Electrical storm: clinical manifestations and management.

Electrical storm is the clustering of hemodynamically destabilizing ventricular tachycardia or ventricular fibrillation that typically requires multiple electrical cardioversions or defibrillations within a 24-hour period. Electrical storm is frequently seen in the acute phase of myocardial infarction, in patients with the genetic arrhythmia syndromes, and in patients with implanted cardioverters-defibrillators. The evaluation and management should focus on the immediate suppression of the arrhythmia, a search for possible reversible causes, and attempts to prevent recurrences. In this review we present the most common conditions associated with electrical storm, therapeutic options for suppression of electrical storm, and new investigational techniques emerging for the treatment of electrical storm in refractory cases. The management of this life threatening arrhythmia typically requires the coordinated efforts of emergency medicine, critical care, cardiology, cardiac electrophysiology, and pacemaker experts.

Two-year case collection of the Brugada syndrome electrocardiogram pattern at a large teaching hospital.

BACKGROUND: Recommendations have recently emerged suggesting that the presence of the Brugada electrocardiographic (ECG) pattern in an otherwise asymptomatic individual warrants electrophysiologic testing for inducible ventricular arrhythmias. However, the prevalence of this pattern in the general population and its specificity for identifying those likely to develop the true Brugada syndrome are not known. HYPOTHESIS: The purpose of this study was to collect ECGs that displayed the Brugada pattern from unselected, noncardiac patients at a single institution to determine whether the implied prevalence in the literature may represent a significant underestimation of the true prevalence. METHODS: We performed a prospective case collection of Brugada-patterned ECGs over a 2-year time period from unselected, noncardiac patients at a large urban teaching hospital. RESULTS: Of approximately 12,000 noncardiac patients, 52 were found to have an ECG pattern fully consistent with the Brugada sign. CONCLUSIONS: The Brugada type ECG pattern is much more prevalent than previously reported when rigorously searched for in a prospective manner. More data are needed on its specificity for predicting future arrhythmic events in asymptomatic individuals before recommendations are made for extensive evaluation in this group.

The power of PACs.

An elderly woman was admitted for palpitation, light-headedness, and syncope. Telemetry strips revealed numerous episodes of supraventricular tachycardia (SVT) as well as premature beats and pauses. Analysis of the effects of spontaneous premature atrial contractions (PACs) on both the sinus discharge rate and on the SVTs revealed strict relationships that helped decipher the electrophysiological mechanisms of the arrhythmias and offered a rational approach to treatment. Invasive electrophysiological evaluation was not needed. A hitherto unreported phenomenon was the predictable termination of reentrant SVTs by spontaneous PACs. This instructional exercise shows the power of PACs in triggering and terminating arrhythmias, as well as their ability to serve as diagnostic tools in arrhythmia analysis.

Brugada-type electrocardiographic pattern induced by cocaine.

Right bundle branch block with coved ST-segment elevation in leads V1 through V3 is the electrocardiographic (ECG) marker of the Brugada syndrome. We describe a healthy young man with a normal baseline ECG in whom a transient Brugada pattern was observed repeatedly after recreational cocaine use. Intravenous administration of procainamide and subsequent intravenous propranolol followed by noradrenaline failed to reproduce the Brugada sign. An electrophysiologic study performed in the presence of the Brugada ECG pattern showed no inducible arrhythmias. This case illustrates that, in susceptible individuals, cocaine may provoke the Brugada sign. The clinical importance of this cocaine-induced ECG abnormality is currently unknown.

Wide-complex tachycardia: continued evaluation of diagnostic criteria.

OBJECTIVE: To evaluate the accuracy of the Brugada algorithm for analysis of wide-complex tachycardia (WCT) when applied by board-certified emergency physicians and board-certified cardiologists. METHODS: A database consisting of 157 electrocardiograms of WCTs were evaluated in a blinded fashion using the Brugada criteria to determine the presence of ventricular tachycardia (VT) or supraventricular tachycardia with aberrancy. These results were then compared with the electrophysiologically proven diagnosis for each tracing. Sensitivity and specificity of the Brugada criteria for diagnosis of VT were calculated. Two board-certified emergency physicians and two board-certified cardiologists analyzed each tracing, and interobserver agreement was determined using the kappa statistic. RESULTS: Sensitivity and specificity for the determination of VT using the Brugada algorithm were 85% [95% confidence interval (95% CI) = 79% to 91%] and 60% (95% CI = 43% to 78%) for cardiologist 1 (C 1) and 91% (95% CI = 86% to 96%) and 55% (95% CI = 37% to 72%) for C 2. Emergency physician (EP 1) achieved a sensitivity of 83% (95% CI = 78% to 91%) and a specificity of 43% (95% CI = 25% to 59%), while EP 2 attained 79% (95% CI = 73% to 87%) and 70% (95% CI = 51% to 84%), respectively. The original authors achieved a sensitivity of 98.7% and specificity of 96.5% when determining VT in their study population. Interobserver agreement for the emergency physicians and the cardiologists in determining VT was 82% and 81%, respectively. CONCLUSIONS: Neither the emergency physicians nor the cardiologists were able to achieve a sensitivity or specificity as high as that reported by the original investigators when using the Brugada algorithm to determine the presence of VT.

Hemodynamic implications of left bundle branch block.

Left bundle branch block (LBBB), traditionally viewed as an electrophysiologic abnormality, is increasingly recognized for its profound hemodynamic effects. LBBB causes asynchronous myocardial activation, which, in turn, may trigger ventricular remodeling. Exercise nuclear studies frequently show reversible perfusion defects in the absence of obstructive coronary artery disease and some patients with intermittent LBBB develop angina coincident with the onset of LBBB. It is uncertain, however, if these phenomena are because of myocardial ischemia or ventricular asynergy. LBBB is associated with impaired systolic and diastolic function. In patients with dilated cardiomyopathy (DCM), LBBB is accompanied by progressive left ventricular (LV) dilatation and mitral regurgitation. It is not known whether LBBB is the cause or the consequence of LV dilatation. DCM patients with LBBB, as compared to those with normal intraventricular conduction, are more likely to have a nonischemic etiology, profound LV dilatation, lower ejection fraction, increased symptomatology, and shorter survival. Patients with DCM and acceleration-dependent LBBB may benefit from restoration of a narrow QRS complex by suppressing the heart rate with beta-blocker. There is extensive research underway in patients with DCM and LBBB to evaluate the short and long-term effects of normalization of ventricular activation sequence with high septal, LV, or biventricular pacing.

Large T wave inversion and QT prolongation associated with pulmonary edema: a report of nine cases.

OBJECTIVES: The purpose of this study is to describe a new clinical electrocardiographic phenomenon characterized by diffuse symmetrical T wave inversion and QT prolongation after recovery from an episode of cardiogenic but nonischemic pulmonary edema. BACKGROUND: A variety of clinical conditions, but not acute pulmonary edema, have been previously associated with giant negative T waves and QT prolongation in the postevent electrocardiogram. METHODS: In nine patients not suspected of having ischemic heart disease, new large or global T wave inversion with QT prolongation was observed after resolution of acute cardiogenic pulmonary edema. Each patient underwent detailed clinical evaluation including testing for myocardial injury and a coronary ischemic etiology. RESULTS: There were seven women and two men with ages ranging from 32 to 79 years. The etiology of pulmonary edema was diverse, but acute myocardial infarction and significant coronary artery disease were ruled out in each case. During the index event, most patients had elevated blood pressure, sinus tachycardia, minimal nonspecific ST and T wave changes and normal QT intervals. Large inverted T waves with marked prolongation of the QT intervals evolved within 24 h after clinical stabilization. The electrocardiographic changes gradually resolved in one week. There was no in-hospital mortality. CONCLUSIONS: Acute cardiogenic but nonischemic pulmonary edema may cause deep T wave inversion and QT prolongation after resolution of the symptoms. The repolarization abnormalities may last for several days. These electrocardiographic changes do not adversely effect short-term prognosis.

Alternate patterns of ventricular activation during supraventricular bigeminy.

Several investigators have previously noted that in the presence of bigeminal atrial extrasystoles, the premature beats may exhibit an alternate pattern of ventricular excitation either in the form of alternating left and right bundle-branch block, or alternating right bundle-branch block and normal intraventricular conduction. However, the association of alternating intraventricular conduction with other types of supraventricular bigeminy has rarely been documented. In this report we present five diverse forms of supraventricular bigeminy exhibiting the phenomenon of alternating ventricular excitation on the early beats. Our findings suggest that the exact mechanism of supraventricular bigeminy is irrelevant in terms of subsequent ventricular events. Practically any type of supraventricular bigeminy may result in an alternate pattern of ventricular activation.

Laser photoablation of experimental post-infarction ventricular tachycardia guided by three dimensional activation mapping.

BACKGROUND AND OBJECTIVE: The purpose of this study was to evaluate the efficacy of epicardially delivered laser energy to ablate induced ventricular tachycardia in a post-infarction canine model. STUDY DESIGN/MATERIALS AND METHODS: In 13 canines, the left anterior wall myocardial infarction was created. Five days later, 240 plunged electrodes were inserted into the heart. Three-dimensional ventricular activation sequences were analyzed on line by a computerized mapping system. RESULTS: Sixteen sustained monomorphic ventricular tachycardias were reproducibly induced in 10 canines. Epicardially contacted Nd:YAG laser irradiated the areas of the final pathway in macro-reentrant activation and the impulse origin in focal excitation. Linear photocoagulation lesions (11-16 x 50-72 mm) were created. Seven macro-reentrant circuits and six of nine focal origins were eliminated (success rate 81%). Pathology showed that laser photocoagulation involved all surviving subepicardial and intramural fibers. CONCLUSION: Epicardially delivered laser energy in conjunction with electrical activation mapping has a high probability of ablating post-infarction ventricular tachycardia.

Epicardial neodymium. YAG laser photocoagulation of ventricular tachycardia without ventriculotomy in patients after myocardial infarction.

BACKGROUND: Surgical ablation of ventricular tachycardia (VT) after myocardial infarction has been reported by different endocardial approaches. The ventriculotomy may increase mortality of the procedure. METHODS AND RESULTS: We report on nine patients who suffered from recurrent VT in the late post-myocardial infarction period. Significant stenoses were detected in all patients. The mean left ventricular ejection fraction was 43.1 +/- 8.3%. Left ventricular scar (n = 9) was seen. The mean NYHA class was 2.2 +/- 0.4. Sustained VT (mean cycle length, 293 +/- 52 ms) occurred spontaneously (n = 9) and could be induced reproducibly. Catheter mapping detected a prematurity of -42 +/- 13 ms in six patients. Clinical VT was inducible during surgery in seven patients. Middiastolic potentials were detected from the epicardial surface (n = 3), and premature potentials were found (n = 8 with prematurity of -108 +/- 46 ms). Application of neodymium/yttrium/argon/ garnet (Nd:YAG) laser energy to early epicardial activation terminated the arrhythmia (n = 7). Ventriculotomy was not performed. Seven patients have been free of VT for a mean follow-up period of 17 +/- 11 months; one patient relapsed and was treated with an implantable cardioverter-defibrillator, as was a second patient with inducible VT after surgery. CONCLUSIONS: Surgical Nd:YAG laser photocoagulation of VT on the epicardial surface of the heart in post-myocardial infarction patients without ventriculotomy is safe and has a high success rate. At the present time, this method is recommended in patients with sustained and tolerated VT who need bypass surgery. This is the first report on epicardial laser ablation of VT in post-myocardial infarction VT.