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AimsSeveral procedural and electrocardiogram (ECG) parameters have been associated with the occurrence of high-degree atrioventricular block (AVB) requiring permanent pacemaker implantation (PPI) after transcatheter aortic valve replacement (TAVR). We hereunder sought to assess if the baseline R-wave amplitude in V1 ECG lead of patients with normal QRS duration undergoing TAVR is associated with a higher patient’s risk for developing high-degree AVB following left bundle branch block (LBBB).Methods and resultsIn this retrospective single-centre study in 720 consecutive patients who underwent TAVR, 141 (19.6%) patients with normal QRS duration developed a new LBBB after TAVR. The 24 (17%) patients who underwent PPI for reasons other than high-degree AVB were excluded from further analysis. In the remaining 117 study patients, 14 (12%) developed high-degree AVB requiring PPI (Group 1) while the remaining 103 (88%) patients did not (Group 2). There were no significant differences in baseline demographic or procedural characteristics nor in PR interval, QRS duration, and QRS axis between these two groups. The incidence of left anterior hemiblock was higher in Group 1 (3 of 14, 21.4%) than that in Group 2 (9 of 103, 8.7%), but the difference was not statistically significant (P = 0.156). The R-wave amplitude in V1 was smaller in Group 1 than that in Group 2 (0.029 ± 0.04 mV vs. 0.11 ± 0.14 mV, P = 0.0316). In the receiver-operating characteristics analysis, the cutoff for R-wave amplitude pre-TAVR was 0.03 mV, area under the curve = 0.7219 (P = 0.0002).ConclusionThe R-wave amplitude in lead V1 during baseline ECG in patients with normal QRS duration may predict the occurrence of high-degree AVB following new LBBB after TAVR.

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Background Arrhythmogenic ventricular cardiomyopathy (AC) is a genetic progressive disease characterized by fibro-fatty replacement of either ventricles in isolation or in combination. Arrhythmogenic ventricular cardiomyopathy is frequently associated with ventricular tachycardia (VT) having a left bundle branch block (LBBB) morphology and much more rarely with VT having right bundle branch block (RBBB) morphology even when the left ventricle is involved. Cardiac magnetic resonance (CMR) imaging plays a key role in the diagnosis of AC. Sustained VT in AC may occur in the concealed stage of the disease before the manifestation of morphological abnormalities on echocardiogram; however, they almost always are accompanied by structural abnormalities of the ventricles on CMR. Case summary A 54-year-old man presented with sustained VT of LBBB configuration consistent with the diagnosis of AC but with no right ventricular (RV) anomalies at repeat CMR. Ten years later, he developed sustained VT with RBBB morphology and structural changes at CMR compatible with RV involvement in the setting of AC. Two years later, he suffered from recurrent identical sustained RBBB-VT with typical CMR signs of left ventricular involvement. Genetic analysis was negative for any known mutation. Discussion In the present report, we describe a patient with AC who first exhibited LBBB- and 10 years later RBBB-sustained VT. Contrasting with what is usually observed in patients with AC, documentations of the VT’s arising from either ventricle were found to precede the structural anomalies in the respective cardiac chambers. This case highlights that normal CMR does not exclude underlying AC contrary to the perceptions of many clinicians. In addition, it strongly encourages repeating CMR after 1–2 years when the diagnosis of AC is highly suspected.

Aims We recently reported that patients with coronary artery disease (CAD) who develop polymorphic ventricular tachycardia (VT) during the healing phase of an acute coronary event, generally fail to respond to revascularization or standard antiarrhythmic therapy but respond immediately to quinidine therapy. Here, we describe that CAD patients presenting with out-of-hospital polymorphic VT without a recent coronary event or an obvious precipitating factor, also respond uniquely to quinidine therapy. Methods and results Retrospective study of patients with unheralded, mainly out-of-hospital, polymorphic VT related to CAD but without evidence of acute myocardial ischaemia. We identified 20 patients who developed polymorphic VT without precipitating factors. The polymorphic VT events were triggered by extrasystoles with short (376 ± 49 ms) coupling interval. Arrhythmic storms occurred in 70% patients. These arrhythmic storms were generally refractory to conventional antiarrhythmic therapy but invariably responded to quinidine therapy. Revascularization was antiarrhythmic in 3 patients despite the absent clinical or ECG signs of ischaemia. During long-term follow-up (range 2 months to 11 years), 3 (15%) of patients not receiving quinidine developed recurrent polymorphic VT. There were no recurrent arrhythmias during long-term quinidine therapy. Conclusions Patients with CAD may develop polymorphic VT in the absence of obvious acute ischaemia or apparent precipitating factors, presenting as out-of-hospital polymorphic VT with high risk of arrhythmic storms that respond uniquely to quinidine therapy.

Aims In arrhythmogenic cardiomyopathy (ACM) sustained monomorphic ventricular tachycardia (VT) typically displays left bundle branch block (LBBB) morphology. Sustained VT with right bundle branch block (RBBB) morphology is very rare despite the frequent left ventricular involvement. The present study sought to assess the prevalence of spontaneous sustained LBBB-VT, RBBB-VT or both as well as clinical and genetic differences associated with these VT types. Methods and results Twenty-six centers from 11 European countries provided information on 952 patients with ACM and >1 episode of sustained VT observed during the patients' clinical course. VT was classified as: LBBB-VT; RBBB-VT or LBBB+RBBB-VT. Among 952 patients, 881 (92.5%) had LBBB-VT alone, 71 (7.5%) had RBBB-VT [alone in 42 (4.4%) patients or with LBBB-VT in 29 (3.0%) patients]. Male prevalence was 90.5%, 79.2% and 55.9% in the RBBB-VT, LBBB-VT and LBBB+RBBB-VT groups, respectively (P=0.001). Patients' age at first VT did not differ amongst the 3 VT groups. ICD implantation was more frequent for the RBBB-VT and the LBBB+RBBB groups (≈90% each) vs. 67.9% for the LBBB-VT group (P=0.001). Death incidence (9.5%–17.2%) was not significantly different between the 3 groups (P=0.425). Plakophylin-2 mutations predominated in the LBBB-VT and LBBB-VT+RBBB-VT groups (47.2% and 27.3%, respectively) and Desmoplakin mutations in the RBBB-VT group (36.7%). Conclusion This large European survey demonstrates: 1) Sustained RBBB-VT is documented in 7.5% patients with ACM; 2) Males markedly predominate in the RBBB-VT and LBBB-VT groups but not in the LBBB+RBBB VT group; 3) Distribution of desmosomal mutations appears to be different in the 3 VT groups. Funding Acknowledgement Type of funding source: None

Aims: Data on predictors of time-to-first appropriate implantable cardioverter-defibrillator (ICD) therapy in patients with Brugada Syndrome (BrS) and prophylactically implanted ICD's are scarce.Methods and results: SABRUS (Survey on Arrhythmic Events in BRUgada Syndrome) is an international survey on 678 BrS patients who experienced arrhythmic event (AE) including 252 patients in whom AE occurred after prophylactic ICD implantation. Analysis was performed on time-to-first appropriate ICD discharge regarding patients' characteristics. Multivariate logistic regression models were utilized to identify which parameters predicted time to arrhythmia ≤5 years. The median time-to-first appropriate ICD therapy was 24.8 ± 2.8 months. A shorter time was observed in patients from Asian ethnicity (P Conclusion: First appropriate therapy in BrS patients with prophylactic ICD's occurred during the first 5 years in 76.6% of patients. Syncope and spontaneous Type 1 Brugada ECG correlated with a shorter time to ICD therapy.

We present a 34-year-old patient with recurrent episodes of drug refractory paroxysmal atrial fibrillation referred for pulmonary vein (PV) isolation at our institution. During isolation of the right superior PV, a dissociated escape rhythm was observed on a portion of the PV that was disconnected, while the rest of the PV showed clear left atrium to PV conduction. This report demonstrates the rare possibility of escape PV rhythm from only partially disconnected PV, highlighting that dissociated PV rhythm does not necessarily reflect complete PV isolation.

A 15-year-old girl with no obvious heart disease and frequent episodes of paroxysmal supraventricular tachycardia (PSVT) underwent electrophysiological study with radiofrequency ablation. Her resting electrocardiogram showed prominent R waves in right precordial leads without obvious pre-excitation (PR=0·16 s) [Fig. 1(a)]. Both right atrial and coronary sinus pacing showed exclusive antegrade conduction over the atrioventricular (AV) node. Sustained AV re-entrant tachycardia (AVRT) at a rate of 220 bpm was reproducibly induced with atrial pacing. The sequence of atrial activation during AVRT suggested the existence of a concealed left lateral accessory pathway. Radiofrequency ablation of the pathway was attempted via a patent foramen ovale during AVRT using a temperaturecontrolled ablation catheter (temperature set at 72 C). At the fifth radiofrequency pulse, AVRT terminated after 4·5 s due to retrograde block in the accessory pathway. A wide QRS complex tachycardia immediately developed upon termination of AVRT (Fig. 2). This tachycardia had a right bundle branch block morphology with right axis, was regular at 190 bpm [Fig. 1(b)], and persisted as long as the radiofrequency pulse lasted (60 s). A few minutes later, conduction over the accessory pathway resumed and AVRT was induced again. Another radiofrequency pulse was administered at the mitral valve annulus at a site very close to the previous site. Again, AVRT terminated after 2·5 s and a regular, wide QRS complex tachycardia, identical in morphology, rate and regularity to that induced previously, was observed and persisted as long as the radiofrequency pulse lasted (60 s). Subsequent right and left ventricular pacing showed exclusive retrograde AV nodal

The clinical significance of sustained nonclinical ventricular tachycardia (VT) induced during electrophysiologic studies was studied in 10 amiodarone-treated patients. Nine patients had previous myocardial infarction while 1 patient had right ventricular dysplasia. All patients had only a single morphologic type of VT recorded during the multiple spontaneous episodes of tachycardia. After serial pharmacological electrophysiologic testing, the patients were placed on antiarrhythmic regimens which included amiodarone in all cases. These drugs did not prevent the induction of nonclinical VT in any of the 10 patients and of sustained clinical VT in 7 patients. Nonclinical VT was sustained, requiring cardioversion (7 patients) or rapid ventricular pacing (3 patients) for termination. After a mean follow-up period of 27 +/- 10 months (range 12 to 36 months), 4 patients did not exhibit recurrent VT, 3 patients with inducible clinical VT experienced a recurrent episode of clinical VT after 16, 27 and 49 months, respectively, 2 patients had nonarrhythmia related deaths after 11 and 12 months, and 1 patient died suddenly after 17 months. These results suggest that laboratory induction of sustained nonclinical VT in amiodarone-treated patients does not imply the likelihood of their future spontaneous occurrence and, therefore, their prevention may not be required.

The influence of aminophylline, a competitive antagonist of adenosine, on the chronotropic and dromotropic effects of adenosine and adenosine triphosphate was studied in pentobarbital anaesthetised dogs under various modifications of the autonomic nervous tone. Adenosine and adenosine triphosphate (3 mumol.kg-1 each) were rapidly (greater than or equal to 1 s) injected into the right atrium during both sinus rhythm and right atrial pacing (cycle length 300 ms) before and after infusion of aminophylline (5 mg.kg-1) (n = 21) as well as after increasing doses of aminophylline (n = 10). Some dogs underwent either muscarinic blockade with atropine (0.2 mg.kg-1) (n = 10), or beta adrenergic blockade with propranolol (1 mg.kg-1) (n = 10), or complete autonomic blockade with atropine and propranolol (n = 10). Aminophylline (5 mg.kg-1) antagonised the negative chronotropic and dromotropic effects of adenosine triphosphate and adenosine in dogs pretreated with atropine or atropine plus propranolol but did not affect them in autonomically intact dogs. In addition, the electrophysiological effects of adenosine were antagonised by only the highest doses of aminophylline in autonomically intact dogs and by aminophylline (5 mg X kg-1) in dogs pretreated with propranolol. It was concluded that (a) alteration of the electrophysiological effects of adenosine triphosphate and adenosine by aminophylline is appreciably influenced by the autonomic nervous tone and (b) autonomic blockade is required for the manifestation of the antagonism by aminophylline of the electrophysiological action of adenosine and adenosine triphosphate.

The antiarrhythmic and haemodynamic effects of tiapamil, a new calcium antagonist, were studied in 28 anaesthetised open chest dogs. Tiapamil (2 mg X kg-1 intravenously over 5 min) was infused 15 min before a 20 min ligature of the left anterior descending coronary artery in 11 dogs. In 17 dogs physiological solution was given instead of tiapamil. In this control group, ventricular fibrillation developed during coronary occlusion in 14 (82%) dogs and after coronary reperfusion in seven of 9 (77%) dogs, which reached this stage. In contrast, in the dogs pretreated with tiapamil, ventricular fibrillation did not develop during coronary occlusion in any of the 11 dogs and did develop after coronary reperfusion in only one (9%). In addition, tiapamil appreciably decreased heart rate and blood pressure and increased cardiac output and stroke volume. These antiarrhythmic and haemodynamic effects of tiapamil suggest that this drug would be useful in the management of patients with coronary artery disease.