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The recognition of the presence, location, and properties of unusual accessory pathways for atrioventricular conduction is an exciting, but frequently a difficult, challenge for the clinical cardiac arrhythmologist. In this third part of our series of reviews, we discuss the different steps required to come to the correct diagnosis and management decision in patients with nodofascicular, nodoventricular, and fasciculo-ventricular pathways. We also discuss the concealed accessory atrioventricular pathways with the properties of decremental retrograde conduction that are associated with the so-called permanent form of junctional reciprocating tachycardia. Careful analysis of the 12-lead electrocardiogram during sinus rhythm and tachycardias should always precede the investigation in the catheterization room. When using programmed electrical stimulation of the heart from different intracardiac locations, combined with activation mapping, it should be possible to localize both the proximal and distal ends of the accessory connections. This, in turn, should then permit the determination of their electrophysiologic properties, providing the answer to the question "are they incorporated in a tachycardia circuit?". It is this information that is essential for decision-making with regard to the need for catheter ablation, and if necessary, its appropriate site.

unster, MGermany Background: We will focus our attention in this article in the ECG changes of classical Prinzmetal angina that occur during occlusive proximal coronary spasm usually in patients with normal or noncritical coronary stenosis. Results: The most important ECG change during a focal proximal coronary spasm is in around 50% of cases the appearance of peaked and symmetrical T wave that is followed, if the spasm persist, by progressive ST-segment elevation that last for a few minutes, and later progressively resolve. The most frequent ECG changes associated with ST-segment elevation are: (a) increased height of the R wave, (b) coincident S-wave diminution, (c) upsloping TQ in many cases, and (d) alternans of the elevated ST-segment and negative T wave deepness in 20% of cases. The presence of arrhythmias is very frequent during Prinzmetal angina crises, especially ventricular arrhythmias. The prevalence and importance of ventricular arrhythmias were related to: (a) duration of episodes, (b) degree of ST-segment elevation, (c) presence of ST-T wave alternans, and (d) the presence of >25% increase of the R wave. Conclusions: The incidence of Prinzmetal angina is much lower then 50 years ago for many reasons including treatment with calcium channel blocks to treat hypertension and ischemia heart disease and the decrease of smoking habits. Ann Noninvasive Electrocardiol 2014;19(5):442-453 electrocardiography; Prinzmethal angina; coronary spasm; ST elevation

Background For many years was considered that negative T wave in ischemic heart disease represents ischemia and for many authors located in subepicardial area. Methods We performed a review based in the literature and in the experience of the authors commenting the real significance of the presence of negative T wave in patients with ischemic heart disease. Results The negative T wave may be of primary or secondary type. Negative T wave observed in ischemic heart disease are of primary origin, therefore not a consequence of abnormal repolarization pattern. The negative T wave of ischemic origin presents the following characteristics: (1) are symmetrical and of variable deepness; (2) present mirror patterns; (3) starts in the second part of repolarization; and (4) may be accompanied by positive or negative U wave. The negative T wave of ischemic origin may be seen in the following clinical settings: (1) postmyocardial infarction due to a window effect of necrotic zone and (2) as a consequence of reperfusion in case of aborted MI when the artery has opened spontaneously, or after fibrinolysis, PCI, or coronary spasm. Conclusion Acute ongoing ischemia do not cause negative T wave. This pattern appears when the ongoing ischemia is vanishing or in the chronic phase. In all these cases the cause of negative T wave is not located in the subepicardial area. Furthermore, positive exercise testing is expressed by ST depression never by isolated negative T wave. There are many circumstances that may present negative T wave outside ischemic heart disease and that have been discussed in this paper.

A 28-year-old male patient with a 3-year history of re-current tachycardia was referred for electrophysiologic eval-uation and catheter ablation. The patient had no other co-morbidities. Propafenone was discontinued 7 days beforeadmission.Electrophysiologic study: normal baseline intervals dur-ing sinus rhythm (PA = 20, AH = 68, HV = 50 ms). Anarrow QRS tachycardia was repeatedly induced by a singleatrial premature beat following a pacing drive of 400 ms, orfollowing 2 premature beats delivered during sinus rhythm.In contrast, a wide QRS tachycardia was always inducedby 2 right ventricular premature beats delivered during sinusrhythm.Thisleftbundlebranchblock(LBBB)-liketachycar-dia with a cycle length of 330–340 ms would spontaneouslychange into a slower, narrow QRS tachycardia with a cyclelengthof370msafterstabilizationoftheRRinterval(Fig.1).Transitionfromwidetonarrowtachycardiawassudden.Thecycle length of the first RR interval after disappearance oftheLBBBpatternwas310msbutincreasedthereafter.Whatwas the mechanism of change in cycle length?

Antidromic Tachycardia in Patients with an Atriofascicular Fiber. Background: The typical and most common tachycardia in patients with atriofascicular pathways is a macro reentrant tachycardia, with anterograde conduction over the decrementally conducting bypass tract and retrograde conduction over the right bundle branch-His-AV node axis resulting in a short V-right bundle branch and short V-H interval. Objectives: To report on changes in rate and QRS configuration when right bundle branch block (RBBB) develops spontaneously during antidromic tachycardia using an atriofascicular fiber. Methods: Three of 25 patients with an antidromic circus movement tachycardia using a right-sided atriofascicular pathway showed episodes of right bundle branch block (RBBB) during ventriculo-atrial conduction. Effect of retrograde RBBB on tachycardia rate and QRS configuration was studied using intracardiac and extracardiac recordings. Results: All 3 patients showed prolongation of their V-A interval when retrograde RBBB occurred during tachycardia, resulting in a longer tachycardia cycle length. The VA time increase ranged from 85 to 100 msec, with a mean 346 ± 5 msec. Two of the 3 patients also showed a change in QRS configuration due to a more leftward shift of the frontal plane QRS axis. Conclusion: Rate changes in antidromic tachycardia in patients with atriofascicular fibers can be based on a shift in VA conduction from one bundle branch to the other. This may be accompanied by changes in the frontal plane QRS axis because of a change in ventricular activation sequence.

Dual Conduction in a Mahaim Fiber. The case of an 8-year-old girl with incessant nonsustained left bundle branch block-like tachycardia refractory to antiarrhythmic drug therapy is reported. Electrophysiologic study revealed the presence of a right-sided accessory atriofascicular pathway. Episodes of nonsustained tachycardia were found to be based upon a dual response in AV conduction over the Mahaim fiber to one P wave. No reentrant tachycardia could be induced. The arrhythmia was cured by catheter ablation targeting a Mahaim potential at the right lateral tricuspid annulus. The findings can be explained by longitudinal dissociation in a single Mahaim fiber, a fiber distally diverging into two fibers with different conduction times, or (less likely) two closely located Mahaim fibers with different conduction times.

Introduction: Automatic rhythms associated with Mahaim fibers usually occur during radiofrequency catheter ablation. The incidence and significance of spontaneous automaticity in Mahaim fibers are unknown. Methods and Results: Spontaneous automatic rhythms were observed in 5 (12.5%) of 40 patients with Mahaim fibers referred for nonpharmacologic therapy because of recurrent episodes of symptomatic tachyarrhythmias, usually antidromic circus movement tachycardia (33/40 patients). Three were female and two were male. Their mean age was 15 ± 7 years compared to 26 ± 13 years of the patients without automaticity (P = 0.09). Three patients had both antidromic tachycardia and asymptomatic spontaneous automatic rhythms recorded during ambulatory ECG (1 patient) or electrophysiologic study (2 patients). In 2 patients, the automatic rhythm triggered antidromic tachycardia. Two other patients had nonsustained repetitive episodes of wide QRS tachycardia due to automaticity arising in the Mahaim fiber, without antidromic tachycardia. All automatic rhythms were abolished by successful catheter ablation of the Mahaim fibers. Conclusion: Spontaneous automaticity occurred in 12.5% of our Mahaim patients and may trigger antidromic tachycardia. Spontaneous automaticity, which is not seen in rapidly conducting accessory pathways, is another argument for the presence of an AV nodal-like structure in Mahaim fibers. (J Cardiovasc Electrophysiol, Vol. 15, pp. 738-744, July 2004)

The introduction of programmed electrical stimulation of the heart and intracardiac activation mapping 35 years ago made it possible to study the site of origin or the pathway of a supraventricular tachycardia and to obtain insight into the mechanism of the tachycardia. Information from these studies has been the basis for the development of new therapies, such as arrhythmia surgery, antitachycardia pacing, and catheter ablation. Correlation of intracardiac findings with the 12-lead ECG recorded during the tachycardia resulted in the recognition of ECG patterns characteristic of the different types of supraventricular tachycardias. Currently, gross localization of the site of origin of the arrhythmia is based on the 12-lead ECG recorded during the arrhythmia, with fine-tuning using intracardiac activation mapping and pacing. These developments during the past 3 decades have made accurate arrhythmia diagnosis possible and allow us to offer curative therapies to many of our patients with a supraventricular tachycardia. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1020-1025, September 2003)

Septal Activation in Patients with LBBB and Heart Failure.Introduction: Little is known about the septal activation pattern in patients with heart failure and left bundle branch block (LBBB-HF). Methods and Results: The right ventricular (RV) and left ventricular (LV) activation patterns of 12 patients (mean age 67 ± 11 years) with LBBB-HF and 5 patients (mean age 45 ± 14) with normal hearts were studied during sinus rhythm using a three-dimensional mapping system. The etiology of HF was myocardial infarction (n = 4) or idiopathic dilated cardiomyopathy (n = 8). In patients with LBBB-HF, endocardial activation usually started before the onset of the surface QRS complex on the RV free wall. Latest RV activation occurred in the basal region, and total RV activation time was longer than in patients with normal hearts. In patients with LBBB-HF, the left septum was activated via slowly conducting LBB or via right-to-left transseptal conduction. In both patients with LBBB-HF and those with normal hearts, latest LV activation occurred either in the posterior or posterolateral-basal region. Conduction velocity was slower in the peri-scar region, in patients with previous myocardial infarct and globally slow, in patients with idiopathic dilated cardiomyopathy. Conclusion: The two types of left septal activation observed in patients with LBBB-HF may have consequences for biventricular hemodynamic performance. Conduction slowing along the LV, regionally or globally, suggests a contribution outside the specific conduction system in the ECG pattern of LBBB. (J Cardiovasc Electrophysiol, Vol. 14, pp. 135-141, February 2003)

Atrial Defibrillation Pathway. Introduction: Previous studies have demonstrated significant failure in converting atrial fibrillation (AF) using a conventional ventricular pathway. The aim of this study was to assess the benefit of incorporating a coronary sinus (CS) lead into the atrial defibrillation pathway in atrial defibrillation threshold (ADFT) reduction in patients with persistent AF. Methods and Results: This study was a prospective, randomized assessment of shock configuration on ADFT in 18 patients undergoing elective internal cardioversion for persistent AF (mean AF duration: 8 ′ 9 months). The lead system included a dual-coil defibrillation lead (Endotak DSP, Guidant) with a distal right ventricular (RV) electrode and a proximal superior vena cava (SVC) electrode, a CS lead (Perimeter, Guidant), and a left pectoral cutaneous electrode (Can). In each patient, dual step-up ADFTs were determined for each of three vectors: (1) RV → SVC+Can; (2) CS → SVC+Can; and (3) RV → CS+SVC+Can (group 1, n = 8) or RV+CS → SVC+Can (group 2, n = 10), using R wave-synchronized biphasic shocks. Successful defibrillation was achieved in all patients without any ventricular proarrhythmia. ADFT of CS -> SVC+Can (11.8 ′ 5.6 J) was significantly lower than ADFT of RV → SVC+Can (16.5 ′ 7.8 J, P = 0.021). ADFT of CS → SVC+Can was similar to RV → CS+SVC+Can (group 1: 12.0 ′ 6.5 J vs 17.4 ′ 4.8 J, P = 0.16), but it was significantly higher than RV+CS → SVC+Can (group 2: 9.0 ′ 3.9 J vs 11.6 ′ 5.0 J, P = 0.049). Conclusion: Patients with persistent AF of substantial duration can be reliably cardioverted using a conventional implantable cardioverter defibrillator (ICD) lead set; however, the incorporation of a CS lead to the conventional ICD lead configuration significantly lowered ADFT. The optimal shock vector that incorporates a CS lead for atrial defibrillation requires future studies.

TSE, H.-F., et al.: Effect of Coexisting Cardiovascular Disease on the Long-Term Efficacy and Safety of the Implantable Atrial Defibrillator. The long-term efficacy and safety of implantable atrial defibrillator (IAD) therapy in patients with AF and cardiovascular disease is unclear. The aim of this study was to evaluate the efficacy and safety of IAD therapy in patients with and without coexisting cardiovascular disease. In 115 patients implanted with an IAD, 85 patients had cardiovascular disease: 41 (48%) patients had 1 cardiovascular abnormality, 29 (35%) patients had 2, 13 (15%) patients had 3, and 2 (2%) patients had 4 different cardiovascular abnormalities. The device was programmed into a rhythm monitoring mode for the first 3-month postimplant period. All defibrillation therapy was performed under physician supervision to monitor safety and efficacy. After this initial monitoring period, patients were allowed to activate their device away from the hospital or clinic. A total of 357 spontaneous AF episodes occurred in 83 (72%) patients during observed operation and the mean shock efficacy was 93.5 ± 20.3% (lower 95% confidence interval [CI] 89.8%). As of the last follow-up, 58 (55%) patients had transition to receive nonphysician observed therapy. Forty-two (72%) patients had experienced 332 episodes of AF for which they had received device therapy away from the hospital/clinic (mean shock efficacy 90.5 ± 39.7%). The presence of hypertension, valvular heart disease, and ischemic heart disease did not affect the shock efficacy of the IAD during physician observed and nonobserved therapy (P > 0.05). However, the presence of congestive heart failure was associated with a lower clinical efficacy during observed and nonobserved therapy (P < 0.05). Overall, 5,262 shocks have been delivered with the IAD without any episode of proarrhythmia. The observed proarrhythmic risk was 0%, with an estimated maximum proarrhythmic risk of 0.06% per shock (95% upper CI). A stand-alone IAD appears to be safe in the presence of cardiovascular disease. The lower clinical efficacy for AF associated with congestive heart failure might be related to a higher rate of early reinitiation of AF after defibrillation.

Predictors of Survival in Postinfarct VT. Introduction: The aim of this study was to determine the predictive value of echocardiographic parameters of systolic left ventricular (LV) dysfunction for survival in a group of patients with “mappable” ventricular tachycardia (VT) after myocardial infarction who underwent radiofrequency ablation (RFA) of their clinical VT(s). Methods and Results: RFA of at least one inducible, “mappable,” and clinical VT was attempted in 61 patients. In total, 63 (79%) of 80 target clinical VTs were ablated successfully, such that clinical VT(s) were noninducible in 49 (80%) of 61 patients. At the last recorded follow-up (range 2 to 98 months; mean 21 ± 20), nonfatal VT recurrences were observed in 11 (22%) patients; 10 (16%) patients died. On univariate analysis, a higher LV end-diastolic volume (LVEDV; P = 0.008) and, by multivariate analysis, applying backward selection of variables, older age (P = 0.03) with a higher LVEDV (P = 0.003) predicted patients more likely to die. When age and LV ejection fraction (LVEF) were excluded, LV end-systolic diameter (LVESD; P = 0.007) was the most significant predictor of survival. Conclusion: In our patient population with postinfarct VT who underwent RFA of mappable clinical VT(s), LVEF did not predict survival. In this group of patients with overall low mean LVEF (

Atrial Channel and VT Therapy in ICD. Introduction: Performance of dual chamber implantable cardioverter defibrillator (ICD) systems bas been judged based on functioning of the ventricular tachycardia:supraventricular tachycardia (VT:SVT) discrimination criteria and DDD pacing. The purpose of this study was to evaluate the use of dual chamber diagnostics to improve the electrical and antiarrhythmic therapy of ventricular arrhythmias. Methods and Results: Information about atrial and ventricular rhythm in relation to ventricular arrhythmia occurrence and therapy was evaluated in 724 spontaneous arrhythmia episodes detected and treated by three types of dual chamber K Ds in 41 patients with structural heart disease. Device programming was based on clinically documented and induced ventricular arrhythmias. In ambulatory patients, sinus tachycardia preceded ventricular arrhythmias more often than in the hospital during exercise testing. The incidence of these VTs could be reduced by increasing the dose of a beta-blocking agent in only two patients. In five patients in whom sinus tachycardia developed after onset of hemodynamic stable VT, propranolol was more effective than Class III antiarrhythmics combined with another beta-blocking agent with regard to the incidence of VT and pace termination. In all but three cases, atrial arrhythmias were present for a longer time before the onset of ventricular arrhythmias. During atrial arrhythmias, fast ventricular rates before the onset of ventricular rate were observed more often than RR irregularities and short-long RR sequences. Dual chamber diagnostics allowed proper interpretation of detection and therapy outcome in patients with different types of ventricular arrhythmia. Conclusion: The advantages of the dual chamber ICD system go further than avoiding the shortcomings of the single chamber system. Information from the atrial chamber allows better device programming and individualization of drug therapy for ventricular arrhythmia.

Atrial Arrhythmias in ICD Patients. Introduction: Devices capable of monitoring and treating atrial taihyarrhythmias provide information about the natural history of the arrbythmias and potentially can influence their natural course by electrical therapy early after onset. Methods and results: Types of atrial arrhythmias and efficacy of device therapies were evaluated in 30 patients implanted with the Medtronic model 7250 Jewel AF implantable cardioverter defibrillator (ICD). All patients had structural heart disease and documented sustained ventricular and atrial arrhythmias (27 with atrial fibrillation [AF]) before implant. Twenty patients were taking amiodarone, and three were taking sotalol. During 20 ± 10 months of follow-up, 600 atrial arrhythmia recurrences were documented in 50% of patients. AF was diagnosed in 19%. fast polymorphic atrial tacbycardia (AT) in 20%, fast monomorpbic AT in 57%. and slow AT in 4% of episodes. The two adaptive pacing therapies, burst and ramp, together with the 50-Hz burst, were successful in 57% of delected atrial arrhythmias. Burst and ramp were responsible for 49% and 50-Hz burst for 51% of successfully treated arrbytbmias; 33% of the episodes terminated spontaneously. No ventricular proarrbythmia was observed due to atrial pacing therapies. In 30% of episodes, dual chamber pacing was required due to post termination bradycardia. Atrial arrhythmia recurrences in patients with dilated cardiomyopathy were not amenable to pacing therapies. Several aspects of atrial arrhythmia diagnosis, therapy, and documentation that are specific for functioning of the Jewel AF arc discussed. Conclusion: Atrial arrhythmias in ICD patients with diseased hearts who are taking Class III antiarrbythmics frequently had longer cycle lengths than AF. Half of these arrhythmias could be terminated with pacing therapies; one third terminated spontaneously.

Normally, ventricular APD exceeds the VERP. However, under specific circumstances this relation may change and can become inverse. This phenomenon of postrepolarization refractoriness may be caused by a decrease in excitability. The threshold current (TC) for pacing has never been quantified as a possible explanation for these observations. Using a MAP pacing catheter in the right ventricular apex, the rate dependent behavior of TC, VERP, and APD before and after procainamide (dose 20 mg/kg in 10 min + 5 mg/min infusion) was determined in 17 dogs with chronic complete AV block. Initially, TC was determined with 0.1 mA accuracy. Using a pacing current of at least twice TC, VERP and APD showed a similar, rate dependent shortening for PCLs 800, 575, and 350 ms. Procainamide treatment led to an equal, rate independent VERP and APD increase: no post repolarization refractoriness. Subsequently, accuracy for TC determination was increased to 0.01 mA. Comparing PCLs 800 and 250 ms, TC doubled from 0.05 +/- 0.01 to 0.10 +/- 0.09 mA during control and almost tripled from 0.06 +/- 0.02 to 0.17 +/- 0.10 mA (P < 0.05) after procainamide. Using a fixed pacing current of exactly twice TC found at 800 ms PCL during control, VERP exceeded APD after procainamide treatment at 300 and 250 ms PCL: postrepolarization refractoriness. Increasing the pacing current to twice the rate dependent TC, the relation between VERP and APD normalized: no postrepolarization refractoriness. We conclude that after procainamide, rate dependent TC increase is of major importance for the phenomenon of postrepolarization refractoriness.

We have described the value of the diastolic slope of the MAP recording at the end of a pacing train as a qualifying marker for the induction of delayed afterdepolarization (DAD) dependent arrhythmias. In the present study (1) the behavior of the slope at different time points during a pacing train was quantified and related to the arrhythmogenic outcome (group A) and (2) termination of DAD dependent VT was related to changes in the slope steepness (group B). In dogs with chronic complete AV block, a MAP was recorded during (1) ventricular pacing, before and after ouabain administration (group A) and (2) 6 spontaneous and 6 lidocaine induced VT terminations (group B). During control (group A), the slope at the end of pacing train was 5 +/- 3 m V/s (mean +/- SD), independent of the pacing duration. During ouabain, this increased to 20 +/- 15 mV/s (P < 0.05), varying with the duration of pacing. The slope was steeper after pacing for 4 seconds, compared to 20 seconds (26 +/- 12 mV/s vs 16 +/- 13 mV/s, P < 0.05) which corresponded with more frequent VT induction. In spontaneously terminating VTs (group B), CL increased from 353 +/- 54 ms at the start to 434 +/- 78 ms (P < 0.05) before VT termination. This corresponded with a decreasing steepness of the slope from 19 +/- 10 mV/s to 6 +/- 5 mV/s (P < 0.05). In lidocaine induced VT termination, the CL and the steepness of the slope showed an identical behavior. There is a dynamic variation in the steepness of the diastolic slope during pacing, which depends on the duration of pacing and predicts arrhythmogenic outcome. Furthermore, a decrease in steepness of the slope during DAD dependent VT can be used to predict VT termination.

Electrode Length for Atrial Defibrillation. Introduction: Catheter-based electrodes have been used previously to terminate episodes of atrial fibrillation in animals and man. Typically, these electrodes span 6 to 7 cm, and lowest energy requirements are achieved when these electrodes are positioned in the distal coronary sinus and in the right atrium. The purpose of this study was to evaluate the use of longer electrode lengths for atrial defibrillation. Methods and Results: In 15 patients, two decapolar catheters were inserted, one into the distal coronary sinus and one in the right atrium. To provide longer electrodes lengths, a third catheter was inserted and alternated positioned in the right atrium or coronary sinus. A 6-cm electrode span was obtained by using the distal 8 rings on the coronary sinus catheter or 8 consecutive electrodes on the right atrial catheter and increased from 6 to 11 cm by connecting consecutive, nonoverlapping rings of the third catheter with the 10 rings of the initial right atrial or coronary sinus catheter. Atrial defibrillation thresholds were determined twice, in a randomized order, in each patient for each of the three combinations of electrode lengths. All 15 patients could he successfully converted to sinus rhythm without complications; however, one patient could be converted reproducibly with only 2 of the 3 electrode combinations. Mean thresholds were 306 ± 102 V, 5.9 ± 4.0 J for the 6 cm/6 cm electrode length combination with an impedance of 72 ± 18 ω. For the electrode combination using the 11-cm electrode in the right atrium, the defibrillation threshold was 296 ± 107 V, 5.8 ± 3.9 J with an impedance of 61 ± 17 ω and was 294 ± 91 V, 5.6 ± 3.6 J with an impedance of 55 ± 11 ω for the 11-cm electrode in the coronary sinus. There were no significant differences in defibrillation voltage or energy (P > 0.05) associated with the longer electrode lengths; however, the longer electrode lengths did significantly lower shock impedance (P < 0.05). Conclusion: The use of longer electrodes, when using the right atrium to coronary sinus shock vector, does not lower the defibrillation requirements for restoration of sinus rhythm.

Sudden death can be the first manifestation of the Wolff-Parkinson-White (WPW) syndrome. The underlying mechanism being atrial fibrillation with a very high ventricular rate, because of a short anterograde refractory period of the accessory atrioventricular pathway (AP), deteriorating into ventricular fibrillation. Information on the anterograde refractory period of the AP is therefore important to recognize asymptomatic people with the WPW ECG at risk for dying suddenly. Several noninvasive tests are available to identify the low risk patient. Decision making when to interrupt the AP in asymptomatic WPW patients not at low risk requires an invasive study to document the electrophysiological properties of the AP and to determine its exact location.

We performed radiofrequency catheter ablation of idiopathic ventricular tachycardia in six children. In four, the ventricular tachycardia originated in the left ventricle, in two it originated in the right ventricular outflow tract. In 5/6 (83%) the RF procedure was successful; there were no complications.

Monomorphic VT in HCM. Introduction: Incessant monomorphic ventricular tachycardia (VT) with a right bundle branch block morphology and a northwest axis is a rare arrhythmic complication in a patient with hypertrophic cardiomyopathy and apical left ventricular aneurysm. Methods and Results: The origin of this VT was localized using the following criteria: the presence of entrainment without fusion, equal internals from the stimulus to the beginning of the QRS complex and from the electrogram to the QRS complex during VT, and the first postpacing interval identical to the tachycardia cycle length. Radiofrequency energy applied to the septoapical part of the apical left ventricular aneurysm terminated the tachycardia within 2 seconds. Conclusion: Using criteria to guide radiofrequency (RF) ablation of VT in patients with coronary artery disease, an incessant monomorphic VT in a patient with hypertrophic cardiomyopathy was successfully ablated.

Objectives: To evaluate the expansion ratio of a self-expanding stem over time, and the chronic effect of stent pressure on the vessel wall. Methods: Self-expanding stents, developed by Medtronic Inc. (Minneapolis, MN, USA) and the Rouen group (Letac, Cribier, France), were implanted in 21 normal pig coronary arteries. Animals were sacrificed after recatheterization at 1 day (group I, n = 4), I week (group 2, n = 3), 3 weeks (group 3, n = 5), or 8 weeks (group 4, n = 4). Histological morphometry of the vessel medial and neointimal layers was performed. Changes were related to the, stent diameter and. its force on the vessel wall. Results: The stent expansion ratio gradually increased from 73% to 93% after 8 weeks, which implicates that radial force decreased concomitantly from 0.10 N to 0.03 N. Media compression under the rods ranged from 4l%-66% immediately after stent implantation. The mean compression was unrelated to stent expansion and remained nearly the same (40%-50%) during follow-up. Individual media rod compression ranged from 5%-95%. The neointimal layer on top of the rods increased until the third week after stent implant (neointimal thickness 211 ± 108 μm). The layer significantly decreased at 8 weeks (neointimal thickness 65 ± 9 μm). The cross-sectional neointimal area increased gradually only at the end of the stent during the 8-week follow-up. Conclusions: The self-expanding stent implanted in normal pig coronary arteries reached a gradual relaxation state 8 weeks after implantation due to the persistent radial force. This radial force induces medial wall compression, which was only positively related to the thickness of the neointimal layer at 3 weeks after implant. (J Interven Cardiol 1996;9:45–52)

This study presents a comparison of three different methods for differentiating between supraventricular and ventricular tachycardias with wide-QRS complex. One set of criteria, derived using classical statistical techniques, was compared with two new self-learning computer techniques: the artificial neural networks and the induction algorithm approach. By analyzing the results obtained in an independent test set, using these new techniques, the criteria defined by the classical method could be improved.

Mode switching algorithms have been developed to avoid tracking of atrial fibrillation (AF) or flutter (AFL) during DDD(R) pacing. Upon recognition of AF or AFL, the mode is switched to a nontracking, sensor driven mode. The Vitatron Diamond model 800 pacemaker does this on a beat-to-beat basis. Atrial events occurring within a “physiological range” (± 15 beats/min) calculated from a running average of the atrial rate are tracked. When atrial events are not tracked the escape interval is either determined by the sensor(s) or by a fallback algorithm thereby preventing large increases in V-V interval during mode switching. Loss of atrioventricular (AV) synchrony by atrial premature beats and after an episode of AF or AFL is prevented by atrial synchronization pulses (ASP), which are delivered after a safe interval (timed out from the sensed premature atrial event) has expired and before delivery of the next ventricular stimulus. We implanted 26 such devices in 18 men and 8 women with symptomatic second- or third-degree AV block and paroxysmal AF or AFL. Their ages ranged from 18–84 years (mean 60), and the follow-up ranged from 2–13 months (mean 8). During pacemaker check-up, exercise testing or 24-hour Holter monitoring one or more episodes of mode switching was documented in 8 patients. In these 8 patients a smooth transition (ventricular rate) from sinus rhythm to AF or AFL was documented on one or more occasions, without inappropriate increase in ventricular rate in the DDDR mode. None of the patients complained of palpitations. Appropriate rate response was seen in all patients during Holter monitoring and exercise. Restoration of AV synchrony with ASP was documented many times. In 2 patients the DDIR mode was programmed due to intermittent synchronization of ventricular stimuli to near incessant supraventricular tachycardia, which sometimes gave rise to asymptomatic slightly irregular ventricular paced rhythms below WO beats/min. Recognition of AF or AFL was reliable. No inappropriate increases in ventricular pacing rate were seen at the onset of or during AF or AFL. ASP is an effective method of maintaining AV synchrony and avoiding competitive atrial pacing.

After an abrupt decrease in pacing cycle length (PCL), the ventricular effective refractory period (VERP) shortens. The pacing protocol needed to determine accurate and reproducible values for the VERP during this process is elaborate and time consuming. In this study, steady-state values of VERP at 800 and 350 msec PCL and dynamic values of VERP due to an abrupt change in PCL from 800 to 350 msec were determined. This was done for 11 different dogs to test the interindividual variation and repetitively in the same dog to test the intraindividual variation. The results for steady-state and dynamic values of the VERP show a wide range for both groups. This means that accurate prediction of steady-state and dynamic values of VERP based on previous measurements is not possible.

Mechanism-Specific Action of Levcromakalim. Introduction: The hypothesis that levcromakalim. a potassium channel (IK-ATP.) activator with antihypertensive properties, has a mechanism-specific antiarrhythmic action against repolarization-dependent ventricular tachycardias (VTs) was tested in dogs. Methods and Results: A low dose of leveromakalim (0.01 mg/kg) was selected, which decreased blood pressure by 25% but had almost no electrophysiologic effect on AV nodal or ventricular conduction or effective refractory period. In dogs with chronic AV block, the antiarrhythmic action of this dose of levcromakalim was evaluated in three models of abnormal impulse formation: (I) dsotalol (2 mg/kg) induced torsades de pointes VT, initiated by early afterdepolarizations (EADs). (2) sustained ouabain-induced VTs, which are dependent on delayed after depolarizations (DADs), and (3) VT occurring 24 hours after left anterior descending coronary artery occlusion, which are likely based on abnormal automaticity. Levcromakalim abolished d-sotalol induced U waves, ventricular ectopic beats, and self-terminating bouts of torsades de pointes. Induction of torsades de pointes by pacing was also completely prevented. The cycle length of the idioventricular rhythm, which was lengthened after d-sotalol from 1490 ± 515 to 1700 ± 610 msec (P < 0.05), remained similar after levcromakalim (1655 ± 580 msec). The QT(U) duration, which was increased after d-sotalol from 410 ± 55 to 550 ± 40 msec (P < 0.05), normalized to 405 ± 70 msec (P < 0.05). Lcvcromakulim did not suppress but rather enhanced ouabain-induced VT by decreasing the cycle length slightly from 315 ± 35 to 290 ± 35 msec (P < 0.05). Pretreatment with a beta Mocker prevented this acceleration in rate. Finally, levcromakalim had no effect on VT 24 hours after infarction. Conclusion: A low dose of levcromakalim has specific antiarrhythmic properties against repolarization-dependent arrhythmias, but it does not affect VTs based on other mechanisms of abnormal impulse formation.

In patients with intermittent AV block and dual chamber pacemakers, a long paced AV interval of 200 msec or more can be selected to prolong pulse generator life (by avoiding the ventricular pace output) and to enable a more physiological and hemodynamically superior activation sequence. This case report describes the potential risks of programming a long paced AV interval in a patient with a DDDR pacemaker. T wave pacing, as described here, can occur if the conducted QRS complex is not sensed because it occurs during the ventricular blanking period (delivery of the atrial stimulus). This can be initiated by the mechanisms that induce apparent and actual P wave undersensing of the conducted QRS complex. In this case report apparent P wave undersensing and subsequent T wave pacing with ventricular capture (in a patient with intermittent AV block) occurred frequently during an exercise test done in the DDDR mode with a paced AV interval of 200 msec, according to the clinical evaluation protocol.

During the last decade dynamic cardiomyoplasty has been introduced as a new method to treat patients with severe heart failure. This procedure consists of the wrapping of the latissimus dorsi (LD) muscle around the heart with electrical stimulation of the muscle synchronous to cardiac contraction. The optimal pacing mode of the muscle, during the conditioning and working period of the LD muscle, is still unclear. The pace protocol, currently used worldwide, has a maximal number of muscle tetanic contractions of 100 per minute. Data are presented on the LD muscle contraction characteristics using that protocol. Both force measurements from six in situ stimulated goat LD muscles and x-ray evaluation of the movement of metallic clips on wrapped LD muscles in two patients were used. Results demonstrate that LD muscle force is well maintained at the maximal rate of 100 contractions per minute but relaxation is severely hampered. This may lead to diminished support of the failing heart and damage of the wrapped muscle. A pacing protocol is proposed using a lower maximal stimulation rate.

Radiofrequency Ablation of Multiple Accessory Pathways. A 19-year-old patient is described having three accessory atrioventricular pathways. All three pathways were ablated using radiofrequency current in a single electrophysiologic investigation. (J Cardiovasc Electrophysiol, Vol. 3, pp. 141–149, April 1992)

An atrial defibrillator was implanted in a patient with congenitally corrected transposition of the great arteries, associated cardiac abnormalities, and persistent atrial arrhythmias. During a 15-month follow-up, 14 of 20 spontaneous episodes of his arrhythmias were successfully treated with the device. Two of these episodes were converted to sinus rhythm during ambulatory use of the device. Successful use of the device required implantation of a third defibrillation lead in the persistent left-sided superior caval vein and rigid control of congestive heart failure. An atrial defibrillator may be a valid treatment option in patients with congenital heart disease crippled by atrial fibrillation.

UNLABELLED At the onset of tachycardia, the refractory period (RP) changes together with the tachycardia termination window. We evaluated dogs with total atrioventricular (AV) block to determine if stimulus-T interval (STI) can be used to adjust the coupling interval(s) of an antitachycardia pacemaker in relation to changes in RP. Endocardial STI was recorded continuously together with six surface ECG leads. Steady-state (greater than 2 min) RP was determined for drive cycle lengths (DCL) 400 msec and 900 msec. The test pulse (TP) coupling interval, with DCL 900 msec, was chosen to be equal to the RP of DCL 400 msec. DCL was then changed to 400 msec until TP captured. STI of DCL of beat before capture was gained was measured. DCL was then changed back to 900 msec and the interval determined when capture was lost. TP was then lengthened by 5 msec and the procedure repeated until TP captured immediately upon changing to DCL 400 msec. RESULTS The difference between RP at onset of pacing at DCL of 400 msec and RP when capture was achieved with the shortest coupling interval was 35-50 (mean 40) msec. This required 35-90 (mean 62) seconds. The correlation coefficient RP to STI was greater than 0.95. CONCLUSIONS (1) RP changed by as much as 35-50 msec at the onset of an abrupt increase in rate in a 35-90-second period; and (2) STI enables estimation of RP on a beat-to-beat basis. Capture can therefore be predicted from the previous beat and the coupling interval adjusted accordingly in an antitachycardia pacing mode.

Alterations in vagal tone can influence the atrial fibrillatory process by changing the atrial refractory period. We observed in a patient with paroxysmal atrial fibrillation (AF) that carotid sinus massage (CSM) changed a "coarse" type of fibrillation into a "fine" type, followed by termination of the arrhythmia. Although coincidental conversion of AF into sinus rhythm could not be excluded, we concluded that it is worth while to try CSM in every patient presenting with AF prior to other interventions to restore sinus rhythm.

Variants of ventricular preexcitation : , Variants of ventricular preexcitation : , کتابخانه دیجیتال جندی شاپور اهواز

In a patient with chronic congestive heart failure, right bundle branch block-shaped QRS complexes occurred in salvos during atrial fibrillation. The site of origin of these complexes could not be determined from the 12-lead ECG alone. Recording of a His bundle electrogram showed that both intraventricular aberrant conduction and ventricular tachycardia were responsible for salvos having the same QRS complexes in the 12-lead ECG.

Pacemaker circus movement tachycardia (PCMT) was a significant problem in first generations of DDD pacemakers. Programmability of the atrial refractory period proved to he an elective tool to prevent PCMT except in patients with very long ventriculoatrial (V-A) conduction intervals, because a long atrial refractory period severely limits the maximum tracking rate. In these patients, extension of the atrial refractory period after a VPB, bipolar atrial sensing, adaptation of atrial refractory period to atrial rate, and VPB synchronous atrial stimulation helped limit the incidence of PCMT. Rate smoothing and fallback behavior have given rise to other forms of PCMT. Once initiated, PCMT can be terminated by a single P wave or by means of an appropriately timed atrial stimulus. Recognition by means of continued upper rate pacing may not be helpful in patients with a long V-A conduction interval because their PCMT rate will be low, thus requiring a low upper rate to trigger. Therefore, (1) absolute prevention of PCMT has not yet been achieved, but PCMT is no longer a significant problem in DDD pacing; (2) recognition of PCMT should not be related to the ventricular upper rate limit.

For over twenty years computer programs have been written for applications in cardiology. Approximately one decade ago the first Expert Systems using knowledge on cardiology were built. The use of Expert System shells enabled a breakthrough. Many systems were developed, each covering a small part of cardiology. In the pacing environment Expert Systems can be used to select the optimal pacemaker therapy or to analyze complex pacemaker electrocardiograms. With the help of these artificial intelligence techniques pacemakers can be designed, that behave in an intelligent way. Finally this knowledge representation enables the reproducible simulation of the heart-pacemaker interaction.

Pacing is becoming an accepted form of treatment for reentry tachycardias. The different pacing modalities available and experience with a patient-activated antitachycardia pacemaker are presented in this paper. This system has bidirectional communication between pacemaker and pacemaker-activator and between pacemaker and prescription formulator (which is a sophisticated portable stimulator used for non-invasive electrophysiological evaluation of the system). This pacemaker was implanted in 18 patients with drug-resistant tachycardias. Six patients had ventricular tachycardia, 3 had A-V nodal reentrant tachycardia, 4 had the concealed accessory pathway, and 5 had the WPW syndrome. In the 3 months before implantation the mean number of admissions for termination of tachycardia was 2.1 per patient-month. During a follow-up period of 3–26 months only 6 patients were admitted once for termination of tachycardia (0.02 admissions per patient-month). The reasons for admission of these 6 patients were: defective pacemaker activator in 2 patients, inadequate control of tachycardia in 2 patients, inappropriate use of the device in 1, and inadequate intake of medication in 1. All these problems were solved easily. Eight pacemaker activators required reprogramming, which was done in 5 patients on an out-patient basis. The interval scanning mode was used in 9 patients. Nine patients required more than 2 stimuli for reproducible termination. A step-wise increase in number of stimuli was used in 5 patients. This system has proven to be a safe and effective form of treatment of drug-resistant supraventricular and ventricular tachycardias and has resulted in marked improvement of the quality of life of these patients.

DDD pacemakers were implanted in 11 patients of whom 5 had the capacity to conduct retrogradely to the atrium. Methods to prevent or terminate pacemaker circus movement tachycardia ( PCMT ) were evaluated in these patients. V-A conduction was assessed before implantation by incremental right ventricular pacing while recording right atrial electrograms. Following implantation and at quarterly outpatient clinic visits, V-A conduction and ability to initiate and sustain PCMT were systematically assessed by non-invasive techniques. PCMT could be induced non-invasively in all 5 patients. The methods used to reduce and terminate the incidence of PCMT were: 1) decreasing the atrial sensitivity; 2) stressing the V-A conduction system by programming a high upper rate with an appropriately short A-V interval; 3) programming a low lower rate; 4) avoiding the Wenckebach response (by programming a high upper rate); 5) medication; and 6) occasionally by using a magnet. PCMT was controlled in all patients, in 2 patients by programming measures only and in 2 with the addition of medication. One patient who refused medication had to be programmed into another pacing mode. We conclude that: 1) the presence of V-A conduction is not an absolute contraindication to the use of a DDD pacing system; 2) pacing the ventricle early enough to cause V-A block was the most useful method to terminate PCMT ; 3) future generation DDD pacemakers should prevent initiation of PCMTs while maintaining the possibility to synchronize to exercise-induced high atrial rates.

A description is given of a mathematical model of impulse conduction through the heart. The model can be used to evaluate the best pacing mode for the individual patient and to develop new pacemakers. This allows study of the influence of different parameters related to the behavior of the heart or pacemaker. Two examples using a model of a DDD pacemaker and two examples describing simulation of an antitachycardia pacing system are given to illustrate how the performance of pacemakers under different conditions can be simulated.

A patient who received a patient-activated pacemaker system for termination of paroxysmal, drug-resistant, ventricular tachycardia is described. During the pre-implant invasive electrophysiological (EP) study and the three post-implant non-invasive EP studies, tachycardias were easily and reproducibly terminated by two stimuli using the interval scanning mode. On the fourth day post-implant, this pacing mode no longer terminated tachycardia at rest. A new pacing mode using more stimuli was then found to terminate the tachycardia reproducibly under various physiological conditions. This case report demonstrated a spontaneous change in the tachycardia terminating window and the usefulness of versatility in antitachycardia pacemaker systems.

During digitalis-induced, sustained, monomorphic ventricular tachycardia, programmed electrical stimulation was performed and the effect on the first post-pacing QRS morphology was determined. Ventricular tachycardia was induced in nine conscious dogs with chronic complete atrioventricular block by administering digoxin i.v. 0.1 mg/kg given in 1-1 1/2 hour. Spontaneous ventricular tachycardia most frequently had a right bundle branch block morphology and an extreme left axis suggesting an origin in the apex of the left ventricle. Less frequently, a left bundle branch block-like configuration with an intermediate axis was observed, compatible with an origin in the basal part of the right ventricle. Following pacing close to one of these predilection sites, the first post-pacing QRS morphology suggested an origin close to the site of stimulation. Pacing distant from these predilection sites resulted in fusion complexes between electrical activation from these predilection sites and the stimulation site. The amount of fusion depended on interstimulus interval and the number of stimuli. Long interstimulus intervals and few stimuli induced a QRS complex similar to that of the spontaneous tachycardia. The faster and longer the stimulation train, the more the QRS complex became similar to the paced QRS complex. Similar findings were also observed on decreasing the last paced interval only. Our findings suggest that triggered activity is the underlying mechanism for the first post-pacing QRS complex. QRS configuration and the relation between the R-R interval and QRS configuration during tachycardia suggest that triggered activity is also the mechanism for the spontaneously occurring ventricular tachycardia during digitalis intoxication. These observations may have important clinical implications.

Termination of atriovontricular nodal (A VN) re-entrant tachycardia by one or two induced premature beats generally occurs within one tachycardia cycle from the last premature beat. Two cases are described in which programmed stimulation during sustained re-entrant AVN tachycardia caused delayed termination in the second or third tachycardia cycle following the extrastimuli. The site of block was the antegrade pathway in one case and the retrograde pathway in the other. The most likely mechanism was induced second degree block in one limb of the tachycardia circuit. Delayed termination provided evidence for concealed penetration of the tachycardia circuit in one case. We conclude that delayed termination of tachycardia is not an indicator of the underlying mechanism of tachycardia. Delayed termination may reveal concealed penetration of the tachycardia circuit. Lastly, in unusual cases programmed stimulation may fail to cause immediate termination of re-entrant tachycardia but may perturb the tachycardia circuit enough to cause termination in subsequent tachycardia cycles.

A patient who received an AAI Activitrax rate variable pacemaker for treatment of symptomatic sinus bradycardia is described. disopyramide prolonged the anterograde effective refractory period of the fast conducting atrioventricular (AV) nodal pathway to such an extent, that conduction switched to the slow AV nodal pathway at low atrial pacing rates. This gave rise to symptoms of the pacemaker syndrome during moderate exercise because the paced atrial event was conducted with a long, spike to Q interval with occurrence of the paced atrial event just after the preceding QRS complex. A change of medication solved this problem. Programming a bipolar electrode configuration avoided sensing of far-field QRS signals with the associated problems of resetting the basic pacing interval as well as the upper rate interval. AAI rate variable pacing requires careful evaluation of AV conduction properties, AV conduction intervals as well as the influence of medication to be given. The use of multiprogrammable pacemakers with marker channel capability will significantly facilitate the understanding and resolution of anomalous behavior.

Different mechanisms of block of impulse propagation in several re-entrant circuits resulted in a major discordance between the "echo-zone" and the "tachycardia-zone" in a patient with intermittent Wolff-Parkinson-White syndrome, dual atrioventricular nodal pathways, and bundle branch re-entry. This case illustrates the delicate balance in electrophysiological properties required between the tissues incorporated in a re-entrant circuit to initiate and sustain the arrhythmia. It also shows how the presence of several reentrant pathways can lead to refractoriness in the circuit responsible for the circus movement tachycardia.