Coronary Artery Revascularization in Patients with Sustained Ventricular Arrhythmias
April 1, 2001 4 minutes read
Coronary Artery Revascularization in Patients with Sustained Ventricular Arrhythmias
Abstract & Commentary
Synopsis: A combination of coronary artery revascularization and antiarrhythmic therapy is required in patients with prior myocardial infarctions who present with sustained ventricular arrhythmias and an indication for revascularization.
Source: Brugada J, et al. J Am Coll Cardiol. 2001;37:529-533.
Brugada and colleagues from Barcelona describe a series of 64 consecutive patients who had a sustained ventricular arrhythmia (sustained monomorphic ventricular tachycardia or ventricular fibrillation with cardiac arrest) in the chronic phase after myocardial infarction who subsequently underwent coronary artery revascularization. Coronary artery revascularization was performed using either coronary artery bypass grafting (46 patients) or single or double percutaneous transluminal coronary angioplasty (16 patients). Patients underwent electrophysiologic testing with programmed ventricular stimulation at the time of coronary angiography and then again 3-15 days after the coronary revascularization was performed. There were no changes in antiarrhythmic drugs or beta-adrenergic blocking agent usage between the first and second studies. Patients with an inducible arrhythmia at the second study were treated with either antiarrhythmic drugs or an implantable cardioverter defibrillator.
Fifty-eight of the 64 patients were men, and the mean age for the entire group was 65 ± 8 years. The mean ejection fraction was 38 ± 9%, with 13 of the patients having ejection fractions less than 30%. The presenting arrhythmia had been sustained monomorphic ventricular tachycardia in 55 patients and ventricular fibrillation in the remaining 9 patients. Percutaneous transluminal coronary angioplasty was successfully performed in 16 patients with single or uncomplicated double-vessel disease. Coronary artery bypass grafting was performed in the remaining 48 patients. Two of the patients who underwent surgical intervention died at the time of surgery.
At the initial electrophysiologic study, 53 of the 55 patients with a clinical presentation of monomorphic ventricular tachycardia had inducible ventricular tachycardia (47) or ventricular fibrillation (6). Only 2 of these patients had no inducible arrhythmia. Among the 9 patients with ventricular fibrillation, 6 had inducible ventricular tachycardia, 2 had inducible ventricular fibrillation and 1 patient had no inducible arrhythmia. Fifty-nine patients with an inducible arrhythmia (ventricular tachycardia, 51 patients; ventricular fibrillation, 8 patients) at the time of the first electrophysiologic study underwent a second electrophysiologic study. At the follow-up electrophysiologic study, 52 of these 59 (88%) patients again had an inducible sustained ventricular arrhythmia. Five of 53 patients with inducible ventricular tachycardia had no inducible arrhythmia at the follow-up study. Two of 8 patients with inducible ventricular fibrillation had no inducible arrhythmia at the follow-up study. Three patients who had no inducible arrhythmia at the first study had no inducible arrhythmia at the follow-up study as well.
Thirty-six patients received an implantable cardioverter defibrillator (ICD) prior to discharge, and 14 of these 36 also received amiodarone. The remaining 26 patients with an inducible arrhythmia after revascularization were treated with either amiodarone (18) or sotalol (8). Among the 52 patients with inducible arrhythmia at the follow-up study, recurrent arrhythmias were documented after discharge in 28 (54%). Four of the 10 patients (40%) who had no inducible arrhythmia at their second study also had recurrent events. Events were somewhat more common in patients with the lowest ejection fractions. Nine of 13 patients (69%) with an ejection fraction of less than 30% had a recurrent arrhythmic event compared with 23 of 49 (47%) with an ejection fraction greater than 30% (P = .02).
Brugada et al conclude that coronary artery revascularization does not improve the arrhythmia substrate in a significant proportion of patients who presented with sustained ventricular arrhythmias. Sustained arrhythmias remain inducible in most patients after revascularization, and there is a high recurrence rate of clinical arrhythmias during follow-up. Brugada et al conclude that a combination of coronary artery revascularization and antiarrhythmic therapy is required in patients with prior myocardial infarctions who present with sustained ventricular arrhythmias and an indication for revascularization.
Comment by John P. DiMarco, MD, PhD
The beneficial effect of coronary revascularization on survival in patients with multivessel disease and decreased left ventricular function is well accepted. Among patients who initially presented with ventricular tachycardia or ventricular fibrillation, Kelly and associates reported that surgical coronary revascularization was an independent predictor of an improved outcome.1 However, the effect of revascularization on the risk of future arrhythmia remains poorly characterized. This paper is the largest study on this issue to date and it clearly indicates that revascularization alone does not favorably influence previously established stable arrhythmia substrates as identified by responses to programmed stimulation and clinical outcome.
Several years ago, the Coronary Artery Bypass Graft (CABG) Patch Trial reported that prophylactic ICD insertion at the time of bypass surgery did not favorably influence mortality during follow-up. A proposed explanation for that observation was that revascularization decreased the frequency of sustained ventricular arrhythmias. The difference from that study and this current one is that the patients in the current study by Brugada et al had already presented with ventricular arrhythmia. Therefore, they had previously defined themselves as a high-risk group with an established substrate for arrhythmia. The patients in the CABG Patch Trial had low ejection fractions but most probably had not yet developed a chronic substrate for ventricular arrhythmias. This study shows that once such a substrate becomes established, it is unlikely to be favorably affected by revascularization.
The conclusion we should take from this paper is that although revascularization may be effective in preventing the development for a substrate of arrhythmia and in preventing arrhythmias due to ischemia, once a stable substrate has developed, revascularization alone is not adequate therapy.
Reference
1. Kelly P, et al. J Am Coll Cardiol. 1990;15:267-273.
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