Shock-induced termination of reentrant cardiac arrhythmias: comparing monophasic and biphasic shock protocols.
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ABSTRACT:
SUBMITTER: Bragard J
PROVIDER: S-EPMC3843767 | biostudies-other | 2013 Dec
REPOSITORIES: biostudies-other
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Project description:Multiple unstable spiral waves rotating around phase singularities (PSs) in the heart, i.e., ventricular fibrillation (VF), is the leading cause of death in the industrialized world. Spiral waves are ubiquitous in nature and have been extensively studied by physiologists, mathematicians, chemists, and biologists, with particular emphasis on their movement and stability. Spiral waves are not easy to terminate because of the difficulty of "breaking" the continuous spatial progression of phase around the PSs. The only means to stop VF (i.e., cardiac defibrillation) is to deliver a strong electric shock to the heart. Here, we use the similarities between spiral wave dynamics and limit cycle oscillators to characterize the spatio-temporal dynamics of VF and defibrillation via phase-resetting curves. During VF, only PSs, including their formation and termination, were associated with large phase changes. At low shock strengths, phase-resetting curves exhibited characteristics of weak (type 1) resetting. As shock strength increased, the number of postshock PSs decreased to zero coincident with a transition to strong (type 0) resetting. Our results indicate that shock-induced spiral wave termination in the heart is caused by altering the phase around the PSs, such that, depending on the preshock phase, sites are either excited by membrane depolarization (phase advanced) or exhibit slowed membrane repolarization (phase delay). Strong shocks that defibrillate break the continuity of phase around PSs by forcing the state of all sites to the fast portion of state space, thus quickly leading to a "homogeneity of state," subsequent global repolarization and spiral wave termination.
| S-EPMC555701 | biostudies-literature
Project description:AimsCurrent treatments of ventricular arrhythmias rely on modulation of cardiac electrical function through drugs, ablation or electroshocks, which are all non-biological and rather unspecific, irreversible or traumatizing interventions. Optogenetics, however, is a novel, biological technique allowing electrical modulation in a specific, reversible and trauma-free manner using light-gated ion channels. The aim of our study was to investigate optogenetic termination of ventricular arrhythmias in the whole heart.Methods and resultsSystemic delivery of cardiotropic adeno-associated virus vectors, encoding the light-gated depolarizing ion channel red-activatable channelrhodopsin (ReaChR), resulted in global cardiomyocyte-restricted transgene expression in adult Wistar rat hearts allowing ReaChR-mediated depolarization and pacing. Next, ventricular tachyarrhythmias (VTs) were induced in the optogenetically modified hearts by burst pacing in a Langendorff setup, followed by programmed, local epicardial illumination. A single 470-nm light pulse (1000?ms, 2.97?mW/mm2) terminated 97% of monomorphic and 57% of polymorphic VTs vs. 0% without illumination, as assessed by electrocardiogram recordings. Optical mapping showed significant prolongation of voltage signals just before arrhythmia termination. Pharmacological action potential duration (APD) shortening almost fully inhibited light-induced arrhythmia termination indicating an important role for APD in this process.ConclusionBrief local epicardial illumination of the optogenetically modified adult rat heart allows contact- and shock-free termination of ventricular arrhythmias in an effective and repetitive manner after optogenetic modification. These findings could lay the basis for the development of fundamentally new and biological options for cardiac arrhythmia management.
| S-EPMC5837774 | biostudies-literature
Project description:IntroductionCannabis use is known to be associated with significant cardiovascular morbidity. We describe three cases of cannabis-related malignant arrhythmias, who presented to the cardiac department at our institution within the last 2 years. All three patients were known to smoke cannabis on daily basis.Case summariesCase 1: A 30-year-old male, presented with recent onset of palpitations. A 12-lead electrocardiogram (ECG), transthoracic echocardiogram (TTE), and blood tests were all normal. During an inpatient exercise treadmill test (ETT) he developed polymorphic ventricular tachycardia (VT), which converted spontaneously to supraventricular tachycardia (SVT) in the recovery phase of the test. Subsequent risk stratification with cardiac magnetic resonance imaging and coronary angiography showed no abnormalities and an electrophysiological study was negative for sustained VT, however, SVT was easily induced with rapid conversion to atrial fibrillation. The patient successfully stopped smoking all tobacco products including cannabis and was treated with beta-blockers, with no further episodes of arrhythmia. Case 2: A 30-year-old male presented to the Emergency Department with palpitations, chest pain, and dizziness that improved during exertion. His initial ECG demonstrated complete atrioventricular block (AVB). Subsequent traces showed Mobitz Type I and second-degree AVB, which converted to atrial flutter after exertion. Routine blood tests, TTE, and an ETT were all normal and he was discharged home with no conduction abnormalities. Case 3: A 24-year-old male presented with two episodes of syncope. Baseline examination was normal, with an ECG showing a low atrial rhythm. Interrogation of his implantable loop recorder showed episodes of early morning bradycardia episodes with no associated symptoms.DiscussionCannabis-related arrhythmia can be multiform regarding their presentation. Therefore, ambiguous combinations of arrhythmia should raise suspicion of underlying cannabis abuse, where clinically appropriate. Although causality with regards to cannabis use cannot be proven definitively in these cases, the temporal relationship between drug use and the onset of symptoms suggests a strong association.
| S-EPMC7793045 | biostudies-literature
Project description:To present the design of a multicenter, randomized trial testing the effects of stress reduction treatment (SRT) on the prevalence of shock-treated ventricular arrhythmias among patients with an implantable cardioverter defibrillator (ICD). Significant adjustment problems secondary to ICD shock can increase the likelihood of arrhythmias requiring shock for termination. Whether SRT can reduce arrhythmias requiring shock for termination in patients with ICDs has not been tested in clinical trials.New ICD recipients and previous recipients who have received an appropriate therapeutic shock in the last 6 months (n = 304) will be enrolled and randomized to either SRT or usual cardiac care. Participants complete a psychosocial questionnaire and undergo laboratory mental stress testing and 24-hour Holter monitoring with diary at study entry and approximately 4 months later. Follow-ups are completed at 6, 12, and 24 months post randomization to assess occurrence of ICD shock for ventricular arrhythmias (primary outcome), antitachycardia pacing events, medication changes, hospitalizations, deaths, and quality of life.Log-rank test and Cox proportional hazards model will be used to test the effects of SRT on time to first shock-treated ventricular arrhythmia, with exploratory analyses testing the effects on overall frequency of ventricular arrhythmia. Secondary analyses will test the effects of SRT on laboratory stress-induced and 24-hour arrhythmogenic electrophysiological indices from pre to post treatment, and both quality of life and measures of anger across the 2 years of the study.The Reducing Vulnerability to ICD Shock-Treated Ventricular Arrhythmias (RISTA) Trial is the first large-scale, randomized, clinical trial designed to evaluate the effect of SRT on the prevalence of shock-treated arrhythmias among patients with an ICD. Results may demonstrate a treatment that can reduce vulnerability to arrhythmia-provoked shock and improve quality of life.
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| S-EPMC1769155 | biostudies-literature
Project description:Early afterdepolarizations (EADs) are an important cause of lethal ventricular arrhythmias in long QT syndromes and heart failure, but the mechanisms by which EADs at the cellular scale cause arrhythmias such as polymorphic ventricular tachycardia (PVT) and torsades de pointes (TdP) at the tissue scale are not well understood. Here we summarize recent progress in this area, discussing (1) the ionic basis of EADs, (2) evidence that deterministic chaos underlies the irregular behavior of EADs, (3) mechanisms by which chaotic EADs synchronize in large numbers of coupled cells in tissue to overcome source-sink mismatches, (4) how this synchronization process allows EADs to initiate triggers and generate mixed focal reentrant ventricular arrhythmias underlying PVT and TdP, and (5) therapeutic implications.
| S-EPMC3005298 | biostudies-literature
Project description:There has been a significant progress in our understanding of the molecular mechanisms by which calcium (Ca2+) ions mediate various types of cardiac arrhythmias. A growing list of inherited gene defects can cause potentially lethal cardiac arrhythmia syndromes, including catecholaminergic polymorphic ventricular tachycardia, congenital long QT syndrome, and hypertrophic cardiomyopathy. In addition, acquired deficits of multiple Ca2+-handling proteins can contribute to the pathogenesis of arrhythmias in patients with various types of heart disease. In this review article, we will first review the key role of Ca2+ in normal cardiac function-in particular, excitation-contraction coupling and normal electric rhythms. The functional involvement of Ca2+ in distinct arrhythmia mechanisms will be discussed, followed by various inherited arrhythmia syndromes caused by mutations in Ca2+-handling proteins. Finally, we will discuss how changes in the expression of regulation of Ca2+ channels and transporters can cause acquired arrhythmias, and how these mechanisms might be targeted for therapeutic purposes.
| S-EPMC5607780 | biostudies-literature
Project description:AimsIn 2003, an Australian woman was convicted by a jury of smothering and killing her four children over a 10-year period. Each child died suddenly and unexpectedly during a sleep period, at ages ranging from 19 days to 18 months. In 2019 we were asked to investigate if a genetic cause could explain the children's deaths as part of an inquiry into the mother's convictions.Methods and resultsWhole genomes or exomes of the mother and her four children were sequenced. Functional analysis of a novel CALM2 variant was performed by measuring Ca2+-binding affinity, interaction with calcium channels and channel function. We found two children had a novel calmodulin variant (CALM2 G114R) that was inherited maternally. Three genes (CALM1-3) encode identical calmodulin proteins. A variant in the corresponding residue of CALM3 (G114W) was recently reported in a child who died suddenly at age 4 and a sibling who suffered a cardiac arrest at age 5. We show that CALM2 G114R impairs calmodulin's ability to bind calcium and regulate two pivotal calcium channels (CaV1.2 and RyR2) involved in cardiac excitation contraction coupling. The deleterious effects of G114R are similar to those produced by G114W and N98S, which are considered arrhythmogenic and cause sudden cardiac death in children.ConclusionA novel functional calmodulin variant (G114R) predicted to cause idiopathic ventricular fibrillation, catecholaminergic polymorphic ventricular tachycardia, or mild long QT syndrome was present in two children. A fatal arrhythmic event may have been triggered by their intercurrent infections. Thus, calmodulinopathy emerges as a reasonable explanation for a natural cause of their deaths.
| S-EPMC7947592 | biostudies-literature
Project description:IntroductionRecent studies suggest cardiac involvement with an increased incidence of arrhythmias in the setting of coronavirus disease 2019 (COVID-19). The aim of this study was to evaluate the risk of potentially lethal arrhythmias and atrial fibrillation in patients with COVID-19-induced acute respiratory distress syndrome (ARDS) and to elicit possible predictors of arrhythmia occurrence.Methods and resultsA total of 107 patients (82 male, mean age 60 ± 12 years, median body mass index 28 kg/m2) treated for COVID-19-induced ARDS in a large tertiary university hospital intensive care unit between March 2020 and February 2021 were retrospectively analyzed. Eighty-four patients (79%) had at least moderate ARDS, 88 patients (83%) were mechanically ventilated, 35 patients (33%) received vvECMO. Forty-three patients (40%) died during their hospital stay. Twelve patients (11%) showed potentially lethal arrhythmias (six ventricular tachycardia, six significant bradycardia). Atrial fibrillation occurred in 27 patients (25%). In a multivariate logistic regression analysis, duration of hospitalization was associated with the occurrence of potentially lethal arrhythmias (p = 0.006). There was no association between possible predictive factors and the occurrence of atrial fibrillation. Invasive ventilation, antipsychotics, and the QTc interval were independently associated with acute in-hospital mortality, but this was not arrhythmia-driven as there was no association between the occurrence of arrhythmias and mortality.ConclusionIn this relatively young population with COVID-19-induced ARDS, the incidence of potentially lethal arrhythmias was low. While overall mortality was high in these severely affected patients, cardiac involvement and arrhythmia occurrence was not a significant driver of mortality.
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