Ventricular Fibrillation Storm Research Articles

Catheter Ablation of Ventricular Fibrillation: State of the Art

Catheter ablation of the triggering ventricular premature beats (VPBs) is feasible for idiopathic and ischemic ventricular fibrillation (VF) and can be used for a bailout therapy of VF storm. Also, it can reduce the number of the shock from an implantable defibrillator, one of the poor prognostic factors. In VF or polymorphic ventricular tachycardia (VT) from right ventricular outflow tract (RVOT), suppression of VF was achieved by catheter ablation at RVOT or pulmonary artery. In the short-coupled variant of torsade de pointes and ischemic VF, VF was suppressed by catheter ablation of the Purkinje network. Focal firing from Purkinje fiber and reentry at the Purkinje network may play an important role in the initiation and perpetuation of VF. The same approach with good short-term results has been reported in a small number of patients with other heart diseases (i.e., amyloidosis, chronic myocarditis, nonischemic cardiomyopathy, Brugada syndrome, Long-QT syndrome, and catecholaminergic polymorphic VT).

Calcium-Handling Protein Phosphorylation Abnormalities in a Rabbit Model with Recurrent Ventricular Fibrillation Storm

Electrical storm (ES), characterized by recurrent ventricular tachycardia/fibrillation (VT/VF), is an increasing problem among implantable cardioverter-defibrillators (ICDs) patients. While acute cessation of ES is generally achievable with medical therapy, ES is associated with a high risk of mortality in a few months after its occurrence, mostly due to non-sudden cardiac causes. The underlying mechanisms are unknown. Here, we investigated ES effects on Ca2+-handling protein expression/phosphorylation in an experimental ES model. Thirty-seven rabbits with chronic complete atrioventricular block, equipped with ICDs, were studied. All had QT-prolongation and ICD-detected VT/VF-episodes. Twenty-two rabbits (59%) developed ES (defined as ≥3 VF-episodes/24-hr period; 108±29 VF-episodes/rabbit). ES-rabbits showed left-ventricular function deterioration, along with striking activation of Ca2+/calmodulin-dependent protein-kinase II (CaMKII) and enhanced protein-phosphatase expression. These alterations produced changes in phosphorylation-pattern, markedly hyperphosphorylation of L-type Ca2+-channel and sarcoplasmic reticulum (SR) Ca2+-release channel ryanodine receptor and dephosphorylation of SR Ca2+-uptake regulator phospholamban (PLB). Repeated VF induction/defibrillation with ICD-shocks in control rabbits reproduced ES-related changes in CaMKII and PLB phosphorylation. Continuous infusion of calmodulin-antagonist W-7 to ES-rabbits reduced CaMKII-activation, suppressed VT/VF-episodes and rescued LV-dysfunction without significantly altering hypertrophic or apoptotic markers. In conclusions, ES causes marked CaMKII-activation and Ca2+-handling protein phosphorylation abnormalities, which may be responsible for adverse outcomes in ES-patients.

A child with influenza A (H1N1)-associated myocarditis rescued by extracorporeal membrane oxygenation

A 6-year-old boy had cold-like symptoms and was diagnosed with influenza A at a clinic. Administration of oseltamivir and azithromycin did not improve the symptoms. He was referred to our hospital and was diagnosed with H1N1 pneumonia. The patient required ventilator support. However, hypoxia and hypercapnia were uncontrollable. To oxygenate and reduce the carbon dioxide concentration, veno-venous extracorporeal membrane oxygenation (ECMO) was applied 24h after admission. We established outflow via the right internal jugular vein and inflow via the right femoral vein. Six hours later, an electrical storm of ventricular fibrillation occurred, probably due to influenza myocarditis. Chest compression was started immediately. Both cardioversion and medication were ineffective in treating the electrical storm. Therefore, we decided to switch the veno-venous ECMO to veno-arterial ECMO to maintain systemic flow. During chest compression, a 6-mm graft was anastomosed to the left common femoral artery, and an outflow tube was connected to the graft. Consequently, veno-arterial ECMO was established via outflow through the left common femoral artery and inflow through both the right jugular vein and right femoral vein. Veno-arterial ECMO terminated the electrical storm, and cardiac output improved. Veno-arterial ECMO was provided for 107h, and was then replaced by veno-venous ECMO. Forty-three hours later, veno-venous ECMO was discontinued. The patient was successfully weaned from the mechanical ventilator on the 9th day after admission. Unfortunately, spinal infarction appeared as a complication. The patient was discharged from the hospital on the 86th day, and has now returned to primary school.

Isoproterenol as an adjunct for treatment of idiopathic ventricular fibrillation storm in a pregnant woman

Idiopathic ventricular fibrillation is a rare entity seen in a very small subset of patients presenting to the emergency department. Management of ventricular arrhythmias in pregnant women is similar to that in nonpregnant women, but special consideration is given to avoid adverse fetal effects when selecting antiarrhythmic agents. Electrical defibrillation is the intervention of choice in both pregnant and nonpregnant patients with ventricular fibrillation of all etiologies. This was not associated with any significant adverse effects for mother or fetus. Although lidocaine and sotalol are Food and Drug Administration category B antiarrhythmics used in pregnancy, Food and Drug Administration category C antiarrhythmics such as β-blockers and category D drugs such as amiodarone can be used as pharmacologic adjuncts to facilitate termination of recurrent ventricular fibrillation where other agents have failed. Isoproterenol has been used to terminate recurrent ventricular fibrillation in patients with Brugada syndrome and torsades de pointes resistant to magnesium therapy. This case report describes a previously healthy 32-year-old pregnant woman with recurrent idiopathic ventricular fibrillation that failed to respond to standard therapy including electrical defibrillation, intravenous lidocaine, metoprolol, and amiodarone but eventually terminated with isoproterenol infusion.

Catheter Ablation for Electrical Storm as Polymorphic Ventricular Tachycardia in a Case with Ischemic Cardiomyopathy after Coronary Artery Bypass Graft

We report a case involving a patient with ischemic cardiomyopathy who developed polymorphic ventricular tachycardia (PVT) and ventricular fibrillation storm after coronary artery bypass graft. Because PVT was initiated by various right bundle branch type premature ventricular contractions (PVCs), we assessed the relatively monomorphic ventricular tachycardia (MVT) during PVT. Electroanatomical mapping revealed that the earliest ventricular activation of the MVT was located in the scar border zone at the posterior septum of the left ventricle. Stable potentials which preceded the MVT were observed. Catheter ablation for the preceding potential suppressed the maintenance of the PVT, although triggered PVCs appeared frequently. Catheter ablation was effective as a bailout therapy in a patient with PVT‐induced cardiomyopathy after cardiac operation.

Worsening Heart Failure in the Setting of Dronedarone Initiation

To describe a challenging patient case in which dronedarone was selected for a patient with atrial fibrillation and heart failure; the drug may have been associated with worsening heart failure, leading to acute renal and hepatic failure. A 47-year-old male with a history of heart failure with New York Heart Association class III-IV symptoms presented to our institution with ventricular fibrillation and ventricular tachycardia storm. Torsade de pointes secondary to a combination of dofetilide and hypokalemia was determined to be the etiology. Upon stabilization, the patient was initiated on dronedarone 400 mg orally twice daily by the electrophysiology service for atrial fibrillation. The patient had a questionable history of amiodarone intolerance. By hospital day 9 (day 4 of dronedarone therapy), the patient demonstrated a clinical picture consistent with acute renal and hepatic failure possibly due to worsening heart failure. Dronedarone was discontinued on hospital day 10. He was subsequently transferred to an outside hospital where he required milrinone therapy for cardiogenic shock. Laboratory markers of renal and hepatic function improved over the remainder of his hospitalization and he was discharged on hospital day 20. Dronedarone is a newly approved antiarrhythmic agent with multichannel blocking properties similar to amiodarone. Use of the Naranjo probability scale determined that this patient's worsening heart failure leading to acute renal and hepatic failure was possibly caused by dronedarone. The implication from the ANDROMEDA trial as well as our experience in this case is that dronedarone should be used cautiously in patients with heart failure and avoided in patients specifically outlined in the product labeling. This case report, to our knowledge, represents the first published postmarketing report of worsening heart failure complicated by multiorgan dysfunction in the setting of dronedarone initiation. Dronedarone use must be approached with caution in patients with a history of heart failure.

Therapeutic hypothermia and ventricular fibrillation storm in early repolarization syndrome

Pronounced J-point elevation is now a well-described characteristic of idiopathic ventricular fibrillation (VF), 1 Haïssaguerre M. Derval N. Sacher F. et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med. 2008; 358: 2016-2023 Crossref PubMed Scopus (1082) Google Scholar , 2 Rosso R. Kogan E. Belhassen B. et al. J-point elevation in survivors of primary ventricular fibrillation and matched control subjects: incidence and clinical significance. J Am Coll Cardiol. 2008; 52: 1231-1238 Abstract Full Text Full Text PDF PubMed Scopus (450) Google Scholar but J waves were previously noted in association with hypothermia and were called Osborn waves. 3 Osborn J.J. Experimental hypothermia: respiratory and blood pH changes in relation to cardiac function. Am J Physiol. 1953; 175: 389-398 PubMed Google Scholar We present the case of a patient with idiopathic VF and J waves in whom therapeutic hypothermia increased J-point elevation and appeared to exacerbate ventricular arrhythmias.

High Efficacy of Disopyramide in the Management of Ventricular Fibrillation Storms in a Patient with Brugada Syndrome

The patient was a 57-year-old man with Brugada syndrome, who had been implanted with a implantable cardioverter defibrillator (ICD). The frequency of ventricular fibrillation (VF) started to increase about 4 years after ICD implantation, occurring, at worst, six times in one night. Immediately after starting oral administration of disopyramide, VF stopped occurring. He then discontinued taking disopyramide, but immediately after the discontinuation VF started occurring again, so he restarted taking disopyramide. Thereafter, VF completely stopped occurring. Findings observed in our case suggest that disopyramide could be added in our arsenal of medications for treating arrhythmic storms in patient with Brugada syndrome.

J wave syndromes.

The J wave, also referred to as an Osborn wave, is a deflection immediately following the QRS complex of the surface ECG. When partially buried in the R wave, the J wave appears as J-point elevation or ST-segment elevation. Several lines of evidence have suggested that arrhythmias associated with an early repolarization pattern in the inferior or mid to lateral precordial leads, Brugada syndrome, or arrhythmias associated with hypothermia and the acute phase of ST-segment elevation myocardial infarction are mechanistically linked to abnormalities in the manifestation of the transient outward current (I(to))-mediated J wave. Although Brugada syndrome and early repolarization syndrome differ with respect to the magnitude and lead location of abnormal J-wave manifestation, they can be considered to represent a continuous spectrum of phenotypic expression that we propose be termed J-wave syndromes. This review summarizes our current state of knowledge concerning J-wave syndromes, bridging basic and clinical aspects. We propose to divide early repolarization syndrome into three subtypes: type 1, which displays an early repolarization pattern predominantly in the lateral precordial leads, is prevalent among healthy male athletes and is rarely seen in ventricular fibrillation survivors; type 2, which displays an early repolarization pattern predominantly in the inferior or inferolateral leads, is associated with a higher level of risk; and type 3, which displays an early repolarization pattern globally in the inferior, lateral, and right precordial leads, is associated with the highest level of risk for development of malignant arrhythmias and is often associated with ventricular fibrillation storms.

Catheter ablation of fatal ventricular tachyarrhythmias storm in acute coronary syndrome—role of Purkinje fiber network

Ventricular fibrillation (VF) or ventricular tachycardia (VT) storm is a life-threatening arrhythmia. Antiarrhythmic drugs (AADs) are not necessarily effective to rescue life from such conditions. Catheter ablation (CA) targeting triggering premature ventricular contractions (PVCs) of VF or VT that originates from Purkinje fiber network (PFN) is reported to be effective, especially in idiopathic patients. However, in condition of acute coronary syndrome (ACS), the efficacy of CA is not well understood. To clarify the usefulness of CA as an alternative way to AADs, we performed CA in four patients with VF or VT storm. The Purkinje potential was seen just before the myocardial ventricular wave during sinus rhythm that became more prominent and double components during the initiating PVC at the targeted area. Following CA, spontaneous episodes of VF or VT were no longer observed. CA is an efficacious way to bail out PFN-related VF or VT storm even in ACS.

Successful catheter ablation of focal ventricular fibrillation originating from the right ventricle

Sudden cardiac death from ventricular fibrillation (VF) typically occurs in patients with structural heart disease, but in 5 to 10 percent VF is "idiopathic," occurring in normal hearts. Recently, there has been the description and growing recognition of patients with VF that has a focal origin, the common sites being in the right ventricular outflow tract (RVOT) and sites in the left ventricle. A focus within the right ventricle outside the RVOT is rare. We present a case of a woman with VF storm that was localized to the inferobasal right ventricle and was successfully treated with radiofrequency ablation.

Role of Left Ventricular Scar and Purkinje‐Like Potentials During Mapping and Ablation of Ventricular Fibrillation in Dilated Cardiomyopathy

Purkinje-like potentials (PLPs) have been described as important contributors to initiation of ventricular fibrillation (VF) in patients with normal hearts, ischemic cardiomyopathy, and early after-myocardial infarction. Of the 11 consecutive patients with VF storm, nonischemic cardiomyopathy (68 +/- 22 years, left ventricular ejection fraction 28 +/- 8%) who were given antiarrhythmic drugs and/or heart failure management, five had recurrent VF and underwent electrophysiology study (EPS) and catheter ablation. At EPS, frequent monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia did not occur. With isoproterenol, VF was induced in three patients, and sustained monomorphic PVCs were induced in one patient. Three-dimensional electroanatomical mapping using CARTO (Biosense-Webster Inc., Diamond Bar, CA) revealed posterior wall scar in four of the five patients. PLP in sinus rhythm were recorded around the scar border in these four patients, and radiofrequency ablation targeting PLP was successfully performed at these sites. The patient without PLP did not undergo ablation. During follow-up (12 +/- 5 months), only the patient without PLP had four VF recurrences requiring implantable cardioverter-defibrillator (ICD) shocks. In patients with VF and dilated cardiomyopathy, left ventricular posterior wall scar in the vicinity of the mitral annulus seems to be a common finding. Targeting PLP along the scar border zone for ablation seems to efficiently prevent VF recurrence in these patients.

Sudden death by storm of ventricular fibrillation in spite of appropriate ICD shock ; two cases report

Sudden death by storm of ventricular fibrillation in spite of appropriate ICD shock ; two cases report

Ablation of Polymorphic Ventricular Tachycardias in Patients with Structural Heart Disease

Monomorphic ventricular premature beats (VPB) originating from the Purkinje network can induce polymorphic ventricular tachycardia (PMVT) and ventricular fibrillation (VF) storm. We hereby report the results of targeted ablation to treat PMVT/VF storms initiated by monomorphic VPB in seven patients with structural heart disease and left ventricular (LV)-dysfunction (n=4 withcoronary artery disease (CAD), n=2 with chronic and remote myocarditis, n=1 after aortic valve replacement). Pace-mapping and activation mapping was used to identify optimal ablation targets. Earliest activation during mapping was found midseptal of LV in three patients, midinferoseptal of LV in two patients. One patient with myocarditis showed earliest activation at free wall of right ventricle, the other one basal midseptal of LV. Local ventricular electrograms at the successful ablation sites were preceded by short, high frequency, low amplitude potentials by 22-90 ms (median 35 ms). The same local potentials were seen in sinus rhythm. Cycle lengths of VT ranged between 200 and 360 ms (median 245 ms). A median of nine radiofrequency (RF)-ablations (range 3-19) were necessary to abolish all local Purkinje potentials at the site of earliest activation. Two patients with CAD died due to refractory heart failure. The other five patients had no recurrence of PMVT and VF during follow up (median 10 months, range 1-27 months). The distal Purkinje network plays an important role in triggering PMVT/VF in patients with structural heart disease. Ablation of the triggering VPB originating from the Purkinje arborization is feasible; prevents recurrence in a long-term follow up; and is potentially life saving in patients with severe LV-dysfunction after myocardial infarction, in patients after aortic valve replacement, or in patients with myocarditis particularly when medical treatment, including antiarrhythmic drugs, failed to suppress electrical storms.

Ventricular fibrillation initiated by premature beats from the ventricular myocardium not associated with the Purkinje system after myocardial infarction

t m t F a v u D s Ventricular fibrillation (VF) can be successfully treated by atheter ablation of the initiating ventricular premature beats VPBs). The dominant source of those initiating VPBs is the urkinje system. This report describes the successful ablation f VF storm by targeting initiating VPBs arising not from the urkinje system, but from the right ventricular (RV) myocarium in a patient after myocardial infarction.

Successful Radiofrequency Catheter Ablation for Electrical Storm of Ventricular Fibrillation in a Patient With Brugada Syndrome

The case of a 41-year-old man with Brugada syndrome (BS) who suffered electrical storms (ES) of ventricular fibrillation (VF) is presented. Although intravenous infusion of isoproterenol (ISP) suppressed the VF occurrence, he consistently experienced recurrence of VF following discontinuation of ISP infusion. Quinidine and cilostazol were ineffective. An analysis of VF episodes on electrocardiogram monitoring revealed that the QRS morphology of the first beat of all VF episodes was identical to that of premature ventricular complexes (PVCs) with a left bundle branch-block morphology and inferior axis, which occurred repetitively before the episodes of VF and were recorded throughout the day. In addition, stored electrograms from the implantable cardioverter defibrillator showed that the first beat of all VF episodes had the same morphology. On electrophysiological study, the VF-triggering PVC was found to originate from the posterior portion of the right ventricular outflow tract area and their elimination, which was achieved with radiofrequency catheter ablation (RFCA), resulted in the suppression of ES. Although several other PVCs were still observed, the patient has been free of VF during the 29-month follow-up period. This case indicates that RFCA of VF-triggering PVCs may be useful in the treatment of drug-resistant ES in patients with BS.

Mapping and Ablation of Trigger Premature Ventricular Contractions in a Case of Electrical Storm Associated with Ischemic Cardiomyopathy

We report a case of polymorphic ventricular tachycardia and ventricular fibrillation (PVT/VF) storm associated with ischemic cardiomyopathy (ICM). The electrocardiogram (ECG) monitor revealed frequent premature ventricular contractions (PVCs) initiated PVT/VF. Electroanatomic mapping revealed the plausible origins of PVCs were located in the scar border zone at the posterior septum of the left ventricle. Purkinje-like potentials (PLPs) always preceded PVCs and a decremental property for the PLPs and infarcted myocardium junction was observed. Ablation at these sites eliminated both PVCs and PVT/VF.

Acute and chronic management in patients with Brugada syndrome associated with electrical storm of ventricular fibrillation

Some patients with Brugada syndrome experience an electrical storm of ventricular fibrillation (VF). The purpose of this study was to investigate the clinical, laboratory, electrocardiographic, and electrophysiologic characteristics, acute and subsequent chronic treatment, and follow-up data of patients with Brugada syndrome associated with electrical storm of VF. Sixty-seven patients with Brugada syndrome (65 men and 2 women, age 46 +/- 14 years) were divided into three groups: 7 patients with a history of electrical storm of VF (group I), 39 symptomatic patients with documented VF and/or syncope (group II), and 21 asymptomatic patients (group III). Electrical storm was defined as three or more episodes of VF per day recorded by the memory of an implantable cardioverter-defibrillator. No significant differences were observed among the three groups with regard to clinical (age at diagnosis, familial history of sudden cardiac death), laboratory (SCN5A mutation and serum potassium level), electrocardiographic and electrophysiologic characteristics, and follow-up duration after diagnosis. However, arrhythmic events during follow-up after diagnosis and number of arrhythmic events per patient were significantly higher in group I compared with groups II and III. Isoproterenol infusion (0.003 +/- 0.003 microg/kg/min for 24 +/- 13 days) completely suppressed electrical storm of VF in all five patients treated and was successfully replaced with oral medications, including denopamine, quinidine, isoproterenol, cilostazol, and bepridil alone or in combination. No specifically clinical, laboratory, electrocardiographic, and electrophysiologic characteristics were recognized in patients with Brugada syndrome associated with electrical storm of VF. Isoproterenol infusion was effective as an acute treatment in suppressing electrical storm of VF and was successfully replaced with chronic oral medications.

Ventricular Fibrillation in a Patient with Prominent J Wave in the Inferior and Lateral Electrocardiographic Leads After Gastrostomy

We describe the case of a 39-year-old man who experienced a ventricular fibrillation storm related to a prominent J wave in the inferior and lateral electrocardiographic leads on the day after gastrostomy. The J wave slowly decreased after amiodarone therapy (400 mg/day) was started, and ventricular fibrillation disappeared.

Catheter Ablation of Ventricular Fibrillation Storm in Patients with Infiltrative Amyloidosis of the Heart

Recent studies have demonstrated that premature ventricular contractions (PVCs) originating from the Purkinje system are responsible for initiation of ventricular fibrillation (VF) in patients with and without structural heart disease. Ablation of the PVCs has been shown to be feasible. We report 2 patients with repetitive VF associated with cardiac amyloidosis. Each episode of ventricular arrhythmia was preceded by monomorphic PVC. The electrical storms were drug resistant. Electrophysiological testing was performed and the sites of earliest activation were localized within the left ventricle in the absence of significant scar tissue. After ablation, PVCs subsided and there were no further VF recurrences.