Stewart RB, Bardy GH, Greene HL.
Wide complex tachycardia: misdiagnosis and outcome after emergent therapy.
Ann Intern Med. 1986 Jun;104(6):766-71. doi: 10.7326/0003-4819-104-6-766.
Abstract/Text
The extent and consequence of misdiagnosis of wide complex tachycardia (QRS, 120 ms or more; heart rate, 100 or more beats/min) presenting emergently were assessed. Forty-six consecutive episodes of wide complex tachycardia were reviewed and their tachycardia mechanisms subsequently established. All 8 episodes of supraventricular tachycardia with aberrant conduction were correctly diagnosed, whereas 15 of 38 episodes of ventricular tachycardia (39%) were misdiagnosed as supraventricular tachycardia at the time initial therapy was given. Ventriculoatrial dissociation was evident in 11 (73%) of the electrocardiograms of misdiagnosed ventricular tachycardia. Patients with misdiagnosed episodes had poorer outcomes than those with episodes correctly diagnosed (p = 0.0003). Verapamil was administered to patients in 13 of the 15 episodes of misdiagnosed ventricular tachycardia; hemodynamic deterioration occurred in all 13 episodes. Wide complex tachycardia is often incorrectly diagnosed as supraventricular tachycardia when, in fact, the 12-lead electrocardiogram strongly suggests ventricular tachycardia. Verapamil is commonly administered in these circumstances and is frequently associated with a poor outcome.
Akhtar M, Shenasa M, Jazayeri M, Caceres J, Tchou PJ.
Wide QRS complex tachycardia. Reappraisal of a common clinical problem.
Ann Intern Med. 1988 Dec 1;109(11):905-12. doi: 10.7326/0003-4819-109-11-905.
Abstract/Text
BACKGROUND AND PURPOSE: Despite available criteria, diagnosis of the mechanisms of wide complex tachycardia is often incorrect. We aimed in this study to identify reasons for misdiagnoses and the value and limitations of clinical and surface electrocardiographic criteria.
DATA IDENTIFICATION: The analyzed data of 150 consecutive patients with wide QRS tachycardia from this study and a literature search of key papers in English since 1960 on clinical and surface electrocardiographic criteria form the basis of this report. The final correct diagnosis was made with intracardiac electrograms.
DATA EXTRACTION AND ANALYSIS: Among the 150 patients, 122 had ventricular tachycardia, 21 had supraventricular tachycardia with aberrant conduction, and 7 had accessory pathway conduction. Only 39 of 122 patients with ventricular tachycardia were correctly diagnosed initially. In others, the diagnoses were supraventricular tachycardia with aberrant conduction (43 of 122) or simply a wide QRS tachycardia (40 of 122). Misdiagnosis in patients with aberrant or accessory pathway conduction was also common. Standard electrocardiographic criteria for ventricular tachycardia had unacceptable sensitivity, poor specificity, or both. Collectively such criteria allowed a correct diagnosis of ventricular tachycardia in 92% of cases. Diagnosis of ventricular tachycardia was also suggested by its association with structural heart disease. Criteria suggestive of ventricular tachycardia included atrioventricular dissociation, positive QRS concordance, axis less than -90 deg to +/- 180 deg, combination of left bundle branch block and right axis, QRS duration of greater than 140 ms with right bundle branch block and greater than 160 ms with left bundle branch block and, a different QRS during tachycardia compared to baseline preexisting bundle branch block.
CONCLUSIONS: Ventricular tachycardia is the commonest underlying mechanism for wide QRS tachycardia. A correct diagnosis can usually be made from clinical and surface electrocardiographic criteria.
Gupta AK, Thakur RK.
Wide QRS complex tachycardias.
Med Clin North Am. 2001 Mar;85(2):245-66, ix-x. doi: 10.1016/s0025-7125(05)70315-1.
Abstract/Text
Wide QRS complex tachycardia is a common clinical occurrence and presents a diagnostic challenge for the physician. History, physical examination, chest radiographs, and electrocardiographic analysis are important in making the correct diagnosis. Diagnosis of ventricular tachycardia is supported by history of prior myocardial infarction or congestive heart failure, physical examination showing cannon A-waves in the jugular venous pulsation or variable heart sounds, chest radiograph showing cardiomegaly or evidence of prior cardiac surgery, and characteristic ECG features: AV dissociation, fusion/capture beats, QRS concordance or typical morphologic features in leads V1 and V6. In this article, a clinical approach to wide QRS complex tachycardias is presented.
Tchou P, Young P, Mahmud R, Denker S, Jazayeri M, Akhtar M.
Useful clinical criteria for the diagnosis of ventricular tachycardia.
Am J Med. 1988 Jan;84(1):53-6. doi: 10.1016/0002-9343(88)90008-3.
Abstract/Text
Misdiagnosis occurs upon initial presentation to medical attention in a considerable number of patients referred for evaluation of wide QRS tachycardia. In order to improve diagnostic accuracy (ventricular versus supraventricular tachycardia), the answers to two key bedside questions were prospectively evaluated: (1) Had the patient experienced a prior myocardial infarction? (2) Did symptoms of tachyarrhythmia start only after the infarction? A patient presenting with a wide QRS tachycardia was considered to have ventricular tachycardia if he or she answered in the affirmative to both of these questions. Of 31 consecutive patients referred with electrocardiographically documented sustained wide QRS tachycardia that was reproduced in the electrophysiology laboratory, the diagnoses made when the patients first presented to medical attention were ventricular tachycardias in 17 patients and supraventricular tachycardias in 14 patients. Following electrophysiologic evaluation, 29 were diagnosed as having ventricular tachycardia and two as supraventricular tachycardia. If the diagnoses were made solely on the basis of responses to the bedside questions mentioned earlier, 28 of the 29 patients having a final diagnosis of ventricular tachycardia would have been correctly identified. It is concluded that the use of these two questions can be very helpful in improving the clinical diagnosis of ventricular tachycardia.
Brooks R, Burgess JH.
Idiopathic ventricular tachycardia. A review.
Medicine (Baltimore). 1988 Sep;67(5):271-94. doi: 10.1097/00005792-198809000-00001.
Abstract/Text
Idiopathic or unexplained VT occurs in a small but important subset of patients without clinically evident heart disease. The majority of these patients appear to have a structurally normal heart. The cause of the arrhythmias in these individuals is unclear and may never be recognized. Other patients with this condition may have minor abnormalities not sufficient to impair overall cardiac function. The significance of these abnormalities to the genesis of the arrhythmia is uncertain. Whether patients with minor abnormalities are more likely to harbor covert heart disease such as myocarditis or a focal defect is not known, nor is it resolved whether such patients warrant a more aggressive search for a structural cause. The question that remains in any patient not subjected to surgical or pathological exploration is whether undetermined heart disease is responsible for the arrhythmia. Continued correlation between functional (electrophysiological) and structural (pathological) data will provide meaningful information concerning the pathophysiology (substrate) of these arrhythmias. Because of the preservation of normal cardiac function, these arrhythmias are generally well-tolerated. Although the condition is usually associated with a favorable prognosis, the occasional deaths reported in patients with apparently idiopathic ventricular arrhythmias may not permit calling this condition benign. It would be important to know the extent to which unrecognized abnormalities play a role in the genesis of these tachycardias, and whether such patients are more predisposed to fatal arrhythmias or have a different natural history. If cases involving undetermined or covert heart disease were excluded from consideration, then a relatively homogeneous disease-free group may be identified with a truly benign condition and a uniformly favorable prognosis. In these cases, a primary electrical abnormality may prove to be the basis for the arrhythmia. These issues remain to be elucidated in future studies.
Ohe T, Aihara N, Kamakura S, Kurita T, Shimizu W, Shimomura K.
Long-term outcome of verapamil-sensitive sustained left ventricular tachycardia in patients without structural heart disease.
J Am Coll Cardiol. 1995 Jan;25(1):54-8. doi: 10.1016/0735-1097(94)00324-j.
Abstract/Text
OBJECTIVES: This study attempted to determine the long-term outcome of verapamil-sensitive sustained left ventricular tachycardia in patients without apparent structural heart disease.
BACKGROUND: Several types of idiopathic ventricular tachycardia have been reported, and their clinical, electrophysiologic and electropharmacologic characteristics are different. It is possible that the prognosis of each type of ventricular tachycardia might also be different.
METHODS: We studied mortality and morbidity in 37 consecutive patients (27 male, 10 female; mean [+/- SD] age 33 +/- 14 years) with verapamil-sensitive sustained left ventricular tachycardia who had no apparent structural heart disease. Patients were followed up for 1 to 13 years (mean 5.8). Verapamil repeatedly terminated ventricular tachycardia in all patients. Ventricular tachycardia originated from the inferior and inferoseptal regions of the left ventricle in 33 patients and the superior and superioseptal regions in 4. Severity of ventricular tachycardia was classified according to the extent to which symptoms limited daily activities. Ventricular tachycardia was mild (minimal limitation) in 14 patients, moderate (some limitation) in 17 and severe (severe limitation) in 6.
RESULTS: Fourteen patients with mild ventricular tachycardia were followed up without any drug therapy, and the ventricular tachycardia remained mild in all patients. Antiarrhythmic therapy was initiated empirically in the 23 patients with moderate and severe ventricular tachycardia (verapamil in 20, propranolol in 2, digoxin in 1). Moderate ventricular tachycardia became mild ventricular tachycardia after drug therapy in all patients, but the six patients with severe ventricular tachycardia showed no improvement. The six patients with severe ventricular tachycardia had nonpharmacologic therapy (cryosurgery in one, catheter ablation in four, antitachycardia pacing device in one). During the follow-up period, all patients remained alive except for one who died suddenly after implantation of an antitachycardia pacing device.
CONCLUSIONS: 1) The long-term prognosis of verapamil-sensitive sustained left ventricular tachycardia in patients without apparent structural heart disease is good. 2) Verapamil is the drug of choice for alleviating symptoms, but nonpharmacologic therapy is necessary in some patients.
Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators.
A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias.
N Engl J Med. 1997 Nov 27;337(22):1576-83. doi: 10.1056/NEJM199711273372202.
Abstract/Text
BACKGROUND: Patients who survive life-threatening ventricular arrhythmias are at risk for recurrent arrhythmias. They can be treated with either an implantable cardioverter-defibrillator or antiarrhythmic drugs, but the relative efficacy of these two treatment strategies is unknown.
METHODS: To address this issue, we conducted a randomized comparison of these two treatment strategies in patients who had been resuscitated from near-fatal ventricular fibrillation or who had undergone cardioversion from sustained ventricular tachycardia. Patients with ventricular tachycardia also had either syncope or other serious cardiac symptoms, along with a left ventricular ejection fraction of 0.40 or less. One group of patients was treated with implantation of a cardioverter-defibrillator; the other received class III antiarrhythmic drugs, primarily amiodarone at empirically determined doses. Fifty-six clinical centers screened all patients who presented with ventricular tachycardia or ventricular fibrillation during a period of nearly four years. Of 1016 patients (45 percent of whom had ventricular fibrillation, and 55 percent ventricular tachycardia), 507 were randomly assigned to treatment with implantable cardioverter-defibrillators and 509 to antiarrhythmic-drug therapy. The primary end point was overall mortality.
RESULTS: Follow-up was complete for 1013 patients (99.7 percent). Overall survival was greater with the implantable defibrillator, with unadjusted estimates of 89.3 percent, as compared with 82.3 percent in the antiarrhythmic-drug group at one year, 81.6 percent versus 74.7 percent at two years, and 75.4 percent versus 64.1 percent at three years (P<0.02). The corresponding reductions in mortality (with 95 percent confidence limits) with the implantable defibrillator were 39+/-20 percent, 27+/-21 percent, and 31+/-21 percent
CONCLUSIONS: Among survivors of ventricular fibrillation or sustained ventricular tachycardia causing severe symptoms, the implantable cardioverter-defibrillator is superior to antiarrhythmic drugs for increasing overall survival.
Connolly SJ, Hallstrom AP, Cappato R, Schron EB, Kuck KH, Zipes DP, Greene HL, Boczor S, Domanski M, Follmann D, Gent M, Roberts RS.
Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials. AVID, CASH and CIDS studies. Antiarrhythmics vs Implantable Defibrillator study. Cardiac Arrest Study Hamburg . Canadian Implantable Defibrillator Study.
Eur Heart J. 2000 Dec;21(24):2071-8. doi: 10.1053/euhj.2000.2476.
Abstract/Text
AIMS: Three randomized trials of implantable cardioverter defibrillator (ICD) therapy vs medical treatment for the prevention of death in survivors of ventricular fibrillation or sustained ventricular tachycardia have been reported with what might appear to be different results. The present analysis was performed to obtain the most precise estimate of the efficacy of the ICD, compared to amiodarone, for prolonging survival in patients with malignant ventricular arrhythmia.
METHODS AND RESULTS: Individual patient data from the Antiarrhythmics vs Implantable Defibrillator (AVID) study, the Cardiac Arrest Study Hamburg (CASH) and the Canadian Implantable Defibrillator Study (CIDS) were merged into a master database according to a pre-specified protocol. Proportional hazard modelling of individual patient data was used to estimate hazard ratios and to investigate subgroup interactions. Fixed effect meta-analysis techniques were also used to evaluate treatment effects and to assess heterogeneity across studies. The classic fixed effects meta-analysis showed that the estimates of ICD benefit from the three studies were consistent with each other (P heterogeneity=0.306). It also showed a significant reduction in death from any cause with the ICD; with a summary hazard ratio (ICD:amiodarone) of 0.72 (95% confidence interval 0.60, 0.87;P=0.0006). For the outcome of arrhythmic death, the hazard ratio was 0.50 (95% confidence interval 0.37, 0.67;P<0.0001). Survival was extended by a mean of 4.4 months by the ICD over a follow-up period of 6 years. Patients with left ventricular ejection fraction < or = 35% derived significantly more benefit from ICD therapy than those with better preserved left ventricular function. Patients treated before the availability of non-thoracotomy ICD implants derived significantly less benefit from ICD therapy than those treated in the non-thoracotomy era.
CONCLUSION: Results from the three trials of the ICD vs amiodarone are consistent with each other. There is a 28% reduction in the relative risk of death with the ICD that is due almost entirely to a 50% reduction in arrhythmic death.
Copyright 2000 The European Society of Cardiology.
