Arrhythmogenic response to isoproterenol testing vs. exercise testing in arrhythmogenic right ventricular cardiomyopathy patients.

Aims: To compare the arrhythmic response to isoproterenol and exercise testing in newly diagnosed arrhythmogenic right ventricular cardiomyopathy (ARVC) patients. Methods and results: We studied isoproterenol [continuous infusion (45 µg/min) for 3 min] and exercise testing (workload increased by 30 W every 3 min) performed in consecutive newly diagnosed ARVC patients. Both tests were evaluated with regard to the incidence of (i) polymorphic premature ventricular contractions (PVCs) and couplet(s) or (ii) sustained or non-sustained ventricular tachycardia (VT) with left bundle branch block [excluding right ventricular outflow tract VT]; and compared to a control group referred for the evaluation of PVCs without structural heart disease. Thirty-seven ARVC patients (63.5% male, age 38 ± 16 years) were included. The maximal sinus rhythm heart rate achieved during isoproterenol testing was significantly lower compared to exercise testing (149 ± 17 bpm vs. 166 ± 19 bpm, P < 0.0001). However, the incidence of polymorphic ventricular arrhythmias was much higher during isoproterenol testing compared to exercise testing [33/37 (89.2%) vs. 16/37 (43.2%), P < 0.0001]. Interestingly, isoproterenol testing was arrhythmogenic in all 15 patients in whom baseline PVCs were reduced or suppressed during exercise testing. During both isoproterenol and exercise testing, control group presented a low incidence of ventricular arrhythmias compared to ARVC patients (8.1% vs. 89.2%, P < 0.0001 and 2.7% vs. 43.2%, P < 0.0001, respectively). Conclusions: The incidence of polymorphic ventricular arrhythmias is significantly higher during isoproterenol compared to exercise testing in newly diagnosed ARVC patients, suggesting its potential utility for the diagnosis.

Prevalence, characteristics, and prognosis role of type 1 ST elevation in the peripheral ECG leads in patients with Brugada syndrome.

BACKGROUND: Despite isolated reports of Brugada syndrome (BrS) in the inferior or lateral leads, the prevalence and prognostic value of ST elevation in the peripheral electrocardiographic (ECG) leads in patients with BrS remain poorly known. OBJECTIVE: To study the prevalence, characteristics, and prognostic value of type 1 ST elevation and ST depression in the peripheral ECG leads in a large cohort of patients with BrS. METHODS: ECGs from 323 patients with BrS (age 47 ± 13 years; 257 men) with spontaneous (n = 141) or drug-induced (n = 182) type 1 ECG were retrospectively reviewed. Two hundred twenty-five (70%) patients were asymptomatic, 72 (22%) patients presented with unexplained syncope, and 26 (8%) patients presented with sudden death (12 patients) or appropriated implantable cardioverter-defibrillator therapies (14 patients) at diagnosis or over a mean follow-up of 48 ± 34 months. RESULTS: Thirty (9%) patients presented with type 1 ST elevation in at least 1 peripheral lead (22 patients in the aVR leads, 2 in the inferior leads, 5 in both aVR and inferior leads, and 1 in the aVR and VL leads). Patients with type 1 ST elevation in the peripheral leads more often had mutations in the SCN5A gene, were more often inducible, had slower heart rate, and higher J-wave amplitude in the right precordial leads. Twenty-seven percent (8 of 30) of the patients with type 1 ST elevation in the peripheral leads experimented sudden death/appropriate implantable cardioverter-defibrillator therapy, whereas it occurred in only 6% (18 of 293) of other patients (P < .0001). In multivariate analysis, type 1 ECG in the peripheral leads was independently associated with malignant arrhythmic events (odds ratio 4.58; 95% confidence interval 1.7-12.32; P = .0025). CONCLUSIONS: Type 1 ST elevation in the peripheral ECG leads can be seen in 10% of the patients with BrS and is an independent predictor for a malignant arrhythmic event.

Electrical storms in Brugada syndrome: review of pharmacologic and ablative therapeutic options.

Electrical storm occurring in a patient with the Brugada syndrome is an exceptional but malignant and potentially lethal event. Efficient therapeutic solutions should be known and urgently applied because of the inability of usual antiarrhythmic means in preventing multiple recurrences of ventricular arrhythmias. Isoproterenol should be immediately infused while oral quinidine should be further administrated when isoproterenol is not effective. In case of failure of these therapeutic options, ablation of the triggering ventricular ectopies should be attempted.

[Mapping and ablation of malignant ventricular arrhythmias]. / Cartographie et ablation des arythmies ventriculaires malignes.

Endocavitary investigations showed that the ventricular extrasystoles originated in the common ventricular myocardium (pulmonary infundibulum) in only 9 cases whereas the majority arose from the Parkinje system either on the anterior wall of the right ventricle or in septal region of the left ventricle. The extrasystoles arising from the Parkinje system and pulmonary infundibulum differed in their duration and polymorphism (128 +/- 18 ms vs 145 +/- 13 ms, p = 0.05; 3.3 +/- 2.7 morphologies vs 1.1 +/- 0.4, p < 0.001, respectively). During the extrasystoles, the local Pukinje potential preceded the ventricular activation by variable intervals, some of which were very long, up to 150 ms. Seven applications of radiofrequency were delivered on average per patient on the most distal part of the Purkinje system leading to ablation of the specific activation. The clinical results were spectacular: 88% of patients had no further episodes of ventricular fibrillation as demonstrated by analysis of the defibrillator with an average follow-up period of more than 34 months.

[The place of ablation in the treatment of atrial fibrillation: where are we and where are we going?]. / Place de l'ablation dans le traitement de la fibrillation auriculaire: où en sommes-nous? où allons-nous?

Atrial fibrillation, the most common arrhythmia, is frequently disabling and drug resistant and is associated with significant complications, especially thromboembolic events. Non-pharmacological approaches including surgery and catheter-based ablation have been developed for the most symptomatic patients. These new treatment strategies have dramatically increased our knowledge of the pathophysiology of this arrhythmia but most importantly have demonstrated that atrial fibrillation is curable. Since 1994, 2 different concepts have been used, aiming to modify the substrate responsible for AF maintenance using linear lesions, or to ablate the triggers located from within the pulmonary veins (PV) in about 90% of cases. The vast majority of the laboratories in the world are now using approaches centred on isolation of the PV. These approaches are far from being perfect but good enough to be offered in routine practice to selected patients in experienced centres. The importance of PVs in the initiation of AF has been clearly demonstrated and they also have a possible role in the maintenance of AF. However, the existence of non venous foci or a prominent substrate for AF maintenance limits the success rate to about 70%. As a consequence, a combination of PV isolation and linear lesions is commonly used. This more complex procedure carries a significantly higher success rate however with an increased risk of tamponade. As a consequence, we need to identify which patients will require linear lesions in addition to PV isolation. At the present time, AF ablation is restricted to symptomatic patients who have failed at least 1-2 antiarrhythmic drugs but future technical improvements based on presently applied concepts are likely to widen the indications for ablation therapy of AF.

[Role of radiofrequency ablation in atrial fibrillation]. / Place de l'ablation par radiofréquence dans la fibrillation auriculaire.

Atrial fibrillation is the most frequently encountered arrhythmia in the human species. Its danger is widely appreciated but it remains for certain patients and their practitioners an awkward or even exasperating problem. Only surgery and radiofrequency ablation allow certain patients to be cured. The surgical approach is of course warranted in the case of an otherwise necessary cardiac intervention. In the absence of a surgical indication, endovenous ablation, which is less aggressive, is preferred. The procedure consists of disconnecting the pulmonary veins which "house" 80 to 95% of the foci, together with the ablation of further non-venous foci, which are always difficult to treat. Side effects in experimental centres are rare and 70% of patients are cured, which allows cessation of antiarrhythmic and anticoagulant treatments. The procedure is currently offered to symptomatic patients having had at least one episode every ten days in spite of antiarrhythmics.

Electrophysiological breakthroughs from the left atrium to the pulmonary veins.

BACKGROUND: The extent of ostial ablation necessary to electrically disconnect the pulmonary vein (PV) myocardial extensions that initiate atrial fibrillation from the left atrium has not been determined. METHODS AND RESULTS: Seventy patients underwent PV mapping with a circumferential 10-electrode catheter during sinus rhythm or left atrial pacing. After assessment of perimetric distribution and activation sequence of PV potentials, ostial ablation was performed at segments showing earliest activation, with the end point of PV disconnection. A total of 162 PVs (excluding right inferior PVs) were ablated. PV potentials were present at 60% to 88% of their perimeter, but PV muscle activation was always sequential from a segment with earliest activation (breakthrough). Radiofrequency (RF) application at this breakthrough eliminated all PV potentials in 34 PVs, whereas a secondary breakthrough required RF applications at separate segments in 77; in others, >2 segments were ablated. A median of 5, 6, and 4 bipoles from the circular catheter were targeted in the right superior, left superior, and inferior PVs, respectively, to achieve PV disconnection. Early recurrence of arrhythmia was observed in 31 patients as a result of new venous or atrial foci or recovery of previously targeted PVs, most related to a single recovered breakthrough that was reablated with local RF application. CONCLUSIONS: Although PV muscle covers a large extent of the PV perimeter, there are specific breakthroughs from the left atrium that allow ostial PV disconnection by use of partial perimetric ablation.

Mapping and ablation of left atrial flutters.

BACKGROUND: Typical right atrial isthmus-dependent flutters have been described in detail, but very little is known about left atrial (LA) flutters. METHODS AND RESULTS: We performed conventional and 3D mapping of the LA for 22 patients with atypical flutters. Complete maps in 17 patients demonstrated macroreentrant circuits (n=15) with 1 to 3 loops rotating around the mitral annulus, the pulmonary veins, and a zone of block or a silent area. In 2 patients, a small reentry circuit with a zone of markedly slow conduction was identified. Linear ablation performed across the most accessible part of the circuit cured 16 patients (73%) with a follow-up of 15+/-7 months. CONCLUSIONS: LA reentrant tachycardias are related to individually varying circuits and are amenable to mapping guided radiofrequency ablation.

High-density mapping of activation through an incomplete isthmus ablation line.

BACKGROUND: Activation mechanisms through gaps in ablation lines and resulting electrograms are poorly understood. METHODS AND RESULTS: Eight patients (all men; age, 59+/-9 years) were studied during a recurrence of typical atrial flutter (cycle length, 233+/-19 ms) after a previous catheter ablation in the cavotricuspid isthmus. High-density 3-dimensional mapping of the isthmus was performed with the Cordis-Biosense EP Navigation system, and local conduction velocity (CV) was estimated. Maps created with 96+/-19 points revealed 0.8+/-0.3-cm gaps of recovered conduction in the ablation line. A broad wave front entered the lateral isthmus with a CV of 1.8+/-0.7 m/s, halted on the lesion line, and penetrated slowly through the gap with a CV of 0.3+/-0.1 m/s. Activation then curved and returned antidromically to activate the downstream flank of the line with a CV of 1.1+/-0.7 m/s. This front fused downstream of the line with slow transverse activation (CV, 0.4+/-0.3 m/s) parallel to it. The ablation line was demarcated by an incomplete line of convergent double potentials with isoelectric intervals (from 123+/-34 to 62+/-16 ms); each potential corresponded to local activation upstream and downstream of the lesions, while the intervening delay was produced by slow conduction through the gap combined with the progressively longer curved pathway of downstream antidromic activation as a function of distance from the gap. CONCLUSIONS: High-density isthmus mapping during recurrent flutter indicates slow conduction through gaps of recovered conduction of varying dimensions in the ablation line followed by a curved front of activation antidromically activating its downstream flank, this detour producing wide double potentials on the line.

A focal source of atrial fibrillation treated by discrete radiofrequency ablation.

BACKGROUND: Atrial fibrillation is usually thought to be due to multiple circulating reentrant wavelets. From previous studies, a focal mechanism is considered to be very unlikely. In this report, focal atrial fibrillation is defined on an ECG pattern of atrial fibrillation and later demonstrated to be due to a focal source. METHODS AND RESULTS: Nine patients (five men and four women, age, 38 +/- 7 years) with paroxysmal focal atrial fibrillation are reported here. All were free of structural heart disease and had frequent episodes of atrial fibrillation despite the use of a mean of 4 +/- 2 antiarrhythmic drugs. Atrial fibrillation was associated with runs of irregular atrial tachycardia or monomorphic extrasystoles. The electrophysiological study demonstrated that all the atrial arrhythmias were due to the same focus firing irregularly and exhibiting a consistent and centrifugal pattern of activation. Three foci were found to be located in the right atrium, two near the sinus node and one in the ostium of the coronary sinus. Six others were located in the left atrium at the ostium of the right pulmonary veins (n = 5) and at the ostium of the left superior pulmonary vein (n = 1). All atrial arrhythmias were successfully treated by use of a mean of 4 +/- 4 radiofrequency pulses. CONCLUSIONS: In some patients, the surface ECG pattern of atrial fibrillation is due to a focal rapidly firing source of activity that can be eliminated by discrete radiofrequency energy applications.