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Biomedical subjects

B B Lerman

Publications and source records attributed to B B Lerman.

At least 19 recordsLinked to original sources
PubMed1999

Comparison of a novel rectilinear biphasic waveform with a damped sine wave monophasic waveform for transthoracic ventricular defibrillation. ZOLL Investigators.

OBJECTIVES: We compared the efficacy of a novel rectilinear biphasic waveform, consisting of a constant current first phase, with a damped sine wave monophasic waveform during transthoracic defibrillation. BACKGROUND: Multiple studies have shown that for endocardial defibrillation, biphasic waveforms have a greater efficacy than monophasic waveforms. More recently, a 130-J truncated exponential biphasic waveform was shown to have equivalent efficacy to a 200-J damped sine wave monophasic waveform for transthoracic ventricular defibrillation. However, the optimal type of biphasic waveform is unknown. METHODS: In this prospective, randomized, multicenter trial, 184 patients who underwent ventricular defibrillation were randomized to receive a 200-J damped sine wave monophasic or 120-J rectilinear biphasic shock. RESULTS: First-shock efficacy of the biphasic waveform was significantly greater than that of the monophasic waveform (99% vs. 93%, p = 0.05) and was achieved with nearly 60% less delivered current (14 +/- 1 vs. 33 +/- 7 A, p < 0.0001). Although the efficacy of the biphasic and monophasic waveforms was comparable in patients with an impedance < 70 ohms (100% [biphasic] vs. 95% [monophasic], p = NS), the biphasic waveform was significantly more effective in patients with an impedance > or = 70 ohms (99% [biphasic] vs. 86% [monophasic], p = 0.02). CONCLUSIONS: This study demonstrates a superior efficacy of rectilinear biphasic shocks as compared with monophasic shocks for transthoracic ventricular defibrillation, particularly in patients with a high transthoracic impedance. More important, biphasic shocks defibrillated with nearly 60% less current. The combination of increased efficacy and decreased current requirements suggests that biphasic shocks as compared with monophasic shocks are advantageous for transthoracic ventricular defibrillation.

Aged↗
PubMed1999

Induction of neurally mediated syncope with adenosine.

BACKGROUND: Tilt testing is used to establish the diagnosis of neurally mediated syncope. However, applicability of the tilt test is limited by test sensitivity and length of time required to perform the test. We hypothesized that adenosine could facilitate the induction of neurally mediated syncope through its sympathomimetic effects and therefore could be used as an alternative to routine tilt testing. METHODS AND RESULTS: In protocol 1, the yield of adenosine tilt testing (12 mg while upright, followed by 60 degrees tilt for 5 minutes) and a 15-minute isoproterenol tilt test were compared in 84 patients with a negative 30-minute drug-free tilt test. In protocol 2, 100 patients underwent an initial adenosine tilt test followed by our routine tilt test (30-minute drug-free tilt followed by a 15-minute isoproterenol tilt). Six additional control patients underwent microneurography of the peroneal nerve to compare the sympathomimetic effects during bolus administration of adenosine and continuous infusion of isoproterenol. In protocol 1, the yields of adenosine (8 of 84, 10%) and isoproterenol (7 of 84, 8%) tilt testing were comparable (P=NS). In protocol 2, the yields of adenosine (19 of 100, 19%) and routine (22 of 100, 22%) tilt testing were also comparable (P=NS). Although the yield of adenosine tilt testing was comparable in both protocols, patients with a negative adenosine tilt test but a positive routine tilt test usually required isoproterenol to elicit the positive response. Microneurography confirmed discordant sympathetic activation after adenosine and isoproterenol administration. CONCLUSIONS: Adenosine is effective for the induction of neurally mediated syncope, with a diagnostic yield comparable to routine tilt testing. However, the discordant results obtained with adenosine and the isoproterenol phase of routine tilt testing suggest that adenosine and isoproterenol tilt testing may have complementary roles in eliciting a positive response. Therefore, a tilt protocol that uses an initial adenosine tilt followed, if necessary, by an isoproterenol tilt would be expected to increase the overall yield and reduce the duration of tilt testing.

Adenosine↗
PubMed1999

Long-term outcome of patients with unexplained syncope treated with an electrophysiologic-guided approach in the implantable cardioverter-defibrillator era.

OBJECTIVES: We evaluated the long-term outcome of patients with coronary artery disease and unexplained syncope who were treated with an electrophysiologic (EP)-guided approach. BACKGROUND: Electrophysiologic studies are frequently performed to evaluate unexplained syncope in patients with coronary artery disease. Patients with this profile who have inducible ventricular tachycardia are considered at high risk for sudden death and increased overall mortality, and therefore are often treated with an implantable cardioverter-defibrillator (ICD). The impact of this EP-guided strategy is unknown because there are no data comparing the long-term outcome of ICD recipients with that of noninducible patients. METHODS: We evaluated 67 consecutive patients with coronary artery disease and unexplained syncope. All patients were treated with an EP-guided approach that included ICD implantation in patients with inducible ventricular tachycardia. RESULTS: Electrophysiologic testing suggested a plausible diagnosis in 32 (48%) of these patients. Inducible monomorphic ventricular tachycardia was the most common abnormality. Despite frequent appropriate therapy with ICDs, the total mortality for patients with inducible monomorphic ventricular tachycardia was significantly higher than for noninducible patients. The respective one- and two-year survival rates were 94% and 84% in noninducible patients and 77% and 45% in inducible patients (p = 0.02). CONCLUSIONS: Electrophysiologic testing suggests an etiology for unexplained syncope in approximately 50% of patients and risk stratifies these patients with regard to long-term outcome. Patients who receive an ICD for the management of inducible ventricular tachycardia have a high incidence of spontaneous ventricular arrhythmias requiring ICD therapy. However, despite ICD implantation and frequent appropriate delivery of ICD therapies, patients with inducible ventricular tachycardia have a significantly worse prognosis than do those who are noninducible.

Aged↗
PubMed1999

Catecholamine facilitated reentrant ventricular tachycardia: uncoupling of adenosine's antiadrenergic effects.

INTRODUCTION: Adenosine has no direct electrophysiologic function in ventricular tissue, but in the presence of cyclic adenosine monophosphate (cAMP), stimulation exerts a potent antiadrenergic effect. This effect has been exploited in the recognition and treatment of ventricular tachycardia (VT) due to cAMP-mediated triggered activity and automaticity, which are respectively terminated and suppressed by adenosine. However, the effects of adenosine on catecholamine-facilitated reentrant VT are unknown. A pivotal issue is whether termination of VT with adenosine is mechanism specific, or whether it represents a nonspecific antiadrenergic effect. The purpose of this study, therefore, was to define the effects of adenosine in a well-characterized group of patients with catecholamine-facilitated reentrant VT. METHODS AND RESULTS: Fourteen patients with catecholamine-facilitated reentry were studied. In the 12 patients with structural heart disease (including two with arrhythmogenic right ventricular dysplasia), adenosine (260 to 550 microg/kg) failed to slow or terminate VT. Two patients without structural heart disease had intrafascicular tachycardia confined to the left posterior fascicle, a calcium-dependent, verapamil-sensitive arrhythmia. In the absence of isoproterenol, verapamil terminated VT but adenosine did not. However, when isoproterenol was subsequently required for facilitation of tachycardia, adenosine terminated VT in both patients. CONCLUSION: Adenosine has no antiadrenergic (antiarrhythmic) effect in patients with catecholamine-facilitated VT due to structural heart disease. Patients with verapamil-sensitive, left posterior intrafascicular reentry have an unusual dual response to adenosine. In the unstimulated state, adenosine has no effect on basal inward calcium current and, therefore, no effect on VT. However, when induction of VT requires amplification of the inward calcium current through stimulation of cAMP, adenosine sensitivity of VT becomes manifest. These results indicate that with few exceptions, termination of VT with adenosine is strongly suggestive of a cAMP-mediated triggered mechanism rather than reentry.

Adenosine↗
PubMed1999

Differential effects of adenosine on focal and macroreentrant atrial tachycardia.

INTRODUCTION: The effects of adenosine on atrial tachycardia (AT) remain controversial, and the mechanistic implications of adenosine termination have not been fully established. The purpose of this study was to elucidate the differential effects of adenosine on focal and macroreentrant AT and describe the characteristics of adenosine-sensitive AT. METHODS AND RESULTS: Thirty patients received adenosine during AT. Tachycardia origins were identified as focal or macroreentrant during invasive electrophysiologic studies. Responses to adenosine were analyzed and characterized as tachycardia termination, transient suppression, or no effect. Electrophysiologic studies demonstrated a focal origin of tachycardia in 17 patients. Adenosine terminated focal tachycardias in 14 patients (dose 7.3 +/- 4.0 mg) and transiently suppressed the arrhythmias in three others (dose 10.0 +/- 6.9 mg). A macroreentrant mechanism was demonstrated in 13 patients; adenosine terminated only one of these tachycardias and had no effect on the remaining 12 patients (dose 10.2 +/- 2.9 mg). Four classes of adenosine-sensitive AT were identified. Class I consisted of nine patients with tachycardia arising from the crista terminalis; these tachycardias also terminated with verapamil (4/4). Class II consisted of four patients with repetitive monomorphic AT arising from diverse sites in the right atrium; these either slowed or terminated in response to verapamil (2/2). Class III consisted of the three patients with transient suppression and demonstrated electropharmacologic characteristics consistent with an automatic mechanism, including insensitivity to verapamil (2/2). In the one patient with macroreentrant AT that was comprised of decremental atrial tissue, adenosine terminated tachycardia in a zone of decremental slow conduction (Class IV); this tachycardia slowed with verapamil. CONCLUSIONS: Adenosine-sensitive AT is usually focal in origin and arises either from the region of the crista terminalis (inclusive of the sinus node) or from diverse atrial sites with an incessant nonsustained repetitive pattern. Although most forms of macroreentrant AT are insensitive to adenosine, rarely macroreentrant AT with zones of decremental slow conduction can demonstrate adenosine sensitivity.

Adenosine↗
PubMed1999

Ventricular response in atrial fibrillation: random or deterministic?

The ventricular response in atrial fibrillation is often described as "chaotic," but this has not been demonstrated in the strict mathematical sense. A defining feature of chaotic systems is sensitive dependence on initial conditions: similar sequences evolve similarly in the short term but then diverge exponentially. We developed a nonlinear predictive forecasting algorithm to search for predictability and sensitive dependence on initial conditions in the ventricular response during atrial fibrillation. The algorithm was tested for simulated R-R intervals from a linear oscillator with and without superimposed white noise, a chaotic signal (the logistic map) with and without superimposed white noise, and a pseudorandom signal and was then applied to R-R intervals from 16 chronic atrial fibrillation patients. Short-term predictability was demonstrated for the linear oscillators, without loss of predictive ability farther into the future. The chaotic system demonstrated high short-term predictability that declined rapidly further into the future. The pseudorandom signal was unpredictable. The ventricular response in atrial fibrillation was weakly predictable (statistically significant predictability in 8 of 16 patients), without sensitive dependence on initial conditions. Although the R-R interval sequence is not completely unpredictable, a low-dimensional chaotic attractor does not govern the irregular ventricular response during atrial fibrillation.

Aged↗
PubMed1998

Right ventricular outflow tract tachycardia due to a somatic cell mutation in G protein subunitalphai2.

Idiopathic ventricular tachycardia is a generic term that describes the various forms of ventricular arrhythmias that occur in patients without structural heart disease and in the absence of the long QT syndrome. Many of these tachycardias are focal in origin, localize to the right ventricular outflow tract (RVOT), terminate in response to beta blockers, verapamil, vagal maneuvers, and adenosine, and are thought to result from cAMP-mediated triggered activity. DNA was prepared from biopsy samples obtained from myocardial tissue from a patient with adenosine-insensitive idiopathic ventricular tachycardia arising from the RVOT. Genomic sequences of the inhibitory G protein Galphai2 were determined after amplification by PCR and subcloning. A point mutation (F200L) in the GTP binding domain of the inhibitory G protein Galphai2 was identified in a biopsy sample from the arrhythmogenic focus. This mutation was shown to increase intracellular cAMP concentration and inhibit suppression of cAMP by adenosine. No mutations were detected in Galphai2 sequences from myocardial tissue sampled from regions remote from the origin of tachycardia, or from peripheral lymphocytes. These findings suggest that somatic cell mutations in the cAMP-dependent signal transduction pathway occurring during myocardial development may be responsible for some forms of idiopathic ventricular tachycardia.

Amino Acid Sequence↗
PubMed1998

Heart rate changes preceding ventricular ectopy in patients with ventricular tachycardia caused by reentry, triggered activity, and automaticity.

OBJECTIVES: Although enhanced sympathetic tone is thought to be proarrhythmic and beta-blockade reduces the risk of sudden cardiac death in survivors of myocardial infarction, the role of the autonomic nervous system in triggering spontaneous ventricular ectopy and ventricular tachycardia (VT) has not been fully elucidated. The purpose of this study was to compare and contrast autonomic tone preceding spontaneous ventricular arrhythmias in patients with reentrant, triggered, and automatic forms of VT. BACKGROUND: The prevailing model of reentrant VT is based on a triggering beat interacting with a fixed substrate. Within this model, cyclic fluctuations in autonomic tone comprise a "third factor" that may initiate the triggering extrasystoles as well as alter the substrate, facilitating perpetuation of tachycardia. Consistent with this model, adrenergic stimulation can facilitate the induction of reentrant arrhythmias as well as arrhythmias resulting from enhanced automaticity and those caused by triggered activity resulting from cyclic adenosine monophosphate-dependent delayed afterdepolarizations. METHODS AND RESULTS: On the basis of the results at electrophysiologic study, 26 patients with coronary artery disease were identified as having reentrant VT, 11 were identified as having idiopathic VT caused by triggered activity, and 4 were identified as having idiopathic VT caused by enhanced automaticity. Each patient underwent 24-hour electrocardiographic monitoring, and the mean sinus R-R intervals immediately preceding each sinus beat as well as the 15 beats preceding sinus beats, premature ventricular contractions (VPCs), and complex ventricular ectopy (couplet/non-sustained VT) were computed. In addition, high-frequency heart rate variability was determined. Heart rate accelerated before spontaneous ventricular ectopy for all three arrhythmia mechanisms. R-R intervals preceding episodes of complex ventricular ectopy were significantly shorter than the corresponding intervals preceding single VPCs in patients with 'riggered VT [p=0.006 and 0.01, R-R(-1) and R-R(-15), respectively] and in those with reentrant VT (p=0.007 and p=0.05). There were no corresponding differences in high-frequency heart rate variability. R-R intervals preceding single VPCs were significantly shorter than the corresponding intervals preceding sinus beats in patients with automatic VT (p=0.0004 and 0.0001, respectively), which was accompanied by a small reduction in high-frequency heart rate variability (p=0.04). CONCLUSIONS: Heart rate accelerates before spontaneous ventricular ectopy in patients with VT. The acceleration is disproportionate to parasympathetic withdrawal, implicating increased endogenous sympathetic tone in the genesis of spontaneous ventricular arrhythmias caused by all three electrophysiologic mechanisms: reentry, triggered activity, and automaticity.

Adolescent↗
PubMed1997

Adenosine-sensitive ventricular tachycardia: right ventricular abnormalities delineated by magnetic resonance imaging.

BACKGROUND: Adenosine-sensitive ventricular tachycardia (VT) is thought to be due to cAMP-mediated triggered activity. It typically originates from the RVOT and occurs in patients with apparently normal hearts. Using magnetic resonance imaging (MRI), we tested the hypothesis that adenosine-sensitive VT occurs in patients without structural heart disease. METHODS AND RESULTS: Fourteen patients (9 women; age, 47+/-19 years) presented with sustained VT (n=3), repetitive monomorphic VT (n=7), or both (n=4). VT terminated with adenosine in each patient and was sensitive to vagal maneuvers in 9 of 11 and verapamil in 10 of 12. VT originated from the right ventricular outflow tract in 10 patients, the right ventricular apex in 1, and the left ventricular septum in 3. Conventional studies included normal signal-averaged ECGs in 9 of 9, normal right ventricular echocardiography in 10 of 10, and normal left ventriculography and coronary angiography in 6 of 7. In contrast, MRI scans were abnormal in 10 of 14 patients. These abnormalities included focal thinning (6), fatty infiltration (4), and wall motion abnormalities (4) of the right ventricle. The most common site of MRI abnormalities was the right ventricular free wall, but there was a poor correlation between the site of MRI abnormalities and the origin of VT. Among 18 control patients without clinical heart disease, thinning of the right ventricular wall was noted in only 1 patient (patients versus control subjects, P=.0001). CONCLUSIONS: Patients with idiopathic adenosine-sensitive VT comprise a heterogeneous group as assessed by MRI, with 70% demonstrating mild structural abnormalities. However, it is unlikely that these findings are causally related to tachycardia, and the functional significance of these anatomic abnormalities is uncertain.

Adenosine↗
PubMed1997

Precordial QT dispersion and inducible ventricular tachycardia.

We compared the performance of precordial QT dispersion, late potentials on the signal-averaged electrocardiogram (ECG), and reduced left ventricular ejection fraction for identification of inducible ventricular tachycardia (VT) in 162 patients undergoing electrophysiologic study (EPS). QT(apex) dispersion in 56 patients with inducible VT (72 +/- 55 msec) was greater than that in 106 patients without inducible VT (55 +/- 36 msec, p < 0.01); dispersion was greater in both groups than in 144 normal subjects (33 +/- 19 msec). A QT(apex) dispersion partition of more than 68 msec, the upper ninety-fifth percentile in normal subjects, identified inducible VT with a specificity of 75% and a sensitivity of 45%. Although the performances of late potentials (specificity 82%, sensitivity 59%) and reduced ejection fraction (specificity 86%, sensitivity 54%) were each stronger than QT dispersion alone for identification of inducible VT, abnormal QT(apex) dispersion remained a significant additional predictor of inducible VT in a logistic regression model that included the three variables (specificity 78%, sensitivity 75%).

Adult↗
PubMed1997

Response of neurocardiac syncope to beta-blocker therapy: interaction between age and parasympathetic tone.

Beta-blockers are a first line therapy for neurocardiac syncope, but are not always effective. The purpose of this study was to determine whether differential autonomic responses to orthostasis predict the response of patients with neurocardiac syncope to beta-adrenergic blockade. We computed the RMS successive difference of the RR intervals (RMSSD: a measure of cardiac parasympathetic tone) during supine and upright phases of the initial tilt test in 28 patients with syncope and positive tilt tests who were treated with atenolol. Follow-up tilt testing was performed to assess the efficacy of the drug in preventing tilt induced neurocardiac syncope. RMSSD did not differ at baseline (supine) between those who did (n = 20) and did not (n = 8) respond to beta-blockade. However, withdrawal of parasympathetic tone in response to tilt varied inversely with age (r = -0.69; P < 0.01). Reduced age adjusted parasympathetic withdrawal during orthostasis was associated with a 47% versus 8% risk of beta-blockade failure (odds ratio = 11; P = 0.01). Patients with diminished age adjusted parasympathetic withdrawal during orthostatic stress are less likely to respond to beta-blocker therapy of neurocardiac syncope than their counterparts. This may reflect a correspondingly greater sympathetic response to orthostasis in these patients, but the mechanism for this interaction is undetermined.

Adrenergic beta-Antagonists↗
PubMed1997

Vasodepressor syncope due to subclinical myocardial ischemia.

INTRODUCTION: Vasodepressor syncope is a common cause of syncope, but the initiating event that triggers the vasodepressor response remains incompletely understood. Although ischemia due to acute right coronary occlusion may precipitate hypotension and bradycardia through the Bezold-Jarisch reflex, an ischemic precipitant for the common vasodepressor faint has not been previously identified. In the present study, we present evidence for a causal relationship between myocardial ischemia and vasodepressor syncope. METHODS AND RESULTS: Two patients referred for evaluation of syncope underwent upright tilt table testing with either ST segment monitoring, sestamibi scintigraphy and echocardiography during the tilt test, or coronary angiography. Both patients had positive tilt table tests during the control study. Patient 1 was documented to have reproducible ischemic ECG changes during atypical chest pressure induced by upright tilt, despite a normal coronary angiogram with ergonovine provocation. Subsequent tilt testing with simultaneous sestamibi perfusion imaging and echocardiography revealed reversible anterolateral hypoperfusion corresponding with anterolateral hypokinesis during upright tilt that preceded syncope. Ischemic ECG changes during incremental rapid atrial pacing further suggested ischemia on the basis of microvascular disease. Follow-up tilt testing on verapamil was negative. Patient 2 developed ischemic ECG changes during the recovery phase of an exercise stress test, which was followed by a vasodepressor response and frank syncope. Coronary angiography revealed a 90% distal right coronary artery stenosis that was successfully dilated, after which follow-up tilt table testing off all other medication was negative. CONCLUSIONS: These two cases illustrate a previously unrecognized causality between myocardial ischemia and clinical vasodepressor syncope, and demonstrate that subtle manifestations of myocardial ischemia, associated with either atypical angina or silent ischemia, can provoke syncope.

Cardiac Pacing, Artificial↗
PubMed1997

Mechanisms of idiopathic left ventricular tachycardia.

Idiopathic left ventricular tachycardia (ILVT) differs from idiopathic right ventricular outflow tract (RVOT) tachycardia with respect to mechanism and pharmacologic sensitivity. ILVT can be categorized into three subgroups. The most prevalent form, verapamil-sensitive intrafascicular tachycardia, originates in the region of left posterior fascicle of the left bundle. This tachycardia is adenosine insensitive, demonstrates entrainment, and is thought to be due to reentry. The tachycardia is most often ablated in the region of the posteroinferior interventricular septum. A second type of ILVT is a form analogous to adenosine-sensitive RVOT tachycardia. This tachycardia appears to originate from deep within the interventricular septum and exits from the left side of the septum. This form of VT also responds to verapamil and is thought to be due to cAMP-mediated triggered activity. A third form of ILVT is propranolol sensitive. It is neither or initiated or terminated by programmed stimulation, does not terminate with verapamil, and is transiently suppressed by adenosine, responses consistent with an automatic mechanism. Recognition of the heterogeneity of ILVT and its unique characteristics should facilitate appropriate diagnosis and therapy in this group of patients.

Humans↗
PubMed1996

Mechanism of ventricular rate control after radiofrequency modification of atrioventricular conduction in patients with atrial fibrillation.

BACKGROUND: Modification of atrioventricular (AV) conduction during atrial fibrillation (AF) may be achieved by radiofrequency ablation in the posteroseptal region of the tricuspid annulus. We tested the hypothesis that elimination of the posterior atrionodal input rather than direct damage to the compact AV node accounts for the decrease in ventricular rate after AV nodal modification. METHODS AND RESULTS: Twenty-four patients with the typical form of AV nodal reentrant tachycardia (AVNRT) underwent selective radiofrequency ablation of the slow AV nodal pathway in the posteroseptal tricuspid annulus. AF was induced before ablation (phase 1), 30 minutes after ablation (phase 2), and during follow-up 24 hours after ablation (phase 3), both with and without concurrent infusion of isoproterenol (4 micrograms/min). Successful elimination of AVNRT was achieved in all patients. During phase 3, 11 patients (46%) had residual dual pathway physiology. AV nodal Wenckebach cycle length (AVNW-CL) increased progressively during each phase of the protocol (356 +/- 72 versus 371 +/- 78 ms versus 432 +/- 104 ms, P < .0001), as did the effective refractory period of the AV node (279 +/- 60 versus 304 +/- 67 ms versus 372 +/- 56 ms, P < .0001). Minimal, mean, and maximal RR intervals during AF progressively increased immediately after ablation and 24 hours later (485 +/- 88 versus 533 +/- 116 ms versus 637 +/- 142 ms for mean RR, P < .0001). The changes in AVNW-CL, AV nodal effective refractory period, and ventricular response during AF were independent of residual dual pathway physiology after ablation. Similar observations were observed during isoproterenol infusion. CONCLUSIONS: Modification of AV nodal conduction during AF by radiofrequency ablation in the posteroseptal tricuspid annulus is independent of the presence or absence of a residual slow AV nodal pathway. On the basis of these observations, the mechanism of AV nodal modification is consistent with elimination of the posterior atrionodal input.

Adult↗
PubMed1996

Posterior fast atrioventricular node pathways: implications for radiofrequency catheter ablation of atrioventricular node reentrant tachycardia.

OBJECTIVES: This study sought to present evidence that fast atrioventricular (AV) node pathways with posterior exit sites may participate in typical AV node reentry. BACKGROUND: Catheter ablation of the slow AV node pathway in the posteroseptal right atrium is the preferred therapeutic approach in patients with AV node reentrant tachycardia. Despite the success achieved with this approach, electrophysiologic changes consistent with fast pathway ablation are occasionally observed. One potential explanation is the presence of an aberrant posterior fast pathway. METHODS: The location of fast and slow AV node pathways was determined by atrial activation mapping along the tricuspid valve annulus during tachycardia and was further confirmed by the effect of radiofrequency catheter ablation. RESULTS: Seven patients with AV node reentrant tachycardia had evidence of a posterior fast pathway near the coronary sinus os. Abolition of anterograde and retrograde fast pathway conduction followed radiofrequency ablation in the posteroseptal region in six patients. Consistent with fast pathway ablation, the AH interval increased from 70 +/- 24 to 195 +/- 35 ms (mean +/- SD), and tachycardia was no longer inducible. Selective slow pathway ablation was performed in one other patient with a posterior fast pathway. CONCLUSIONS: Functionally fast AV node pathways may be located in the posteroseptal right atrium, where slow pathway modification is performed. These data delineate the limitation of an anatomically guided slow pathway ablative approach and emphasize the importance of detailed mapping and localization of the retrograde fast pathway exit site before ablation. Failure to recognize the presence of posterior fast AV node pathways may account for sporadic examples of AV block, complicating posteroseptal ablation in patients with AV node reentry.

Adult↗
PubMed1996

Idiopathic right ventricular outflow tract tachycardia: a clinical approach.

Right ventricular outflow tract (RVOT) tachycardia is the most common form of idiopathic ventricular tachycardia (VT). Phenotypically, RVOT tachycardia segregates into two predominant forms, one characterized by repetitive monomorphic nonsustained VT and the other by paroxysmal exercise induced sustained VT. There is an increasing body of evidence to support the concept that both forms of tachycardia reflect disparate clinical manifestations of an identical cellular mechanism (i.e., cAMP-mediated triggered activity), which is identified clinically by the tachycardia's sensitivity to adenosine. The clinical characteristics, natural history, and approaches to therapy of RVOT tachycardia are delineated herein.

Adenosine↗