Recurrent Episodes Of Ventricular Fibrillation Research Articles

Injectable contraceptive Depo-Provera induces erratic beating patterns in patient-specific induced pluripotent stem cell–derived cardiomyocytes with long QT syndrome type 2

Long QT syndrome type 2 (LQT2) is caused by pathogenic variants in KCNH2. LQT2 may manifest as QT prolongation on an electrocardiogram and present with arrhythmic syncope/seizures and sudden cardiac arrest/death. Progestin-based oral contraceptives may increase the risk of LQT2-triggered cardiac events in women. We previously reported on a woman with LQT2 and recurrent cardiac events temporally related and attributed to the progestin-based contraceptive medroxyprogesterone acetate ("Depo-Provera" [Depo] MilliporeSigma, Catalog# 1378001, St. Louis, MO). The purpose of this study was to evaluate the arrhythmic risk of Depo in a patient-specific induced pluripotent stem cell-derived cardiomyocyte (iPSC-CM) model of LQT2. An iPSC-CM line was generated from a 40-year-old woman with p.G1006Afs∗49-KCNH2. A CRISPR/Cas9 gene-edited/variant-corrected isogenic control iPSC-CM line was generated. FluoVolt (Invitrogen, F10488, Waltham, MA) was used to measure the action potential duration after treatment with 10 μM Depo. Erratic beating patterns characterized as alternating spike amplitudes, alternans, or early afterdepolarization-like phenomena were assessed using multielectrode array (MEA) after 10 μM Depo, 1 μM isoproterenol (ISO), or combined Depo + ISO treatment. Depo treatment shortened the action potential duration at 90% repolarization of G1006Afs∗49 iPSC-CMs from 394 ± 10 to 303 ± 10 ms (P < .0001). Combined Depo + ISO treatment increased the percentage of electrodes displaying erratic beating in G1006Afs∗49 iPSC-CMs (baseline: 18% ± 5% vs Depo + ISO: 54% ± 5%; P < .0001) but not in isogenic control iPSC-CMs (baseline: 0% ± 0% vs Depo + ISO: 10% ± 3%; P = .9659). This cell study provides a potential mechanism for the patient's clinically documented Depo-associated episodes of recurrent ventricular fibrillation. This invitro data should prompt a large-scale clinical assessment of Depo's potential proarrhythmic effect in women with LQT2.

Abstract 12044: Injectable Contraceptive, Medroxyprogesterone Acetate, Produces Erratic Beating Patterns in Patient-Specific Re-Engineered Heart Cells With Type 2 Long QT Syndrome

Background: Type 2 long QT syndrome (LQT2) is an inherited arrhythmia syndrome caused by pathogenic variants in the KCNH2 gene which result in QT prolongation and confers susceptibility to arrhythmic syncope/seizures and sudden cardiac arrest/death. Oral progestin-based contraceptives increase the risk of cardiac events in women with LQT2 and we previously reported the case of a LQT2 woman with recurrent cardiac events attributed to the use of the progestin-based contraceptive, Medroxyprogesterone Acetate (“Depo-Provera”, Depo). Objective: To evaluate the arrhythmic-risk of Depo in a LQT2-specific, induced pluripotent stem cell-derived cardiomyocyte (iPSC-CM) model. Methods: An iPSC-CM line was generated from the previously reported woman (KCNH2-G1006A*fs) as well as a control line. Voltage-sensing dye was used to assess the optical action potential duration (APD) with 10 μM Depo. 3-D erratic beating patterns were then assessed using multiple electrode array (MEA) with Depo and isoproterenol (ISO) to mimic an adrenergic surge. Results: Addition of Depo to the G1006A*fs iPSC-CMs decreased the optical APD from baseline 438±14 ms (n=6) to 363±35 ms (n=12; p=0.0001). Despite the APD shortening at baseline, in the setting of ISO, Depo administration induced erratic beating patterns in MEA, characterized as alternating spike amplitudes, alternans, or early after depolarization-like phenomena. Combined Depo and ISO treatment increased the percent of electrodes displaying erratic beating in G1006A*fs [baseline 8%±13 vs. Depo + ISO 38%±40 (p=0.0097)] but not in controls [baseline 2%±5 vs. Depo + ISO 7%±11 (p=0.14)]. Neither Depo nor ISO alone changed beating patterns in G1006A*fs [baseline 8%±13, Depo 30%±41 (p=0.08), ISO 21%±30, (p=0.17)] and controls [baseline 2%±5, Depo 3%±7 (p=0.61), ISO 0%±0 (p=0.4)]. Conclusion: This patient-specific, re-engineered heart cell study provides a potential mechanism for the patient’s clinically documented, Depo-associated episodes of recurrent ventricular fibrillation. This in-vitro data should prompt a large-scale clinical assessment of Depo’s potential pro-arrhythmic effect in women with LQT2.

Autoimmune Myocarditis and Arrhythmogenic Mitral Valve Prolapse: An Unexpected Overlap Syndrome

Background: both myocarditis and mitral valve prolapse (MVP) are known uncommon causes of ventricular arrhythmias in young patients. Aim: to report the first clinical case of endomyocardial biopsy (EMB)-proven autoimmune myocarditis and associated arrhythmogenic MVP in a patient with recurrent ventricular fibrillation (VF) episodes. Methods: myocarditis was diagnosed both by cardiac magnetic resonance (CMR) and EMB. Arrhythmogenic MVP was documented by transthoracic echocardiogram, CMR, and electroanatomical mapping of the trigger premature ventricular contractions (PVCs). Results: a 22-year-old woman underwent immunosuppressive therapy after EMB-proven diagnosis of autoimmune myocarditis with VF onset and early implantable cardioverter defibrillator (ICD) placement. Three years later, she experienced two VF recurrences and persistent PVCs, despite no signs of myocarditis recurrence. An echocardiogram revealed bileaflet MVP with high arrhythmic risk features. Finally, electroanatomical mapping and ablation of the trigger PVC were successfully performed. Conclusion: in patients with recurrent VF episodes despite evidence-based medical treatment for myocarditis, MVP should be considered as an alternative arrhythmogenic substrate, and warrants early ICD implant and PVC-targeted therapy.

Radiofrequency ablation in Brugada syndrome.

Radiofrequency ablation in Brugada syndrome.

Dynamic Changes in Electrocardiogram Parameters After Epicardial Substrate Catheter Ablation of Brugada Syndrome.

Catheter ablation (CA) is effective for recurrent episodes of ventricular fibrillation (VF) in Brugada syndrome (BrS). VF development in BrS is associated with several electrocardiogram (ECG) abnormalities. This study investigated changes in ECG parameters in high-risk BrS patients who underwent epicardial CA.Methods and Results:In all, 27 BrS patients were implanted with an implantable cardioverter-defibrillator (ICD). Patients were divided into 2 groups: (1) an ablation group (n=11) that underwent epicardial CA because of VF recurrence; and (2) a primary prevention (PP) group (n=16) with ICD implantation only. ECG parameters were evaluated before and 12 months after CA and compared with ECG parameters in the PP group. The T wave peak-to-end interval was significantly longer and the number of abnormal spikes in leads V1-V3 at the second, third, and fourth intercostal spaces was greater in the ablation than PP group. After ablation, ST levels and the sum of abnormal spikes in leads V1-V3 were significantly decreased. The mean (±SD) number of ICD shocks decreased markedly during a mean follow-up period of 42.0 months (from 3.8±3.7 to 0.2±0.4/year). Four patients had an ICD shock following the ablation procedure. Greater reductions in ST-segment elevation and abnormal spikes were observed in the group without than with VF recurrence. Improvements in surface ECG parameters appear to be associated with successful ablation in high-risk BrS patients.

Coronary vasospasm as an etiology of recurrent ventricular fibrillation in the absence of coronary artery disease: a case report

ABSTRACT Background: Vasospastic angina (VA), or Prinzmetal’s angina, is characterized by symptoms of coronary angina caused by coronary vasospasm, usually in the absence of atherosclerotic changes. It typically presents with chest pain, which can be accompanied by transient electrocardiographic changes, if visualized during the attack. It can also rarely present with severe manifestations of acute myocardial angina, ventricular fibrillation, or cardiac arrest. Case presentation:We present a case of a 50-year-old Caucasian male who initially presented to the hospital with chest pain and was diagnosed with VA. Later, he was brought to the hospital by emergency medical services later with ventricular fibrillation, despite normal coronary anatomy on angiogram. He was managed with placement of an intra–cardiac defibrillator (ICD) for secondary prevention. The patient continued to have recurrent episodes of ventricular fibrillation with associated ICD shocks, and had multiple admissions to the hospital with similar presentations. Symptoms and arrhythmia improved after optimizing antianginal therapy. Conclusions:Ventricular fibrillation can be an uncommon but severe manifestation during VA crises. In cases with normal coronary vasculature, it is important to recognize VA as a cause of recurrent ventricular fibrillation in order to optimize medical management for prevention of fatal arrhythmias.

Myocardial infarction and ventricular fibrillation due to iatrogenic right coronary artery occlusion following tricuspid valve annuloplasty: a case report.

BackgroundIatrogenic right coronary artery (RCA) injury is a rare complication of tricuspid valve annuloplasty. Given that surgical intervention is increasingly favoured for tricuspid regurgitation, it is of great importance to recognize potential complications following tricuspid valve surgery.Case summaryA 72-year-old man underwent surgical mitral and tricuspid valve repair. The early post-operative course was complicated by recurrent ventricular fibrillation episodes. Due to haemodynamic instability, a re-sternotomy and another cardiopulmonary bypass run were required. The patient subsequently underwent coronary angiography study which confirmed RCA occlusion. The occluded posterior left ventricular (PLV) branch was reopened by balloon angioplasty. However, despite multiple attempts it was not possible to pass a coronary guide wire into the posterior descending artery (PDA). An intravascular ultrasound examination revealed that the ostium of the PDA was compressed by external factors leaving a narrow slit-like appearance with no accessible lumen. Subsequently, a drug-eluting stent was placed into the PLV branch. The PDA was not accessible on repeated re-canalization attempts. The patient later successfully recovered from the right ventricular myocardial infarction.DiscussionRight coronary artery occlusion should be considered as a differential diagnosis for significant rhythm disturbances and haemodynamic instability in the peri- and post-operative period following tricuspid valve annuloplasty. A low threshold for diagnostic angiography is needed to avoid potential delay in life-saving revascularization.

Mapping and Ablation of Ventricular Fibrillation Associated With Early Repolarization Syndrome.

We conducted a multicenter study to evaluate mapping and ablation of ventricular fibrillation (VF) substrates or VF triggers in early repolarization syndromes (ERS) or J-wave syndrome (JWS). We studied 52 patients with ERS (4 women; median age, 35 years) with recurrent VF episodes. Body surface electrocardiographic imaging and endocardial and epicardial electroanatomical mapping of both ventricles were performed during sinus rhythm and VF for localization of triggers, substrates, and drivers. Ablations were performed on VF substrates, defined as areas that had late depolarization abnormalities characterized by low-voltage fractionated late potentials, and VF triggers. Fifty-one of the 52 patients had detailed mapping that revealed 2 phenotypes: group 1 had late depolarization abnormalities predominantly at the right ventricular (RV) epicardium (n=40), and group 2 had no depolarization abnormalities (n=11). Group 1 can be subcategorized into 2 groups: Group 1A included 33 patients with ERS with Brugada electrocardiographic pattern, and group 1B included 7 patients with ERS without Brugada electrocardiographic pattern. Late depolarization areas colocalize with VF driver areas. The anterior RV outflow tract/RV epicardium and the RV inferior epicardium are the major substrate sites for group 1. The Purkinje network is the leading underlying VF trigger in group 2 that had no substrates. Ablations were performed in 43 patients: 31 and 5 group 1 patients had only VF substrate ablation and VF substrates plus VF trigger, respectively (mean, 1.4±0.6 sessions); 6 group 2 patients and 1 patient without group classification had only Purkinje VF trigger ablation (mean, 1.2±0.4 sessions). Ablations were successful in reducing VF recurrences (P<0.0001). After follow-up of 31±26 months, 39 (91%) had no VF recurrences. There are 2 phenotypes of ERS/J-wave syndrome: one with late depolarization abnormality as the underlying mechanism of high-amplitude J-wave elevation that predominantly resides in the RV outflow tract and RV inferolateral epicardium, serving as an excellent target for ablation, and the other with pure ERS devoid of VF substrates but with VF triggers that are associated with Purkinje sites. Ablation is effective in treating symptomatic patients with ERS/J-wave syndrome with frequent VF episodes.

Fatal 5-APB and 5-APDB overdose: A case report with clinical, analytical and forensic documentation

5-APB and 5-APBD belong to the benzofuran group of new psychoactive substances (NPS). Used for their entactogen and stimulant properties, benzofurans are related to phenethylamines and displayed sympathetic activity, with possible neurologic and cardiovascular complications [1] . We describe a fatal poisoning with 5-APB and 5-APDB as the only drugs involved. A 25-year-old woman, with history of recreative ecstasy abuse, was referred to an emergency department (ED) after a malaise during a party. Her medical condition abruptly worsened with tonico-clonic seizure followed by a first resuscitated cardiorespiratory arrest. In intensive care unit, there was a major hemodynamic instability with hypotension and she experienced recurrent episodes of ventricular fibrillation with iterative cardiac arrests. She eventually died a few hours after admission in ED. According to friends, she consumed Ecstasy during the party. The autopsy showed non-specific signs of asphyxia, signs of multi-organ failure and of hemodynamic shock, without revealing any previous condition that may have contributed to the fatality. Cardiac/femoral blood, urine, vitreous humor, bile, gastric content and hair were collected for toxicological forensic analysis. Immunoassay for amphetamine, methamphetamine, cocaine, opiates and cannabinoids was performed on urine. Identification and quantification of major amphetamine derivatives in blood was performed by GC-MS. General unknown screening (GUS) was performed on blood and gastric contents by GC-MS and LC-DAD after liquid-liquid extraction. 5-APB and 5-APDB were quantified in blood by GC-MS/MS, using MDA-d5 as internal standard, after assay validation for linearity, selectivity, limits of detection, precision and accuracy at 3 concentration levels. Blood ethanol/other volatile compounds analysis was performed on HS-GC-FID. Urine immunoassay was positive for amphetamine, but confirmation analysis for major amphetamine derivatives was negative. An APB isomer was detected on GUS by GC-MS. It was identified as 5-APB studying urine metabolites. A 2nd compound, 5-APDB, was highlighted in urine, with confirmation after 5-APDB commercial standard injection. 5-APB and 5-APDB respective peripheral blood/urine concentrations were as follows: 1429/34,469 ng/mL and 111/3770 ng/mL. No other drugs/toxins, including ethanol or volatile compounds, have been identified. As far as we know, this is the first reported case with no other compound detected but benzofurans 5-APB and 5-APDB. The latter, suspected by McIntyre et al. [2] was formally identified without ruling out the hypothesis of a 5-APB metabolite or a synthesis/conditioning impurity.

Case report: electrical storm during induced hypothermia in a patient with early repolarization

BackgroundPopulation based studies showed an association of early repolarization in the electrocardiogram (ECG) and a higher rate of sudden cardiac death presumably due to ventricular fibrillation. The triggers for ventricular fibrillation in patients with early repolarization are not fully understood.Case presentationWe describe the case of a young patient with a survived ventricular fibrillation arrest while asleep followed by multiple episodes of recurrent ventricular fibrillation. The admission ECG showed an early repolarization pattern with substantial J-point elevation in most of the ECG-leads. After initiation of a hypothermia protocol, the patient developed an electrical storm with multiple ventricular fibrillation episodes requiring multiple cardioversions. Intravenous isoproterenol infusion successfully suppressed the malignant arrhythmia.ConclusionHypothermia appears proarrhythmic in patients with early repolarization and may trigger ventricular fibrillation. This knowledge is particularly important when initiating temperature management protocols in patients after a survived cardiac arrest. During the acute phase of an early repolarization associated electrical storm, isoproterenol is the most effective treatment suppressing the ventricular fibrillation-inducing premature ventricular complexes at higher heart rates.

Management of Aborted Sudden Cardiac Arrest with J Wave Syndrome

We report the case of a 19-year-old male who successfully recovered from sudden cardiac arrest. Careful evaluation did not reveal any electrical or structural abnormalities. He underwent implantable cardioverter defibrillator (ICD) implantation, with a diagnosis of idiopathic ventricular fibrillation (VF). Three months later, VF recurred and was successfully terminated by ICD shock. Electrocardiogram (ECG) revealed a slurred type J point elevation at the inferolateral leads with a horizontal/descending ST segment change, which was not present during the initial hospitalization. Cilostazol was prescribed to prevent further lethal ventricular arrhythmias. Subsequently, no arrhythmic events were reported, and the J wave disappeared at the follow-up ECG. However, recurrent VF episodes with an interval of 1–2 weeks occurred 1 year later, and were terminated by ICD shock. Simultaneous ECG revealed a J point elevation at the inferolateral leads. Cilostazol was replaced by quinidine. Subsequently, no arrhythmic event recurred for over 12 months. Serial follow-up ECG is needed to identify masked inherited primary arrhythmic syndromes in sudden cardiac arrest survivors diagnosed with idiopathic VF. Cilostazol and quinidine might be good therapeutic options to prevent further lethal events in cases where the J wave syndrome is present with recurrent ventricular arrhythmias.

Sudden Cardiac Death in a Dialysis Patient: Hyperkalemia Reconsidered

BackgroundTo many physicians, hyperkalemia is the first diagnosis ascribed to any patient with end-stage renal disease and abnormal electrocardiographic morphologies or dysrhythmias. Case ReportA 52-year-old man with end-stage renal disease presented in cardiac arrest. The patient was initially presumed to have hyperkalemia, based on the appearance of wide QRS complexes on the monitor. The diagnosis of hyperkalemia was incorrect; the patient was severely hypokalemic and suffered recurrent episodes of ventricular fibrillation and torsades de pointes. Why Should an Emergency Physician Be Aware of ThisAn emergency physician's differential diagnosis of sudden cardiac arrest in the patient with end-stage renal disease should not be limited to hyperkalemia and myocardial infarction. Hypokalemia should also be considered. Hypokalemia may be an under-recognized cause of sudden cardiac death in this patient population.

Mapping and ablation of ventricular fibrillation—how and for whom?

The involvement of the Purkinje system in a subset of patients with idiopathic ventricular fibrillation or polymorphic VT/VF related to structural heart disease was first demonstrated in the pioneering work of Michel Haissaguerre and co-workers (Circulation 106:962-967, 2002 and Lancet 359:677-678, 2002). It is very important to identify these patients with recurrent episodes of ventricular fibrillation and/or ICD shocks with regard to the presence of triggering premature ventricular contractions (PVC), which may be amenable to mapping and catheter ablation by screening Holter and ICD recordings. The practical problem, which is frequently encountered, is the absence of these PVCs when the patients are brought to the EP lab. However, catheter ablation is an important adjunctive tool to antiarrhythmic drug treatment, beta blocker therapy, and general anesthesia in this setting. Local electrogram criteria related to this phenomenon have been identified guiding mapping and ablation (e.g., low amplitude, high-frequency Purkinje potentials preceding a closely coupled ventricular signal (Fig.1a)). The favorable long-term follow-up after catheter ablation has been demonstrated in the setting of right and left ventricular Purkinje-related PVCs leading to polymorphic VT/VF (Leenhardt et al., Circulation 89:206-215, 1994) and also following myocardial infarction (Baensch et al., Circulation 108:3011-3016, 2003) and right ventricular outflow tract-associated VF (Noda et al., Journal of the American College of Cardiology 46:1288-1294, 2005). Most recently, epicardial ablation strategies leading to suppression of polymorphic VT/VF episodes related to the Brugada syndrome have been described irrespective to the presence of premature ventricular beats (Nademanee et al., Circulation 123:1270-1279, 2011).

Cardiac Arrest due to Recurrent Ventricular Fibrillation Triggered by Unifocal Ventricular Premature Complexes in a Silent Myocardial Infarction

A 51-year-old male patient was referred for a sudden out-of-hospital cardiac arrest. Upon arrival, he was conscious and had no chest pain complaints. There was no abnormality in initial electrocardiographic and echocardiographic examinations. However, episodes of recurrent ventricular fibrillation (VF) were documented on rhythm monitoring. Each VF episode was triggered by an isolated monomorphic ventricular premature complex (VPC). Suspecting idiopathic VF, emergency radiofrequency catheter ablation was planned for the VPCs. However, when coronary angiography was performed to exclude silent ischemia, the results showed a total occlusion of the right coronary artery posterolateral branch, which is thought to supply the left ventricular inferior and septal wall. After successful reperfusion, VF episodes and the triggering VPCs disappeared. We are documenting this case to emphasize the potential for silent myocardial infarction to cause out-of-hospital sudden cardiac arrest even in a patient without any symptom or sign of acute coronary syndrome.

Direct Left Ventricular Endocardial Pacing: An Alternative When Traditional Resynchronization Via Coronary Sinus Is Not Feasible or Effective

Biventricular pacing through the coronary sinus (CS) is effective for the treatment of patients with heart failure and left bundle-branch block. However, this approach is not always feasible. Although surgical epicardial lead implantation is an alternative, the technique may be deleterious in some patients. Thus, direct left ventricular (LV) endocardial pacing under local anesthesia may be an option. We describe our technique and analyze the results of direct LV endocardial pacing. Fourteen patients with failed resynchronization via CS (April 2006-September 2011) were selected. Using a femoral approach, we performed transseptal puncture and LV mapping, then fixed the active lead where the longest electrical delay was observed; the generator was placed in the anterior thigh. For resynchronization, eight patients with a device previously implanted through the upper veins received a single-chamber generator that was set to the VVT mode to sense the subclavian pacing spike. Six patients received a complete femoral resynchronization system with either a defibrillator or pacemaker. Patients were followed for 6-54 months. The LV lead was successfully implanted in all cases. Two patients experienced excessive bleeding and two died during follow-up. All except one improved at least one New York Heart Association class and experienced improved left ventricle ejection fraction. One patient with recurrent episodes of ventricular fibrillation was asymptomatic. Direct LV endocardial pacing is safe and may be a less risky, more efficient alternative than surgical epicardial lead implantation for resynchronization via CS.

Pseudo-PJRT in an 8 year-old boy with severe decompensated heart failure and recurrent episodes of ventricular fibrillation

We present a case of 8 year-old boy with several episodes of ventricular fibrillation in the course of tachycardia-mediated cardiomyopathy and severe decompensated heart failure. The cardiomyopathy was caused by incessant long-RP tachycardia that was resistant to pharmacotherapy. Despite initial suspition that the arrhythmia was permanent junctional reciprocating tachycardia (PJRT) electrophysiology study revealed atypical atrioventricular nodal reentrant tachycardia. Due to clinical and electrocardiographical presentation mimicking PJRT such arrhythmia merits the name 'pseudo PJRT'.

ORAL PRESENTATION

ORAL PRESENTATION

Performance of a rectilinear biphasic waveform in defibrillation of presenting and recurrent ventricular fibrillation: A prospective multicenter study

Objectives We tested the hypothesis that shock success differs with initial and recurrent episodes of ventricular fibrillation (VF). Methods From September 2008 to March 2010 out-of-hospital cardiac arrest patients with VF as the initial rhythm at 9 study sites were defibrillated by paramedics using a rectilinear biphasic waveform. Shock success was defined as termination of VF within 5 s post-shock. We used generalized estimating equation (GEE) analysis to assess the association between shock type (initial versus refibrillation) and shock success. Results Ninety-four patients presented in VF. Mean age was 65.4 years, 78.7% were male, and 80.9% were bystander-witnessed. VF recurred in 75 (79.8%). There were 338 shocks delivered for initial ( n = 90) or recurrent ( n = 248) VF available for analysis. Initial shocks terminated VF in 79/90 (87.8%) and subsequent shocks in 209/248 (84.3%). GEE odds ratio (OR) for shock type was 1.37 (95% CI 0.68–2.74). After adjusting for potential confounders, the OR for shock type remained insignificant (1.33, 95% CI 0.60–2.53). We observed no significant difference in ROSC (54.7% versus 52.6%, absolute difference 2.1%, p = 0.87) or neurologically intact survival to hospital discharge (21.9% versus 33.3%, absolute difference 11.4%, p = 0.31) between those with and without VF recurrence. Conclusions Presenting VF was terminated with one shock in 87.8% of cases. We observed no significant difference in the frequency of shock success between initial versus recurrent VF. VF recurred in the majority of patients and did not adversely affect shock success, ROSC, or survival.

Brugada-like ECG pattern in a patient with isolated right ventricular infarction

A 55-year-old female patient collapsed at home with sudden cardiac death. Upon arrival of the emergency physician, the patient was defibrillated for ventricular fibrillation (VF). After successful mechanical resuscitation, the patient was transferred to our intensive care unit requiring high-dose vasopressor support. The electrocardiogram (ECG) at presentation showed atrial fibrillation with right bundle branch block and cove-type ST segment elevation in leads V1 and V2, ECG abnormalities suggestive of Brugada syndrome (Figure 1). Transthoracic echocardiography showed left ventricular hypertrophy and preserved systolic left ventricular function without significant wall motion abnormalities. Right ventricular function was, however, markedly reduced. Myoglobin at presentation was 1,287 mg/l with a creatine kinase of 134 U/l and a troponin I of 0.02 ng/ml. Because of the conspicuous ECG changes, Brugada syndrome was initially suspected and coronary angiography was delayed in order to stabilize the patient hemodynamically. During the next hours, the patient developed recurrent episodes of VF, which were refractory to amiodarone and could finally be prevented by transjugular venous pacing at 90 beats per minute. Laboratory analysis exhibited a significant rise in cardiac markers and the patient underwent coronary angiography. Coronary angiography revealed proximal thrombotic occlusion of a small nondominant right coronary artery (Figure 2a), which could be successfully recanalized (Figure 2b). Isolated right ventricular infarction is an extremely rare event. It has been associated with unusual ECG appearances which may be misinterpreted or even missed if not suspected. Ischemia of the right ventricular free wall to the outflow tract may cause ST segment elevations in leads V1–V3 similar to Brugada syndrome, as in the present case. Similar Brugada-like ECG pattern may also occur in hypothermic patients or patients that have undergone mechanical resuscitation. In the literature, there have been several case reports highlighting that Brugada syndrome can be mistaken for acute myocardial infarction. This case illustrates that the reverse may also occur. Address for Correspondence Dr. Holger Eggebrecht Department of Cardiology University of Duisburg-Essen Hufelandstrase 55 45122 Essen Germany Phone (+49/201) 723-3363, Fax -5931 e-mail: holger.eggebrecht@uk-essen.de 1 Department of Cardiology, West-German Heart Center Essen, University of Duisburg-Essen, Essen, Germany.

A high peak current 150-J fixed-energy defibrillation protocol treats recurrent ventricular fibrillation (VF) as effectively as initial VF

We tested the hypothesis that the frequency of shock success differs between initial and recurrent episodes of ventricular fibrillation (VF). Out-of-hospital cardiac arrest patients presenting with VF from December 1996 to February 2007 defibrillated using an AED with a fixed-energy protocol (150 J) (Philips Medical Systems, Seattle, WA) were included for analysis. We defined shock success as termination of VF within 5s post-shock (either asystole or organized rhythm). Generalized estimating equation (GEE) analysis was used to adjust for the interrelatedness of shocks within each patient. One hundred and three events occurred during the study period. Patient characteristics included: mean age 64.4 years, 82.5% male, and 81.6% bystander witnessed. Synchronized call-to-shock time was 6.4+/-2.3 min (mean+/-S.D.). VF recurred in 64 (62.1%) patients. Two hundred and fifty-seven shocks delivered for initial (101) or recurrent (156) VF were available for analysis. Initial shocks terminated VF in 93/101 (92.1%); subsequent shocks terminated recurrent VF in 140/156 (89.7%). GEE odds ratio for shock type (initial versus refibrillation) was 1.10 (95% CI 0.37-3.24, p=0.87). After adjusting for potential confounders, shock type remained insignificant (OR 1.14, 95% CI 0.41-3.2, p=0.80). We observed no significant difference in ROSC (34.4% versus 46.2%, p=0.23) or survival (37.5% versus 41.0%, p=0.72) between those with and without VF recurrence. We observed no significant difference in the frequency of shock success between initial and recurrent episodes of VF using this AED with a 150 J fixed-energy protocol. VF recurrence is common and does not adversely affect shock success, ROSC or survival.