Bibliothek

Notizen: Introduction: We previously have shown that a 3-minute single-stage adenosine tilt test has a diagnostic yield comparable to a two-stage protocol consisting of a 30-minute drug-free tilt followed by a 15-minute isoproterenol tilt. In this study, we sought to further define the clinical utility of adenosine tilt testing in patients with unexplained syncope by prospectively evaluating test specificity and determining predictors of a positive test response. Methods and Results: The specificity of single-stage adenosine tilt testing was determined using 30 control subjects. To determine the diagnostic yield of this protocol, adenosine tilts were performed in 129 patients with unexplained syncope. The adenosine tilt test protocol had high specificity (100%) but a low overall diagnostic yield (18%). However, the yield was affected significantly by age. In patients ≤40 years of age, the tilt test was positive in 15 (41%) of 37 patients, which was significantly greater than the yield in patients between the ages of 41 and 64 years (6/41 patients [15%], P = 0.012) and those ≥65 years of age (2/41 patients [5%], P 〈 0.0001). Conclusion: These data support single-stage adenosine tilt testing in patients ≤40 years of age because the diagnostic yield of the test is maximal in this group and the test can be completed in ≤3 minutes. Conversely, the diagnostic yield of adenosine tilt testing in patients 〉40 years of age is low, suggesting that the clinical utility of this protocol is limited in these patients. (J Cardiovasc Electrophysiol, Vol. 15, pp. 1-4, June 2004)

Notizen: Ventricular Tachycardia After Revascularization. Introduction: Two randomized trials (Multicenter Automatic Defibrillator Implantation Trial [MADIT] and Multicenter Unsustained Tachycardia Trial [MUSTT]) suggest that implantable cardioverter defibrillator (ICD) placement is associated with improved survival in patients with coronary artery disease, depressed left ventricular function, and nonsustained ventricular tachycardia (VT) who also have inducible sustained VT. However, neither study directly addresses the management of such patients who develop nonsustained VT early after revascularization. Methods and Results: We evaluated 109 consecutive patients who underwent electrophysiologic testing to evaluate nonsustained VT, which occurred 5 ± 4 days following revascularization. Sustained monomorphic VT was inducible in 46 (42%) patients; these patients received an ICD. The remaining 63 (58%) noninducible patients received neither antiarrhythmic drug therapy nor an ICD. During 27 ± 12 months of follow-up, 15 (33%) of 45 patients with an implanted ICD received at least one appropriate therapy from the device and 26 (24%) of the 109 study patients died. The 1- and 2-year freedom from ventricular tachycardia/fibrillation or sudden death in noninducible patients (97% and 93%) was significantly greater than that of inducible patients (84% and 71%; P = 0.001). However, no difference was observed in total mortality. Conclusion: Patients with nonsustained VT during the early postrevascularization period who have inducible VT have a high incidence of arrhythmic events. Although this study was not designed to assess the impact of ICD placement on the total mortality of inducible patients, the finding that one third of these patients received appropriate ICD therapy suggests that the device may have a protective effect in these patients.

Notizen: Catecholamine Facilitated Reentry. 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 μ/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.

Notizen: 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 local 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 cither 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.

Notizen: Adenosine-Sensitive VT. Idiopathic ventricular tachycardia (VT) is a term that refers to tachycardia that arises from ventricles devoid of apparent structural abnormalities. This form of VT is now recognized to be related to several distinct entities and includes a reentrant form typically located in the region of the left posterior fascicle, an automatic form that may originate from either ventricle, and a form that originates from the right ventricular outflow tract. This last type can account for up to 80% of cases of idiopathic VT and with few exceptions can be further subdivided into repetitive monomorphic VT and paroxysmal stress-induced VT, Evidence has accumulated suggesting that both forms of VT are related to cAMP-mediated triggered activity. The experimental underpinnings of this conclusion as well as the clinical characteristics of this form of idiopathic VT are elucidated in this review.

Notizen: Vasodepressor Syncope. 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.

Notizen: AV Nodal-His-Purkinje Reentry. Introduction: Bundle branch reentry (BBR) typically occurs in patients with dilated cardiomyopathy and infra-Hisian conduction system disease. The macroreentrant circuit of BBR is confined to the His-Purkinje system (HPS) and ventricular myocardium. As such, the atrioventricular (AV) node plays no role in the tachycardia circuit. Methods and Results: In the present study, we identified a novel form of wide complex tachycardia in a patient with coronary disease and severe aortic regurgitation. The tachycardia morphology was right bundle branch block with a left superior axis. Ventriculoatrial block was present during tachycardia. An unusual feature of this rhythm was two sequential His-bundle deflections (H and H′) for each ventricular beat of tachycardia. The H′V interval was identical to the HV interval during supraventricular rhythm. Changes in the ventricular cycle length (VV) preceded changes in the HH interval, consistent with retrograde activation of the first His-bundle deflection. Changes in the H ‘H’interval preceded changes in the VV interval, consistent with anterograde activation of the second His-bundle deflection. Tachycardia could be terminated with ventricular extrastimuli that did not capture the proximal HPS as well as with ventricular extrastimuli that advanced the His deflection, consistent with block in the HPS and in the AV node, respectively. Reproducible termination of the tachycardia following the first His deflection was demonstrated with adenosine, consistent with an upper pivot in the AV node. Conclusions: We have identified a new form of reentrant tachycardia in which the AV node, HPS, and ventricular myocardium each obligatorily participates in the tachycardia circuit, with the left posterior fascicle and right bundle functioning as the anterograde and retrograde limbs, respectively. Unlike BBR, however, the His bundle is activated twice as the wavefront pivots in the AV node. This model requires longitudinal dissociation at the levels of the AV node and His bundle.

Notizen: 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 β-adrenergic blockade. We computed the RMS successive difference of the BB intervals (BMSSD: 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. BMSSD did not differ at baseline (supine) between those who did (n = 20) and did not (n = 8) respond to β-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 β-blockade failure (odds ratio = 11; P = 0.01). Patients with diminished age adjusted parasympathetic withdrawal during orthostatic stress are less likely to respond to β-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.

Notizen: Withdrawal of parasympathetic tone has been reported after ablation in the posteroseptal right atrium and has been attributed to injury of vagal efferent fibers. The purpose of this study was to assess the time course and predictors of autonomic dysfunction after slow pathway ablation. In 30 patients with AV nodal reentrant tachycardia, time- and frequency-domain measures of heart rate variability (HRV) were measured before, 30 minutes after, and 1 day after slow pathway ablation. There were significant reductions in mean RR interval (724 ± 163 vs 836 ± 164 ms, P 〈 0.05), SD of RR intervals (29 ± 17 vs 40 ± 18 ms, P 〈 0.05), root mean squared difference (15 ± 8 vs 29 ± 17 ms, P 〈 0.05), and high frequency power (4.1 ± 0.4 vs 4.5 ± 0.6 log10ms2, P 〈 0.05) 30 minutes after ablation. However, these parameters returned to baseline 1 day after ablation. Multivariate regression identified isoproterenol dose during the diagnostic study (P = 0.02) and radiofrequency duration (P = 0.02) as statistically significant predictors of heart rate change (R2= 0.45). These findings suggest that changes in autonomic tone after ablation in the posteroseptal right atrium are transitory and resolve within 1 day of the procedure. These short-term changes may be related to procedural variables rather than direct injury to vagal efferent fibers.

Notizen: 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 he 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 he 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 he due to cAMP-mediated triggered activity. A third form of ILVT is propranolol sensitive. It is neither 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.