R on T Phenomenon Causing Ventricular Fibrillation during LV Angiography.
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ABSTRACT:
SUBMITTER: Garg N
PROVIDER: S-EPMC3089831 | biostudies-literature | 2010 Oct
REPOSITORIES: biostudies-literature
Publications
R on T Phenomenon Causing Ventricular Fibrillation during LV Angiography.
Garg Naveen N Moorthy Nagaraja N
Heart views : the official journal of the Gulf Heart Association 20101001 3
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Project description:Sudden cardiac death (SCD) from ventricular fibrillation (VF) during coronary artery disease (CAD) is a leading cause of total and cardiovascular mortality, and in more than half of SCD cases VF occurs as the first symptom of CAD. Several epidemiological studies have shown that sudden death of a family member is a risk factor for SCD and VF during acute myocardial infarction (MI), independent of traditional risk factors including family history of MI, suggesting a genetic component in the susceptibility to VF. To prevent SCD and VF due to MI, we need a better understanding of the genetic and molecular mechanisms causing VF in this apparently healthy population. Even though new insights and technologies have become available, the genetic predisposition to VF during MI remains poorly understood. Findings from a variety of different genetic studies have failed to reach reproducibility, although several genetic variants, both common and rare variants, have been associated to either VF or SCD. For this review, we searched PubMed for potentially relevant articles, using the following MeSH-terms: "sudden cardiac death", "ventricular fibrillation", "out-of-hospital cardiac arrest", "myocardial infarction, myocardial ischemia", "coronary artery disease", and "genetics". This review describes the epidemiology and evidence for genetic susceptibility to VF due to MI.
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| S-EPMC7328414 | biostudies-literature
Project description:BackgroundOut-of-hospital ventricular fibrillation (VF) cardiac arrest is a leading cause of death. Quantitative analysis of the VF electrocardiogram (ECG) can predict patient outcomes and could potentially enable a patient-specific, guided approach to resuscitation. However, VF analysis during resuscitation is confounded by cardiopulmonary resuscitation (CPR) artifact in the ECG, challenging continuous application to guide therapy throughout resuscitation. We therefore sought to design a method to predict VF shock outcomes during CPR.MethodsStudy data included 4577 5-s VF segments collected during and without CPR prior to defibrillation attempts in N = 1151 arrest patients. Using training data (460 patients), an algorithm was designed to predict the VF shock outcomes of defibrillation success (return of organized ventricular rhythm) and functional survival (Cerebral Performance Category 1-2). The algorithm was designed with variable-frequency notch filters to reduce CPR artifact in the ECG based on real-time chest compression rate. Ten ECG features and three dichotomous patient characteristics were developed to predict outcomes. These variables were combined using support vector machines and logistic regression. Algorithm performance was evaluated by area under the receiver operating characteristic curve (AUC) to predict outcomes in validation data (691 patients).ResultsAUC (95% Confidence Interval) for predicting defibrillation success was 0.74 (0.71-0.77) during CPR and 0.77 (0.74-0.79) without CPR. AUC for predicting functional survival was 0.75 (0.72-0.78) during CPR and 0.76 (0.74-0.79) without CPR.ConclusionA novel algorithm predicted defibrillation success and functional survival during ongoing CPR following VF arrest, providing a potential proof-of-concept towards real-time guidance of resuscitation therapy.
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Project description:BackgroundThe relationship between the ventricular rate (VR) during atrial fibrillation (AF) and skin sympathetic nerve activity (SKNA) remains unclear.ObjectiveThe purpose of this study was to test the hypothesis that SKNA bursts accelerate VR during AF.MethodsWe simultaneously recorded electrocardiogram and SKNA in 8 patients (median age 66.0 years [interquartile range {IQR} 59.0-77.0 years]; 4 men [50%]) with 30 paroxysmal AF episodes (all >10-minute long) and 12 patients (73.0 years [IQR 60.5-80.0 years]; 6 men [50%]) with persistent AF. The average amplitude of SKNA (aSKNA [μV]) during AF was analyzed in 1-minute windows and binned, showing 2 Gaussian distributions. We used the mean + 3SD of the first Gaussian distribution as the threshold that separates burst from baseline (nonburst) SKNA. All 1-minute aSKNA values above the threshold were detected, and the area between aSKNA and baseline of every 1 minute was calculated and added as burst area.ResultsVR was higher during SKNA bursts than during the nonburst period (103 beats/min [IQR 83-113 beats/min] vs 88 beats/min [IQR 76-101 beats/min], respectively; P = .003). In the highest quartile of the burst area during persistent AF, the scatterplot of maximal aSKNA and VR during each SKNA burst shows higher aSKNA and VR. The overall estimate of the correlation between maximal VR and aSKNA during bursts show a positive correlation in the highest quartile of the burst area (0.64; 95% confidence interval 0.54-0.74; P < .0001).ConclusionSKNA bursts are associated with VR acceleration. These SKNA bursts may be new therapeutic targets for rate control during AF.
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Project description:Quantitative analysis has demonstrated five temporal stages of activation during the first 10 min of ventricular fibrillation (VF) in dogs. To determine whether these stages exist in another species, we applied the same analysis to the first 10 min of VF recorded in vivo from two 504-electrode arrays, one each on left anterior and posterior ventricular epicardium in six anesthetized pigs. The following descriptors were continuously quantified: 1) number of wavefronts, 2) wavefront fractionations, 3) wavefront collisions, 4) repeatability, 5) multiplicity index, 6) wavefront conduction velocity, 7) activation rate, 8) mean area activated by the wavefronts, 9) negative peak rate of voltage change, 10) incidence of breakthrough/foci, 11) incidence of block, and 12) incidence of reentry. Cluster analysis of these descriptors divided VF into four stages (stages i-iv). The values of most descriptors increased during stage i (1-22 s after VF induction), changed quickly to values indicating greater organization during stage ii (23-39 s), decreased steadily during stage iii (40-187 s), and remained relatively unchanged during stage iv (188-600 s). The epicardium still activated during stage iv instead of becoming silent as in dogs. In conclusion, during the first 10 min, VF activation can be divided into four stages in pigs instead of five stages as in dogs. Following a 16-s period during the first minute of VF when activation became more organized, all parameters exhibited progressive decreased organization. Further studies are warranted to determine whether these changes, particularly the increased organization of stage ii, have clinical consequences, such as alteration in defibrillation efficacy.
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Project description:Oxidative stress with hydrogen peroxide (H(2)O(2)) readily promotes early afterdepolarizations (EADs) and triggered activity (TA) in isolated rat and rabbit ventricular myocytes. Here we examined the effects of H(2)O(2) on arrhythmias in intact Langendorff rat and rabbit hearts using dual-membrane voltage and intracellular calcium optical mapping and glass microelectrode recordings. Young adult rat (3-5 mo, N = 25) and rabbit (3-5 mo, N = 6) hearts exhibited no arrhythmias when perfused with H(2)O(2) (0.1-2 mM) for up to 3 h. However, in 33 out of 35 (94%) aged (24-26 mo) rat hearts, 0.1 mM H(2)O(2) caused EAD-mediated TA, leading to ventricular tachycardia (VT) and fibrillation (VF). Aged rabbits (life span, 8-12 yr) were not available, but 4 of 10 middle-aged rabbits (3-5 yr) developed EADs, TA, VT, and VF. These arrhythmias were suppressed by the reducing agent N-acetylcysteine (2 mM) and CaMKII inhibitor KN-93 (1 microM) but not by its inactive form (KN-92, 1 microM). There were no significant differences between action potential duration (APD) or APD restitution slope before or after H(2)O(2) in aged or young adult rat hearts. In histological sections, however, trichrome staining revealed that aged rat hearts exhibited extensive fibrosis, ranging from 10-90%; middle-aged rabbit hearts had less fibrosis (5-35%), whereas young adult rat and rabbit hearts had <4% fibrosis. In aged rat hearts, EADs and TA arose most frequently (70%) from the left ventricular base where fibrosis was intermediate ( approximately 30%). Computer simulations in two-dimensional tissue incorporating variable degrees of fibrosis showed that intermediate (but not mild or severe) fibrosis promoted EADs and TA. We conclude that in aged ventricles exposed to oxidative stress, fibrosis facilitates the ability of cellular EADs to emerge and generate TA, VT, and VF at the tissue level.
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