Biomedical subjects

D E Kopp

Publications and source records attributed to D E Kopp.

11 recordsLinked to original sources

PubMed1999

Retrograde fast pathway ablation for atrioventricular nodal reentry associated with markedly prolonged PR intervals.

Three patients with typical atrioventricular nodal reentrant tachycardia (AVNRT) and markedly prolonged PR intervals (>300 ms) without dual pathway physiology at baseline or during isoproterenol infusion underwent successful fast pathway ablation and remained asymptomatic without recurrent AVNRT, atrioventricular block, or symptomatic bradycardia for a mean of 19 months. In patients with recurrent AVNRT and markedly prolonged PR intervals, selective ablation of the retrograde fast pathway can eliminate AVNRT without further impairment of anterograde atrioventricular nodal function.

Adrenergic beta-Agonists↗

PubMed1999

Frozen shoulder syndrome associated with subpectoral defibrillator implantation.

Pectoral implantation of transvenous non-thoracotomy internal cardioverter defibrillators (ICD) has resulted in very few complications whether placed subpectorally or subcutaneously. We report the case of a 68 year old man with a subpectorally implanted MINI-plus (Cardiac Pacemakers, Incorporated, St. Paul, Mn.) transvenous ICD who developed nearly instantaneous severe ipsilateral shoulder pain and immobilization. The symptoms progressed despite aggressive physical therapy. We elected to remove the device from the pectoral site and place it in a traditional abdominal position due to the severity, duration and refractoriness of his symptoms. This procedure utilized the chronic Endotak DSP (Model 0125, Cardiac Pacemakers, Incorporated) transvenous lead, a compatible Endotak DSP lead extender (Model 6952, Cardiac Pacemakers, Incorporated) and the above described ICD. Immediate relief of symptoms was accomplished by relocation of the device to an abdominal site. This intervention should be reserved for patients with severely debilitating symptoms. Prospective comparison of subpectoral and subcutaneous surgical approaches with respect to patient comfort and acceptance and complications may be warranted.

Aged↗

PubMed1998

Atrial fibrillation after radiofrequency ablation of type I atrial flutter: time to onset, determinants, and clinical course.

BACKGROUND: The occurrence of atrial fibrillation after ablation of type I atrial flutter remains an important clinical problem. To gain further insight into the pathogenesis and significance of postablation atrial fibrillation, we examined the time to onset, determinants, and clinical course of atrial fibrillation after ablation of type I flutter in a large patient cohort. METHODS AND RESULTS: Of 110 consecutive patients with ablation of type I atrial flutter, atrial fibrillation was documented in 28 (25%) during a mean follow-up of 20.1+/-9.2 months (cumulative probability of 12% at 1 month, 23% at 1 year, and 30% at 2 years). Among 17 clinical and procedural variables, only a history of spontaneous atrial fibrillation (relative risk 3.9, 95% confidence intervals 1.8 to 8.8, P=0.001) and left ventricular ejection fraction <50% (relative risk 3.8, 95% confidence intervals 1.7 to 8.5, P=0.001) were significant and independent predictors of subsequent atrial fibrillation. The presence of both these characteristics identified a high-risk group with a 74% occurrence of atrial fibrillation. Patients with only 1 of these characteristics were at intermediate risk (20%), and those with neither characteristic were at lowest risk (10%). The determinants and clinical course of atrial fibrillation did not differ between an early (< or = 1 month) compared with a later onset. Atrial fibrillation was persistent and recurrent, requiring long-term therapy in 18 patients, including 12 of 19 (63%) with prior atrial fibrillation and left ventricular dysfunction. CONCLUSIONS: Atrial fibrillation after type I flutter ablation is primarily determined by the presence of a preexisting structural and electrophysiological substrate. These data should be considered in planning postablation management. The persistent risk of atrial fibrillation in this population also suggests a potentially important role for atrial fibrillation as a trigger rather than a consequence of type I atrial flutter.

Aged↗

PubMed1997

What can we expect from prophylactic implantable defibrillators?

Death due to ventricular tachyarrhythmia (VT) remains an important public health problem; patients with prior myocardial infarction (MI) constitute the largest identifiable population for prophylactic interventions. Targeting of progressively higher-risk subgroups of post-MI survivors carries inevitable tradeoffs with respect to the global impact of interventions on overall mortality. Therapy with aspirin, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors comprise the benchmark against which all additional interventions, including implantable defibrillators, must be measured. Initial enthusiasm for empiric amiodarone therapy has been tempered by the limited benefit demonstrated in recent randomized trials. Trials of other class III antiarrhythmic drugs, including both d,l-sotalol and d-sotalol, have also failed to demonstrate survival benefit. The Multicenter Automatic Defibrillator Implantation Trial (MADIT) demonstrated significantly improved survival associated with defibrillators in a small subgroup of post-MI survivors with a high short-term risk of death. The ultimate number and optimal criteria for selection of patients who may benefit from prophylactic defibrillator therapy after MI will undergo continued evolution as new data from current and ongoing trials become available.

Amiodarone↗

PubMed1997

Adenosine-sensitive bundle branch reentry.

INTRODUCTION: Bundle branch reentry is an uncommon mechanism for ventricular tachycardia. More infrequently, both fascicles of the left bundle may provide the substrate for such macroreentrant bundle branch circuits, so-called interfascicular reentry. The effect of adenosine on bundle branch reentrant mechanisms of tachycardia is unknown. METHODS AND RESULTS: A 59-year-old man with no apparent structural heart disease and history of frequent symptomatic wide complex tachycardias was referred to our center for further electrophysiologic evaluation. During electrophysiologic study, a similar tachycardia was reproducibly initiated only during isoproterenol infusion, which had the characteristics of bundle branch reentry, possibly using a left interfascicular mechanism. Intravenous adenosine reproducibly terminated the tachycardia. Application of radiofrequency energy to the breakout site from the left posterior fascicle prevented subsequent tachycardia induction and rendered the patient free of spontaneous tachycardia during long-term follow-up. CONCLUSIONS: Patients with ventricular tachycardia involving a bundle branch reentrant circuit may be sensitive to adenosine. These results suggest that adenosine may not only inhibit catecholamine-mediated triggered activity but also some catecholamine-mediated reentrant ventricular arrhythmias.

Adenosine↗

PubMed1995

Catheter ablation of the mitral isthmus for ventricular tachycardia associated with inferior infarction.

BACKGROUND: Intraoperative mapping studies suggest that an isthmus of myocardium between the mitral valve annulus and the border of inferior myocardial infarction may play a role in the genesis of ventricular tachycardia. We examined the frequency with which a slow conduction zone within the mitral isthmus was critical to the maintenance of ventricular tachycardia associated with remote inferior infarction in patients undergoing catheter ablation. METHODS AND RESULTS: In 4 of 12 patients, a critical zone of slow conduction was identified within the mitral isthmus. In each of these patients, two characteristic and morphologically distinct tachycardias were induced: a left bundle (rS in V1, R in V6), left superior axis morphology and a right bundle (R in V1, QS in V6), right superior axis morphology (cycle length, 610 to 320 ms). In each patient, a zone of slow conduction, shared by both morphologies, was characterized by diastolic potentials with electrogram-QRS intervals of 85 to 161 ms (21% to 47% of tachycardia cycle length) and entrainment with concealed fusion during pacing associated with stimulus-QRS intervals of 81 to 400 ms (20% to 91% of tachycardia cycle length). In each patient, a single radiofrequency energy application at the shared site of slow conduction eliminated inducibility of both morphologies. During follow-up of 1 to 11 months, no patient had recurrent tachycardia. CONCLUSIONS: The mitral isthmus contains a critical region of slow conduction in some patients with ventricular tachycardia after inferior myocardial infarction, providing a vulnerable and anatomically localized target for catheter ablation. Characteristic tachycardia morphologies may provide clinical markers for this underlying mechanism.

Cardiac Catheterization↗

PubMed1995

Predictors of defibrillation energy requirements with nonepicardial lead systems.

The determinants of high defibrillation energy requirements (DER) using nonepicardial lead systems (NELS) have not been well characterized. The goal of this study was to examine prospectively the influence of clinical, radiographic, echocardiographic, and procedural variables on DER during NELS placement. Data from 100 consecutive patients undergoing attempted NELS implantation were analyzed. Transvenous leads, subcutaneous patches, and monophasic shock devices from two manufacturers were used. Leads were successfully positioned for testing in 95% of patients. An adequate DER (< or = 25 J) was obtained in 73 of 95 (77%) of patients. Univariate analysis identified amiodarone therapy and left ventricular mass as predictors of high DER. With multivariate analysis, amiodarone therapy was the sole significant predictor of high DER (P = 0.002, odds ratio 5.46). The 22 patients with high NELS DER also had high epicardial DER (mean 24 +/- 9 J). The two patch epicardial DER was > 25 joules in 12 of 22 patients. Thus, adequate DER with monophasic shock waveforms can be obtained in most patients undergoing NELS testing. However, amiodarone therapy significantly increases the probability of obtaining high DER.

Amiodarone↗

PubMed1993

Use of multiple patches during implantation of epicardial defibrillator systems.

During implantation of epicardial automatic defibrillator systems, occasional patients have difficulty in obtaining adequate defibrillation thresholds. Of 236 consecutive patients undergoing implantation of epicardial defibrillator systems, 18 patients received a 3-patch (n = 15) or 4-patch (n = 3) defibrillator system. Twelve patients who received a multiple-patch defibrillator system had a best 2-patch defibrillation energy requirement of > or = 30 J; in the remaining 6 patients less stringent clinical criteria were used in the decision to add a third defibrillator patch (defibrillation energy requirement > 18 J in 4 patients, and > 20 J in 2 patients). Technically, multiple-patch systems were made possible with either the use of Y-connectors or defibrillators allowing output to 3 patches. In 3 patients, addition of a third epicardial patch still resulted in a defibrillation energy requirement of > or = 30 J; in these 3 patients, addition of a fourth patch resulted in a defibrillation energy requirement of < or = 20 J. All patients receiving a multiple-patch defibrillator system had a reduction in defibrillation energy requirement, and 12 patients had a reduction in defibrillation energy requirement of > or = 10 J over the best 2-patch defibrillation energy requirement. In the patients who eventually had placement of a multiple-patch system, the best 2-patch defibrillation energy requirement was > 18 J in 4 patients, > 20 J in 2 patients, > or = 30 J in 9 patients, and > 40 J in 3 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗

PubMed1992

Palpitations and arrhythmias. Separating the benign from the dangerous.

Palpitations are a nonspecific symptom and do not necessarily imply serious heart disease. The vast majority of palpitations are benign. Goals in evaluation include detecting and identifying an arrhythmia, clarifying symptom severity, and defining the extent of underlying heart disease. If palpitations are infrequent and not accompanied by angina, congestive heart failure, or syncope, outpatient transtelephonic monitoring yields useful clinical information in most patients and is more cost-effective than Holter monitoring. Patients with major symptoms require hospitalization for aggressive cardiac evaluation and, possibly, electrophysiologic testing to guide treatment.

Arrhythmias, Cardiac↗

PubMed1986

In vivo and in vitro assessment of the role of leukotriene B4 as a mediator of rat cutaneous late-phase reactions.

Mast cell-dependent late-phase reactions (LPR) occur in rat skin and are characterized histologically by an early (1 to 8 hours) neutrophil-rich infiltrate, which is essential to a later (24 hours) infiltration by mononuclear cells. Although the ability of preformed mast cell-granule constituents alone to elicit LPR is clearly established, the relative pathogenetic contributions of newly generated lipid mediators to rat LPR are unknown. Leukotriene B4 (LTB4) may be generated by stimulated mast cells in a number of species and might potentially contribute to the neutrophil ingress. In order to examine this possibility in a well-characterized animal model of LPR, the capacity of LTB4 to influence rat cutaneous inflammation was studied. LTB4 (0.1 to 100 ng) alone did not induce vasopermeability in rat skin nor potentiate the blueing response to histamine. Intracutaneous LTB4 (0.1 to 100 ng) did not cause significant infiltration of neutrophils 3 to 4, 6 to 8, or 24 hours after injection; increased numbers of mononuclear leukocytes were not appreciated through 24 hours. In the same animals intracutaneous anti-IgE and intact mast cell granules both produced intense biphasic infiltration characteristic of rat LPR. In order to examine if rat polymorphonuclear leukocytes were capable of responding to LTB4, several in vitro studies were performed. Rat peritoneal and peripheral blood neutrophils migrated toward formyl-methionyl-leucyl-phenyl-alanine in vitro but not to purified human or synthetic LTB4. Rat peripheral blood and elicited peritoneal neutrophils bound only 32% and 27%, respectively, of the quantity of [3H]LTB4 bound by human neutrophils.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Flavonoid modulation of human neutrophil function.

Flavonoids are naturally occurring plant compounds that have been demonstrated to possess a variety of anti-inflammatory effects. We studied the effects of flavonoids on three aspects of neutrophil function that are commonly considered to be associated with inflammation: the release of lysosomal enzymes, the chemiluminescence (CL) response, and the production of superoxide anion. Quercetin and eight other flavonoids at a 10(-5)M concentration inhibited the neutrophil CL response to opsonized zymosan particles by approximately 60% or more. In contrast, the release of lysosomal beta-glucuronidase from neutrophils stimulated with opsonized zymosan was only inhibited by two flavonoids, quercetin and chalcone, and only at concentrations of 1.5 X 10(-4)M to 2 X 10(-4)M. Quercetin also inhibited the generation of superoxide anion by neutrophils but to a lesser degree than its effect on CL. The present studies demonstrated that certain flavonoids are not uniformly active in inhibiting neutrophil CL, beta-glucuronidase release, or superoxide generation. The effects of flavonoids on neutrophil functions probably depend on many variables including the response measured, the activating stimulus, and specific flavonoid structural features.

Cyclic AMP↗