers of SCD can be of considerable benefit to reduce premature mortality in high risk patients in a cost-effective manner. MYOCARDIAL FIBROSIS; A NEW TARGET FOR SCD PREVENTIONFibrosis is characterized by increased deposition of collagenous septa forming insulating barriers within bundles of myocardial cells, and increased density of myocardial fibroblasts and their differentiated active phenotype, myofibroblasts. Myocardial fibrosis is a common feature of diverse types of cardiac diseases that are associated with increased risk of VT and VF causing SCD (1). These conditions i...

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“…It is not clear whether it is the beta-blocking effect or the class III effect that is important for sotalol. In the SWORD Trial, d-sotalol resulted in more arrhythmic deaths than placebo in patients with left ventricular ejection fraction c40% and either a recent (6-42 days) myocardial infarction or symptomatic heart failure with a remote (>42 days) myocardial infarction [33,34] . Antz et al suggested from their randomized study that metoprolol (16 patients) is as effective as dl-sotalol (18 patients) in patients with documented sustained ventricular tachycardia [35] .…”

Section: Efficacy Of Sotalol and Amiodarone In Preventing Death From mentioning

confidence: 99%

Comparison of sotalol with amiodarone for long-term treatment of spontaneous sustained ventricular tachyarrhythmia based on coronary artery disease

Kovoor

Eipper

Cooper

et al. 1999

European Heart Journal

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Aim To compare the efficacy of sotalol versus amiodarone for long-term treatment of ventricular tachyarrhythmias.Methods Patients (n=75) with spontaneous, sustained ventricular tachyarrhythmias secondary to remote myocardial infarction were studied. After intravenous electrophysiological testing, both sotalol and amiodarone were predicted to be ineffective in 50 (67%) patients. Five patients were excluded. Forty-five patients were randomized to receive sotalol (n=22) or amiodarone (n=23) for maintenance therapy. The primary outcome variable was the time to first recurrence of sustained ventricular tachyarrhythmia.Results At 36 months, 75% of those allocated sotalol remained free of ventricular tachyarrhythmia compared with 38% of those allocated amiodarone (P=0·05). On multivariate analysis the risk of recurrence of ventricular tachyarrhythmia for patients on amiodarone was 5·9 times higher (P=0·008) than that for patients on sotalol.Conclusion Sotalol is superior to amiodarone for longterm treatment of ventricular tachyarrhythmia secondary to coronary artery disease when both drugs have been predicted to be ineffective at intravenous electrophysiological testing. Randomized trials in larger numbers of patients with ventricular tachyarrhythmia need to be performed comparing the two agents directly. (Eur Heart J 1999; 20: 364-374)

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Survival with oral d-Sotalol in patients with left ventricular dysfunction after myocardial infarction: Rationale, design, and methods (the SWORD trial)

Cited by 106 publications

References 25 publications

Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT

Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT

Serum transforming growth factor-ß1 as a risk stratifier of sudden cardiac death

Comparison of sotalol with amiodarone for long-term treatment of spontaneous sustained ventricular tachyarrhythmia based on coronary artery disease

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