Reinder Evertz

Scar Dechanneling New Method for Scar-Related Left Ventricular Tachycardia Substrate Ablation

Background—Ventricular tachycardia (VT) substrate ablation usually requires extensive ablation. Scar dechanneling technique may limit the extent of ablation needed. Methods and Results—The study included 101 consecutive patients with left ventricular scar–related VT (75 ischemic patients; left ventricular ejection fraction, 36±13%). Procedural end point was the elimination of all identified conducting channels (CCs) by ablation at the CC entrance followed by abolition of residual inducible VTs. By itself, scar dechanneling rendered noninducibility in 54.5% of patients; ablation of residual inducible VT increased noninducibility to 78.2%. Patients needing only scar dechanneling had a shorter procedure (213±64 versus 244±71 minutes; P=0.027), fewer radiofrequency applications (19±11% versus 27±18%; P=0.01), and external cardioversion/defibrillation shocks (20% versus 65.2%; P<0.001). At 2 years, patients needing scar dechanneling alone had better event-free survival (80% versus 62%) and lower mortality (5% versus 11%). Incomplete CC-electrogram elimination was the only independent predictor (hazard ratio, 2.54 [1.06–6.10]) for the primary end point. Higher end point-free survival rates were observed in patients noninducible after scar dechanneling (log-rank P=0.013) and those with complete CC-electrogram elimination (log-rank P=0.013). The complications rate was 6.9%, with no deaths. Conclusions—Scar dechanneling alone results in low recurrence and mortality rates in more than half of patients despite the limited ablation extent required. Residual inducible VT ablation improves acute results, but patients who require it have worse outcomes. Recurrences are mainly related to incomplete CC-electrogram elimination.

Time Course of Atrial Fibrillation in Patients With Congenital Heart Defects

Background—The incidence of atrial fibrillation (AF) is rising in the aging patients with congenital heart defects (CHD). However, studies reporting on AF in patients with CHD are scarce. The aim of this multicenter study was to examine in a large cohort of patients with a variety of CHD: (1) the age of onset and initial treatment of AF, coexistence of atrial tachyarrhythmia and (2) progression of paroxysmal to (long-standing) persistent/permanent AF during long-term follow-up. Methods and Results—Patients (n=199) with 15 different CHD and documented AF episodes were studied. AF developed at 49±17 years. Regular atrial tachycardia (AT) coexisting with AF occurred in 65 (33%) patients; 65% initially presented with regular AT. At the end of a follow-up period of 5 (0–24) years, the ECG showed AF in 81 patients (41%). In a subgroup of 114 patients, deterioration from paroxysm of AF to (long-standing) persistent/permanent AF was observed in 29 patients (26%) after only 3 (0–18) years of the first AF episode. Cerebrovascular accidents/transient ischemic attacks occurred in 26 patients (13%), although a substantial number (n=16) occurred before the first documented AF episode. Conclusions—Age at development of AF in patients with CHD is relatively young compared with the patients without CHD. Coexistence of episodes of AF and regular AT occurred in a considerable number of patients; most of them initially presented with regular AT. The fast and frequent progression from paroxysmal to (long-standing) persistent or permanent AF episodes justifies close follow-up and early, aggressive therapy of both AT and AF.

Dual ventricular response: another road to supraventricular tachycardia in dual atrioventricular nodal physiology.

Dual atrioventricular nodal (AVN) physiology is an established cause of AVN reentrant tachycardias, of which the slow-fast variant is the most frequent. We present a patient with a mistaken diagnosis of AVN reentrant tachycardia referred for ablation. She actually had a tachycardia due to dual ventricular response, an uncommon presentation of tachycardia due to the presence of dual AVN physiology. We present this case to emphasize the importance of a thorough analysis of the electrocardiogram (ECG) because this tachycardia is frequently misdiagnosed, especially for atrial fibrillation. A 54-year-old woman without structural heart disease was referred to our center for an electrophysiology study and possible ablation of an AVN reentrant tachycardia because of persistent rapid palpitations despite treatment with a beta-blocker. On reviewing the ECG we noted a regular irregularity in the ventricular interval and the presence of P-waves, preceding every 2 QRS complexes. This and the positive morphology of the P-waves in the inferior leads ruled out a diagnosis of AVN reentrant tachycardia. A differential diagnosis of sinus rhythm with a dual ventricular response due to the presence of dual AVN physiology, junctional extrasystoles in bigeminy or (less likely) atrial tachycardia was made (Fig. 1). The intracardiac tracing of the electrophysiology study with a catheter positioned at the His showed the same phenomenon of dual ventricular response. A clear electrogram of the atrium (A) can be seen followed by 2 His potentials (H) and 2 ventricular electrograms (V). Because of the fixed relationship of both Hisand V potentials to the preceding A, the diagnosis of dual atrioventricular response was found to be most likely (Fig. 2). We proceeded to perform an ablation of the slow pathway, eliminating the dual ventricular response. With programmed stimulation, as previously described in this journal, the absence of dual AVN physiology could be confirmed. Dual ventricular response to a single supraventricular impulse is a rare presentation of dual AVN physiology. Every supraventricular beat is conducted anterograde both through the fast and the slow pathway. To allow dual ventricular response there has to be retrograde unidirectional block in at least the slow pathway, but probably in both pathways, and critical conduction delay of the slow pathway that is at least greater than the refractory period of the distal common pathway. We excluded the presence of an (atypical) AVN reentrant tachycardia with 2:1 conduction to the atrium because of the positive morphology of the P-waves on Rev Esp Cardiol. 2013;66(2):145–154

Non-sustained ventricular tachycardia in patients with congenital heart disease: An important sign?

BACKGROUND Sustained ventricular tachycardia (susVT) and ventricular fibrillation (VF) are observed in adult patients with congenital heart disease (CHD). These dysrhythmias may be preceded by non-sustained ventricular tachycardia (NSVT). The aims of this study are to examine the 1] time course of ventricular tachyarrhythmia (VTA) in a large cohort of patients with various CHDs and 2] the development of susVT/VF after NSVT. METHODS In this retrospective study, patients with VTA on ECG, 24-hour Holter or ICD-printout or an out-of-hospital-cardiac arrest due to VF were included. In patients with an ICD, the number of shocks was studied. RESULTS Patients (N=145 patients, 59% male) initially presented with NSVT (N=103), susVT (N=25) or VF (N=17) at a mean age of 40 ± 14 years. Prior to VTA, 58 patients had intraventricular conduction delay, 14 an impaired ventricular dysfunction and 3 had coronary artery disease. susVT/VF rarely occurred in patients with NSVT (N=5). Fifty-two (36%) patients received an ICD; appropriate and inappropriate shocks, mainly due to supraventricular tachycardia (SVT), occurred in respectively 15 (29%) (NSVT: N=1, susVT: N=9, VF: N=5) and 12 (23%) (NSVT: N=4, susVT: N=5, VF: N=3) patients. CONCLUSIONS VTA in patients with CHD appear on average at the age of 40 years. susVT/VF rarely developed in patients with only NSVT, whereas recurrent episodes of susVT/VF frequently developed in patients initially presenting with susVT/VF. Hence, a wait-and-see treatment strategy in patients with NSVT and aggressive therapy of both episodes of VTA and SVT in patients with susVT/VF seems justified.

Tachyarrhythmia in patients with congenital heart disease: inevitable destiny?

The prevalence of patients with congenital heart disease (CHD) has increased over the last century. As a result, the number of CHD patients presenting with late, postoperative tachyarrhythmias has increased as well. The aim of this review is to discuss the present knowledge on the mechanisms underlying both atrial and ventricular tachyarrhythmia in patients with CHD and the advantages and disadvantages of the currently available invasive treatment modalities.

Frequent atrial extrasystolic beats predict atrial fibrillation in patients with congenital heart defects

Aims Atrial fibrillation (AF) is increasingly observed in patients with congenital heart defects (CHDs) who survive nowadays into adulthood. Yet, predictors of AF are scarce in this high-risk population. This study therefore examined the predictive ability of atrial extrasystole (AES) for development of AF in CHD patients. Methods and results Adult CHD patients who had a 24 h Holter registration were followed to determine who developed AF. A total of 573 patients (49% male, mean age 35 ± 12 years) were included; they had a simple/complete repaired CHD (n = 279), complex repaired CHD (n = 251), or univentricular heart (UVH, n = 43). Ageing (P < 0.0001), female gender (P = 0.028), UVH (P = 0.0010), and left atrial dilatation (P = 0.0025) were associated with the number of AES. During a median follow-up of 51.6 months (interquartile range 22.8-85.7), 29 patients (5%) developed de novo AF. An one-point increase in the number of logtotal-AES was associated with a two-fold higher risk of AF development (hazard ratio 1.95; 95% confidence interval 1.21-3.13; P = 0.016). C-statistic for left atrial dilatation, complexity, and age had a good discriminative ability for the incidence of AF with a C-statistic of 84.5%. The addition of the total number of AES/24 h to this model increased C-statistic to 88.4%. Conclusion Atrial extrasystole occur relatively frequent in adult CHD patients compared with patients with other cardiac diseases. This is the first study that showed an association between an increased AES frequency and a higher risk of AF development in CHD patients.

Differential diagnosis between dual ventricular response and bigeminy arising from the bundle of His. Response.

We have read with attention the scientific letter published by Evertz et al. entitled ‘‘Dual Ventricular Response: Another Road to Supraventricular Tachycardia in Dual Atrioventricular Nodal Physiology’’. As the authors clearly explain, their case concerned a form of supraventricular ‘‘pseudotachycardia’’ in which they established a differential diagnosis involving 2 conditions: atrial tachycardia (quickly ruled out during the electrophysiological study) and bigeminy arising from the bundle of His. The latter diagnosis is not easily differentiated. The authors ruled out premature contractions of the bundle of His due to the consistent relationship of the His and ventricular action potentials to the preceding atrial action potential. However, in the description of the electrocardiographic recording shown in Figure 1 of their letter, the authors mention certain irregularity of up to 50 ms in the PR2 interval. As they state in the text, the diagnosis of dual nodal physiology was more evident once the dual ventricular response had disappeared following ablation of the slow pathway. Our group reported a case of frequent extrasystoles arising from the bundle of His in which, as in that described by Evertz et al., the patient had been referred to us with palpitations and supraventricular tachycardia. Our patient showed a wider variability in the H1-H2 interval, which contributed to the presence of a greater number of beats with aberrant conduction and facilitated the differential diagnosis. Moreover, in our case, the presence of blocked P waves and ‘‘pseudoblock’’ of atrioventricular conduction was incompatible with the existence of dual nodal physiology. By way of this letter, we wish to stress how difficult it is on occasion to differentiate between these two conditions during the diagnostic stage of the electrophysiological study performed prior to ablation. The diagnosis of premature beats arising from the bundle of His can be confirmed using a detailed map of the region

Female Aspects of Electrocardiography and Cardiac Arrhythmias

Normograms of the ECG are derived from the standard male patient. Women have a longer duration of the P-wave and PR-interval, while the QRS complex is smaller with a lower voltage. Non-specific ST-T changes are more often present in women than in men and vary by age. Paroxysmal supraventricular tachycardia’s (PSVT) are later diagnosed in women than in men. Women with atrial fibrillation (AF) have more symptoms, undergo fewer cardioversions and have a worse quality of life than men. Women more often develop Torsades de pointes (TdP) with some antiarrhythmic drugs. Although implantable defibrillator devices (ICD) therapy in secondary prevention are equally beneficial in both genders, they are less often applied in women. The quality of mammograms may be reduced by the presence of an implanted medical device.

Broad complex rhythm with a salty taste

A 65-year-old female patient with a medical history of stroke and paroxysmal atrial fibrillation presented to the neurologist at the emergency department of our hospital because of progressive weakness, dyspnoea, and fatigue. Her fluid intake had been minimal because of her malaise. She had no history of syncope. She used the following medications: warfarin, flecainide, and metoprolol. Initial physical examination showed a blood pressure of 105/65mmHg, a heart rate of 90/min, and no fever. She was clinically mildly decompensated: she had bilateral pulmonary rales and ankle oedema. A CT scan of the brain did not show any significant abnormalities. Laboratory results showed:

Erratum to: Tachyarrhythmia in patients with congenital heart disease: inevitable destiny

Erratum to: Neth Heart J (2016) DOI 10.1007/s12471-015-0797-z In the version of the article originally published online, the members of the DANARA study group were appended to the list of authors. The author line should have read: Christophe P. Teuwen, MD1; Yannick J.H.J. Taverne, MD2; Charlotte Houck, Msc1; Marco Gotte, MD, PhD3; Bianca J.J.M. Brundel, PhD4,5; Reinder Evertz, MD6; Maarten Witsenburg, MD, PhD1; Jolien W. Roos-Hesselink, MD, PhD1; Ad J.J.C. Bogers, MD, PhD2; Natasja M.S. de Groot, MD, PhD1; DANARA Study Investigators Collaborators: Sander G. Molhoek, MD, PhD7; Tanwier T.T.K. Ramdjan, MSc1; Wim A. Helbing, MD, PhD8; Janneke A.E. Kammeraad, MD, PhD8; H.G. Reinhart Dorman, MD9; Jurren M. van Opstal, MD, PhD10; Thelma C. Konings, MD11; Joris W.J. Vriend, MD, PhD3; Pepijn van der Voort, MD12; 1Dept of Cardiology, Erasmus University Medical Center, Rotterdam, The Netherlands; 2Dept of Cardio-Thoracic Surgery, Erasmus University Medical Center, Rotterdam, The Netherlands; 3Dept of Cardiology, Haga Hospital, The Hague, The Netherlands; 4Dept of Clinical Pharmacy and Pharmacology, University Medical Center Groningen, Groningen, The Netherlands; 5Dept of Physiology, Institute of Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands; 6Dept of Cardiology, University Medical Center St. Radboud, Nijmegen, The Netherlands; 7Dept of Cardiology, Amphia Hospital, Breda, The Netherlands; 8Dept of Pediatrics, Division of Pediatric Cardiology, Erasmus Medical Center – Sophia Children’s Hospital, Rotterdam, The Netherlands; 9Dept of Cardiology, Bravis Hospital, Rosendaal, The Netherlands; 10Dept of Cardiology, Medisch Spectrum Twente, Enschede, The Netherlands; 11Dept of Cardiology, VU University Medical Center, Amsterdam, The Netherlands; 12Dept of Cardiology, Catharina Hospital, Eindhoven, The Netherlands;