Showing papers on "Cardiac arrhythmia published in 2002"

Mother rotors and fibrillatory conduction: a mechanism of atrial fibrillation

Abstract: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and the major cardiac cause of stroke. Recent studies in patients with paroxysmal AF have shown that the arrhythmia is triggered by focal sources localized usually in one of the cardiac veins. However, in chronic AF, the prevailing theory is that multiple random wavelets of activation coexist to create an unorganized atrial rhythm. Experiments in isolated hearts have demonstrated that stable, self-sustained rotors can exist in the atria and that high frequency activation by such rotors results in the complex patterns of activation that characterize AF. Studies in animals and patients support the view that at least some cases of paroxysmal and chronic AF are the result of the uninterrupted periodic activity of discrete reentrant sites. In this brief review article, we examine historical data and more recent experimental evidence behind the hypothesis that AF may be organized by one, or a small number of high-frequency reentrant sources localized in the left atrium. We then discuss the potential implications and evidence supporting such a hypothesis for human AF. Finally, we suggest future studies designed to unravel the detailed molecular, cellular and pathophysiological mechanisms responsible for AF initiation and maintenance. The work discussed may open potentially exciting new diagnostic and therapeutic possibilities.

Variant of SCN5A sodium channel implicated in risk of cardiac arrhythmia.

Abstract: Every year, ∼450,000 individuals in the United States die suddenly of cardiac arrhythmia. We identified a variant of the cardiac sodium channel gene SCN5A that is associated with arrhythmia in African Americans (P = 0.000028) and linked with arrhythmia risk in an African-American family (P = 0.005). In transfected cells, the variant allele (Y1102) accelerated channel activation, increasing the likelihood of abnormal cardiac repolarization and arrhythmia. About 13.2% of African Americans carry the Y1102 allele. Because Y1102 has a subtle effect on risk, most carriers will never have an arrhythmia. However, Y1102 may be a useful molecular marker for the prediction of arrhythmia susceptibility in the context of additional acquired risk factors such as the use of certain medications.

Prospective multicenter study of pregnancy outcomes in women with Heart disease

Abstract: Either the mother or fetus may decompensate as a result of maternal heart disease, but available risk figures are based chiefly on retrospective studies or have focused on a particular cardiac disorder. This study prospectively enrolled 562 pregnant women with heart disease at 13 Canadian cardiac and obstetrical teaching hospitals. Pregnancies totaled 617. Women with congenital or acquired cardiac lesions or cardiac arrhythmia were eligible for the study. Follow-up assessments were made in the second and third trimesters of pregnancy, the peripartum period, and after 6 weeks and 6 months. Primary cardiac events included pulmonary edema, sustained symptomatic tachyarrhythmia or bradyarrhythmia requiring treatment, stroke, cardiac arrest, and cardiac death. Baseline features did not in any way distinguish the 18 pregnancies ending in miscarriage. Among 546 women having 599 completed pregnancies (more than 20 weeks' gestation), the major cardiac lesion was congenital in 74%, acquired in 22%, and arrhythmic in 4%. Surgery had been performed in 46% of study pregnancies before conception. Cardiac medication, aspirin, or anticoagulants were being taken at baseline in 100 pregnancies (17%) and were initiated in the prepartum period in another 87. The rate of primary cardiac events in completed pregnancies was 13%; more than half took place in the prepartum period. Most of these events were pulmonary edema and/or cardiac arrhythmia. There were four embolic strokes. Predictors of these events included a past cardiac event or arrhythmia; New York Heart Association (NYHA) class III or higher dysfunction or cyanosis; left heart obstruction; and an ejection fraction less than 40%. Secondary cardiac events (NYHA functional deterioration of two or more stages compared with baseline or an urgent need for invasive cardiac procedures) occurred in 6% of study pregnancies. Neonatal events, most commonly premature birth, occurred in 20% of pregnancies. Predictors included NYHA class more than II or cyanosis at baseline, maternal left heart obstruction, smoking during pregnancy, multiple gestations, and anticoagulant therapy throughout pregnancy. Cardiac intervention should be considered in advance of conception when a woman is at high risk for cardiac events but the risk-benefit ratio is favorable. Women at substantial risk might well do best receiving ongoing care at a regional center. Women at low cardiac risk who lack lesion-specific risk factors can safely deliver at a community hospital.

Cardiac arrhythmia classification using autoregressive modeling

Abstract: Computer-assisted arrhythmia recognition is critical for the management of cardiac disorders. Various techniques have been utilized to classify arrhythmias. Generally, these techniques classify two or three arrhythmias or have significantly large processing times. A simpler autoregressive modeling (AR) technique is proposed to classify normal sinus rhythm (NSR) and various cardiac arrhythmias including atrial premature contraction (APC), premature ventricular contraction (PVC), superventricular tachycardia (SVT), ventricular tachycardia (VT) and ventricular fibrillation (VF). AR Modeling was performed on ECG data from normal sinus rhythm as well as various arrhythmias. The AR coefficients were computed using Burg's algorithm. The AR coefficients were classified using a generalized linear model (GLM) based algorithm in various stages. AR modeling results showed that an order of four was sufficient for modeling the ECG signals. The accuracy of detecting NSR, APC, PVC, SVT, VT and VF were 93.2% to 100% using the GLM based classification algorithm. The results show that AR modeling is useful for the classification of cardiac arrhythmias, with reasonably high accuracies. Further validation of the proposed technique will yield acceptable results for clinical implementation.

Molecular Mechanisms of Remodeling in Human Atrial Fibrillation

Abstract: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia in humans. Most frequently, AF occurs in conjunction with other cardiovascular disease, such as hypertension, ischemic heart disease, valve disease or cardiac failure. However, in 20-50% of the patients AF is not associated with any underlying disease [1]. One of the most intriguing properties of AF is its tendency to become more persistent over time [2]. Consequently, a large percentage of patients with paroxysmal AF will develop persistent AF [2]. Also, conversion to and maintenance of sinus rhythm by pharmacological or electrical methods becomes increasingly difficult the longer the arrhythmia exists[3].

Method and apparatus for treatment of atrial fibrillation

Abstract: Methods and apparatus of embodiments of the invention are adapted to treat tissue inside a patient's body. Aspects of the invention can be used in a wide variety of applications, but certain embodiments provide minimally invasive alternatives for treating atrial fibrillation by delivering a tissue-damaging agent to selected areas of the heart. One exemplary embodiment of the invention provides a method of treating cardiac arrhythmia. This method includes positioning a distal tissue-contacting portion of a body in surface contact with a tissue surface of cardiac tissue; detecting the surface contact between the tissue-contacting portion and the tissue surface; and thereafter, injecting a tissue-ablating agent into the cardiac tissue through the tissue-contacting portion of the body.

Cellular electrophysiology of atrial fibrillation

Abstract: Time for primary review 23 days. Atrial fibrillation (AF) is presently the most common cardiac arrhythmia in clinical practice. Its treatment is inadequate. Maintenance of normal sinus rhythm (SR) is obviously the optimal approach, but is difficult to achieve without drugs that have the potential to cause ventricular proarrhythmia and increase mortality. Non-pharmacological therapy is attractive, but to date has not reached the same level of efficacy as in the treatment of arrhythmias other than AF. In order to improve therapeutic approaches, it is important to understand the detailed pathophysiology of the arrhythmia. A key component to the pathophysiology of any cardiac arrhythmia is the cellular milieu in which it occurs. Changes in ion transport processes, including pumps, channels and exchangers, are central to alterations in action potential properties that govern the occurrence of arrhythmias like AF. Action potential duration (APD) determines the refractory period and is therefore a key determinant of the likelihood of reentry. Maximum Na+-current ( I Na) governs phase 0 upstroke velocity, determining conduction velocity (CV) and contributing to the likelihood of reentry. Delayed and early afterdepolarizations produce abnormal activity that can in themselves produce tachyarrhythmias and can trigger reentrant arrhythmia. This paper reviews these aspects of the cellular electrophysiology of AF, attempting to summarize what is known, what remains to be explored and what this information can teach us about why AF occurs and how to treat it. The identification of the molecular structure of many ion channels involved in cardiac excitability and their functional correlation with native ionic currents have made it possible to study the effects of pathophysiological conditions, like AF, at different levels from genes to ionic currents. The different steps underlying the expression of an ion channel are depicted in Fig. 1 and have recently been reviewed by Roden and … * Corresponding author. Tel.: +49-7071-298-3196; fax: +49-7071-294-121 ralph.bosch{at}uni-tuebingen.de

Anomalies of cardiac venous drainage associated with abnormalities of cardiac conduction system

Abstract: The embryological development of the superior vena cava (SVC) is complex. If the left common cardinal vein fails to occlude it can, along with the left duct of Cuvier form a left SVC, which frequently drains into the coronary sinus. This may result in abnormalities in the anatomy of this structure. A persistent left SVC occurs in 0.5% of the normal population, and 3% to 4.3% of patients with congenital heart anomalies. The pacemaking tissue of the heart is derived from two sites near the progenitors of the superior vena cava. The right-sided site forms the sinoatrial node, the left-sided site is normally carried down to an area near the coronary sinus. Out of 300 patients with cardiac rhythm abnormalities, who have undergone electrophysiological studies (EPS), or permanent pacemaker insertion (PPI), we identified 12 patients with cardiac conduction abnormalities and anomalies of venous drainage. Anomalies of the coronary sinus may be associated with abnormalities of the conduction system of the heart. This may be due to the close proximity of the coronary sinus to the final position of the left-sided primitive pacemaking tissue. In our series of 300 patients, 4% had an associated left SVC, a similar incidence to that found in previous studies of congenital heart disease.

Methods and apparatus employing ionizing radiation for treatment of cardiac arrhythmia

Abstract: Method and apparatus are disclosed employing ionizing radiation for forming lines of ablation or lesions in cardiac tissue to treat atrial fibrillation or other electrophysiological problems with the heart. The apparatus may include a catheter in which the radiation source is advanced hydraulically after the catheter is in place within the heart. Various fixation devices are also disclosed for fixing the location of the catheter within the heart.

Correction of ionized plasma magnesium during cardiopulmonary bypass reduces the risk of postoperative cardiac arrhythmia.

Abstract: We conducted this randomized controlled trial to determine whether the intraoperative measurement and correction of ionized plasma magnesium can reduce the risk of cardiac arrhythmia after cardiopulmonary bypass. Eighty-five patients presenting for coronary artery bypass grafting were randomly assig

Stroke and cardiac arrhythmias.

Abstract: Stroke is frequently followed by electrocardiographic (ECG) changes. The aim of the present study was to evaluate the global incidence of these changes after ischemic or hemorrhagic strokes, but it focused on cardiac arrhythmias. In ischemic strokes, these were correlated with the side of the lesion(s). The study was retrospective, and 450 patients (out of 971 examined) were entered in the study based on the following inclusion criteria: (1) "completed" stroke (352 ischemic and 98 hemorrhagic), (2) ECG on admission, and (3) at least 1 previous ECG. We also examined 71 patients with carotid or vertebro-basilar transient ischemic attacks (TIA). As controls, 71 patients suffering from nonvascular neurologic diseases were examined. The results were as follows: In stroke patients, new-onset ECG abnormalities were present in 75% of cases, and cardiac arrhythmias accounted for 28.7%. Cardiac arrhythmias were observed in 21.9% of ischemic strokes (26.8% of patients with right hemispheric lesion and 14.3% of those with left hemispheric lesion) and in 20.4% of hemorrhagic strokes, with the highest incidence in subarachnoid hemorrhage (37.5%). The mechanisms of genesis of cardiac arrhythmias occurring after stroke are still not well understood. Some evidence supports the hypothesis of a "cardiac cortical rhythm control site," probably lying within the middle cerebral artery territory. Vascular damage to this area could be followed by cardiac arrhythmias related to a disinhibition of the right insular cortex with resulting increased sympathetic tone. Our data seem to indicate that ischemic involvement of the right hemisphere induces a higher risk for cardiac arrhythmia occurrence than that of the left hemisphere.

The cardiac ryanodine receptor (calcium release channel): emerging role in heart failure and arrhythmia pathogenesis.

Abstract: The cardiac sarcoplasmic reticulum calcium release channel, commonly referred to as the ryanodine receptor, is a key component in cardiac excitation-contraction coupling, where it is responsible for the release of calcium from the sarcoplasmic reticulum. As our knowledge of the ryanodine receptor has advanced an appreciation that this key E-C coupling component may have a role in the pathogenesis of human cardiac disease has emerged. Heart failure and arrhythmia generation are both pathophysiological states that can result from deranged excitation-contraction coupling. Evidence is now emerging that hyperphosphorylation of the cardiac ryanodine receptor is an important event in chronic heart failure, contributing to impaired contraction and the generation of triggered ventricular arrhythmias. Furthermore the therapeutic benefits of beta blockers in heart failure appear to be partly explained through a reversal of this phenomenon. Two rare inherited arrhythmogenic conditions, which can cause sudden death in children, have also been shown to result from mutations in the cardiac ryanodine receptor. These conditions, catecholaminergic polymorphic ventricular tachycardia and arrhythmogenic right ventricular cardiomyopathy (subtype 2), further implicate the ryanodine receptor as a potentially arrhythmogenic substrate and suggest that this channel may offer a new therapeutic target in the treatment of both cardiac arrhythmias and heart failure.

Hypertension and arrhythmia: blood pressure control and beyond.

Abstract: Arrhythmias are common problems in hypertensive patients. The presence and complexity of both supraventricular and ventricular arrhythmias may influence morbidity, mortality, as well as the quality of life of patients. Diastolic dysfunction of the left ventricle, left atrial size and function, and left ventricular hypertrophy have been suggested as the underlying risk factors for supraventricular and ventricular arrhythmias in hypertensives. Recently, several non-invasive electrocardiographic parameters have been defined and widely investigated to identify the hypertensive patient at risk for the development of arrhythmias. These parameters include signal averaged analysis of P wave, QT interval dispersion, heart rate variability, ventricular late potentials and T wave morphology analysis. The aim of this review was to evaluate the relationships between high blood pressure, ventricular and supraventricular arrhythmias, relevant non-invasive cardiac parameters for risk assessment in hypertensive patients and the effects of blood pressure control. Copyright 2002 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved .

Unraveling the genetics and mechanisms of cardiac arrhythmia

Abstract: In this issue of the PNAS, Papadatos et al. (1) analyze the mechanism of arrhythmia in the heart after targeted disruption of the cardiac sodium channel, Scn5a. They combine a wide variety of techniques (including genetic deletion, cellular electrophysiology, morphology, and electrocardiography) in an integrated approach to unravel the sequence of events all of the way from the genetic to the whole organism level. They are therefore able to show that the effect of the deletion is to reduce the ionic current carried by sodium channels, so that the propagation among cardiac cells is slowed. This slowing generates arrhythmia because it allows more time for a wavefront to encounter cells that are reexcitable before the wavefront dies out. A sustained rapid reentrant circuit can then be established. This is called a tachycardia and can be fatal.

Embryonic arrhythmia by inhibition of HERG channels: a common hypoxia-related teratogenic mechanism for antiepileptic drugs?

Abstract: PURPOSE: There is evidence that drug-induced embryonic arrhythmia initiates phenytoin (PHT) teratogenicity. The arrhythmia, which links to the potential of PHT to inhibit a specific potassium channel (Ikr), may result in episodes of embryonic ischemia and generation of reactive oxygen species (ROS) at reperfusion. This study sought to determine whether the proposed mechanism might be relevant for the teratogenic antiepileptic drug trimethadione (TMO). METHODS: Effects on embryonic heart rhythm during various stages of organogenesis were examined in CD-1 mice after maternal administration (125-1,000 mg/kg) of dimethadione (DMO), the pharmacologically active metabolite of TMO. Palatal development was examined after administration of a teratogenic dose of DMO and after simultaneous treatment with DMO and a ROS-capturing agent (alpha-phenyl-N-tert-butyl-nitrone; PBN). The Ikr blocking potentials of TMO and DMO were investigated in HERG-transfected cells by using voltage patch-clamping tests. RESULTS: DMO caused stage-specific (gestation days 9-13 only) and dose-dependent embryonic bradycardia and arrhythmia at clinically relevant maternal plasma concentrations (3-11 mM). Hemorrhage in the nasopharyngeal part of the embryonic palate (within 24 h) preceded cleft palate in fetuses at term. Simultaneous treatment with PBN significantly reduced the incidence of DMO-induced cleft palate, from 40 to 13%. Voltage patch-clamping studies showed that particularly DMO (70% inhibition), but also TMO, had Ikr blocking potential at clinically relevant concentrations. CONCLUSIONS: TMO teratogenicity, in the same way as previously shown for PHT, was associated with Ikr-mediated episodes of embryonic cardiac arrhythmia and hypoxia/reoxygenation damage.

Clinical pharmacology: drugs as a benefit and/or risk in sudden unexpected death in epilepsy?

Abstract: Death may be the consequence of natural or unnatural causes, such as accidents, homicide, and suicide, which have no relationship to the disease of epilepsy. Direct causes of death include status epilepticus, and indirect causes may be head trauma or drowning subsequent to a seizure. When death occurs suddenly and without explanation, the term sudden unexpected unexplained death is used. Unexplained is a term that clinicians and research scientists are working to clarify. Numerous preclinical animal studies have been conducted as models for sudden death and have led to clinical studies in persons with epilepsy. These studies show that sympathetic nerve stimulation, ouabain, or coronary occlusion increased temporal dispersion of recovery of ventricular excitability and led to an underlying electrical instability that predisposed the ventricularmyocardium to arrhythmia. Cardiac arrhythmias in an animal model for ouabain-induced toxicity were associated with neural autonomic dysfunction. Neural discharges were characterized by increases, decreases, or no change in the discharge of postganglionic cardiac sympathetic nerves monitored simultaneously, predisposing to cardiac arrhythmia. Stimulation of the sympathetic ventrolateral cardiac nerve produced a shift in the origin of the pacemaker and tachyarrhythmias because the nerve is not uniformly distributed to the various regions of the heart but is localized to the atrioventricular junctional and ventricular regions. Such nonuniform distribution of sympathetic nerves would also contribute to initiation of arrhythmia as a nonuniform neural discharge occurred. Studies examining the physiology and pharmacology of this finding in multiple animal models found that subconvulsant, interictal discharge was associated with autonomic cardiac neural non-uniform discharge and cardiac arrhythmias. As a result of further investigations, Lathers and Schraeder edited a book in 1990 that summarized the clinical problem of sudden unexpected death and epilepsy (SUDEP). The contributors concluded that there was a paucity of clinical data addressing the mechanism of death. Regulatory response resulting from the consequent increased awareness of SUDEP occurred in 1993, when the FDA focused attention of practitioners and pharmaceutical manufacturers on the question of whether use of anticonvulsant drugs contributes to or prevents sudden unexpected death in epileptic persons. The FDA-convened panel of scientists considered the prevalence of sudden unexpected death in patients involved in studies associated with developing new anticonvulsant drugs and reviewed data on the risk of sudden unexpected death in patients taking lamotrigine. The risk of SUDEP was no different from thatfound in the young epilepsy population in general. Estimated SUDEP rates in patients receiving the new anticonvulsant drugs lamotrigine, gabapentin, topiramate, tigabine, and zonisamide were found to be similar to those in patients receiving standard anticonvulsant drugs, suggesting that SUDEP rates reflect population rates and not a specific drug effect. The FDA required warning labels on the risk of SUDEP in association with the use of each of the above-mentioned drugs. Another effect of bringing SUDEP to the attention of epilepsy researchers has been the expansion of basic science and the development of epidemiological and clinical studies directed at this phenomenon. Results from some of these studies are discussed in this article.

A method to quantify the dynamics and complexity of re-entry in computational models of ventricular fibrillation

Abstract: Ventricular fibrillation is a deadly cardiac arrhythmia. There is evidence that electrical activity in cardiac tissue is sustained during fibrillation by re-entrant waves that rotate around filaments. In this paper we develop a method for identifying and tracking filaments in a computational model of ventricular fibrillation. This method identifies the birth, death, bifurcation and amalgamation of filaments and these events are summarized on a directed graph. The approach described in this study provides ways to quantify the complex patterns of electrical activity seen in computational models of fibrillation, to relate the behaviour of computational models to experimental data and thus to gain insights into the underlying mechanisms of this dangerous arrhythmia.

Method and system for evaluating arrhythmia risk with qt-rr interval data sets

Abstract: A method (40a-48a and 40b-48b) of assessing the cardiac arrhythmia risk in a subject to provide a measure of cardiac or cardiovascular health in that subject is described herein.

Complex patterns of abnormal heartbeats.

Abstract: Individuals having frequent abnormal heartbeats interspersed with normal heartbeats may be at an increased risk of sudden cardiac death. However, mechanistic understanding of such cardiac arrhythmias is limited. We present a visual and qualitative method to display statistical properties of abnormal heartbeats. We introduce dynamical "heartprints" which reveal characteristic patterns in long clinical records encompassing approximately 10(5) heartbeats and may provide information about underlying mechanisms. We test if these dynamics can be reproduced by model simulations in which abnormal heartbeats are generated (i) randomly, (ii) at a fixed time interval following a preceding normal heartbeat, or (iii) by an independent oscillator that may or may not interact with the normal heartbeat. We compare the results of these three models and test their limitations to comprehensively simulate the statistical features of selected clinical records. This work introduces methods that can be used to test mathematical models of arrhythmogenesis and to develop a new understanding of underlying electrophysiologic mechanisms of cardiac arrhythmia.

Ventricular dyssynchrony and mechanisms of resynchronization therapy

Abstract: Patients with dilated cardiomyopathy (DCM) that is further complicated by intra-ventricular conduction delay with discoordinate wall motion have increased mortality risk as compared with the general DCM population. Dyssynchrony reduces cardiac systolic function while increasing oxygen consumption, and may be a source of arrhythmia. The recent development of endocardial lead systems to activate the left ventricle prematurely has yielded the novel therapeutic option of resynchronization therapy to correct cardiac dyssynchrony. Using either biventricular or left ventricular pre-excitation, systolic function and energetic efficiency can be substantially enhanced in heart failure patients who have underlying discoordinate contraction. The present review addresses the pathophysiology of cardiac dyssynchrony and the mechanisms that underlie resynchronization treatment.

Risk of severe cardiac arrhythmia in male utility workers: A nationwide Danish cohort study

Abstract: To address concern about the potential cardiovascular effects of occupational exposure to electromagnetic fields in the 50- to 60-Hz frequency band, the authors launched an epidemiologic study of the incidence of severe cardiac arrhythmia, as indicated by the need for a pacemaker, in a nationwide cohort of Danish utility workers. The cohort of 24,056 men employed at utility companies between 1900 and 1993 was linked to the nationwide, population-based Danish Pacemaker Register, and the numbers of persons who had undergone pacemaker implantation between 1982 and 2000 were compared with corresponding numbers in the general population. In addition, the data on the utility workers were fitted to a multiplicative Poisson regression model in relation to estimated levels of exposure to 50-Hz electromagnetic fields. Overall, based on 135 men with pacemakers (140 expected), there was no increased risk of severe cardiac arrhythmia among the utility employees; the risk estimate was 0.96 (95% confidence interval: 0.81, 1.14). No clear dose-response pattern emerged with increasing levels of exposure to electromagnetic fields or with duration of employment. These results are largely reassuring, since they do not support the hypothesis of a link between occupational exposure to electromagnetic fields and an excess risk of severe cardiovascular arrhythmia leading to permanent implantation of a pacemaker.

Atrio-ventricular block: a possible explanation of sudden unexpected death in epilepsy

Abstract: Tigaran S, Molgaard H, Dam M. Atrio-ventricular block: a possible explanation of sudden unexpected death in epilepsy. Acta Neurol Scand 2002: 106: 229–233. © Blackwell Munksgaard 2002 Introduction– This is the third case report describing the occurrence of total atrio-ventricular (AV)-block as a life threatening cardiac arrhythmia complicating epileptic seizures. Case report– A 56-year-old right-handed man was admitted to our hospital for surgical assessment of his medically intractable epilepsy. During the hospitalization he was enrolled in a study investigating cardiac complication of epileptic seizures as the possible cause of sudden unexplained death among epileptics. Discussion– To the best of our knowledge, we are the first to employ simultaneous video-electroencephalogram-, Holter- and pulse oximetry-recordings of our patients in the description of this complication. These recordings allowed us to discuss the evidence and consequences of this particular cardiac abnormality as an explanation of sudden unexplained death in epileptic seizures, especially those of temporal origin.

New Bayesian discriminator for detection of atrial tachyarrhythmias.

Abstract: Background— Accurate, rapid detection of atrial tachyarrhythmias has important implications in the use of implantable devices for treatment of cardiac arrhythmia. Currently available detection algorithms for atrial tachyarrhythmias, which use the single-index method, have limited sensitivity and specificity. Methods and Results— In this study, we evaluated the performance of a new Bayesian discriminator algorithm in the detection of atrial fibrillation (AF), atrial flutter (AFL), and sinus rhythm (SR). Bipolar recording of 364 rhythms (AF=156, AFL=88, SR=120) at the high right atrium were collected from 20 patients who underwent electrophysiological procedures. After initial signal processing, a column vector of 5 features for each rhythm were established, based on the regularity, rate, energy distribution, percent time of quiet interval, and baseline reaching of the rectified autocorrelation coefficient functions. Rhythm identification was obtained by use of Bayes decision rule and assumption of Gaussian...

Compound for treatment of cardiac arrhythmia, synthesis, and methods of use

Abstract: The subject invention pertains to novel compounds (and salts thereof), and compositions comprising the compounds, for the treatment of cardiac arrhythmias. The subject invention further concerns methods of making the novel compounds. The novel compounds are rapidly metabolized analogs of amiodarone, having the distinct and advantageous characteristic of being metabolized to a less lipophilic compound. This results in an improved safety profile. The new compounds have particular utility for treating life-threatening ventricular tachyarrhythmias, especially in patients with congestive heart failure (CHF). The compounds also provide effective management for ventricular arrhythmias and supraventricular arrhythmias, including atrial fibrillation and re-entrant tachyarrhythmias involving accessory pathways.