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Biomedical subjects

M R Lauer

Publications and source records attributed to M R Lauer.

At least 19 recordsLinked to original sources
PubMed2000

Sudden cardiac death syndrome: diagnosis and management.

Sudden cardiac death (SCD) can be caused by a variety of cardiac and noncardiac disorders. The diagnostic work-up includes detailed history, physical examination, electrocardiography (ECG), chemistry panel, 24-hour Holter ECG recording, and echocardiography. In selected patients, treadmill-exercise testing, electrophysiologic study, cardiac catheterization with coronary angiography, magnetic resonance imaging, and endomyocardial biopsy are performed. The treatment strategy is rationalized according to the underlying disorder and clinical presentation. Correction of reversible causes such as hypoxia, myocardial ischemia, electrolyte imbalance, congestive heart failure, and proarrhythmic effects of drugs is essential. In patients with arteriosclerotic heart disease, coronary revascularization, using percutaneous coronary angioplasty with stenting or aortocoronary bypass grafting, and optimization of hemodynamics are often necessary. For survivors of SCD syndrome (secondary prevention), implantation of a cardioverter/defibrillator (ICD) is the treatment of choice, with or without adjunct antiarrhythmic drug therapy. Reduction of the sympathetic influence such as with beta-adrenergic blockade and control of hypertension or congestive heart failure may abate the triggering mechanism, thereby reducing the rate of arrhythmia reemergence. Because of the ease of the implantation technique and refined programmability, the current trend is to apply ICD therapy in patients deemed at high risk of SCD, with the aim of primary prevention.

Arrhythmias, Cardiac↗
PubMed1998

Demonstration of a posterior atrial input to the atrioventricular node during sustained anterograde slow pathway conduction.

OBJECTIVES: This study sought to demonstrate electrophysiologic evidence for the existence of different anatomic atrial input sites of fast and slow conduction pathways in patients with dual atrioventricular (AV) node physiology. BACKGROUND: Although a separate posterior exit site exists for a retrograde slow AV node pathway, it remains unresolved whether a separate atrial input site into the AV node actually exists in patients with dual anterograde AV node pathway physiology. METHODS: In 10 patients with dual AV node pathway physiology, atrial pacing at three chosen drive cycle lengths (DCL1, DCL2 and DCL3) was performed at an anterior site (A) just above the His bundle recording site and at a posterior atrial site (P) just below the coronary sinus ostium. DCL3 was chosen as the one cycle length that resulted in a long AH interval consistent with slow pathway conduction. The stimulus to His bundle conduction times (SH) at both sites (SH(P) and SH(A), respectively) and their differences (deltaSH = SH(P) - SH(A)) at each of the three drive cycle lengths were analyzed. RESULTS: The mean +/- SD deltaSH values for DCL1 and DCL2 measured 9 +/- 16 and 8 +/- 18 ms, respectively, and the mean deltaSH value at DCL3 measured -34 +/- 24 ms, which was significantly different from the mean deltaSH values at DCL1 and DCL2 (both p < 0.05). CONCLUSIONS: The significant change in the deltaSH (SH(P) - SH(A)) value during slow pathway conduction could be accounted for by a corresponding shift of anterograde input from an anterior to a posterior entry site to the AV node. These findings support the notion that a separate anterograde entry site of the slow pathway does exist in patients with dual AV node pathway physiology.

Atrioventricular Node↗
PubMed1998

Multiple atrioventricular nodal pathways in humans: electrophysiologic demonstration and characterization.

INTRODUCTION: Multiple AV nodal pathway physiology can be demonstrated in certain patients with clinical AV reentrant tachycardia. METHODS AND RESULTS: Evidence suggesting multiple AV nodal pathway conduction was present in seven (two males; age range 15 to 75 years) of 78 patients (9%) who underwent electrophysiologic studies for AV nodal tachycardia. The presence of two discrete discontinuities in the AV nodal conduction curves suggested triple AV nodal pathway conduction. Detailed mapping of their retrograde atrial activation sequence was performed along the tricuspid annulus from the coronary sinus ostium to the His-bundle electrogram recording site. Three zones (anterior, middle, and posterior) correspond to the upper, middle, and lower third of the triangle of Koch, respectively. The fast pathway exits were determined as anterior (4/7) or middle (3/7), the intermediate pathway exits as middle (4/7) or posterior (3/7), and the slow pathway exits as middle (1/7) or posterior (6/7). Other evidence suggesting multiple AV nodal pathway conduction includes: (1) triple ventricular depolarizations from a single atrial impulse; (2) sequential dual ventricular echoes; (3) spontaneous transformation between the slow-fast and fast-slow forms of AV nodal reentrant tachycardia; and (4) persistent cycle length alternans during AV nodal reentrant tachycardia. In four patients, all three pathways were shown to be involved in AV nodal echoes or reentrant tachycardia. CONCLUSION: Multiple AV nodal pathways are not uncommon and can be identified by careful electrophysiologic elucidation and mapping technique.

Adolescent↗
PubMed1996

Correlation of P-wave polarity with underlying electrophysiologic mechanisms of long RP' tachycardia.

Analysis of surface electrocardiograms from patients with long RP' tachycardia due to either atypical atrioventricular node reentrant tachycardia, permanent junctional reciprocating tachycardia, or low atrial tachycardia was performed. Although a negative P wave in the inferior leads is common to all 3 mechanisms, the results suggest that a positive or isoelectric P wave in electrocardiographic lead I strongly supports a diagnosis of atypical atrioventricular node reentrant tachycardia, whereas a negative or biphasic P wave in lead I argues against this mechanism.

Adult↗
PubMed1996

Spectrum of electrophysiologic and electropharmacologic characteristics of verapamil-sensitive ventricular tachycardia in patients without structural heart disease.

Verapamil-sensitive ventricular tachycardia (VT) is a well-recognized clinical entity that some authorities believe may result from triggered activity. Despite its uniform response to verapamil, however, there is evidence that this uncommon form of VT may not be as homogeneous as first believed. Standard intracardiac electrophysiologic techniques were used to study verapamil-sensitive VT in 32 patients (aged 38 years +/- 20 years) without evidence of structural heart disease. More than half of these patients (69%) exhibited VT with a right bundle branch block-type QRS pattern, with the remainder (31%) displaying VT with a left bundle branch block pattern. In 31% of the patients the VT could be induced by fixed-cycle length atrial pacing, whereas in 59% of patients fixed-cycle length ventricular pacing was necessary. A critical range of cycle lengths for VT induction was required in 66% of the patients. Ventricular tachycardia was initiated with single atrial premature extrastimuli in 16% of patients, single ventricular extrastimuli in 50% of patients, and double ventricular premature extrastimuli in 9% of patients. Ventricular tachycardia displaying cycle-length alternans was observed in 28% of patients. In only 19% of patients was it possible to entrain VT during pacing from the right ventricular apex. Isoproterenol infusion was required for tachycardia induction in 50% of patients, 44% of whom had VT with a left bundle branch block QRS pattern, with the remaining 56% exhibiting VT with a right bundle branch block pattern. Beta-adrenergic blockers suppressed 53% of verapamil-sensitive VT in patients tested, whereas adenosine terminated VT in 50% of patients, with 81% of these patients exhibiting either a left bundle branch block QRS pattern or isoproterenol dependence. Ventricular tachycardia exhibiting a left bundle branch block pattern was more likely to be isoproterenol dependent (p <0.05) and adenosine sensitive (p <0.001). However, verapamil-sensitive, catecholamine-dependent VT was no more likely to be adenosine sensitive than the catecholamine-independent form of the arrhythmia (p >0.5). Verapamil-sensitive VT exhibits properties expected of both a reentrant and triggered arrhythmia, and it is inconsistently dependent on both exogenous catecholamines for induction and intravenous adenosine for termination. Verapamil-sensitive VT encompasses a heterogeneous group of tachycardias that may result from multiple cellular electrophysiologic mechanisms.

Adenosine↗
PubMed1996

Ventricular pacing threshold and refractoriness after defibrillation shocks in patients with implantable cardioverter-defibrillators.

The aim of this study was to examine the effect of ventricular fibrillation and a subsequent defibrillation shock on ventricular excitability and refractoriness in human beings. We studied 16 consecutive patients with implantable cardioverter-defibrillators undergoing follow-up studies. The pre- and post-shock pacing threshold, ventricular effective refractory period, monophasic action potential duration, and serum catecholamine levels were measured. Compared with the baseline state, immediately after ventricular fibrillation, and a successful defibrillation shock: (1) the ventricular effective refractory period decreased from 251 +/- 24 ms to 222 +/- 30 ms (p < 0.01), (2) the monophasic action potential duration decreased from 210 +/- 16 ms to 179 +/- 23 ms (P < 0.01) at 50% repolarization and from 274 +/- 24 ms to 240 +/- 26 ms (P< 0.01) at 90% repolarization, (3) the pacing threshold was not significantly altered and, (4) serum levels of epinephrine and norepinephrine were elevated. These results show that although ventricular fibrillation and subsequent defibrillation had no effect on the ventricular pacing threshold in human beings, it was associated with a decrease in post-shock monophasic action potential duration and ventricular effective refractory period, contrary to some previously reported findings.

Action Potentials↗
PubMed1996

Localization of the origin of the atrioventricular junctional rhythm induced during selective ablation of slow-pathway conduction in patients with atrioventricular node reentrant tachycardia.

During radiofrequency catheter ablation of slow atrioventricular node pathway conduction in patients with atrioventricular node reentrant tachycardia, an atrioventricular junction rhythm is frequently observed. The origin and relation to ablation success of this junctional rhythm was examined in this study. By using standard intracardiac electrophysiology techniques, we studied the radiofrequency energy-induced atrioventricular junctional rhythm in 43 consecutive patients with atrioventricular node reentrant tachycardia undergoing selective ablation of slow-pathway conduction. The frequency of atrioventricular junctional activity was correlated with successful and unsuccessful attempts at ablation of slow-pathway conduction. Also, we compared the sequence of retrograde atrial activation of radiofrequency energy-induced atrioventricular junctional beats in a subgroup of 22 patients with the retrograde activation sequence observed during pacing from the right ventricular apex and the site of successful ablation of slow-pathway conduction. A total of 201 radiofrequency-energy applications was delivered in 43 patients with > or = 5 atrioventricular junctional beat(s) induced during 110 (55%) of 201 ablation attempts. Atrioventricular junctional activity was noted during 98% of successful ablations but only 43% of the unsuccessful attempts (sensitivity, 98%; specificity, 57%; negative predictive value, 99%). The mean time to appearance of atrioventricular junctional beats was 8.8 +/- 4.1 sec (mean +/- SD) after the onset of radiofrequency-energy application. In 22 (100%) of 22 patients in whom detailed atrial mapping was performed, the retrograde atrial activation sequence of the radiofrequency-induced atrioventricular junctional beats was earliest in the anterior atrial septum, identical to that seen during pacing from the right ventricular apex. Earliest retrograde atrial activation was at the posterior septum in all patients during pacing from the successful ablation site, a markedly different activation pattern compared with that seen during either radiofrequency ablation or ventricular pacing. Whereas the occurrence of atrioventricular junctional activity during radiofrequency ablation does not necessarily herald a successful ablation of slow atrioventricular node pathway conduction, its absence strongly suggests that the energy is being applied in an unsuccessful fashion. Furthermore, it appears that radiofrequency energy-induced atrioventricular junctional beats originate not from the endocardium in contact with the ablating catheter tip but instead appear to exit remotely from the anterior atrial septal region. This finding supports the existence of specialized tissues in the atrioventricular junction that preferentially transmit the effects of radiofrequency energy to an anterior exit site, possibly identical to the atrial exit site of the retrograde fast atrioventricular node conduction pathway.

Atrioventricular Node↗
PubMed1996

Electrophysiologic significance of discrete slow potentials in dual atrioventricular node physiology: implications for selective radiofrequency ablation of slow pathway conduction.

Atrioventricular (AV) node reentrant tachycardia is now routinely cured by selective radiofrequency ablation of slow AV node pathway conduction. However, debate remains concerning the optimum method for localizing the site at which radiofrequency energy should be delivered to eliminate slow-pathway conduction. Some investigators have proposed simple anatomy-guided ablations posteriorly near the ostium of the coronary sinus, whereas others suggest an electrophysiology-guided ablation using either recorded "slow potentials" or mapping of the retrograde atrial exit site of slow AV note pathway conduction when possible. To examine these issues, we systematically studied slow potentials recorded in the AV junction of patients undergoing radiofrequency catheter ablation for medically refractory AV node reentrant tachycardia. In 67 patients with the slow-fast form of AV note reentrant tachycardia, we performed detailed atrial mapping along the tricuspid annulus within the triangle of Koch. Two types of slow potentials were identified. Low-amplitude, low-frequency potentials, found in 48% of patients, were localized to the mid to posterior portions of the triangle of Koch, whereas high-amplitude, high-frequency potentials, observed in 22% of patients, were located only posteriorly near the ostium of the coronary sinus. In response to a bolus infusion of adenosine or incremental atrial pacing-induced AV node Wenckebach periodicity, the low-amplitude, low-frequency potentials showed an increased duration and further reduction in amplitude and frequency and often totally disappeared. In contrast, in spite of these maneuvers, the high-amplitude and high-frequency potentials remained unchanged. Of the 25 (37%) of 67 patients in whom the earliest retrograde atrial activation during ventriculoatrial slow AV nodal pathway conduction could be recorded, no patient exhibited low-amplitude, low-frequency potentials, and only 7 (28%) of 25 of these patients showed high-amplitude, high-frequency potentials. High-amplitude, high-frequency potentials persisted after successful radiofrequency ablation of slow pathway conduction. Fewer applications of radiofrequency energy were required for successful elimination of slow pathway conduction in patients in whom the retrograde atrial exit site of slow-pathway conduction could be localized, compared with those patients who only exhibited retrograde fast AV nodal pathway conduction. We conclude that high-amplitude, high-frequency potentials are part of atrial activity, whereas the origin of low-amplitude, low-frequency potentials is unclear and may represent either true intranodal biophysical electrical activity or merely artifact or far-field potentials. Regardless, the recording of high-amplitude or low-amplitude potentials is not required for successful ablation of slow-pathway conduction, although the ability to localize the retrograde atrial exit of slow-pathway conduction may assist in the ablation procedure.

Adolescent↗
PubMed1995

Electrophysiologic mechanisms of the long QT interval syndromes and torsade de pointes.

PURPOSE: To review the current understanding of the mechanisms and treatment of the long QT interval syndromes and torsade de pointes. DATA SOURCES: Personal databases of the authors and a search of the MEDLINE database from 1966 to 1994. STUDY SELECTION: Experimental and clinical studies and topical reviews on the electrophysiologic mechanisms and treatment of torsade de pointes were analyzed. RESULTS: The long QT interval syndromes have been classified into acquired and hereditary forms, both of which are associated with a characteristic type of life-threatening polymorphic ventricular tachycardia called torsade de pointes. The acquired form is caused by various agents and conditions that reduce the magnitude of outward repolarizing K+ currents, enhance inward depolarizing Na+ or Ca2+ currents, or both, thereby triggering the development of early afterdepolarizations that initiate the tachyarrhythmia. The hereditary form appears to result from an abnormal response to adrenergic or sympathetic nervous system stimulation. At least some cases of the hereditary long QT interval syndromes may result from a single gene defect that alters the intracellular regulatory proteins responsible for the modulation of K+ channel function. Treatment of the acquired form is primarily directed at identifying and withdrawing the offending agent, although emergent therapy using maneuvers and agents that favorably modulate transmembrane ion currents can be lifesaving. In torsade de pointes associated with the hereditary long QT interval syndromes, early diagnosis leading to treatments designed to both shorten the QT interval and block the beta-adrenergic-induced instability of the QT interval is essential. CONCLUSIONS: The long QT interval syndromes and torsade de pointes are potentially life-threatening conditions caused by various agents, conditions, and genetic defects. The mechanisms responsible for these conditions and available treatment options for them are reviewed.

Electrophysiology↗
PubMed1994

Ventricular fibrillation induced by low-energy shocks from programmable implantable cardioverter-defibrillators in patients with coronary artery disease.

Many of the newest implantable cardioverter-defibrillators (ICDs) provide the option of programmable low-energy cardioversion for monomorphic ventricular tachycardia (VT). Whereas these devices may provide less myocardial damage and increased comfort in patients receiving frequent shocks for VT, the proarrhythmic effects of low-energy cardioversion from ICDs in patients with structural heart disease are not clear. The purpose of this study was to determine prospectively the per-patient incidence of ventricular fibrillation (VF) induction after low-energy cardioversion of VT by ICDs in patients with coronary artery disease. The estimated cardioversion energy requirement was determined during the course of routine predischarge ICD testing in 40 patients with newly implanted ICDs. Two groups of patients were identified during determination of the cardioversion energy requirement: (1) a non-VF group consisting of 26 of 40 patients (65%) without VF induced by low-energy shock and, (2) a VF group consisting of 14 of 40 patients (35%) who developed VF during low-energy cardioversion. There was no difference between the 2 groups in terms of patient age, sex, concurrent antiarrhythmic drug therapy, VT cycle length, or type of ICD system implanted. Compared with the non-VF group, the VF group was more likely to have both a lower ejection fraction (25 +/- 5% vs 33 +/- 8%; p = 0.005) and a cardioversion energy requirement > 2 J (79 vs 27%; p = 0.005). Our results suggest that low-energy cardioversion is associated with a high per-patient risk of VF induction, and the risk is higher in patients with poorer left ventricular function and, possibly, higher cardioversion energy requirement.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Efficacy of adenosine in terminating catecholamine-dependent supraventricular tachycardia.

The purpose of this study was to determine if adenosine is equally effective in terminating catecholamine-dependent and independent supraventricular tachycardia (SVT). The effect of adenosine on termination of SVT was studied in 21 patients: 12 with atrioventricular (AV) reciprocating tachycardia, and 9 with AV node reentrant tachycardia. Group 1 comprised 13 patients who had SVT induced in the absence of exogenous catecholamines, whereas group 2 comprised 8 who needed isoproterenol (1.6 +/- 0.4 micrograms/min) for induction. There was no statistical difference between the 2 groups regarding age, weight, mean arterial pressure during sinus rhythm and SVT, cycle length of SVT, or norepinephrine and epinephrine levels during sinus rhythm and SVT. Cycle length during sinus rhythm was significantly decreased in group 2. The mean dose of adenosine needed to terminate SVT was 52 +/- 6 micrograms/kg of body weight in group 1, and 61 +/- 12 micrograms/kg in group 2 (p > 0.05). In addition to isoproterenol not altering the minimal dose of adenosine necessary to terminate SVT, there was also no correlation between the dose of adenosine (mean 55 +/- 6 micrograms/kg) of each patient, and the corresponding endogenous epinephrine (273 +/- 59 pg/ml) (r = -0.19) and norepinephrine (400 +/- 58 pg/ml) (r = 0.01) levels during SVT, or cycle length of SVT (323 +/- 9 ms) (r = -0.35). The results show that adenosine is equally effective in terminating catecholamine-dependent and independent SVT; higher adenosine doses should not be needed to manage catecholamine-dependent SVT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1994

Atrioventricular node reentry: current concepts and new perspectives.

With the advent of RF catheter modification of AV node conduction for the treatment of AV node reentrant tachycardia, considerable advances have been made with better understanding of the AV junctional anatomy, electrophysiology, and mechanism responsible for AV node reentrant tachycardia. Future studies should be designed to uncover the basic cellular electrophysiological mechanisms responsible for fast and slow AV node conduction, to define the exact tissue components of the reentrant circuit in order to make ablative procedures safer, and to study the long-term effects of RF catheter ablation on AV conduction. Special caution should be directed toward pediatric patients with more stringent indications for catheter ablation of the AV junctional area in these patients.

Animals↗