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Biomedical subjects

B Olshansky

Publications and source records attributed to B Olshansky.

At least 19 recordsLinked to original sources
PubMed2001

Apoptosis in the genesis of cardiac rhythm disorders.

Programmed cell death has provided a potential pathogenetic mechanism that could play a role in several diseases of the cardiac conduction system and the myocardium that are clinically expressed as disorders of the cardiac rhythm (Fig. 4). Most of these studies have been descriptive. The exact nature of the triggers for apoptotic cell death is not well understood and is a subject of current investigation. Alterations in the architecture of the myocardium play an important role in the pathogenesis of ventricular arrhythmias that are responsible for a large proportion of sudden cardiac deaths. Although apoptosis is essential for normal development, excessive apoptosis resulting from pathological triggers may result in destruction of tissues and in the development of heart disease in which a fatal arrhythmic event may be a final common pathway. At present, the triggers for programmed cell death in disorders of the cardiac rhythm are not understood completely. Because diverse conditions trigger apoptosis, treatment strategies may have to be directed toward attenuating such triggers and, in some instances, toward modifying the process itself. If future therapies that can favorably modulate the apoptotic process in conditions such as dilated cardiomyopathy and postmyocardial infarction are developed, they will have the potential to prevent the pathologic alteration of myocardial architecture that is conducive to arrhythmogenesis.

Apoptosis↗
PubMed2001

Apparent bidirectional conduction block following radiofrequency catheter ablation of typical atrial flutter.

OBJECTIVE: The purpose of this study is to determine the reliability of activation sequence mapping in assessing the presence of bidirectional conduction block (BCB) in typical atrial flutter (AFL) ablation. INTRODUCTION: Radiofrequency ablation (RFA) can cure typical AFL by creating BCB across the right atrial isthmus. Effective conduction block across this region can prevent AFL recurrence, but accurate assessment of isthmus conduction may be flawed. METHODS: BCB was measured before and after RFA by pacing at multiple rates on both sides of the isthmus during sinus rhythm. Pacing was performed from a low lateral tricuspid annulus site (proximal to the isthmus) and a coronary sinus Os site (distal to the isthmus), while recording simultaneously from 8-10 right atrial sites bordering the isthmus (4-5 free wall sites; 4-5 septal sites) as well as from an isthmus site. After ablation reinduction of atrial flutter was attempted from both sides of the block with rapid atrial pacing after BCB was established in all patients. In some patients lines of conduction block were evident at the isthmus (using the ablation catheter to map). RESULTS: Of 65 patients undergoing RFA of AFL, 59 had typical AFL. In all 59 patients, BCB was demonstrated at all pacing cycle lengths 30 min after RFA applications. In 6 of these 59, AFL was inducible with atrial pacing despite apparent BCB. Further RFA resulted in non inducibility in all 6 patients. In the remaining 53/59 patients, BCB was associated with noninducibility at 30 min. A total of 8 recurrences were seen during a mean 19.3 +/- 8.3 (SD) month follow-up. CONCLUSION: Apparent BCB as determined by activation sequence mapping outside of the isthmus is an excellent marker, but, as measured, may be a misleading method of assessing the presence or absence of conduction through the isthmus. It is necessary to attempt reinduction of AFL after apparent success. Elimination of typical AFL does not preclude other AFLs.

Adult↗
PubMed2001

Implantable cardioverter defibrillator practices and costs at an academic medical center.

This study addresses current costs of implanting implantable cardioverter defibrillators (ICDs) at one large medical center and documents actual costs using two methodologies. To determine the actual cost of ICD therapy, we studied all ICD implants performed in the procedure room (similar to an electrophysiology laboratory) who met accepted secondary prevention (AVID) indications for a 1-year period at Loyola University Medical Center. The study period coincided with the facility's shift of this procedure out of the operating room to a procedure room. Costs were analyzed two ways: a cost-based analysis and a cost-to-charge ratio analysis based on the facility's Medicare Cost Report. Twenty-four patients (14 inpatients and 10 outpatients) met the study inclusion criteria. Length of stay averaged 5.8 days for inpatients and 1.1 days for outpatients. In the cost-based analysis, the mean costs of the ICD implant (device, implant procedure, and preimplant and postimplant stay) were $33,509 for inpatient and $28,078 for outpatient implants. In the cost-to-charge ratio analysis, the mean costs for the inpatient hospitalization were $35,623. This is one of the first studies to document cost of ICD therapy and may serve as a benchmark for other facilities.

Academic Medical Centers↗
PubMed2001

Report of the NASPE policy conference on arrhythmias and the athlete.

INTRODUCTION: This consensus statement summarizes the proceedings of The Expert Consensus Conference on Arrhythmias in the Athlete of the North American Society of Pacing and Electrophysiology (NASPE) on detecting, evaluating, and treating athletes with cardiovascular disorders that predispose to cardiac arrhythmias. METHODS AND RESULTS: The participants in the open policy conference were selected by the codirectors (Drs. Estes and Olshansky) based on expertise and contributions to the literature. All participants provided a referenced summary of their presentation. The writing group used the information from all published scientific studies, clinical trials, registries, clinical experience, and expert opinion to make recommendations regarding screening, evaluation, management, eligibility for competition, and a range of other medical, social, and legal issues regarding the recreational and competitive athlete. The codirectors of the symposium synthesized the participants' reports for this and made revisions according to suggestions of all members of the writing committee. The manuscript was reviewed by four independent reviewers assigned by the NASPE Committee for the Development of Position Statements and NASPE Board of Trustees. CONCLUSION: Despite considerable advances in knowledge regarding the diagnosis, therapy, and mechanisms of arrhythmias in the athlete, much remains unknown. Continued basic, clinical, and epidemiologic research is needed. Current screening techniques to detect athletes lack sensitivity and specificity. Evaluation of standardized screening programs with tracking of long-term outcomes is needed. Officials from athletic, academic, medical, and legal institutions need to form strategic partnerships to develop policy related to assessment of risk and assumption of responsibility for athletic activities.

Arrhythmias, Cardiac↗
PubMed2001

Ventricular tachycardia with QRS configuration similar to that in sinus rhythm and a myocardial origin: differential diagnosis with bundle branch reentry.

INTRODUCTION: Tachycardia with a QRS configuration which resembles that in sinus rhythm is usually thought to be supraventricular. Ventricular tachycardia, with a similar QRS configuration to that in sinus rhythm on the 12-lead ECG, can occur. The mechanisms of this form of ventricular tachycardia have not been previously reported. METHODS AND RESULTS: The mechanism of ventricular tachycardia was defined during electrophysiological study in five patients. During sinus rhythm, all patients had a wide QRS complex (>0.12 s) on the 12-lead ECG. The morphology remained grossly unchanged during spontaneous, symptomatic tachycardia. Four of the five patients had coronary artery disease and left ventricular dysfunction. The remaining patient had idiopathic dilated cardiomyopathy. The relationship between the His bundle, deflection, the right bundle branch and the QRS complex was evaluated during tachycardia. Atrial and ventricular pacing, and ventricular activation mapping were performed during tachycardia to define the tachycardia mechanism. The tachycardia induced at electrophysiological testing, which was similar to the clinical tachycardia, was proven to be ventricular tachycardia in each patient. The morphology of ventricular tachycardia was right bundle branch block in two patients and left bundle branch block in three patients. The median tachycardia cycle length was 300 ms (range: 260-480 ms). His bundle activation occurred in a 1:1 relationship with ventricular activation during tachycardia in all patients at least intermittently. The tachycardias were thought initially to be bundle branch reentry tachycardia. With further intervention and continued observation, it became clear that His bundle activation was passive and was not required for the tachycardia to sustain. During tachycardia, His bundle activation appeared to precede the local ventricular activation. Instead, the His bundle was activated slowly from the previous ventricular beat causing a long ventricular-His (VH) interval. This was shown by: (1) activation patterns, (2) response to pacing, (3) intermittent VH dissociation, and (4) termination of ventricular tachycardia. CONCLUSION: A unique form of ventricular tachycardia is described. The QRS complex morphology on the 12-lead ECG during tachycardia was grossly similar to that during sinus rhythm. The His bundle activation was passive and occurred with a long activation time from the ventricle to the His bundle. Although it mimics usual bundle branch reentry, this form of ventricular tachycardia appears to be due to a different mechanism in which the His bundle is not obligatory for the continuation of the reentrant phenomenon.

Adult↗
PubMed2000

Location of death (in-hospital or out-of-hospital) and type of death (arrhythmic, nonarrhythmic, noncardiac) after inducible sustained ventricular tachyarrhythmias after syncope, sustained ventricular tachycardia, or nonfatal cardiac arrest (the ESVEM trial).

The ESVEM Trial evaluated methods to guide antiarrhythmic drug use in patients with spontaneous, inducible sustained tachyarrhythmias at electrophysiologic testing and frequent ventricular premature complexes (VPCs) per hour (>/=10). We assessed the relation between location (in-hospital or out-of-hospital) and classification of death (arrhythmic, nonarrhythmic, cardiac and/or noncardiac) for 486 randomized patients. Deaths were classified as out-of-hospital arrhythmic deaths if arrhythmic death occurred out-of-hospital, or if an arrhythmia preceded hospital admission and directly caused death. Of the 486 randomized patients, 188 (39%) died during 6 years of follow-up. The location and type of death could be determined clearly in 171 patients (91%). Ninety-one deaths were in-hospital (53%); 80 were out-of-hospital (47%). Arrhythmic deaths occurred in 85% out-of-hospital patients and in 30% in-hospital patients (p <0.001). Baseline characteristics were comparable for patients with out-of-hospital and in-hospital arrhythmic deaths. Twenty-seven of 95 arrhythmic deaths occurred in-hospital (28%); 72% occurred out-of-hospital. Out-of-hospital arrhythmic death accounted for 40% of deaths for which location and type of information were available. The 1- and 4-year actuarial out-of-hospital arrhythmic death rates were 9% and 18%, respectively. Of nonarrhythmic cardiac deaths, 91% were in-hospital and 9% were out-of-hospital. Of noncardiac deaths, 74% were in-hospital and 26% were out-of-hospital. Similar results were seen in the 296 patients for whom a drug was considered to be effective. Thus, over half the deaths in the ESVEM trial occurred in-hospital. The long-term actuarial risk of out-of-hospital arrhythmic death in ESVEM was unexpectedly low.

Actuarial Analysis↗
PubMed2000

Practical guidelines for clinicians who treat patients with amiodarone. Practice Guidelines Subcommittee, North American Society of Pacing and Electrophysiology.

Amiodarone has become an important drug for the treatment of supraventricular and ventricular arrhythmias, in short-term inpatient and outpatient settings. It may also have a role in affecting outcome in patients at high risk for arrhythmic events and sudden death; its place among available therapies is being established in clinical trials.

Administration, Oral↗
PubMed2000

Case 4: a patient with symptomatic bradycardia.

Both the clinical and electrocardiographic presentations of sick sinus syndrome are highly variable. As illustrated by this month's case of Interactive Grand Rounds, the initial challenge to the clinician is to establish the correct diagnosis in the patient who has symptomatic bradyarrhythmias.

Aged↗
PubMed2000

Radiofrequency application to the posteroseptal region alters retrograde accessory pathway activation.

INTRODUCTION: Radiofrequency applications to the posteroseptal region can ablate the atrioventricular accessory pathway residing in this area. In conjunction with the adjacent anatomic structures, however, ablative lesions which do not effectively ablate the accessory pathway could markedly alter retrograde atrial activation sequence and confound interpretation of further mapping of an accessory pathway. METHODS AND RESULTS: Electrophysiologic studies, endocardial activation mapping and radiofrequency catheter ablation were undertaken in three patients with recurrent supraventricular tachycardia. Patients were initially thought to have a single posteroseptal accessory pathway; earliest ventrioatrial activation during tachycardias and during ventricular pacing was at the coronary sinus ostium, but initial radiofrequency applications were unsuccessful to ablate the pathway. After initial radiofrequency applications to the posteroseptal region, the earliest retrograde atrial activation changed to the right atrial free wall in two patients. Additional radiofrequency application to the posteroseptal area was able to ablate the single posteroseptal accessory pathway in one patient. Radiofrequency application to the right atrial free wall was required to stop tachycardia initiation in other patient. The third patient was suspected of having a slow-slow atrioventricular nodal reentry tachycardia. Radiofrequency application to the posteroseptal area changed the earliest retrograde atrial activation to the distal coronary sinus recording site, mimicking an accessory pathway at the left atrial free wall. Radiofrequency application to the anteroseptum was able to ablate the concealed accessory pathway. CONCLUSION: Radiofrequency applications to the posteroseptal region can markedly alter retrograde atrial activation, thereby confounding further mapping of the accessory pathway.

Adolescent↗