Cardiac Arrhythmia Suppression Trial

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The Cardiac Arrhythmia Suppression Trial (CAST) was a double-blind, randomized, controlled study designed to test the hypothesis that suppression of premature ventricular complexes (PVC) with class I antiarrhythmic agents after a myocardial infarction (MI) would reduce mortality. It was conducted between 1986 and 1989 and included over 1700 patients in 27 centres.[1] The study found that the tested drugs increased mortality instead of lowering it as was expected.[2] The publication of these results in 1991/92, in combination with large follow-up studies for drugs that had not been tested in CAST, led to a paradigm shift in the treatment of MI patients. Class I and III antiarrhythmics are now only used with extreme caution after MI, or they are contraindicated completely.[3] Heart Rhythm Society Distinguished Scientist D. George Wyse was a member of the CAST trial's steering and executive committees.[citation needed]

Background

The study was prompted by the fact that patients who suffer from myocardial infarctions (MIs) have a high risk of sudden death, presumably due to

arrhythmia. Around the time of the study onset (1986), an estimated 8 to 15% of patients would die in the subsequent year following an MI, with about half of those deaths resulting from arrhythmia. This warranted the investigation as to whether PVC suppression could improve outcomes in post-MI patients. The trial was conducted by the National Heart, Lung, and Blood Institute.[citation needed
]

Study design

CAST was a multicenter, double-blind,

sudden cardiac death, and the secondary endpoint was all-cause mortality.[citation needed
]

The second Cardiac Arrhythmia Suppression Trial (CAST II) modified the enrollment criteria to include patients at higher risk for serious arrhythmia.

left ventricular ejection fraction lower than 40%, 3) prior to enrollment, suppression of PVCs had occurred with the drugs (vs. placebo) using a double-blinded design, and 4) patients having more serious arrhythmias would also be included.[citation needed
]

Results

The drugs used (encainide, flecainide, and moracizine) successfully reduced the amount of PVCs, but led to more arrhythmia-related deaths. Total mortality was significantly higher with both encainide and flecainide at a mean follow-up period of 10 months. Within about two years after enrollment, encainide and flecainide were discontinued because of increased mortality and sudden cardiac death. CAST II compared moracizine to placebo, but was also stopped because of early (within two weeks) cardiac death in the moracizine group, and long-term survival seemed highly unlikely. The excess mortality was attributed to proarrhythmic effects of the agents. Class I antiarrhythmics are proarrhythmic during

heart ischemia in animals. [5]

References

  1. PMID 2473403
    .
  2. PMID 1900101
    .
  3. ISBN 3-8047-1763-2
    .
  4. PMID 7851106
    .
  5. PMID 7994829
    .

External links
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