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A previously healthy 29-year-old man was admitted with palpitations, dizziness, and near-syncope after he had recently started taking weight loss pills purchased on the internet. The pills contained caffeine and ephedrine. An electrocardiogram and telemetry revealed multiple episodes of non-sustained monomorphic ventricular tachycardia, which was successfully treated with amiodarone. In conclusion, unauthorized weight loss pills can be harmful. In particular, ephedrine-containing drugs carry a risk of ventricular tachycardia and should be discouraged.
Adenosine has become widely used because of its diagnostic and therapeutic value in the emergency management of arrhythmias. It produces transient heart block by slowing conduction through the AV node and thus terminates supraventricular tachycardias that involve the atrioventricular node. Bradyarrhythmias of short duration are common side effects of the use of this drug. Premature atrial and ventricular beats have also been reported. The very short half-life and lack of serious adverse effects generally lead to the consideration that adenosine is a safe drug. We describe a 56-year-old woman with a supraventricular tachycardia. To terminate this rhythm disorder intravenous adenosine was given. Interruption of the supraventricular tachycardia was followed by non-sustained polymorphic ventricular tachycardia.
Ventricular tachycardia is unusual in infancy. Three infants are described in whom this arrhythmia was documented by electrophysiologic studies. The ability to start and terminate this rhythm by critically timed premature ventricular stimulation suggests a reentrant mechanism. All three patients have remained free of arrhythmias on oral propranolol therapy.
Differentiation between early-phase arrhythmogenic right ventricular cardiomyopathy (ARVC) and right ventricular outflow tract (RVOT)-ventricular tachycardia (VT) can be challenging, and correct diagnosis is important. We compared electrocardiogram (ECG) parameters and morphological right ventricular (RV) abnormalities and investigated if ECG and cardiac imaging can help to discriminate early-phase ARVC from RVOT-VT patients.
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a devastating inherited disorder characterized by episodic syncope and/or sudden cardiac arrest during exercise or acute emotion in individuals without structural cardiac abnormalities. Although rare, CPVT is suspected to cause a substantial part of sudden cardiac deaths in young individuals. Mutations in RYR2, encoding the cardiac sarcoplasmic calcium channel, have been identified as causative in approximately half of all dominantly inherited CPVT cases. Applying a genome-wide linkage analysis in a large Swedish family with a severe dominantly inherited form of CPVT-like arrhythmias, we mapped the disease locus to chromosome 14q31-32. Sequencing CALM1 encoding calmodulin revealed a heterozygous missense mutation (c.161A>T [p.Asn53Ile]) segregating with the disease. A second, de novo, missense mutation (c.293A>G [p.Asn97Ser]) was subsequently identified in an individual of Iraqi origin; this individual was diagnosed with CPVT from a screening of 61 arrhythmia samples with no identified RYR2 mutations. Both CALM1 substitutions demonstrated compromised calcium binding, and p.Asn97Ser displayed an aberrant interaction with the RYR2 calmodulin-binding-domain peptide at low calcium concentrations. We conclude that calmodulin mutations can cause severe cardiac arrhythmia and that the calmodulin genes are candidates for genetic screening of individual cases and families with idiopathic ventricular tachycardia and unexplained sudden cardiac death.
Biallelic variants of the CASQ2 are known to cause the autosomal recessive form of catecholaminergic polymorphic ventricular tachycardia (CPVT), an inherited disease that predisposes young individuals to syncope and sudden cardiac death. To date, only about 24 CASQ2 variants have been reported in association with CPVT pathogenesis; furthermore, studies in Asians, especially in the Chinese population, are relatively rare. The aim of this study was to detect CASQ2 variants in Chinese patients with CPVT.
Reperfusion-induced lethal ventricular arrhythmias are observed during relief of coronary artery spasm, with unstable angina, exercise-induced ischemia, and silent ischemia. Accordingly, significant efforts are underway to understand the mechanisms responsible for reperfusion-induced lethal arrhythmias and mice have become increasingly important in these efforts. However, although reperfusion-induced sustained ventricular tachycardia leading to ventricular fibrillation (VF) has been recorded in many models, reports in mice are sparse and of limited success. Importantly, none of these studies were conducted in intact, conscious mice. Accordingly, a chronically instrumented, intact, conscious murine model of reperfusion-induced lethal arrhythmias has the potential to be of major importance for advancing the concepts and methods that drive cardiovascular therapies. Therefore, we describe, for the first time, the use of an intact, conscious, murine model of reperfusion-induced lethal arrhythmias. Male mice (n = 9) were instrumented to record cardiac output and the electrocardiogram. In addition, a snare was placed around the left main coronary artery. Following recovery, the susceptibility to sustained ventricular tachycardia produced by 3 min of occlusion and reperfusion of the left main coronary artery was determined in conscious mice by pulling on the snare. Reperfusion culminated in sustained ventricular tachycardia, leading to VF, in all nine conscious mice. The procedures conducted in conscious C57BL/6J mice, a strain commonly used in transgenic studies, can be utilized in genetically modified models to enhance our understanding of single gene defects on reperfusion-induced lethal ventricular arrhythmias in intact, conscious, and complex animals.
In a patient with right ventricular outflow tract (RVOT) tachycardia, we identified a heterozygous point mutation in the selectivity filter of the stretch-activated K2P potassium channel TREK-1 (KCNK2 or K2P2.1). This mutation introduces abnormal sodium permeability to TREK-1. In addition, mutant channels exhibit a hypersensitivity to stretch-activation, suggesting that the selectivity filter is directly involved in stretch-induced activation and desensitization. Increased sodium permeability and stretch-sensitivity of mutant TREK-1 channels may trigger arrhythmias in areas of the heart with high physical strain such as the RVOT We present a pharmacological strategy to rescue the selectivity defect of the TREK-1 pore. Our findings provide important insights for future studies of K2P channel stretch-activation and the role of TREK-1 in mechano-electrical feedback in the heart.
Ventricular tachycardia due to prior myocardial infarction is caused by reentry. Intraoperative mapping at the time of arrhythmia surgery has shown that the reentry circuits are diverse in size and location. Many circuits are large, extending over several square centimeters. Endocardial excision guided by activation sequence mapping, fractionated sinus rhythm electrograms, or visual identification of scarred subendocardium renders 69% to 95% of patients free from inducible ventricular tachycardia, but with an operative mortality that exceeds 8% at most centers. Catheter ablation is difficult due to limitations of catheter mapping, relatively small size of lesions produced with current techniques, and limited access to intramural and epicardial portions of the reentry circuits. Many problems need to be overcome for catheter ablation to achieve success comparable to that of surgery. At present, only hemodynamically tolerated ventricular tachycardias can be mapped. Progress is being made, and it is likely that catheter ablation will become a viable therapy for subgroups of patients with postmyocardial infarction ventricular tachycardia.
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a severe inherited cardiac disorder caused by mutations predominantly in the ryanodine receptor (RyR2) gene. We sought to identify mutations in genes affecting cardiac calcium cycling in patients with CPVT and in less typical familial exercise-related ventricular arrhythmias.
Nowadays, catheter-based ablation in patients with post-ischemic ventricular tachycardia (VT) is performed in arrhythmogenic sites identified by electrophysiologists by visual inspection during electroanatomic mapping. This work aims to present the development of machine learning tools aiming at supporting clinicians in the identification of arrhythmogenic sites by exploiting innovative features that belong to different domains. This study included 1584 bipolar electrograms from nine patients affected by post-ischemic VT. Different features were extracted in the time, time scale, frequency, and spatial domains and used to train different supervised classifiers. Classification results showed high performance, revealing robustness across the different classifiers in terms of accuracy, true positive, and false positive rates. The combination of multi-domain features with the ensemble tree is the most effective solution, exhibiting accuracies above 93% in the 10-time 10-fold cross-validation and 84% in the leave-one-subject-out validation. Results confirmed the effectiveness of the proposed features and their potential use in a computer-aided system for the detection of arrhythmogenic sites. This work demonstrates for the first time the usefulness of supervised machine learning for the detection of arrhythmogenic sites in post-ischemic VT patients, thus enabling the development of computer-aided systems to reduce operator dependence and errors, thereby possibly improving clinical outcomes.
Arrhythmias originating in scarred ventricular myocardium are a major cause of death, but the underlying mechanism allowing these rhythms to exist remains unknown. This gap in knowledge critically limits identification of at-risk patients and treatment once arrhythmias become manifest. Here we show that potassium voltage-gated channel subfamily E regulatory subunits 3 and 4 (KCNE3, KCNE4) are uniquely upregulated at arrhythmia sites within scarred myocardium. Ventricular arrhythmias occur in areas with a distinctive cardiomyocyte repolarization pattern, where myocyte tracts with short repolarization times connect to myocytes tracts with long repolarization times. We found this unique pattern of repolarization heterogeneity only in ventricular arrhythmia circuits. In contrast, conduction abnormalities were ubiquitous within scar. These repolarization heterogeneities are consistent with known functional effects of KCNE3 and KCNE4 on the slow delayed-rectifier potassium current. We observed repolarization heterogeneity using conventional cardiac electrophysiologic techniques that could potentially translate to identification of at-risk patients. The neutralization of the repolarization heterogeneities could represent a potential strategy for the elimination of ventricular arrhythmia circuits.
The first stereotactic arrhythmia radioablation (STAR) of ventricular tachycardia (VT) was delivered at Stanford on a robotic radiosurgery system (CyberKnife® G4) in 2012. The results warranted further investigation of this treatment. Here we compare dosimetrically three possible treatment delivery platforms for STAR.
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic cardiac disease that leads to ventricular tachycardia (VT), a life-threatening heart rhythm disorder. Treating ARVC remains challenging due to the complex underlying arrhythmogenic mechanisms, which involve structural and electrophysiological (EP) remodeling. Here, we developed a novel genotype-specific heart digital twin (Geno-DT) approach to investigate the role of pathophysiological remodeling in sustaining VT reentrant circuits and to predict the VT circuits in ARVC patients of different genotypes. This approach integrates the patient's disease-induced structural remodeling reconstructed from contrast-enhanced magnetic-resonance imaging and genotype-specific cellular EP properties. In our retrospective study of 16 ARVC patients with two genotypes: plakophilin-2 (PKP2, n = 8) and gene-elusive (GE, n = 8), we found that Geno-DT accurately and non-invasively predicted the VT circuit locations for both genotypes (with 100%, 94%, 96% sensitivity, specificity, and accuracy for GE patient group, and 86%, 90%, 89% sensitivity, specificity, and accuracy for PKP2 patient group), when compared to VT circuit locations identified during clinical EP studies. Moreover, our results revealed that the underlying VT mechanisms differ among ARVC genotypes. We determined that in GE patients, fibrotic remodeling is the primary contributor to VT circuits, while in PKP2 patients, slowed conduction velocity and altered restitution properties of cardiac tissue, in addition to the structural substrate, are directly responsible for the formation of VT circuits. Our novel Geno-DT approach has the potential to augment therapeutic precision in the clinical setting and lead to more personalized treatment strategies in ARVC.
Objectives. Doxapram hydrochloride is a respiratory stimulant that has an inhibitory effect on myocardial IK1 potassium channels and is thought to increase membrane instability and excitability in myocardial cells. We examined the arrhythmogenic effects of doxapram hydrochloride in a rat model of halothane adrenaline-induced arrhythmia. Methods. Thirteen female Wistar rats (12-14 weeks old) were used in the study. Animals were anesthetized with inhalation of halothane to permit observation of the effects of doxapram hydrochloride on halothane adrenaline-induced arrhythmia. Time-dependent changes in ECG repolarization characteristics (QT, QTc, JTp, JT, and Tp-e intervals) were studied. Results. Doxapram hydrochloride itself did not induce arrhythmia but did induce bidirectional ventricular tachycardia after addition of adrenaline. Conclusion. Drug-induced impairment of intracellular Ca(2+) regulation caused BVT in the absence of genetic abnormalities in proteins in the sarcoplasmic reticulum.
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