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Abstract & Commentary
Synopsis: Patients considered to have either a transient or a correctable cause for life-threatening VT or VF remain at high risk during follow-up.
Source: Wyse DG, et al. J Am Coll Cardiol. 2001;38: 1718-1724.
Wyse and colleagues from the antiarrhythmics vs. Implantable Defibrillators (AVID) study analyzed survival data for patients who were initially identified by the AVID investigators as having ventricular tachycardia (VT) or ventricular fibrillation (VF) associated with a transient or correctable cause.
The AVID trial was a study that compared antiarrhythmic drug therapy to defibrillator implantation as primary therapy in patients with either cardiac arrest or hypotensive VT. In addition, investigators at the 56 clinical sites were requested to screen patients with sustained VT or VF at their hospital and include them in a registry even if they were not eligible for randomization or refused enrollment. One of the exclusion criteria was VT or VF caused for identified factors believed to be transient or reversible in nature. Examples of such reversible causes included a new Q wave or non-Q wave myocardial infarction (MI), an acute ischemic event without infarction, a proarrhythmic drug reaction, severe electrolyte imbalance, or other situations including illicit drug use, hypoxia, electrocution, or drowning. In this paper, Wyse et al compare outcomes in patients who had an out-of-hospital episode of sustained VT or VF that was reported as being due to a transient or correctable cause to other patients with sustained arrhythmias who were included in the trial and registry.
During the course of the trial, 4450 patients were entered in the registry. Only patients whose index arrhythmias occurred out-of-hospital were included in this analysis. Patients who were in the randomized portion of AVID were seen in follow-up by the study investigators. Mortality data for the patients in the nonrandomized portion of the study were obtained using the National Death Index Service. There were 2013 registry patients who had out-of-hospital sustained VT or VF that was not thought to be due to a transient or correctable cause, called "primary VT/VF" and 278 patients with VT or VF thought to have a transient or correctable cause.
An acute ischemic event, including a new MI, was the most common reversible cause identified in 183 of 278 patients (66%). Electrolyte imbalance (27 patients, 9.7%), antiarrhythmic drug reactions (18 patients, 6.5%), and miscellaneous causes (50 patients, 17.9%) were the other reversible causes identified. Patients with VT or VF thought due to reversible causes tended to be slightly younger and have better ejection fractions than did the other patients. The patients with primary VT or VF also less frequently had histories of MI, congestive heart failure, prior revascularization, or prior arrhythmias. When cumulative survival was measured, there was no difference in survival between the patients with transient vs. primary VT/VF. However, because of baseline imbalances between the 2 groups, survival was adjusted for 5 variables known to affect survival (age, ejection fraction, coronary artery disease, prior coronary artery bypass grafting, and use of aspirin). After adjustment, survival in the group with transient causes was actually worse than among those with primary VT and VF. Wyse et al however noted that the local investigators were also uncertain about the reversible nature of the causes of VT and VF in their patients. Forty-six percent of these patients were on either an antiarrhythmic drug or had received defibrillator at the time of discharge.
Wyse et al concluded that patients considered to have either a transient or a correctable cause for life-threatening VT or VF remain at high risk during follow-up. This high mortality risk argues for aggressive therapy directed at the potentially reversible causes, but it also argues for ICD implantation should corrective therapy fail.
There are many uncertainties involved in the evaluation of patients resuscitated with life-threatening ventricular arrhythmias. Ischemia, electrolyte imbalance, other electrophysiologic abnormalities (preexcitation), etc, may all serve as triggers for potential arrhythmias. However, most patients with VT or VF also have an abnormal substrate that makes them susceptible to recurrence under a variety of circumstances. This paper points out that identical or similar triggers for arrhythmia are likely to occur in many patients and simply directing therapy at a single identified trigger may not be sufficient.
There clearly are some patients who have a completely reversible cause for a cardiac arrest. The patient with Wolff-Parkinson-White syndrome who develops rapid preexcited AF with rapid rates, which then degenerates to VF, would be one example. A procedure to ablate the accessory pathway should completely eliminate the risk of recurrence. A patient with normal baseline ventricular function who arrests with ischemic chest pain during exercise and is then completely revascularized is also unlikely to require long-term antiarrhythmic therapy. In most patients, however, there is an abnormal underlying substrate due to either coronary disease or myocardial disease, and if this disease is severe, either the same trigger or another trigger may occur and again result in VT or VF.
This paper underlines the need for a comprehensive evaluation for patients with arrhythmias who are resuscitated from a life-threatening arrhythmia. They require a comprehensive evaluation that is directed to both prevention of transient events that trigger arrhythmias as well as some long-term antiarrhythmic strategy for all except the lowest-risk patients. At the present time, defibrillator therapy provides the most beneficial protection for most of these individuals.
Dr. DiMarco is Professor of Medicine, Division of Cardiology, University of Virginia, Charlottesville.