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Concept: Ventricular tachycardia


Background Early defibrillation plays a key role in improving survival in patients with out-of-hospital cardiac arrests due to ventricular fibrillation (ventricular-fibrillation cardiac arrests), and the use of publicly accessible automated external defibrillators (AEDs) can help to reduce the time to defibrillation for such patients. However, the effect of dissemination of public-access AEDs for ventricular-fibrillation cardiac arrest at the population level has not been extensively investigated. Methods From a nationwide, prospective, population-based registry of patients with out-of-hospital cardiac arrest in Japan, we identified patients from 2005 through 2013 with bystander-witnessed ventricular-fibrillation arrests of presumed cardiac origin in whom resuscitation was attempted. The primary outcome measure was survival at 1 month with a favorable neurologic outcome (Cerebral Performance Category of 1 or 2, on a scale from 1 [good cerebral performance] to 5 [death or brain death]). The number of patients in whom survival with a favorable neurologic outcome was attributable to public-access defibrillation was estimated. Results Of 43,762 patients with bystander-witnessed ventricular-fibrillation arrests of cardiac origin, 4499 (10.3%) received public-access defibrillation. The percentage of patients receiving public-access defibrillation increased from 1.1% in 2005 to 16.5% in 2013 (P<0.001 for trend). The percentage of patients who were alive at 1 month with a favorable neurologic outcome was significantly higher with public-access defibrillation than without public-access defibrillation (38.5% vs. 18.2%; adjusted odds ratio after propensity-score matching, 1.99; 95% confidence interval, 1.80 to 2.19). The estimated number of survivors in whom survival with a favorable neurologic outcome was attributed to public-access defibrillation increased from 6 in 2005 to 201 in 2013 (P<0.001 for trend). Conclusions In Japan, increased use of public-access defibrillation by bystanders was associated with an increase in the number of survivors with a favorable neurologic outcome after out-of-hospital ventricular-fibrillation cardiac arrest.

Concepts: Cardiac arrest, Cardiopulmonary resuscitation, Asystole, Ventricular tachycardia, Ventricular fibrillation, Defibrillation, Automated external defibrillator, Fibrillation


Our purpose was to analyze evidence related to timing of cooling from studies of targeted temperature management (TTM) after return of spontaneous circulation (ROSC) after cardiac arrest and to recommend directions for future therapy optimization. We conducted a preliminary review of studies of both animals and patients treated with post-ROSC TTM and hypothesized that a more rapid cooling strategy in the absence of volume-adding cold infusions would provide improved outcomes in comparison with slower cooling. We defined rapid cooling as the achievement of 34°C within 3.5 hours of ROSC without the use of volume-adding cold infusions, with a ≥3.0°C/hour rate of cooling. Using the PubMed database and a previously published systematic review, we identified clinical studies published from 2002 through 2014 related to TTM. Analysis included studies with time from collapse to ROSC of 20-30 minutes, reporting of time from ROSC to target temperature and rate of patients in ventricular tachycardia or ventricular fibrillation, and hypothermia maintained for 20-24 hours. The use of cardiopulmonary bypass as a cooling method was an exclusion criterion for this analysis. We compared all rapid cooling studies with all slower cooling studies of ≥100 patients. Eleven studies were initially identified for analysis, comprising 4091 patients. Two additional studies totaling 609 patients were added based on availability of unpublished data, bringing the total to 13 studies of 4700 patients. Outcomes for patients, dichotomized into faster and slower cooling approaches, were determined using weighted linear regression using IBM SPSS Statistics software. Rapid cooling without volume-adding cold infusions yielded a higher rate of good neurological recovery than slower cooling methods. Attainment of a temperature below 34°C within 3.5 hours of ROSC and using a cooling rate of more than 3°C/hour appear to be beneficial.

Concepts: Myocardial infarction, Cardiac arrest, Cardiopulmonary resuscitation, Asystole, Ventricular tachycardia, SPSS, Ventricular fibrillation, Defibrillation


The aim of this study was to investigate the prognostic impact of acute-phase ventricular tachycardia and fibrillation (VT/VF) on ST-segment elevation myocardial infarction (STEMI) patients in the percutaneous coronary intervention (PCI) era.Methods and Results:Using the database of the Osaka Acute Coronary Insufficiency Study (OACIS), we studied 4,283 consecutive patients with STEMI who were hospitalized within 12 h of STEMI onset and underwent emergency PCI. Acute-phase VT/VF, defined as ≥3 consecutive ventricular premature complexes and/or VF within the 1st week of hospitalization, occurred in 997 (23.3%) patients. In-hospital mortality risk was significantly higher in patients with acute-phase VT/VF than inthose without (14.6% vs. 4.3%, adjusted hazard ratio (HR) 1.83, P=0.0013). Among patients discharged alive, 5-year mortality rates were comparable between patients with and without acute-phase VT/VF. Subgroup analysis showed that acute-phase VT/VF was associated with increased 5-year mortality after discharge in high-risk patients (GRACE Risk Score ≥115; adjusted HR 1.60, P=0.043), but not in intermediate- or low-risk patients.

Concepts: Myocardial infarction, Atherosclerosis, Cardiology, Percutaneous coronary intervention, Ventricular tachycardia, Acute coronary syndrome, Ventricular fibrillation, Premature ventricular contraction


Background Antiarrhythmic drugs are used commonly in out-of-hospital cardiac arrest for shock-refractory ventricular fibrillation or pulseless ventricular tachycardia, but without proven survival benefit. Methods In this randomized, double-blind trial, we compared parenteral amiodarone, lidocaine, and saline placebo, along with standard care, in adults who had nontraumatic out-of-hospital cardiac arrest, shock-refractory ventricular fibrillation or pulseless ventricular tachycardia after at least one shock, and vascular access. Paramedics enrolled patients at 10 North American sites. The primary outcome was survival to hospital discharge; the secondary outcome was favorable neurologic function at discharge. The per-protocol (primary analysis) population included all randomly assigned participants who met eligibility criteria and received any dose of a trial drug and whose initial cardiac-arrest rhythm of ventricular fibrillation or pulseless ventricular tachycardia was refractory to shock. Results In the per-protocol population, 3026 patients were randomly assigned to amiodarone (974), lidocaine (993), or placebo (1059); of those, 24.4%, 23.7%, and 21.0%, respectively, survived to hospital discharge. The difference in survival rate for amiodarone versus placebo was 3.2 percentage points (95% confidence interval [CI], -0.4 to 7.0; P=0.08); for lidocaine versus placebo, 2.6 percentage points (95% CI, -1.0 to 6.3; P=0.16); and for amiodarone versus lidocaine, 0.7 percentage points (95% CI, -3.2 to 4.7; P=0.70). Neurologic outcome at discharge was similar in the three groups. There was heterogeneity of treatment effect with respect to whether the arrest was witnessed (P=0.05); active drugs were associated with a survival rate that was significantly higher than the rate with placebo among patients with bystander-witnessed arrest but not among those with unwitnessed arrest. More amiodarone recipients required temporary cardiac pacing than did recipients of lidocaine or placebo. Conclusions Overall, neither amiodarone nor lidocaine resulted in a significantly higher rate of survival or favorable neurologic outcome than the rate with placebo among patients with out-of-hospital cardiac arrest due to initial shock-refractory ventricular fibrillation or pulseless ventricular tachycardia. (Funded by the National Heart, Lung, and Blood Institute and others; number, NCT01401647 .).

Concepts: Myocardial infarction, Cardiology, Cardiac arrest, Ventricular tachycardia, Supraventricular tachycardia, Amiodarone, Ventricular fibrillation, Defibrillation


Background The role of trypanocidal therapy in patients with established Chagas' cardiomyopathy is unproven. Methods We conducted a prospective, multicenter, randomized study involving 2854 patients with Chagas' cardiomyopathy who received benznidazole or placebo for up to 80 days and were followed for a mean of 5.4 years. The primary outcome in the time-to-event analysis was the first event of any of the components of the composite outcome of death, resuscitated cardiac arrest, sustained ventricular tachycardia, insertion of a pacemaker or implantable cardioverter-defibrillator, cardiac transplantation, new heart failure, stroke, or other thromboembolic event. Results The primary outcome occurred in 394 patients (27.5%) in the benznidazole group and in 414 (29.1%) in the placebo group (hazard ratio, 0.93; 95% confidence interval [CI], 0.81 to 1.07; P=0.31). At baseline, a polymerase-chain-reaction (PCR) assay was performed on blood samples obtained from 1896 patients; 60.5% had positive results for Trypanosoma cruzi on PCR. The rates of conversion to negative PCR results (PCR conversion) were 66.2% in the benznidazole group and 33.5% in the placebo group at the end of treatment, 55.4% and 35.3%, respectively, at 2 years, and 46.7% and 33.1%, respectively, at 5 years or more (P<0.001 for all comparisons). The effect of treatment on PCR conversion varied according to geographic region: in Brazil, the odds ratio for PCR conversion was 3.03 (95% CI, 2.12 to 4.34) at 2 years and 1.87 (95% CI, 1.33 to 2.63) at 5 or more years; in Colombia and El Salvador, the odds ratio was 1.33 (95% CI, 0.90 to 1.98) at 2 years and 0.96 (95% CI, 0.63 to 1.45) at 5 or more years; and in Argentina and Bolivia, the odds ratio was 2.63 (95% CI, 1.89 to 3.66) at 2 years and 2.79 (95% CI, 1.99 to 3.92) at 5 or more years (P<0.001 for interaction). However, the rates of PCR conversion did not correspond to effects on clinical outcome (P=0.16 for interaction). Conclusions Trypanocidal therapy with benznidazole in patients with established Chagas' cardiomyopathy significantly reduced serum parasite detection but did not significantly reduce cardiac clinical deterioration through 5 years of follow-up. (Funded by the Population Health Research Institute and others; number, NCT00123916 ; Current Controlled Trials number, ISRCTN13967269 .).

Concepts: Clinical trial, Myocardial infarction, Cardiology, Randomized controlled trial, Implantable cardioverter-defibrillator, Chagas disease, Ventricular tachycardia, Ventricular fibrillation


We performed a systematic review of the literature to compare the efficacy of different drug therapies for the termination of stable, monomorphic ventricular tachycardia (VT).

Concepts: Medicine, Therapy, Pharmacotherapy, Classification of Pharmaco-Therapeutic Referrals, Ventricular tachycardia, Supraventricular tachycardia, Tachycardia, Therapy?


Rationale: Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) is caused by mutations in cardiac ryanodine receptor (RyR2) or calsequestrin (Casq2) genes. Sinoatrial node dysfunction associated with CPVT may increase the risk for ventricular arrhythmia. Objective: To test the hypothesis that CPVT is suppressed by supraventricular overdrive stimulation. Methods and Results: Using CPVT mouse models (Casq2-/- and RyR2(R4496C)+/- mice), the effect of increasing sinus heart rate was tested by pretreatment with atropine and by atrial overdrive pacing. Increasing intrinsic sinus rate with atropine before catecholamine challenge suppressed ventricular tachycardia (VT) in 86% of Casq2-/- mice (6/7) and significantly reduced the ventricular arrhythmia (VA) score (atropine: 0.6±0.2 vs. vehicle: 1.7±0.3, p<0.05). Atrial overdrive pacing completely prevented VA in 16/19 (84%) Casq2-/- and in 7/8 (88%) RyR2(R4496C)+/- mice and significantly reduced ventricular premature beats in both CPVT models (p<0.05). Rapid pacing also prevented spontaneous calcium waves and triggered beats in isolated CPVT myocytes. In humans, heart-rate dependence of CPVT was evaluated by screening a CPVT patient registry for antiarrhythmic drug-naïve individuals that reached >85% of their maximum predicted heart rate during exercise testing. All 18 CPVT patients who fulfilled the inclusion criteria exhibited VA before reaching 87% of maximum heart rate. In six CPVT patients (33%), VA were paradoxically suppressed as sinus heart rates increased further with continued exercise. Conclusions: Accelerated supraventricular rates suppress VAs in two CPVT mouse models and in a subset of CPVT patients. Hypothetically, atrial overdrive pacing may be a therapy for preventing exercise-induced VT in treatment-refractory CPVT patients.

Concepts: Cardiology, Heart, Ventricular tachycardia, Supraventricular tachycardia, Heart rate, Sinoatrial node, Tachycardia, Bradycardia


Short-coupled variant of torsade de pointes (TdP) is an uncommon variant of polymorphic ventricular tachycardia with unknown etiology. It is initiated by a closely coupled premature ventricular complex (<300 ms) in the absence of QT prolongation and structural heart disease. Verapamil seems to be the only drug able to suppress the arrhythmia but, as it does not reduce the risk of sudden death, implantation of a cardioverter-defibrillator (ICD) is recommended. We describe the case of a 46-year-old woman referred to our Emergency Department because of palpitations. The initial ECG showed a non-sustained polymorphic ventricular tachycardia with a borderline QTc interval (450 ms). After admission, the patient experienced an episode of TdP that started after short-coupling interval (280 ms) between the last sinus beat and the ventricular premature beat (VPB). DC-shock restored sinus rhythm. Physical examination, exercise testing, echocardiography and cardiac magnetic resonance were all normal, and she had no family history of sudden cardiac death. Baseline ECG showed sinus rhythm and unifocal VPBs with the same morphology of the VPB of TdP. The patient received an ICD and was treated medically with verapamil. She was discharged from the hospital on oral therapy with verapamil (240 mg/day), and she was free of recurrence 12 months later when an electrical storm occurred. The verapamil dose was therefore increased to 480 mg/day. Unifocal VPBs disappeared from her body surface ECG, and the subsequent 3-year follow-up was uneventful.

Concepts: Myocardial infarction, Cardiology, Cardiac electrophysiology, Long QT syndrome, QT interval, Ventricular tachycardia, Ventricular fibrillation, Premature ventricular contraction


Objectives. Recent-onset (duration ≤ 1 week) atrial fibrillation (AF) has a high rate of spontaneous conversion to sinus rhythm (SR); still anti-arrhythmic drugs (AAD) are given for conversion purposes. We assessed the effect of AADs by reviewing the literature regarding conversion rates of available drugs in a systematic manner. Design. PubMed searches were performed using the terms “drug name”, “atrial fibrillation”, and “clinical study/RCT”, and a list of 1302 titles was generated. These titles, including abstracts or complete papers when needed, were reviewed for recent-onset of AF, the use of a control group, and the endpoint of SR within 24 hours. Postoperative and intensive care settings were excluded. Results. Five AADs were demonstrated to have an effect, and these were Amiodarone, Ibutilide (only one study and risk of torsade de pointes), Flecainide and Propafenone (only to be used in patients without structural heart disease) and Vernakalant. The time taken for conversion differed markedly; Vernakalant converted after 10 minutes, while Amiodarone converted only after 24 hours; Propafenone and Flecainide had conversion times in-between. Conclusions. For a rapid response in a broad group of patients, Vernakalant appears to be a reasonable first choice, while Flecainide and Propafenone can be used in patients without structural heart disease.

Concepts: Pharmacology, Heart, Atrial fibrillation, Ventricular tachycardia, Antiarrhythmic agent, Amiodarone, Antiarrhythmic agents, Flecainide


The mind-boggling progress in the understanding of the molecular mechanisms underlying the long QT syndrome (LQTS) has been the subject of many articles and reviews. Still, when it comes to the management of the patients affected by this life-threatening disorder, too many errors still take place, both in the diagnostic process and in the therapeutic choices. The price of these errors is paid by the patients and their families. This review is not directed to the relatively small number of LQTS experts who know what to do. It does not deal with genetics, with epidemiology, or with the well-known clinical manifestations. We have focused solely on the approach to diagnosis and therapy and we have directed this review to the average clinical cardiologist who, in his/her practice, sees occasionally patients affected or suspected to be affected by LQTS; the cardiologist who may know enough to manage them but not enough to be completely confident on his/her most critical choices. We have provided our personal views without making any attempt to blend differences whenever present. On most issues we agree fully but where we do not, we make it clear to the reader by indicating who is thinking what. The result may be unconventional, but it mirrors the challenges, often severe, that we all face in managing and protecting these patients from sudden death while also helping them live and thrive despite their diagnosis. We trust that this unabashed presentation of our clinical approach will be useful for both cardiologists and patients.

Concepts: Medicine, Cardiology, Long QT syndrome, Short QT syndrome, QT interval, Jervell and Lange-Nielsen syndrome, Management, Ventricular tachycardia