bluuebunny/crossref_metadata_2025 huggingface dataset:
Abuse Against Women in Rural Minnesota
Authors: Kershner Marion , Long Dianne , Anderson Jon E.
Published: May 2007

ABSTRACT The purpose of this study was to examine the prevalence of physical, emotional, and sexual abuse in women seeking care in rural medical clinics and WIC supplemental food program sites, as well as to examine demographic and health characteristics related to abuse. This was a descriptive, cross‐sectional study using a self‐administered, anonymous survey. Data were collected in 8 medical clinics and 17 WIC supplemental food program sites in 9 counties of west‐central Minnesota during January and February, 1997. The survey instrument asked brief screening questions on physical, emotional, and sexual abuse as well as demographic and health related questions designed to reflect the rural population and characteristics. The survey results showed that in the prior 12 months, 109 (6.6%) of the respondents reported physical abuse, 347 (21.1%) reported emotional/verbal abuse, and 35 (2.1%) reported sexual abuse. Proportional increases in risk of current abuse relative to married women were 2.1 for single, 2.5 for divorced, and 6.5 for separated women, after adjusting for other important variables. Single women with a recent status change had significantly higher risk of current abuse than women with a recent status change at all other marital status levels in adjusted analyses. Women who reported some form of abuse before age 18, and women reporting abuse as an adult prior to the last 12 months, were significantly more likely to report current abuse in all analyses. Prior abuse as an adult was the single best predictor of current abuse in a final logistic regression model.
An Anthropological Study about Epilepsy in Native Tribes from Central and South America
Authors: Carod‐Artal Francisco Javier , Vázquez‐Cabrera Carolina Benigna
Published: May 2007

Summary:  Purpose: Epilepsy was a well‐recognized disease in pre‐Columbian cultures. However, anthropological studies about epilepsy in native cultures living at the present time are scarce. The objective of this paper was to study native perception and myths about epilepsy, their magic‐religious healing rites and ceremonies, and the natural treatments that archaic cultures used.

Methods: An anthropological fieldwork was performed in Central and South America with Tzeltal Maya (Chiapas, Mexico, 1995), Kamayurá (Matto Grosso, Brazil, 1999) and Uru‐Chipaya people (Bolivian Andes, 2004). We collected information from shamans and medicine men about epilepsy beliefs and the use of traditional treatments.

Results: Epilepsy is called tub tub ikal by Tzeltal people. It is caused by an attack suffered by the animal spirit who accompanies the person, after a fight between the spirits who serve the forces of good and evil. People with chronic epilepsy are considered witches. Epilepsy is called teawarup by Kamayurá, and is caused by the revenge of the spirit (mama'e) of the armadillo killed by a huntsman. It is treated with two roots, tsimó and wewurú, kneaded and diluted in water. Epilepsy is called tukuri by the Chipaya people, and is originated by a witchcraft that enters into the nose and the head, as a wind. Tukuri is treated with a ritual animal sacrifice called willancha, and by taking several dried insect infusions and bird's blood.

Conclusion: These American native cultures have developed a system of orally transmitted knowledge about epilepsy based on magic‐religious traditions.
Epilepsy and Recreational Scuba Diving: An Absolute Contraindication or Can There Be Exceptions? A Call for Discussion
Authors: Almeida Maria do Rosario G. , Bell Gail S. , Sander Josemir W.
Published: May 2007

Summary:  Recreational scuba diving is a popular sport, and people with epilepsy often ask physicians whether they may engage in diving. Scuba diving is not, however, without risk for anyone; apart from the risk of drowning, the main physiological problems, caused by exposure to gases at depth, are decompression illness, oxygen toxicity, and nitrogen narcosis. In the United Kingdom, the Sport Diving Medical Committee advises that, to dive, someone with epilepsy must be seizure free and off medication for at least 5 years. The reasons for this are largely theoretical. We review the available evidence in the medical literature and diving websites. The risk of seizures recurring decreases with increasing time in remission, but the risk is never completely abolished. We suggest that people with epilepsy who wish to engage in diving, and the physicians who certify fitness to dive, should be provided with all the available evidence. Those who have been entirely seizure‐free on stable antiepileptic drug therapy for at least 4 years, who are not taking sedative antiepileptic drugs and who are able to understand the risks, should then be able to consider diving to shallow depths, provided both they and their diving buddy have fully understood the risks.
Bacterial screening of apheresis platelets and the residual risk of septic transfusion reactions: the American Red Cross experience (2004‐2006)
Authors: Eder Anne F. , Kennedy Jean M. , Dy Beth A. , Notari Edward P. , Weiss John W. , Fang Chyang T. , Wagner Stephen , Dodd Roger Y. , Benjamin Richard J. ,   American Red Cross Regional Blood Centers
Published: May 2007

BACKGROUND: The American Red Cross initiated systemwide bacterial testing of all apheresis platelet (PLT) collections in March 2004, yet continues to receive reports of septic reactions after transfusion of screened components.

STUDY DESIGN AND METHODS: The rates of confirmed bacterial contamination of apheresis PLT collections detected by prospective quality control (QC) testing, and by surveillance of reported septic reactions to screened‐negative apheresis PLTs, were analyzed according to the technology utilized for collection.

RESULTS: Between March 1, 2004, and May 31, 2006, bacterial culture testing was performed on 1,004,206 donations; of these, 186 (1:5,399) had confirmed‐positive culture results. Transfusion of all but 1 of the associated 293 components was prevented. A significantly higher rate of confirmed‐positive bacterial cultures was seen with products collected utilizing two‐arm collection procedures compared to one‐arm procedures (22.7 vs. 11.9 per 105 donations; odds ratio [OR], 1.9; 95% confidence interval [CI], 1.4‐2.7). During this period, 20 septic transfusion reactions were reported, including 3 fatalities (1:498,711 fatalities per distributed component), which implicated screened‐negative apheresis PLT products. The frequency of septic reactions was 4.7‐fold higher for collections utilizing two‐arm procedures (1:41,173; 95% CI, 1:25,000‐1:66,667) compared to collections from one‐arm procedures (1:193,305; 95% CI, 1:52,632‐1:500,000; OR, 4.7; 95% CI, 1.2‐18.4); most septic reactions (16 of 20) were due to Staphylococcus spp. and occurred on Day 5 (13 of 20) after collection.

CONCLUSION: PLT contamination with bacteria that evade detection by QC culture remains a significant residual transfusion risk, in particular for older PLTs and skin‐commensal bacteria in components collected by two‐arm apheresis procedures during the study period.
The United States' potential blood donor pool: estimating the prevalence of donor‐exclusion factors on the pool of potential donors
Authors: Riley William , Schwei Matthew , McCullough Jeffrey
Published: May 2007

BACKGROUND: Efforts to ensure donor and recipient safety have reduced the population of eligible voluntary blood donors. The current method for determining eligible blood donors in a population using only age as the criterion for excluding donors poorly reflects the large constellation of factors known to cause donor deferrals. An epidemiologic model has been developed to determine the prevalence of donor exclusions and thus improve the estimate of total eligible blood donors in the nation.

STUDY DESIGN AND METHODS: Epidemiologic databases were selected to enumerate the population prevalence of 31 donor exclusionary factors which correspond to the AABB standards. Prevalence data were adjusted for age, duration of exclusion, and comorbidities. This method yields the number of excluded individuals to calculate the number of eligible blood donors.

RESULTS: The conventional method of calculating eligible donors indicates that there are approximately 177 million eligible blood donors in the US population. This study indicates that this method erroneously includes 66 million individuals who are ineligible due to known exclusionary factors. Only 111 million individuals in the US population are eligible to donate blood.

CONCLUSION: The conventional method of determining eligible blood donors overestimates eligible donor prevalence by approximately 59 percent (111 million eligible individual blood donors rather than 177 million eligible individuals). It is recommended that a method similar to the one described in this study be utilized to additionally exclude potential donors not meeting AABB donation standards to improve accuracy of eligible blood donor estimations.
Automated programs for collection of mononuclear cells and progenitor cells by two separators for peripheral blood progenitor cell transplantation: comparison by a randomized crossover study
Authors: Ikeda Kazuhiko , Ohto Hitoshi , Kanno Takahiro , Ogata Takashi , Noji Hideyoshi , Ogawa Kazuei , Maruyama Yukio
Published: May 2007

BACKGROUND: Although automated programs have been increasingly used to collect peripheral blood (PB) progenitor cells (PBPCs), differences among them remain unclear. The automated programs of Amicus (Baxter Healthcare) and Spectra (software Version 6.1, Gambro BCT) apheresis machines were compared in a crossover study.

STUDY DESIGN AND METHODS: The patients for autologous and donors for allogeneic PBPC transplantation mobilized with granulocyte–colony‐stimulating factor were randomly assigned into two groups. PBPCs were collected by the Amicus on the first day and the Spectra on the second of 2 consecutive days in Group I, and the reverse order was used in Group II. Of 39 patients or donors enrolled, 17 reached their collection goal with only one procedure and did not participate in the paired study. Thus, 44 paired procedures of the remaining 22 subjects were evaluated.

RESULTS: The product yields of white blood cells (WBCs; p < 0.005), mononuclear cells (MNCs; p < 0.02), and CD34+ PBPCs (p < 0.0002) from patients or donors were higher in the Amicus collections than those in the Spectra collections. The collection efficiencies of WBCs (p < 0.03), MNCs (p < 0.02), and CD34+ PBPCs (p < 0.03) were higher in the Amicus collections. The numbers of contaminating platelets (PLTs) in the Amicus collections were lower than those in the Spectra collections (p < 0.05) with a greater decrease in PB PLT counts after apheresis with the Spectra (p < 0.01). The Amicus had a longer running time than the Spectra for processing similar volumes (p < 0.005).

CONCLUSION: The automated program of the Amicus may be better than that of the Spectra for collecting MNCs and CD34+ PBPCs and avoiding apheresis‐induced thrombocytopenia.
Short‐term liquid storage of CD14+ monocytes, CD11c+, and CD123+ precursor dendritic cells produced by leukocytapheresis
Authors: Strasser Erwin F. , Keller Benjamin , Hendelmeier Martin , Ringwald Jürgen , Zingsem Jürgen , Eckstein Reinhold
Published: May 2007

BACKGROUND: This prospective study compared white blood cell (WBC) storage in polyvinylchloride (PVC) bags and in polyolefin (POF) bags. After leukapheresis, CD14+ monocytes, CD11c+, and CD123+ precusor dendritic cells (DCs) were analyzed under platelet (PLT) storage conditions.

STUDY DESIGN AND METHODS: Twenty‐five leukapheresis procedures were performed on blood cell separators (AS.TEC204 [PVC; Fresenius HemoCare GmbH] and the COBE Spectra [POF, Gambro BCT]). Blood cell counts, glucose, lactic acid, pO2, pCO2, and pH were measured in mononuclear cell (MNC) harvests on Days 0, 1, 3, and 5. WBCs were analyzed by flow cytometry.

RESULTS: The WBC yields of the AS.TEC204 harvests were 25 percent higher (13.4 × 109 ± 2.7 × 109 WBCs) compared to the COBE Spectra (9.9 × 109 ± 2.5 × 109 WBCs). During 5‐day storage, WBC counts (PVC bags) decreased significantly (24%). Storage in POF bags showed more consistent results (WBC loss, 6%). Loss of CD14+ monocytes and CD11c+ precursor DCs did not differ significantly in leukapheresis products. CD123+ precursor DCs stored in PVC bags dropped by more than 90 percent (POF bags, 24%). Lactic acid concentrations exceeded 20 mmol per L after 24 hours in PVC bags and after 72 hours in POF bags. The mean pH value on Day 5 was 6.2 (PVC) and 6.3 (POF). On Day 1, the product glucose concentration decreased by 76 percent after storage in PVC bags and by 16 percent in POF bags.

CONCLUSIONS: Storage of MNCs within 72 hours in the original harvest container assures stable WBC content and is easy to perform. POF bags should be preferred in the case of extended WBC storage. Patient studies should clarify changes in efficiency of hematopoietic reconstitution that might occur over time during MNC storage.
The Precision of Electrophysiological Mapping: Localizing Depolarization Wave Fronts from Digitized Extracellular Eleetrograms and the Role of Data Sampling Rate
Authors: ROSENBAUM DAVID S. , KAPLAN DANIEL T. , WILBER DAVID J. , SAUL J. PHILIP , RUSKIN JEREMY N. , GARAN HASAN
Published: May 2007

The Precision of Electrophysiological Mapping: Localizing Depolarization Wave Fronts from Digitized Extracellular Electrograms and the Role of Data Sampling Rate. Electrophysiological mapping uses extracellular electrograms to estimate the timing of local cellular depolarization. To measure the precision of localizing propagating wave fronts with this technique and determine its dependence on data sampling rate, extracellular electrograms were recorded with a laboratory computer from 61 bipolar epicardial and endocardial electrodes during 10 morphologically distinct episodes of ventricular tachycardia (VT) in 10 chronically infarcted dogs. Four investigators assigned local activation times to 610 computer displayed local electrograms (61 from each of 10 VTs) sampled at 1,000 Hz (trial 1). With the investigators blinded to the result of the first trial, activation mapping was again repeated in serial independent trials using identical eleetrograms displayed at the data acquisition rate (1,000 Hz), in addition to sampling rates of 500 Hz, 250 Hz, and 125 Hz. The temporal precision of activation mapping (± 10 msec, 95% confidence) was derived from the reproducibility of measuring local activation time from maximally sampled (1,000 Hz) extracellular electrograms. Multivariate analysis revealed decreased precision at epicardial (P <0,02) and infarcted sites, which was attributed to fractionated eleetrograms observed in these regions. Nonetheless, map guided localization of the anatomic breakthrough site of each tachycardia varied by only 1.0 ± 1.2 cm between trials. This value was consistent with the spatial resolution (± 0.5 to + 1.0 cm) that was predicted from the measured temporal precision. Extracellular electrograms contained minimal frequency content above 150 Hz resulting in negligible distortion of waveform morphology at sampling rates as low as 250 Hz. Moreover, the accuracy of activation mapping was not significantly impaired until sampling rate was slowed to 125 Hz.
Ventriculoatrial Conduction Time During Bundle Branch Reentrant Beat Initiating Orthodromic Tachycardia: A Simple and Reliable Method for Localization of Accessory Pathways
Authors: JAZAYERI MOHAMMAD R. , TCHOU PATRICK , CACERES JOSE , MCKINNIE JAMES , AVITALL BOAZ , GILBERT CAROL , WERNER PAUL , AKHTAR MASOOD
Published: May 2007

VA Interval Via Accessory Pathway During Bundle Branch Reentry. Bundle branch reentrant (BBR) complex is commonly induced during programmed ventricular stimulation with single ex‐trastimulus. In patients with atrioventricular accessory pathway, BBR beat frequently triggers orthodromic tachycardia. This study was designed to determine whether evaluation of the ventriculoatrial conduction time during BBR (VABBR) induced with right ventricular extrastimulation (i.e., left bundle branch block morphology) can separate left free‐wall (LFW) accessory pathways from left posteroseptal (LPS) or right‐sided pathways. Thirty‐eight patients with single atrioventricular accessory pathways were included. There were 28 men and 10 women with a mean age of 26 years. The accessory pathway was localized in LFW in 23 patients (group I) and LPS in seven (group ID. Eight patients (group III) had pathways located in the right side. In each patient, VABBR was determined and compared with the following: (1) V2A2 interval exclusively via accessory pathway; and (2) ventriculoatrial conduction time during orthodromic tachycardia with narrow QRS complex (VANQ), left bundle branch block plus normal axis (VALB‐NA) or left axis (VALB‐LA). In group I, VABBR values (170–245 msec, mean 196.1 ± 20.5 msec) were 0–25 msec longer than V2A2 (170–245 msec, mean 191.3 ± 19.1 msec) and 45–125 msec greater than VANQ (100–155 msec, mean 125.6 ± 14.1 msec). VABBR was identical to VALB‐LA but 25–55 msec greater than VA,LB‐NA (140–205 msec, mean 160.9 ± 20.8 msec). In group II, VABBR values (100–140 msec, mean 118.6 ± 14.3 msec) were 15–30 msec shorter than V2A2 (125–165 msec, mean 140.7 ± 14.3 msec) and 15–25 msec longer than VANQ (85–120 msec, mean 100.7 ± 12.0 msec). Comparing VABBR with VALB‐NA or VALB‐LA did not show any statistically significant difference. In group III, VABBR values were consistently shorter than V2A2 and identical to VANQ. Thus, assessment of VABBR is a simple and useful method that can be reliably utilized to differentiate LFW pathways from LPS or right‐sided pathways. Furthermore, these data provide new insights into the electrophysiological characteristics of bundle branch reentry. (J Cardiovasc Electrophysiol, Vol. 1, pp. 121–131, April 1990)
Early Afterdepolarizations: Newer Insights into Cellular Mechanisms
Authors: JANUARY CRAIG T. , SHOROFSKY STEPHEN
Published: May 2007

Early Afterdepolarizations. Early afterdepolarizations (EADs) are a type of bradycardia‐dependent triggered activity postulated to cause certain cardiac arrhythmias. The cellular mechanism(s) that underlie EADs have, until recently, remained obscure. Recent evidence has shown that EADs arise from a cellular mechanism rather than cell‐to‐cell interactions. At least two types of EADs exist that appear to be separable by voltage‐ (and time‐) dependent properties. EADs that arise near action potential plateau voltages depend critically on L‐type Ca2+ current for depolarization. Studies of Ca2+ currents in single heart cells have provided a basis for explaining the potential roles of L‐ and T‐type Ca2+ currents in EADs. (J Cardiovasc Electrophysiol. Vol. 1. pp. 161–169, April 1990)
Electrophysiology of Ethacizin: Effects on Arrhythmias in the In Situ Heart and Transmembrane Action Potentials of Purkinje Fibers and Ventricular Muscle Cells
Authors: DANGMAN KENNETH H. , ZAIM SINA , HOFFMAN BRUCE N. , HOFFMAN BRIAN F.
Published: May 2007

Therapeutic and Toxic Effects of Ethacizin. Ethacizin is a new antiarrhythmic drug that is a derivative of ethmozine. We confirmed the early findings that ethacizin reduces the arrhythmias that occur in dogs 24 hours after ligation of the left anterior descending coronary artery. However, we found that QRS duration and R‐on‐T beats were increased by ethacizin, and that sudden death occurred in one‐third of the dogs. In control experiments, etbmozine (n = 6) and quinidine (n = 6) produced antiarrhythmic effects comparable to those of ethacizin, but sudden death did not occur. Studies then were carried out on canine cardiac tissues using standard microelectrode techniques. Ethacizin 300 ng/mL decreased dV/dtmax in Purkinje fibers and ventricular muscle. These decreases were rate dependent. Ethacizin decreased action potential plateau duration (APD‐60 mV) in false tendon Purkinje fibers, and increased it in ventricular muscle. In spontaneously firing Purkinje fibers, ethacizin consistently decreased high‐potential (normal) and low‐potential (abnormal) automaticity to 14% and 12% of control, respectively. The effects of ethacizin on catecholamine‐enhanced high‐potential automaticity were more variable. Automaticity decreased in about half of the fibers, but did not change greatly in the remainder. The antiarrhythmic actions of ethacizin may result from reduction of impulse initiation or conduction in Purkinje fibers or myocardial cells. (J Cardiovasc Electrophysiol, Vol. 1, pp. 411–425, October 1990)
Atrioventricular Nodal Response to Retrograde Activation in Atrial Fibrillation
Authors: WITTKAMPF FRED H.M. , JONGSTE MIKE J.L. DE , MEIJLER FRITS L.
Published: May 2007

Atrioventricular Nodal Reset. Retrograde (ventriculoatrial) conduction that reaches the atrioventricular node simultaneous with, or just before an atrial impulse ean facilitate subsequent anterograde conduction. However, a spontaneous or programmed ventricular extrasystule during atrial nbrillation is generally followed by a compensatory pause indicating subsequent delayed anterograde transmission. This characteristic response was used as a model to study the mechanism of atrioventricular nodal behavior during atrial fibrillation. In eight medically‐treated patients with chronic atrial fibrillation and a relatively slow but random ventricular response, single premature right ventricular stimuli were delivered after every eighth spontaneous R wave during at least 1 hour. A fixed coupling interval of the ex‐trastimulus, considerably shorter than the shortest spontaneous RR interval, was used. The histograms of the postextrasystolic intervals were compared with those of the spontaneous noninterrupted RR intervals. The average postextrasystolic interval was 180 to 300 msec longer than the mean control RR interval, and in six of eight patients, the shape of the histogram of the postextrasystolic cycles was insignificantly different from that of the spontaneous RR intervals. This suggests that In those six patients, the retrograde impulse had reset the random timing cycle of atrioventricular nodal discharge during atrial fibrillation. This observation is compatible with the hypothesis that electrotonically‐mediated propagation across a weakly coupled junctional area within the atrioventricular node, rather than decremental conduction and extinction of anterograde atrial impulses at different levels within the node, may be the mechanism of atrioventricular transmission in atrial fibrillation. (J Curdiovasc Electrophysiol, Vol. 1, pp. 437–447, October 1990)
The Mechanism of Simulated Torsade de Pointes in a Computer Model of Propagated Excitation
Authors: ABILDSKOV J.A. , LUX ROBERT L.
Published: May 2007

Mechanism of Torsade de Pointes. A computer model that simulated propagation, nonuniform cycle length dependent recovery of excitability, and slow propagation during incomplete recovery in cardiac muscle has been shown to exhibit behavior similar to torsade de pointes. The conditions required in the model resembled those in long QT syndromes with regionally prolonged ventricular repolarization. In the model, premature excitation of a path with relatively short refractory periods resulted in sequential reentry of that path from a region with longer refractory periods. Sites of reentry become progressively more distal to the site of initiation. The episodes terminated spontaneously when reentrant excitation reached the end of unclosed paths or collided in closed paths. Each reentry site moved away from its initial position in the short recovery path because the distance traversed by propagation in that path exceeded the distance at which reentry occurred via the longer recovery region. The migrating sites of reentry resulted in changing QRS waveform in calculated electrocardiograms including changing QRS polarity when calculated from appropriate sites. Variations of the basic behavior occurred with nonuniform distribution of refractory periods within relatively short and long refractory period regions and included unidirectional progression of reentry sites and multiple circuits of reentry in closed paths. Termination of serial reentry at times other than those when activation reached the end of unclosed paths or collided in closed paths also occurred with nonuniform distribution of refractory periods. Findings provide a plausible explanation for the changing QRS waveform, spontaneous termination, and association of torsade de pointes with long QT syndromes but do not elucidate the mechanism of initiation of the tachyarrhythmia.
Mechanisms of Arrhythmias in Ventricular Hypertrophy
Authors: ARONSON RONALD S.
Published: May 2007

Mechanisms of Arrhythmias in Ventricular Hypertrophy. Cardiac hypertrophy is an adaptative process by which the heart accommodates to abnormal pressure and volume overloads. However, hypertrophy of the left ventricle is associated with a high incidence of ventricular arrhythmias and sudden death. The cellular mechanisms responsible for the abnormal rhythmic activity in hypertrophied myocardium has not been clearly defined, but left ventricular hypertrophy is associated with characteristic electrical abnormalities in experimental models and in hypertrophied human tissue. The most consistent electrical alteration is prolonged duration of the action potential in hypertrophied myocardium. The prolonged duration of depolarization predisposes hypertrophied tissue to develop early afterdepolarizations, which can encourage the development of arrhythmias by a variety of mechanisms. Early afterdepolarizations interrupt repolarization and can lead directly to sustained triggered activity. Early afterdepolarizations can depolarize adjacent excitable fibers and thereby induce triggered activity. The prolonged duration of repolarization can enhance influx of calcium, which can in turn lead to delayed afterdepolarizations that can give rise to triggered activity. Early afterdepolarizations can also produce conduction block or delay, which could contribute to the development of reentrant arrhythmias. Early afterdepolarizations are the most likely electrical abnormality to arise from the prolonged time course of repolarization in hypertrophied myocardium. Therefore, therapeutic measures aimed at preventing the development of early afterdepolarizations in hypertrophied myocardium could prove to be a fruitful approach to inhibiting the development of arrhythmias. The development of agents that selectively reduce the duration of the action potential requires a better understanding of the ionic mechanisms responsible for prolonging the action potential in hypertrophied myocardium. In the meantime, avoiding factors known to favor the development of afterpotentials (e.g., extremes of heart rate, electrolyte abnormalities, certain antiarrhythmic drugs) in patients with left ventricular hypertrophy seems prudent.
Chaos in Cardiology
Authors: KAPLAN DANIEL T. , GOLDBERGER ARY L.
Published: May 2007

Chaos in Cardiology. The field of nonlinear dynamics, including chaos theory, has received considerable attention of late. There is a growing body of research relating chaos to basic and clinical cardiology. We present some of the concepts underlying nonlinear dynamics at an introductory level, and review the research relating chaos to cardiology in three areas: cellular‐level cardiac electrophysiology; ventricular fibrillation; and sinus rhythm.
Adrenergic Induction of Delayed Afterdepolarizations in Ventricular Myocardial Cells: β Induction and α Modulation
Authors: MARCHI STEFANO , SZABO BELA , LAZZARA RALPH
Published: May 2007

Adrenergic Afterdepolarizations in Ventricular Cells. Introduction: The purpose of these studies was to expose canine multicellular ventricular endocardial preparations and disaggregated myocytes to adrenergic agonists and antagonists, and to investigate the generation of delayed afterdepolarizations and triggered action potentials. Methods and Results: We used multicellular preparations and disaggregated myocytes from canine ventricles. The threshold concentration for induction of delayed afterdepolarizations in isolated myocytes for norepinephrine was between 1 × 10−8 M and 5 × 10−5 M, with 50% of the cells showing delayed afterdepolarizations at 4.3 × 10−8 M. Higher concentrations of epinephrine are required with 50% of the cells responding to 8.3 × 10−8 M. The threshold concentrations for induction of delayed afterdepolarizations in myocardial cells of multicellular preparations were an order of magnitude higher. Delayed afterdepolarizations could not be induced in Purkinje fibers with concentrations up to 10−4 M with norepinephrine. Adrenergic delayed afterdepolarizations were inhibited promptly by reduction of pO2 in superfusate that was equilibrated with N2 (95%) in place of O2. The amplitudes of adrenergic delayed afterdepolarizations and the propensity to triggered action potentials were inversely related to cycle length down to the shortest cycle length tested (330 msec). Adrenergic delayed afterdepolarizations were induced by isoproterenol but not by α‐adrenergic agonists (methoxamine or phenylephrine). They were inhibited by a β antagonist (propranolol) but not by α antagonists (prazosin or yohimbine). Delayed afterdepolarizations induced by isoproterenol were inhibited by α agonists (methoxamine or phenylephrine). The α‐adrenergic inhibitory effects on β‐adrenergic delayed afterdepolarizations could be reversed by prazosin, but not by yohimbine. Conclusions: We conclude the natural catecholamines norepinephrine and epinephrine generate delayed afterdepolarizations in myocardial cells, but not in Purkinje cells, by activating β receptors, but activation of α1 receptors inhibits adrenergic delayed afterdepolarizations. Individual myocytes exhibit widely varying sensitivities for induction of adrenergic delayed afterdepolarizations, but some cells respond to concentrations similar to those that may exist in vivo. Therefore, sympathetic activation in vivo may generate delayed afterdepolarizations, triggered action potentials, and arrhythmias.
Arrhythmias in Hypertrophic Cardiomyopathy
Authors: STEWART JAMES T. , McKENNA WILLIAM J.
Published: May 2007

Arrhythmias in Hypertrophic Cardiomyopathy. Arrhythmias, particularly atrial fibrillation and nonsustained ventricular tachycardia, are common in adult patients with hypertrophic cardiomyopathy. Atrial fibrillation has long been thought to herald an ominous prognosis, but this is probably not the case, and in the majority of patients atrial fibrillation can be controlled without accelerated symptomatic deterioration. Uncontrolled observations indicate that low dose amiodarone may be the most useful drug in paroxysmal and chronic atrial fibrillation. The detection of nonsustained ventricular tachycardia on ambulatory electrocardiogram monitoring remains the single most useful indicator of the risk of sudden death in the adult patient, and the treatment of choice is again low dose amiodarone. The mechanism of sudden death, and the mode of action of amiodarone in preventing it, are not known for certain in the majority of patients. The risk of sudden death is higher in children and adolescents, but arrhythmias are less common, and no useful predictive marker of increased risk has been found. The role of invasive electrophysiological studies and the place of the implantable cardioverter‐defibrillator in hypertrophic cardiomyopathy have not yet been established.
Cardiac Pain, Sympathetic Afferents, and Life‐Threatening Arrhythmias
Authors: SCHWARTZ PETER J. , FOREMAN ROBERT D.
Published: May 2007

Cardiac Pain, Sympathetic Afferents, and Life‐Threatening Arrhythmias. Myocardial ischemia activates receptors of sympathetic and vagal afferent fibers. Although both afferent pathways are excited, this article primarily focuses on the sympathetic pathways. Increased sympathetic afferent activity to cells of the spinal cord can lead to cardiac pain and reflex sympathetic hyperactivity that can be quite arrhythmogenic. Complicating factors that affect the relationship arises from activation of vagal afferent fibers. Sympathetic afferent fibers in the ventricle appear to be composed of mechanosensitive and chemosensitive receptors. Sympathetic afferent fibers excite cells of origin of the spinothalamic tract, the classical pain pathway that transmits information about noxious somatic and visceral episodes to areas of the brain involved with pain perception. Activation of selected brainstem nuclei, the vagus, and the dorsal columns can suppress afferent information from the heart that excites spinothalamic tract cells. Excitation of sympathetic afferent fibers initiates a series of cardiovascular reflexes, some of which may affect cardiac electrical stability significantly. Increased arrhythmogenesis can be reduced when C8‐T5 dorsal roots are transected. Stimulation of cardiac nerves that involve the left stellate ganglion can produce life‐threatening arrhythmias, particularly if combined with myocardial ischemia or infarction. Through reflex mechanisms, activation of sympathetic afferent fibers can suppress activity of vagal efferent fibers. If prevention of cardiac pain through reduced firing or inhibition of cells in the spinothalamic tract reduces afferent sympathetic activity that occurs during acute myocardial ischemia, it would be logical to surmise that another significant benefit would follow, namely reduced risk for malignant arrhythmias.
Medullo‐Spinal Modulation of Sympathetic Output and Spinal Afferent Input
Authors: SCHRAMM LAWRENCE P. , POREE LAWRENCE R.
Published: May 2007

Associated Inhibition of Sympathetic and Afferent Activities. In intact animals, it is important that most “tonic” sympathetic activity be regulated by brainstem systems that have access to “central commands” from higher centers and to highly specific cranial nerve afferents. The importance of this supraspinal regulation is manifested by severe derangements of sympathetic regulation after spinal cord injury. A major component of these derangements is an exaggerated responsiveness of sympathetic neurons to visceral and somatic afferent activity. Although much is known about medullo‐spinal systems that excite sympathetic preganglionic neurons, little is known about those systems that, in intact animals, isolate preganglionic neurons from spinal afferent input. This brief review will consider the evidence that either identical or cospatial medullary systems regulate the output of sympathetic preganglionic neurons and afferent input to the spinal cord. Further, evidence from this laboratory is presented, which indicates that a recently described system in the rostral cervical spinal cord, perhaps in concert with medullary systems, may play an important role in regulating the excitation of sympathetic preganglionic neurons by spinal afferents.
Localization of a Coronary Stenosis, Left Ventricular Function, and Pain Perception During Myocardial Ischemia in Patients with One‐Vessel Disease
Authors: DROSTE CONRAD , GREENLEE MARK W. , RUF GÜNTHER , ROSKAMM HELMUT
Published: May 2007

Silent Myocardial Ischemia and Endogenous Pain Modulation.A total of 97 patients with asymptomatic and 69 patients with symptomatic myocardial ischemia and one‐vessel disease were compared with respect to the location of coronary stenosis and left ventricular wall motion abnormalities. All symptomatic and asymptomatic patients exhibited reproducible objective signs of myocardial ischemia in exercise tests, ischemia being always silent in the asymptomatic group. Right coronary artery stenosis (and left circumflex artery stenosis) was more frequently observed in asymptomatic patients, left artery descending stenosis more often in symptomatic patients. Left ventricular wall movement abnormalities with posterobasal or diaphragmatic localization were significantly more often associated with the absence of angina pectoris pain. The present results could contribute to the understanding of the mechanisms underlying the absence of pain in silent myocardial ischemia. A possible explanation for these results would be that stimulation of inhibitory vagal afferents, which are preferentially distributed in the inferior ventricle wall, may play a role of the suppression of pain perception in myocardial ischemia.
Wide QRS Complexes: Electrophysiologic Basis of a Common Electrocardiographic Diagnosis
Authors: JAZAYERI MOHAMMAD R. , SRA JASBIR J. , AKHTAR MASOOD
Published: May 2007

Wide QRS Complexes. Wide QRS complex tachycardia is a commonly encountered arrhythmia and its appropriate diagnosis often poses a challenge to most physicians. The origin of a wide QRS complex is either supraventricular with abnormal ventricular activation or ventricular. This review addresses the main electrophysiologic mechanisms involved in the genesis of a wide QRS complex and its maintenance as a sustained arrhythmia. (J Cardiovasc Electrophysiol, Vol. 3, pp. 365–393, August 1992)
Cardiac Electrophysiology in Duchenne Muscular Dystrophy: From Basic Science to Clinical Expression
Authors: PERLOFF JOSEPH K. , MOISE N. SYDNEY , STEVENSON WILLIAM G. , GILMOUR ROBERT F.
Published: May 2007

Cardiac Electrophysiology in Duchenne Muscular Dystrophy. Duchenne muscular dystrophy is an X‐linked recessive neuromuscular disorder that involves striated muscle fibers (skeletal, cardiac), smooth muscle Fibers (vasculature), and nervous system (neurons of central brain and cortex). The Duchenne dystrophy gene has been identified on the Xp21 locus of the short arm of the X chromosome. Dystrophin, the protein product of the gene, is present on and limited to myogenic cells in every tissue tested except the central nervous system, and is absent or nearly so in Duchenne dystrophy. However, the function of dystrophin and the pathogenesis of Duchenne dystrophy remain unclear. There is convincing morphological (gross, histologic, ultrastructural) and metabolic evidence (positron emission tomography) that myocardial involvement is found initially in the posterobasal left ventricular wall (cardiac phenotype). This regional localization of myocardial dystrophy is believed to account for the distinctive 12‐lead scalar electrocardiogram (ECG). Abnormalities of cardiac rhythm and conduction have been reported in Duchenne muscular dystrophy, but the pathogenesis of the electrophysiologic disturbances has not been established. Two variables are relevant to cardiac electrophysiologic involvement in Duchenne dystrophy: (1) the small vessel coronary arteriopathy (medial hypertrophy, luminal narrowing); and (2) abnormalities that might originate in the specialized cardiac tissues. The role of the coronary arteriopathy is presently speculative, and it is not currently known whether dystrophin is normally present on the cell membrane of normal cardiac specialized tissues, and if so, whether those tissues are dystrophin deficient in Duchenne dystrophy. Animal models (mouse, cat, dog) have shed light on the pathogenesis of skeletal muscle and myocardial involvement, less so on involvement of cardiac specialized tissues. The determinants of calcium homeostasis in dystrophin‐deficient myogenic cells (skeletal or cardiac) is unclear, and the relationship between dystrophin deficiency, calcium homeostasis, cellular response and phenotypic expression in skeletal muscle and myocardium is imperfectly understood. The purpose of this report is to bring together current genetic, molecular biological, biochemical, histopathological, and clinical information from human Duchenne dystrophy and from animal models bearing on the electrophysiologic expressions of the neuromuscular disease. (J Cardiovasc Electrophysiol, Vol. 3, pp. 394–409, August 1992)
Early Afterdepolarizations in the Familial Long QTU Syndrome
Authors: ZHOU JIN‐TAI , ZHENG LIANG‐RONG , LIU WEI‐YU , ZHANG GUI‐LING , ZHAO JING , SHI JIA‐LING , WANG ZHI‐YI , ZHANG YU‐SHU
Published: May 2007

Early Afterdepolarizations in Long QTU Syndrome. Torsade de pointes‐induced syncopal episodes were almost invariably precipitated by emotional stress or menses in a 17‐year‐old female. U wave accentuation occurred during periods of heigbtened sympathetic tone. To document tbe role of early afterdepolarizations (EADs), monopbasic action potentials were recorded during ventricular extrasystoles and torsade de pointes occurring spontaneously and induced by ventricular pacing in tbe control state and after intravenous lidocaine. The effects of verapamil, propranolol, and epinephrine were observed. Our data show that: (1) EADs may play a significant role in the genesis of familial long QTU syndrome and torsade de pointes; (2) a faster ventricular pacing rate for a longer duration is related to tbe emergence of subsequent pause‐dependent EADs, U waves, and torsade de pointes; (3) atrial pacing with Wenckebach block can provoke large postpause U waves, thus eliciting dual ventricular tachycardia; (4) EADs are enhanced by epinepbrine infusion in the absence of pause; and (5) EAD‐triggered firing is inhibited by verapamil and propranolol but not by lidocaine. (J Cardiovasc Electrophysiol. Vol. 3, pp. 431–436, October 1992)
Prevention of Sudden Cardiac Death After a First Myocardial Infarction by Pharmacologic or Surgical Antiadrenergic Interventions
Authors: SCHWARTZ PETER J. , MOTOLESE MARIO , POLLAVINI GIORGIO , LOTTO ANTONIO , RUBERTI UGO , TRAZZI RINALDO , BARTORELLI CESARE , ZANCHETTI ALBERTO , GROUP THE ITALIAN SUDDEN DEATH PREVENTION
Published: May 2007

Antiadrenergic Interventions and Prevention of Sudden Death after MI.

Introduction: Growing evidence points to sympathetic hyperactivity as one critical trigger for life‐threatening arrhythmias among postmyocardial infarction patients.

Methods and Results: We have evaluated, in a placebo‐controlled multicenter study, the efficacy of a β‐adrenergic blocking agent (oxprenolol 160 mg) and of a selective left cardiac sympathetic denervation in preventing sudden death in patients with a first and anterior myocardial infarction. Two patient groups were studied. The high‐risk group included 144 patients who survived a myocardial infarction complicated by either ventricular tachycardia or fibrillation. The relatively low‐risk group included 869 patients whose myocardial infarction did not have these complications; they were allocated only to placebo or oxprenolol. Randomization took place 30 days postmyocardial infarction; mean follow‐up was 22 months. In the high‐risk group the sudden cardiac death (crude rate) in the placebo subgroup was indeed high (21.3%), and was strikingly reduced to 2.7% and to 3.6% by oxprenolol and by left cardiac sympathetic denervation, respectively (P < 0.05). In the low‐risk group the sudden cardiac death (crude rate) in the placebo subgroup was 5.2% and was still reduced by oxprenolol to 1.6% (P < 0.05). The results for total mortality were quite similar to those for sudden death iu both groups.

Conclusion: This study, unique for the populations studied and for one of the treatments used, demonstrates that pharmacologic and surgical antiadrenergic interventions significantly reduce sudden cardiac death in postmyocardial infarction patients at high and at low risk. With due consideration to the relatively small size of the high‐risk group, it seems reasonable to suggest that left cardiac sympathetic denervation may be considered as a possible alternative for high‐risk patients with contraindications to beta blockers. (J Cardiovasc Electrophysiol, Vol 3, pp. 2–16, February 1992)
Radiofrequency Catheter Ablation of Three Accessory Pathways in a Single Session
Authors: ODRIGUEZ LUZ MARIA , SMEETS JOEP L.M , SCHLÄPFER JÜRG , KATSIVAS APOSTOLOS , DIJKMAN BARBARA , HILLOU CHRISTIAN DE , ORNING OTTO M. , WELLENS HEIN J.J.
Published: May 2007

Radiofrequency Ablation of Multiple Accessory Pathways. A 19‐year‐old patient is described having three accessory atrioventricular pathways. All three pathways were ablated using radiofrequency current in a single electrophysiologic investigation. (J Cardiovasc Electrophysiol, Vol. 3, pp. 141–149, April 1992)
Various Electrocardiographic and Electrophysiologic Presentations of Normal and Abnormal Sinus Node
Authors: ANG YONG‐GAO , HARIMAN ROBERT J. , WILBER DAVID J. , OLSHANSKY BRIAN , HWANG MING H. , KOPP DOUGLAS , LOEB HENRY S.
Published: May 2007

Electropbysiology of the Sinus Node. Differentiation of normal from abnormal sinus nodal function is frequently difficult because the electrocardiographic and electrophysiologic presentations of abnormal and normal sinus nodal function are quite diverse. The autonomic nervous system greatly influences sinus nodal function, making this differentiation even more complicated. Data obtained from the recording of sinus nodal electrogram in animals and humans have helped in elucidating changes in automaticity and conduction of the sinus node. In this review, we provide examples of rhythms related to normal and abnormal sinus nodal function. (J Cardiovasc Electrophysiol, Vol. 3, pp. 187–197, April 1992)
The Effects of Unilateral Stellate Ganglion Blockade on Human Cardiac Function During Rest and Exercise
Authors: GARDNER MARTIN J. , KIMBER SHANE , JOHNSTONE DAVID E. , SHUKLA ROMESH C. , HORACEK B. MILAN , FORBES CHERYL , ARMOUR J. ANDREW
Published: May 2007

Unilateral Stellate Block. Introduction: Left sided stellate ganglion predominance has been proposed as a mechanism responsible for lethal ventricular arrhythmias, due to hetaerae nouns ventricular repolarization. To determine the cardiovascular effects of such asymmetric sympathetic ganglion innervations in man, studies were performed in 15 patients undergoing unilateral stellate ganglion blockade for the management of chronic arm pain.

Methods and Results: Standard 12‐lead ECGs, systemic blood pressure, body surface potential mapping, and radionuclide angiography were performed during rest and graded exercise before and after blockade. Successful unilateral blockade was accomplished in 13 of the patients, 11 of whom had right‐sided blockade and two left‐sided blockade. No significant changes due to blockade of stellate ganglia, including QT intervals, were detected during rest or graded exercise in standard ECGs. No cardiac rhythm disturbances occurred in these states, Body surface potential maps and arterial blood pressure were similar during resting supine and upright positions, as well as immediately after exercise before and after blockade. Unilateral ganglion blockade did not modify resting or exercise cardiac ejection fractions.

Conclusion: Unilateral stellate blockade in man does not induce untoward cardiovascular effects during rest or exercise.
Activation Mapping of Reentry Around an Anatomical Barrier in the Canine Atrium:
Authors: BOYDEN PENELOPE A. , GRAZIANO JOSEPH N.
Published: May 2007

d‐Sotalol and Atrial Reentry. Introduction: In the chronically instrumented animal and the isolated blood perfused heart, atrial reentry via a fixed path around an anatomical obstacle has been described and is terminated by the Class III antiarrhythmic agent, d‐sotalol. The precise mechanism by which d‐sotalol terminates this arrhythmia is not known.

Methods and Results: In the present study, right atrial (RA) activation sequences in the isolated, coronary artery perfused canine heart during episodes of sustained flutter (n = 7) and drug administration were determined. A fixed array of bipolar electrodes was used to record endocardial electrograms from 96 sites on the RA simultaneously. Maps of all control flutters showed that the rhythm was due to persistent circus movement of the impulse around the tricuspid valve ring. D‐sotalol was effective in terminating atrial reentry in this model. In all episodes, block of the excitatory impulse in a specific region of the reentrant circuit accompanied these terminations. However, the events preceding the occurrence of block of the impulse were not similar. Two different modes of termination are described.

Conclusion: The Class III antiarrhythmic agent d‐sotalol can terminate atrial reentry in several ways. In one mode, complete conduction block of he reentering impulse within the fixed path occurs to terminate the rhythm. In the other mode, interruption of the original reentrant circuit occurs when there is failure of a lateral boundary. Often in this latter case, interruption of the original circuit is by an extra impulse that is secondary to a change in the path of the impulse. In both modes cycle length oscillations are observed.