Podcast: Amiodarone for preventing sudden cardiac death

A new Cochrane Review from December 2015 examines the effects of the drug amiodarone on the prevention of sudden cardiac death. The lead author, Juan Carlos Claro, from the Pontificia Universidad Católica de Chile, in Santiago, Chile, describes the review and its findings in this podcast.

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John: A new Cochrane Review from December 2015 examines the effects of the drug amiodarone on the prevention of sudden cardiac death. The lead author, Juan Carlos Claro, from the Pontificia Universidad Católica de Chile, in Santiago, Chile, describes the review and its findings in this Evidence Pod.

Juan Carlos: Sudden death is one of the main causes of cardiac death. It is most frequently provoked by coronary heart disease or structural heart abnormalities, which can facilitate the onset of ventricular arrhythmias that cause the heart to suddenly stop beating. Its prevention depends mainly on preventing coronary disease and reducing the onset of these arrhythmias. The most effective strategy for the latter is the Implantable Cardicac Defibrillator, but it’s very expensive and isn’t widely available in low and middle-income countries. One alternative is to use antiarrhythmic drugs, such as amiodarone, which we specifically examine in our review. Amiodarone is already known to be less effective than the Implantable Cardiac Defibrillator, but it is more available in non-wealthy countries. However, uncertainty about its relative effectiveness compared to other antiarrhythmics or placebo led to our review and we’ve found evidence that it might be beneficial.
We investigated the effects of amiodarone for primary prevention in patients at high risk of a cardiac arrest who have not suffered one previously, and for secondary prevention in people who had a cardiac arrest but recovered from it. We looked at comparisons with other antiarrhythmic drugs, placebo or no intervention. We were most interested in the effects on sudden cardiac death, any cardiac death, and all-cause mortality. We wanted to investigate quality of life as well, but there was insufficient evidence to do so. We also looked at adverse effects, because amiodarone has the potential to cause harms to various organs.
We found 24 randomized trials including a total of just under 10,000 participants. There were 18 studies in primary prevention, and the other 6 studies tested amiodarone for secondary prevention. The minimum follow-up in the included studies was 6 months, and many followed their participants for 1 year. We assessed the overall quality of the evidence as low because of the high risk of bias in the included studies and selective, biased reporting of findings.
For primary prevention, amiodarone was more effective than other antiarrhythmics or placebo or no intervention in reducing sudden cardiac death, cardiac death and all-cause mortality during the follow-up period. However, for secondary prevention, amiodarone was no better than placebo or other antiarrhythmics for any of these main outcomes. Turning to adverse effects, amiodarone increased the risk of pulmonary and thyroid problems, but there was insufficient information to allow us explore the severity of these side effects.
In summary, our review shows that amiodarone is moderately effective in reducing the risk of sudden cardiac death and deaths from all causes compared to placebo or other antiarrhythmic drugs for primary prevention in the medium term, but is not superior for these outcomes in secondary prevention. It increases the risk of pulmonary or thyroid side effects, but the severity of these effects remains uncertain.

John: If you would like to read more about the findings of the review, and access information on each of the included studies, go online to Cochrane Library dot com and search for 'amiodarone and cardiac death'.

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