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Myocardial perfusion SPECT (MPS) is frequently used for cardiovascular risk stratification. The significance of MPS in patients with abnormal electrical ventricular activation is often questionable. This review assesses the value of MPS for risk stratification of patients with intrinsic left bundle branch block or that due to right ventricular apical pacing. We reviewed the literature by a search of the MEDLINE database (January 1980 to September 2010). The terms prognosis or prognostic value were combined with SPECT and LBBB or pacing or pacemakers. MPS was categorised as low and high risk according to the original definitions. We identified 11 studies suitable for review. A low-risk MPS is associated with a low risk of cardiac events whereas high-risk MPS carries a 4.8-fold increased risk, 95% CI [3.2 - 7.2] (p < 0.0001). Despite secondary prevention and an improved medical and interventional care, these figures have hardly changed over time. A low-risk MPS permits a policy of watchful waiting whereas a high-risk MPS requires further analysis and treatment. The persistent high cardiac death and acute myocardial infarction rate after a high-risk MPS suggest that the current management of these patients does not suffice and needs reconsideration.

Remote monitoring of implanted cardiac devices is an evolving method for regular checks of their electronic integrity and functioning. The communication with the devices is carried out unsupervised with wireless trans-telephonic or cable-dependent linkage. The interrogation of the device examines several programmed functions and harvests the stored data of numerous events. The collected data constitute the base to decide whether the implanted device is operating properly and can give some information about the physical condition of the device recipient. Preliminary short-term results show favourable effects in terms of safety and cost and time saving as compared with the current face-to-face visits of conventional patient follow-ups. Remote monitoring of implanted devices will extend markedly in the coming years and its development touches many questions ranging from technical accuracy, patient benefit, cost-effectiveness and responsibilities of the provider and receivers of the delivered device data, to the role of the cardiologist and allied professionals and of course privacy rules. In this point of view, these questions are discussed in order to explore the consequences of device remote monitoring with nationwide Trials. (Neth Heart J 2009;17:434-7.19949713)

Background. Correct pacemaker (PM) diagnosis of paroxysmal atrial tachyarrhythmias is crucial for their prevention and intervention with specific atrial pacing programmes. The PM mode switch to only ventricular pacing after detection of atrial tachyarrhythmias is often used as the parameter to quantify the ‘burden’ of atrial tachyarrhythmias. Objectives. This review addresses potential errors in the detection and diagnosis of atrial tachyarrhythmias, sometimes resulting in incorrect mode switches. The interpretation of PM-stored data of patients with atrial tachyarrhythmias and the results of trials of pace prevention and intervention can be better appreciated with more insight into the technical options and pitfalls. Results. Literature and clinical experience demonstrate that the correctness of PM-derived diagnosis of atrial tachyarrhythmias depends on 1) the sensitivity setting to detect the onset and perpetuation of atrial tachyarrhythmias frequently characterised by variable and low-voltage signals, 2) the rejection of far-field R wave sensing by the atrial sense amplifier, 3) the facility for verification of mode switches by a high-quality intracardiac registration of the nonmodified atrial electrogram. The configuration of the atrial lead also contributes to the diagnostic performance of the PM. Conclusion. Not only pacing algorithms and diverse technical PM features but also the atrial lead configuration are currently the limiting factors to the fully reliable, automated detection and diagnosis of atrial tachyarrhythmias. If these technical shortcomings can be improved, better signal processing will result. Then atrial pacing to prevent or suppress atrial tachyarrhythmias will be more justified. (Neth Heart J 2008;16:201-10.)

The diagnostic programmes of modern pacemakers have increased our knowledge of atrial tachyarrhythmias (ATAs) in chronically paced patients. These programmes also support the evaluation of the effects of pharmacological treatment of ATAs. The success of interruption and/or prevention of ATAs with pacemakers depends strongly on the diagnostic accuracy and the properties of the pacing algorithms, their individual programming and the site and configuration of the pacing leads. Atrial septum pacing can be beneficial in patients with paroxysmal atrial fibrillation and prolonged P wave duration. Recent large-scale studies on preventive and interruptive atrial pacing of ATAs show modestly positive or no results. Therefore, atrial pacing therapy for ATAs should be considered cautiously, serving as an adjuvant to pharmacological treatment rather than as a primary intervention. This also applies for pacing interventions for ATAs in cardiac resynchronisation therapy. The pacemaker algorithms for the detection of ATAs and atrial lead configuration are crucial for the success of pacemaker-mediated prevention or interruption of ATAs. The success of these interventions is dependant on future improvements of pacemaker technology. (Neth Heart J 2008;16 (suppl 1): S20-S24.)

Aims Despite an annual rise in the numbers of patients receiving their first pacemaker (PM), the risks of the implantation procedure remains unclear. The purpose of this prospective study is to estimate the incidence of in-hospital events after first PM implantation and to determine the predictors of these events. Methods and results Patients with conventional pacing diagnosis were included in the Dutch multicentre FOLLOWPACE PM registry that prospectively documented patients’ prognosis and quality of life, and PM events after first implantation. From these registry characteristics, implantation data and in-hospital findings were analysed as potential predictors for events in a sample of 1198 patients. In 111 patients studied, at least one serious in-hospital event occurred (incidence 10.1%, 95%CI: 8.9–12.3). Six variables, i.e. a lower body mass index, presence of heart failure in medical history, main indication for implantation, vena subclavia use for venous access, active atrial lead fixation, and the implantation of a dual chamber system, were found to be independent predictors of events after first PM implantation. The overall multivariable model yielded an ROC area of 0.65 (95%CI: 0.60–0.70). Conclusion This large prospective multicentre study identified six variables as independent predictors for serious in-hospital events after first implantation. This may assist the implanting cardiologist and surgeon to identify patients at higher risk, during and immediately after PM implantation.

Background —Radiofrequency (RF) catheter ablation provides curative treatment for idiopathic ventricular tachycardia (VT). Methods and Results —Nineteen consecutive patients with an idiopathic VT underwent RF catheter ablation. An integrated 3-phase mapping approach was used, consisting of the successive application of online 62-lead body surface QRS integral mapping, directed regional paced body surface QRS integral mapping, and local activation sequence mapping. Mapping phase 1 was localization of the segment of VT origin by comparing the VT QRS integral map with a database of mean paced QRS integral maps. Mapping phase 2 was body surface pace mapping during sinus rhythm in the segment localized in phase 1 until the site at which the paced QRS integral map matched the VT QRS integral map was identified (ie, VT exit site). Mapping phase 3 was local activation sequence mapping at the circumscribed area identified in phase 2 to identify the site with the earliest local endocardial activation (ie, site of VT origin). This site became the ablation target. Ten VTs were ablated in the right ventricular outflow tract, 2 at the basal LV septum, and 7 at the midapical posterior left ventricle. A high long-term ablation success (mean follow-up duration, 14±9 months) was achieved in 17 of the 19 patients (89%) with a low number of RF pulses (mean, 3.3±2.2 pulses per patient). Conclusions —This prospective study shows that integrated 3-phase mapping for localization of the site of origin of idiopathic VT offers efficient and accurate localization of the target site for RF catheter ablation.

Late Results of Surgery for AF. Introduction: Currently, surgery- and catheter-mediated ablation is applied when drug refractoriness of atrial fibrillation is evident, although little is known about the long-term incidence of new atrial arrhythmia and the preservation of sinus node function. Methods and Results: To address this issue, 30 patients with successful corridor surgery for lone paroxysmal atrial fibrillation and normal preoperative sinus node function were followed in a single outpatient department. Five years after surgery, the actuarial proportion of patients with recurrence of atrial fibrillation arising in the corridor was 8%± 5%, with new atrial arrhythmias consisting of atrial flutter and atrial tachycardia in the corridor 27%± 8%, and with incompetent sinus node requiring pacing therapy 13%± 6%. Right atrial transport was preserved in 69% of the patients without recurrence of atrial fibrillation and normal sinus node function. Stroke was documented in two patients. Conclusions: Corridor surgery for atrial fibrillation is a transient or palliative treatment instead of a definitive therapy for drug refractory atrial fibrillation. This observation strongly affects patient selection for this intervention and constitutes a word of caution for other, non-pharmacologic interventions for drug refractory atrial fibrillation.

OBJECTIVE: To evaluate exercise capacity of patients with chronic atrial fibrillation in whom His bundle ablation followed by ventricular rate response pacing (VVIR) was carried out because of drug refractoriness. DESIGN: Prospective study. PATIENTS: 25 consecutive patients, all with chronic symptomatic drug refractory atrial fibrillation, underwent His bundle ablation. Before this intervention all patients were on antiarrhythmic drugs to attain acceptable heart rate control and to relief symptoms. MAIN OUTCOME MEASURES: Exercise capacity, including measurements of VO2, was examined before and after a mean interval of seven months following His bundle ablation. RESULTS: Exercise capacity after His bundle ablation increased from a mean of 109 (SD 49) W to 118 (46) W (P < 0.002), but VO2 at peak exercise did not change significantly. Maximum exercise capacity was achieved with a significantly lower maximum driven heart rate than the spontaneous heart rate before ablation. CONCLUSIONS: Exercise capacity of patients who underwent His bundle ablation followed by VVIR pacing remained unchanged or improved during a mean follow up of seven months. Larger patient populations with longer follow up are necessary to examine determinants of improved exercise capacity.

Background Postinfarction ventricular tachycardias (VTs) may degenerate into ventricular fibrillation (VF), but this does not happen in all patients. The underlying mechanism is not exactly known, but dispersion of refractory periods is considered a major factor in both induction and persistence of reentrant arrhythmias in general. Hypertrophied, noninfarcted myocardium has altered electrophysiological characteristics. We hypothesized that noninfarcted ventricular tissue may provide the heterogeneities that cause the transition from VT into VF. Local fibrillation intervals, ie, the average interval between local activations during VF, have previously been shown to correlate well with local refractoriness in human and canine atrium and in porcine and canine ventricle and may therefore be used as an index of local refractoriness. This technique permits simultaneous assessment of refractoriness at multiple sites. Methods and Results We measured local fibrillation intervals at 32 to 64 sites in the noninfarcted part of the left ventricle in patients undergoing antiarrhythmic surgery for symptomatic, drug-refractory, postinfarction ventricular tachyarrhythmias. The grid of electrodes (interelectrode distance, 7 mm) was attached to the epicardium of the left ventricle remote from the infarcted tissue. Group 1 consisted of 7 patients with hemodynamically tolerable sustained VT (VT group). Group 2 consisted of 7 patients with cardiac arrest and documented VF (VF group). With the patients on cardiopulmonary bypass, VF was induced by multiple premature stimulation. The VF interval was not significantly different in the two study groups (VT group, 136±5.5 ms; VF group, 129±3.4 ms, mean±SEM). However, spatial dispersion of the VF intervals (remote from the infarcted area) expressed as the coefficient of variation of VF intervals (SD×100/mean VF interval in each heart) was significantly larger in the VF group. It was 3.63±0.56 in the VF group and 1.55±0.40 in the VT group (mean±SEM; P P P Conclusions This study shows larger dispersion in VF intervals and therefore suggests larger dispersion of refractory periods in parts of the myocardium remote from the infarction in patients with postinfarction VF than in patients with postinfarction VT.

Elevated levels of N-terminal pro BNP (NT-proBNP) excreted by stretched cardiomyocytes are attributed to increased cardiac filling pressures arising, for example, in left ventricular relaxation disorders. These conditions elicit higher atrial wall stress which in turn can initiate mechanisms causing atrial fibrillation (AF). However, the presence of AF itself can also produce increased levels of NT-proBNP, as was demonstrated by a drop of the peptide levels when sinus rhythm resumed after converted AF [1]. Not surprisingly, therefore, in the past decade NT-proBNP has received much attention as a potential new marker for AF detection and management [2]. In 2008, Asselbergs and coworkers reported data of the Groningen PREVEND study and showed that newly detected AF could be related to elevated NT-proBNP 4 years earlier at baseline [3]. A new AF-independent predictor was born but its significance was debatable for several reasons [4]. Some studies examined the relation of the duration or time of onset of AF to NT-proBNP levels, whereas other papers demonstrated variable outcomes of the relationship between success rates of AF cardioversion and the peptide levels (see publications of reference [5]). Conflicting results could not promote the role of NT-proBNP as the ideal guide for AF detection or management due to the dubious cause-effect relationship. The success rate of drug-administered cardioversion of AF depends on many factors such as gender, duration of AF, presence of structural heart disease and so forth. According to our guidelines for drug-administered cardioversion of AF (see www.NVVC.nl), intravenous flecainide, propafenone, ibutilide, or vernakalant are recommended (Class 1, level A) when pharmacological cardioversion is preferred and there is no or minimal structural heart disease. The conversion success rate of flecainide is 67–92 % at 6 hours provided AF is of 48 hours after the onset [6]. Symptomatic

BACKGROUND The purpose of this study was to assess the value of body surface mapping and the standard 12-lead ECG in localizing the site of origin of postinfarction ventricular tachycardia (VT) during endocardial pace mapping of the left ventricle. METHODS AND RESULTS Simultaneous recordings of 62-lead body surface QRS integral maps and scalar 12-lead ECG tracings were obtained in 16 patients with prior myocardial infarction during a total of 26 distinct VT configurations and during subsequent left ventricular catheter pace mapping at 9 to 24 different endocardial sites. Anatomic pacing site locations were computed by means of a biplane cineradiographic method and plotted on a polar projection of the left ventricle. The QRS integral map and the QRS complexes of the 12 standard leads of each VT morphology obtained in a particular patient were compared independently with the different paced QRS integral maps and paced QRS complexes of the 12-lead ECG generated in that same patient. The stimulus site locations of the best matching paced QRS integral map and paced QRS complexes of the 12-lead ECG were indicated on the polar projection and subsequently compared with the endocardial location of the corresponding site of VT origin identified during intraoperative (surgical ablation) or catheter activation sequence mapping (catheter ablation). The localization resolution of pace mapping was established separately for each electrocardiographic technique by computing the size of endocardial areas with similar morphological features of the QRS complex. Pace mapping advocated with body surface mapping or the 12-lead ECG enabled adequate reproduction of the VT QRS morphology in 24 of 26 VTs (92%) and 25 of 26 VTs (96%), respectively. Activation sequence mapping identified the site of origin in 12 of 26 previously observed VT configurations (46%). Ten and 11 VTs were localized by activation sequence mapping and pace mapping combined with body surface mapping or the 12-lead ECG, respectively. Pace mapping applied with body surface mapping identified the site of origin correctly (distance < or = 2 cm) in 8 of 10 compared VTs (80%); an adjacent site (distance between 2 and 4 cm) or a disparate site (distance > or = 4 cm) was identified in the remaining 2 of 10 VTs (20%). Pace mapping used with the 12-lead ECG localized the site of origin correctly in 2 of 11 VTs (18%); the site of origin was identified correctly next to an additional adjacent site in 5 of 11 VTs (55%); and an adjacent site or a disparate site was found in 1 of 11 VTs (9%) and 2 of 11 VTs (18%), respectively. The difference in localization accuracy of both electrocardiographic techniques was statistically significant (P = .02). The mean size of endocardial areas where a comparable QRS morphology was obtained during pace mapping was 6.0 +/- 4.5 cm2 with the application of body surface mapping and 15.1 +/- 12.0 cm2 with the use of the 12-lead ECG. CONCLUSIONS These results demonstrate that application of the 62-lead instead of the 12-lead ECG during endocardial pace mapping enhances the localization resolution of this mapping technique and enables more precise identification of the site of arrhythmogenesis in the majority of compared postinfarction VT episodes.

Self-terminating ventricular fibrillation was recorded in a 47 year old woman without coronary artery or other structural heart disease. Reperfusion was thought to be responsible for the ventricular fibrillation because the arrhythmia started while the ST segment was returning to the baseline during an episode of silent ischaemia that was probably caused by coronary spasm. This case shows that potentially lethal arrhythmias can arise during reperfusion and that ventricular fibrillation during reperfusion may be self-terminating.

Around 1904 remote monitoring of electrical cardiac activity was carried out for the first time by Willem Einthoven: he recorded the one-lead ECG of a patient admitted to the Leiden University Clinic in his Physiology Laboratory at a distance of 1.5 km from the hospital. Rightly he called this recording the tele-cardiogram (1). Hundred years later remote monitoring has expanded markedly by tremendous technical achievements, information technology, and the worldwide internet, components that underlie the chain between the cardiac implanted electronic device (CIED), the patient at home or outdoors, and the hospital staff responsible for technical controls. The first series of successive outcome studies indicates that remote monitoring and follow-up either at regular periods replacing the in-hospital technical controls (2), or 24-h monitoring to detect timely device failures is safe, highly reliable, prompts replies to failures, and reduces the incidence of inappropriate ICD shocks. Thus remote follow-up and monitoring can be classified as a valuable additional tool for patient care. Afterwards several randomised studies underscored this favourable outcome whereas moderate cost saving (3, 4) could be demonstrated. Consequently a consensus document for remote CIED monitoring was composed for the Dutch cardiology profession that can be applied in daily practice (5). Despite the favourable messages of these papers, several obstacles block the employment of CIED remote monitoring in Western general practice. The overwhelming amount of data that can arrive at the desk of the cardiologist or allied professional 24 h a day/7 days a week (6) and wait for reply or action or not, together with the sometimes unknown potential clinical relevance of the automated generated plots and graphs are serious pitfalls. In addition, lack of justifiable and fair reimbursement, and of legal arrangements of various parties, and in particular the contested willingness of some CIED patients to participate in remote monitoring inhibit further employment of this remote care (7). However, several studies did show obvious patient satisfaction and acceptance of remote ICD follow-up (8), while younger patients and smaller clinics (7), and probably other physical and mental characteristics, are associated with noncompliance and preference for in-hospital checks. In this issue Versteeg and co-workers present the rationale and design of the REMOTE-CIED study that attempts to establish the patient perspective on remote ICD monitoring which ‘could help to support patient-centred care in the future’ and to calculate cost effectiveness of this method (9). In this multicentre, prospective European study patients with a first ICD or CRT-ICD for primary or secondary prevention from fatal arrhythmias, and who have a left ventricular ejection fraction 2 years. To assess patient attitudes and perception of CIED remote monitoring, randomisation between in-hospital follow-up only or the combined patient remote follow-up and annual in-hospital control will be carried out. Several validated questionnaires have to be filled out at scheduled time intervals. Demographic, medical and CIED-related events and failures will be noted to determine factors associated with the perception of remote monitoring of the participants. This study is specifically focused on patient feelings because according to the investigators: ‘previous trials have fallen short in their patient-centredness and have left an important question unanswered: namely what do patients think about remote monitoring?’ (9). This is indeed true because this subject was only studied in (small) outcome studies in selected patients (8) or the patient satisfaction with telemedicine was neither clearly defined nor assessed with validated methods (10). Because patient perception about remote CIED follow-up is without doubt strongly determined by human influences - of the cardiologist, allied professional or family-, the progress of the underlying heart disease, unsatisfying contribution of CRT to the failing cardiac muscle (in about 30 %), comorbidity and negative effects of ageing, inappropriate ICD treatment and so forth, the ultimate comparison of the results of both study arms can become a scientific puzzle and not a clear yes/no answer. This potential problem can be solved by a much longer follow-up of at least 5 years that better reflects real life. Furthermore medicalisation and wish-fulfilling medicine evoked by remote monitoring and follow-up are not addressed at all in this study. Attention to these potential side effects is justified because the Western health care system is under pressure. Third, because the study will be conducted in five European countries assessment of cost-effectiveness is complex and confusing due to large variations in cost calculations of all care components in the participating countries. This part of the objectives has already been sufficiently covered showing clear cost saving in most countries (3, 4). Despite these obstacles, this study warrants implementation and participation of Dutch hospitals with a CIED license and experience because we eventually want to get validated insight into the characteristics of patients who will most profit or not from CIED remote monitoring. These data are strongly desired to also convince health insurance companies that remote ICD follow-up justifies reimbursement and promotes sustainable care with high and measurable quality. In the meantime we go forwards to encourage our CIED patients to profit from remote technical follow-up with the annual medical visit in stable patients while care of heart failure patients with CIED is routinely covered in the specific outpatient departments. In conclusion, we need more and detailed facts to convince ICD and CRT-ICD recipients that remote follow-up is worthwhile and that the patient is more than a computer file (7).

VAN DESSEL, P.F., et al.: Successful Surgical Ablation of Sustained Ventricular Tachycardia Associated with Mitral Valve Prolapse Guided by a Multielectrode Basket Catheter. Ventricular tachycardia occurs frequently in patients with mitral valve prolapse. If antiarrhythmic drug therapy fails or mitral valve surgery is indicated, concomitant arrhythmia surgery may be considered. This report describes the first clinical use of an atrial transseptally inserted multielectrode basket catheter, placed across the mitral valve, to guide intraoperative mapping and ablation of monomorphic sustained ventricular tachycardia in association with mitral valve prolapse. Endocardial covering and signal quality of this percutaneous mapping catheter were of good quality, allowing an accurate localization of the site of origin of the tachycardia.

Mechanical dyssynchrony has proven to be superior to QRS duration in predicting response to cardiac resynchronisation therapy (CRT). Whether time to peak longitudinal strain delay between the mid-septum and mid-lateral left ventricular wall better predicts CRT response than tissue Doppler imaging (TDI) is unclear. This study compares the value of the two methods for the assessment of mechanical dyssynchrony and prediction of CRT responders. 66 clinical responders and 17 nonresponders to CRT with severe systolic heart failure (LVEF 130 ms with left bundle branch block were evaluated by peak longitudinal strain and TDI. Doppler echocardiograms and electromechanical time delay (EMD) intervals were acquired before and after pacemaker implantation. In all responders EMD measured by peak longitudinal strain was >60 ms before implantation, compared with 76% of the patients measured by TDI. Nonresponders had EMD 60 ms. Peak longitudinal strain delay appears to be superior to TDI to predict the response to CRT. (Neth Heart J 2010;18:574-82.)

To improve electrocardiographic localization of the site of origin of ectopic left ventricular (LV) impulse formation in the heart with prior myocardial infarction, 62-lead body surface QRS integral maps were studied during LV pacing at a total of 221 endocardial sites in 14 patients with previous anterior (AMI), inferior (IMI), lateral (LMI), or anterior and inferior (AMI/IMI) myocardial infarction. The anatomic location of each pacing site was computed using digitized biplane fluoroscopic images and plotted on standardized LV endocardial polar projections. A data base of characteristic AMI and IMI mean QRS integral maps was developed after visually selecting subgroups with nearly identical QRS integral morphology from the ectopic activation sequences produced at 110 sites in eight patients with AMI and at 66 sites in four patients with IMI. Intrasubgroup pattern uniformity and intersubgroup pattern variability were statistically verified. The endocardial pacing site locations belonging to each AMI and IMI subgroup were depicted as segments on the respective LV polar projections. In patients with AMI, a total of 18 typical mean QRS integral patterns were obtained, whereas 22 different mean total QRS integral patterns showing more substantial intersubgroup variation were acquired in patients with IMI. Posterolateral regions exhibited a relatively low electrocardiographic sensitivity (six AMI and five IMI patterns) as compared with anteroseptal regions (12 AMI and 17 IMI patterns). Total QRS integral patterns obtained at 24 sites in one patient with LMI were largely compatible with the IMI mean total QRS integral patterns, whereas the majority of total QRS integral patterns acquired at 21 sites in one patient with AMI/IMI corresponded with the AMI mean total QRS integral patterns. The results show that total body surface QRS integral maps generated during LV pacing in patients with prior myocardial infarction cluster by pattern and that each QRS integral pattern is related to a circumscribed endocardial segment of ectopic impulse formation. The relation between a given QRS integral pattern and the position and size of the corresponding paced segment is dependent on infarct location. The present infarct-specific data base of characteristic total body surface QRS integral patterns provides a clinical tool to obtain detailed electrocardiographic localization of ventricular arrhythmias in patients with previous myocardial infarction.

Cardiac resynchronisation therapy (CRT) aims to restore left ventricular electrical/mechanical dyssynchrony, which can underlie impaired systolic left ventricular (LV) function and congestive heart failure. Several large prospective studies were able to document clearly that chronic electrical synchronisation does improve the systolic dysfunction and ameliorates symptoms, patient functioning and prognosis. If the conventional criteria are applied, this positive response can be observed in roughly 70% of patients, depending on the definition used for ‘positive response’.

Endocardial mapping of electrical activity was carried out in 150 patients to guide antiarrhythmic surgery for drug-resistant ventricular tachycardia in the chronic phase of myocardial infarction. In 20 of these patients, the activation pattern of 27 distinct tachycardias was focal and diastolic potentials were recorded at three or more sites. In 26 tachycardias, the sequence of diastolic potentials progressed from the area of latest activation of one cycle toward the “origin” of the next cycle. In two patients, the heart was stimulated during tachycardia, resulting in entrainment of the tachycardia in both. Late potentials were recorded during entrainment at sites where diastolic potentials occurred during tachycardia.In 11 of the 20 patients, endocardial mapping was performed during sinus rhythm. In four of these, late potentials were observed during sinus rhythm at sites where diastolic potentials were recorded during tachycardia. In two patients without late potentials during sinus rhythm, late potentials were observed during stimulation and induced ectopic beats.The results support the concept that the mechanism of several of these tachycardias is based on reentry in a macrocircuit comprising a tract of surviving tissue traversing the infarct and the remaining healthy tissue. They also indicate that the absence of late potentials during sinus rhythm does not guarantee the absence of arrhythmogenic pathways.

We report our combined experience with operative therapy for atrioventricular nodal tachycardia using an anatomically guided procedure. The operative rationale was to dissect the AV node with the intent of modifying perinodal tissues (skeletonization). The anterior septal and posterior septal regions were initially approached epicardially to facilitate endocardial dissection. Under normothermic cardiopulmonary bypass, the right atrial septum was mobilized and the intermediate AV node was exposed anterior to the tendon of Todaro. Ablation of concomitant accessory pathways was done prior to AV nodal skeletonization. Forty-six patients aged 9-71 years (mean 36) were operated upon. Five patients had accessory pathways in addition to AV nodal reentry. At electro-physiological study prior to discharge, no patient had an AV block although anterograde and retrograde Wenckebach cycle lengths were significantly prolonged. Ten patients had a retrograde AV block. The 46 patients were free of arrhythmia and not taking antiarrhythmic medication after a follow-up of 1-45 months (mean 17). Three patients had a recurrence of the tachycardia 10 days, 2 months and 7 months post-operatively, respectively. All patients had a subsequently successful reoperation.

Background: Radiofrequency (1717) catheter ablation is highly effective with a low complication rate. However, lesions created by RF energy are irreversible, inhomogeneous, and therefore potentially proarrhythmic. Objectives: The aim of this study was to examine the magnitude and importance of long-term proarrhythmic effects of RF energy. Methods and Results: Between 1991 and 1995, 120 patients underwent RF ablation for atrioventricular nodal reentrant tachycardia (AVNRT). Patient data were collected by contacting patients and/or filling out a questionnaire, and medical files were screened for recurrent, documented arrhythmias, pharmacological treatment, and repeated EP study. Referring cardiologists were asked about recurrences of tachyarrhythmias. Fourteen patients (11%) were lost to follow-up. During a mean follow-up of 10 years, six patients died. Recurrences of AVNRT were not any more observed after 3 years after ablation. A total of 29 patients (24%) suffered from new arrhythmias, 6 from type 1 atria] flutter, 6 from atrial tachycardia, 9 from atrial fibrillation, and finally 16 from symptomatic premature atria] contractions (PACs), needing medical treatment or a combination of these arrhythmias. Nine patients underwent pacemaker implantation, 4 after developing procedural atrioventricular (AV) conduction disturbances, 2 after His ablation for permanent atria] fibrillation, 1 patient for sick sinus syndrome, and another 2 patients after developing late AV block, respectively, 7 and 9 years after ablation. Conclusion: During long-term follow-up after RF ablation for AVNRT, no AVNRT recurrences were observed, but 29 patients (24%) suffered from new arrhythmias or late AV block. This potential proarrhythmic effect of RF energy promotes the application of alternative energy sources for ablative therapies for cardiac arrhythmias.

In this study we reviewed the history of the surgical treatment of atrial fibrillation (AF). Of the various types, the maze operation has become nowadays the most successful surgical treatment of AF with or without concomitant cardiac surgery. We report on our 10-year experience with conventional maze III surgery: 203 patients were operated on without in-hospital mortality and acceptable morbidity. Success defined as the freedom of AF and other supraventricular arrhythmias was 80.1% for the patients with lone AF and 64.5% for the patients with concomitant AF after a mean of 4 years after surgery. We conclude that despite the complexity of the maze III operation this approach remains the golden standard from which future surgical and other ablative treatments of AF will be derived.

Our current knowledge of the arrhythmic genesis of atrial fibrillation (AF) converges to the AF multiple wavelets concept of Moe and Allessie of the 1970s, which was further elaborated by many other investigators. Around 1990, spontaneous automaticity arising in muscular sleeves of pulmonary veins was documented by Haissaguerre and his rhythm experts of Bordeaux. Therefore, it made sense that after failed antiarrhythmic drug treatment to prevent or suppress AF, these concepts were translated into invasive therapy. Around 1985, cardiac surgeons Cox and Guiraudon were the first to eliminate the type of AF based on the multiple wavelets concept with different cut-and-sew approaches. Due to the large impact of surgery, catheter ablation to eliminate automaticity with pulmonary vein isolation and (gradually more) atrial ablation lines followed. The assumption that the percutaneous approach would be a promising, less aggressive alternative for surgery, however, evaporated due to the inferior long-term results compared with current minimal invasive surgery [1]. These disappointing results conceivably prompted many groups to explore additional measures for the eradication of AF, such as energy sources different from radiofrequency, ablation of the cardiac nervous ganglia and elimination of zones of slow or non-uniform conduction guided by voltage differences or fragmentation mapping of atrial tissue [2]. Fragmented atrial signals and low electrogram voltages are often recordable in AF [3] for example after repair of congenital heart disease and various AF types and manifestations [2]. Their documentation with modern automated signal analysis and 3D mapping raises questions such as their relation to the amount and depth of scarred tissue, stability during sinus rhythm (P wave characteristics) and/or other types of AF and/or atrial tachycardia. Most crucial for therapeutic application is their reproducible contribution to the onset and perpetuation of AF with critical conduction pathways. Studies showed that the incidence and duration of fragmentation are larger in ‘chronic’ compared with ‘paroxysmal’ AF patients and are also related to ageing, left atrial dilatation, shorter excitable periods and non-uniform conduction or anisotropy in atrial tissue. Non-uniform conduction is caused by fibrosis and observed at higher ages and increased atrial pressure. Evidence also exists that mapping of fragmented P waves in sinus rhythm also points to patients prone to or known to have atrial tachyarrhythmias, reflecting functional or structural changes. These observations strongly suggest that fragmentation can potentially guide the ablation procedure in drug refractory AF. In this issue, De Vries et al. [4]. report on a comparative study of RF catheter ablation with pulmonary vein isolation and left atrial lines with or without additional ablative ‘shaving’ of atrial sites with fragmented signals in patients with chronic AF, the so-called defragmentation method. Because this approach takes more time and burning, it is not surprising that more (minor) complications occurred in the defragmentation group. However, it is unclear why defragmentation could not bring out a better result in terms of suppression of AF at 3, 6 and 12 months after the procedure. The report by De Vries et al. [4]. cannot be compared with the results of previous studies, because the applied method of additional defragmentation has not been carried out before. The authors attributed the lack of increased success to resumed conduction from the automatic foci in the pulmonary veins or through the atrial ablation lines, despite all procedural measurements of (successful) conduction block. Furthermore they discussed the risk of ‘insufficient defragmentation’, an ill-defined term, and speculated whether more defragmentation would have ameliorated the outcome. Unfortunately, the authors did not correlate the findings of atrial mapping with the number of recurrences of AF. Finally, weighting the 12-month AF outcome versus complication rate and prolonged procedural time, they concluded that defragmentation should not be considered a routine part of catheter ablation for AF. It should be emphasised that this advice results from a retrospective study of two Dutch invasive arrhythmia groups that undermines the power of this advice. Second, because defragmentation is guided by analysis of endocardial atrial signals, information about the epicardial conduction is missing. Simultaneous endocardial and epicardial recordings of atrial arrhythmias in the dog heart showed a clear discordant activation. Another study in the goat showed that this dissociation is related to an increase in separation between the epicardial layer and endocardial bundles and it is suggested that the thin epicardial layer of the atrial wall can conduct fibrillatory waves [5]. This layer is probably not (always) reachable or too risky with current ablative techniques. Third, our knowledge of the degree of structural and functional temporo/spatial differences of (slow) conduction or block and its relation to the ‘severity’ of AF is limited. More experimental work is necessary to understand the significance of fragmented signals in the individual patient at a certain time of the AF disease. Therefore, before classifying defragmentation a bridge too far, more investigations are needed. We learn little from success but more from failures, reason to thank the authors and the Journal for publication of this initially unsuccessful therapeutic method. The investigators are encouraged to contact the experimental lab to study fragmented atrial signals and to consider a prospective, well-defined, study in a comparable group of AF patients after they have gained more insight into the role of these fragmented atrial signals.

The annual absolute number of cardiovascular implantable devices (CIEDs) is steadily increasing and is expected to rise even further, mostly due to the ageing demographic changes. [1] Consequently this will have a major impact on the post-implantation follow-up of monitor device function and patient condition both in terms of time and personnel. In a recent survey in 14 European countries remote monitoring (RM) was used in about 85% of all centres and the responding centres estimated that this percentage will increase to 93% by 2015. [2] In the same survey, guidelines and/or recommendations for the use of RM available from national scientific societies were reported to be totally absent in 93%. This lack of structural guidelines and/or recommendations will undoubtedly lead to a wide heterogeneity among centres using RM for the optimal care of patients after implantation. In addition responsibility related to remote follow-up is not clearly defined and leaves the device specialist and allied professionals in doubt with respect to the legal issues of RM. In 2009 the Netherlands Heart Rhythm Association (NHRA) took the initiative to develop a consensus document for RM in order to make a more uniform approach for RM and remote follow-up of the device patient. Close to 60 individuals have contributed to this expert consensus report. All aspects related to RM were divided into subgroups focussing on well-defined issues. The following subgroups were defined: Description of remote CIED monitoring Indications, benefits and limitations of remote CIED monitoring Patient perception of remote CIED monitoring Contribution of manufacturer to remote CIED monitoring Costs and reimbursement of remote CIED monitoring Preliminary recommendations for remote CIED monitoring For each subgroup a working group was formed. For each working group a chairperson was appointed and 5 to 8 members were carefully selected based on personal experience and individual expertise in the field. During half-day sessions working groups focussed on their specific subject which resulted in a concept document which was subsequently distributed by the chairperson for additional review. All sessions were also attended by the first three authors of the final expert consensus documents (CdC, JE and NvH) for process surveillance without interference with the contents. Finally the concept consensus report was reviewed during half-day sessions with all chairpersons. Despite the fact that RM was introduced more than 10 years ago, guidelines are available in only 5% of European countries, although RM is already widely implemented in medical practice. [2] A uniform approach to patients with CIED permitting RM is essential for a safe and optimal treatment. Clear and standardised information to the patient is also needed for optimal transmissions. In the CONNECT trial up to 45% of all alerts were not transmitted simply because the setup of the system was inappropriate.[3] In the Dutch expert consensus document a brochure is presented with patient instructions and education emphasising the responsibilities of the patient with respect to RM. [4] In addition a minimal set of parameters and alerts has been defined which may impose early medical treatment and prevent appropriate and inappropriate shocks. [5] Furthermore the introduction of RM into a device clinic needs a tailored organisation with structured appointments on scheduled or unscheduled visits, reason and type of device reprogramming etc. Of interest, the present expert consensus document has made a clear statement that RM can and will not be capable to be used as a 24/7 emergency system. The Heart Rhythm Society/European Heart Rhythm Association expert consensus document on monitoring of CIEDs was published in 2008 and lacks a clear statement on 24/7 surveillance, which fuelled concern with respect to legal issues for alerts. Finally, reimbursement will be a key issue for a wide implementation of RM. For private insurance companies and national health services the major challenge is in demonstrating improved health care with no rise in health rise costs. [6] In 82% of the countries in Europe there is no reimbursement structure despite the fact that preliminary studies demonstrated the cost effectiveness of RM and a high patient acceptance and satisfaction. [7] More prospective studies are needed with health economic costs as one of the primary endpoints before RM will be standard of care for all patients after device implantation. [8, 9]

Background Tissue mass and structure are relevant for initiation and persistence of fibrillation. Modification of the right atrium during maze surgery may change the arrhythmogenic substrate of atrial fibrillation (AF). Methods and Results Epicardial mapping was performed in 9 patients undergoing unmodified maze III surgery for lone paroxysmal AF. Simultaneous recording of AF on the right and left. atrium was carried out with two spoon-electrodes each harbouring 64 terminals. Activation maps of AF were made to study AF wavelet organization. The recording position on right and left atria was outside the surgical field and remained unchanged before and after surgery. Before surgery, mean right and left fibrillatory intervals were 174 +/- 123 ms, and 175 +/- 26 ms, respectively, and did not differ. After completed right atrial surgery, these fibrillary intervals remained unchanged. Mean right and left atrial dispersion of refractoriness (expressed as the coefficient of variation) were 4.2 +/- 0.8 and 5.2 +/- 3.8 ms. Only right atrial dispersion of refractoriness increased significantly after right-sided surgery. Prior to surgery, activation patterns of the left atrium were more complex than that of the right atrium. The left activation patterns became less complex afterwards; the right atrial activation patterns did not change. Conclusion The right atrial modification of maze III surgery neither affects atrial refractoriness during human lone AF nor changes AF wavelet organization. Thus, right atrial surgery does not modify the arrhythmogenic substrate of AF. These findings may imply that maze surgery can be restricted to the left atrium. (C) 2003 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved.

Little information is available about short-term and none about long-term follow-up of cardiac rhythm after percutaneous mitral balloon valvotomy (PTMV).We studied the long-term course of the supraventricular rhythm in 137 consecutive patients with severe mitral stenosis, who underwent PTMV. The rhythm before PTMV was sinus rhythm (SR) in 55% and chronic AF in 45% of patients. The mean follow-up time was 3.7+/-2.5 years (n=126). In patients with SR before PTMV, SR persisted in 91% of patients at the end of follow-up. In patients with chronic AF before PTMV, 84% of these patients were still in chronic AF at the end of follow-up, spontaneous conversion to SR did not occur. In 12 of 14 patients (85%), selected for cardioversion, SR was achieved, by DC cardioversion (n=11) or by drugs alone (n=1). After 2 years this outcome persisted, but after 4 years only 38% remained in SR.Pre-procedural SR will persist following PTMV. However in patients with chronic AF PTMV is not associated with reversion to SR, suggesting that measures should be undertaken to restore sinus rhythm.

Body surface mapping (BSM) can be used to identify the site of earliest endocardial activation of ventricular tachycardias (VTs). The multielectrode QRS morphology during VT is determined by both the site of earliest activation and the subsequent spread of electrical activation through the ventricles. This study investigated the relationship between the site of earliest endocardial activation, endocardial spread of activation, and the morphology of the multielectrode surface map in patients with remote myocardial infarction. In 14 patients with VT late (8.2+/-5.2 years) after myocardial infarction, BSM and simultaneous left ventricular 64-site basket endocardial mapping was performed during a total of 17 monomorphic VTs. In addition, multisite pacing by sequential use of the 64 basket electrodes was performed in 9 patients. BSM and basket mapping revealed the same endocardial breakthrough sites in 8 (47%) of 17 VTs and 189 (59%) of 322 pacing sites; adjacent sites were found in 2 (12%) of 17 VTs and 36 (11%) of 322 pacing sites. Large zones of conduction block explained the mismatch in localization in 2 (12%) of 17 VTs and 52 (16%) of 322 pacing sites. Regional differences in endocardial electrogram amplitudes were found as a cause for dissimilarity in 3 (18%) of 17 VTs and 73 (23%) of 322 pacing sites. Multiple endocardial breakthrough sites were found in 1 (6%) of 17 VTs and 8 (2%) of 322 pacing sites Finally, an epicardial exit site was suggested in 3 (18%) of 17 VTs as an explanation for mismatch, as no early endocardial activity could be recorded. Zones of conduction block, regional differences in signal amplitude, and multiple endocardial breakthrough sites are frequent causes for mismatch between BSM and basket catheter activation mapping

For a long time, it was a matter of debate whether fast rate or ventricular irregularity during atrial fibrillation (AF) was primarily responsible for the perception of palpitations, development of cardiomyopathy, and system emboli from the fibrillating atria. Recent studies have shown that ventricular irregularity associated with AF and manifested by random QRS intervals that constitute the diagnostic clue in scalar electrocardiography, can elicit symptoms and cardiomyopathy regardless of the rate. 1,2 Reduction of ventricular irregularity in AF patients in addition to control of fast ventricular rates, therefore, appears sensible to reduce symptoms and minimize the risk of cardiomyopathy. The underlying mechanisms of ventricular irregularity are uncertain and include concealed conduction within the atrioventricular (AV) node secondary to decremental conduction or electrical modulation of AV nodal propagation or pacemaker activity in the AV node. 1 If rate control is preferred to rhythm control, suppression of AV conduction with pharmacologic treatment and ablation of the AV junction are nowadays the established methods according to guidelines. However, the side effects and non-compliance associated with drug treatment or pacemaker dependency after ablation with potentially unfavourable effects of long-term right ventricular apical pacing often undermine the effectiveness of these therapies. These disadvantages urge the search for other therapeutic modalities for a safe and easy reduction of ventricular irregularity in AF. In 1983, Wittkampf and De Jongste 3 showed that continuous pacing in the right ventricle reduced the irregularity of QRS intervals during AF; faster pacing rates produced even more regularity by elimination of a large proportion of longer QRS intervals observed during slower ventricular rates. This phenomenon of rate stabilization is attributed to suppression or delay in AV nodal conduction by retrograde penetration of ventricular stimuli. This concept was incorporated in rate smoothing pacing algorithms that indeed significantly reduced variability of successive QRS intervals in AF patients. Unfortunately, the application of this algorithm was associated with a concomitant increase in mean heart rate by 21‐29%. 3 This drawback limited the widespread use of rate smoothing algorithms in paced patients with paroxysmal or permanent AF. In 1997, we tested a new rate smoothing programme delivered by the former Vitatron company, that uses a dynamic average of successive sensed or paced heart rates as a reference point. 4 The pacing rate followed the average heart rate and started pacing when the average ventricular rate dropped by 2.5 bpm. In addition, the algorithm prevented the occurrence of sudden brady- or tachyarrhythmia by pacing at a decelerating or accelerating rate at 2 bpm. In the acute pacing study, we observed that variability of the RR intervals could be reduced by 73% while the heart rate during pacing did not increase significantly (2%) compared with the preceding period without pacing. 5 In the unpublished randomized, single-blinded cross-over trial of patients with permanent (n ¼ 91) and paroxysmal AF (n ¼ 93), we observed a significant reduction in the variance of RR intervals in both patients categories. 6 However, quality of life, measured

Aim In patients with and without a permanent pacemaker His bundle ablation was performed for symptomatic drug-refractory atrial fibrillation. This study was performed to examine the complications of temporary pacing in patients without an already implanted pacemaker. Methods and Results Between January 1996 and December 1998, 152 consecutive patients, both referred and our own (non-referred), underwent His bundle ablation for drug-refractory atrial fibrillation. Primary end-point complications were temporary lead dislodgement requiring immediate repositioning (1), severe arrhythmia (2), death (3) and persistent damage to an already implanted pacing system (4). Secondary end-points were malsensing and malpacing of the temporary lead, and blood vessel problems. Lead dislodgement of the temporary pacemaker occurred in three patients (2·9%), all of whom were in the referred group. Severe arrhythmia and death did not occur. Persistent damage of the already implanted pacing system was not observed. Secondary end-points occurred in 15·8% of the patients and were successfully managed by a conservative approach. Conclusion Permanent pacemaker implantation is recommended prior to His bundle ablation in order to avoid haemodynamic deterioration due to dislocation of the temporary pacemaker lead. RF current used for His bundle ablation caused no permanent damage to permanent pacing systems.

Left ventricular (LV) dysfunction can occur due to chronic right ventricular apical pacing. Upgrading of the pacemaker to biventricular pacing is an option to reverse LV dysfunction but reprogramming of the atrioventricular (AV) timing can also be favourable. In this case report we describe the effect of AV-time reprogramming in a patient with LV function deterioration that emerged two years after implantation of a dual chamber system for sick sinus syndrome. Echocardiographc studies demonstrated a tremendous improvement in LV function during two years follow-up whereas the percentage of right ventricular pacing diminished dramatically. Careful analysis of the cause of LV deterioration can avoid unnecessary upgrading to biventricular pacing. (Neth Heart J 2010;18:604-5.).

Recent studies have indicated that nomen were less likely to receive sophisticated pacemaker devices than men. These differences could not be fully explained by demographic and clinical variables. The purpose of the present study was to assess whether a gender related difference might exist in pacemaker mode selection in patients undergoing their first implantation in The Netherlands. Records of first implants (n = 39,217) collected from 1988 through 1997 covering 93'% of all implantations in The Netherlands. From this population 33,564 (85.6%) patients were included for final analysis. I We observed no significant sex differences in pacemaker selection in patients with atrioventricular conduction disorders and bundle branch block. In patients with sick sinus syndrome, only very old women (greater than or equal to 85 years) had more atrial systems implanted than men of similar age (6.5% vs 3.5%), whereas men received more double chamber pacemakers (12.3% vs 10.3%) (P = 0.002). However, the relative distribution of physiological versus nonphysiological pacemakers in this subgroup rr as similar for men and women. In patients with chronic atrial fibrillation/flutter associated with bradycardia, sex differences were only apparent in the age group of 75-85 years; women received more dual chamber pacemakers (8.8% vs 5.3%) whereas men received more single chamber ventricular pacemakers (94.2% vs 89.8%) (P = 0.0011). With increasing age, sex differences in pacemaker selection rt ere absent, but there n as a considerable drop in implantation rate of dual chamber systems. Our study showed no major sex differences in the selection of pacemaker devices. Physicians select pacemaker devices by age rather than gender, which might be a rational choice

Aims Although arrhythmia surgery and radiofrequency catheter ablation to cure atrioventricular nodal reentrant tachycardia differ in technical concept, the late results of both methods, in terms of elimination of the arrhythmogenic substrate and procedure-related new and different arrhythmias, have never been compared. This constituted the purpose of this prospective follow-up study. Methods and Results Between 1988 and 1992, 26 patients were surgically treated using perinodal dissection or ‘skeletonization’, and from 1991 up to 1995, 120 patients underwent radiofrequency modification of the atrio-ventricular node for atrioventricular nodal reentrant tachycardia. The acute success rates of surgery and radiofrequency catheter ablation were 96% and 92%, respectively. Late recurrence rate in the surgical and radiofrequency catheter ablation groups was 12% and 17%, respectively. Mean follow-up was 53 months in the surgical group and 28 months in the radiofrequency catheter ablation group. The final success rate after repeat intervention was 100% in the surgical group and 98% in the radiofrequency catheter ablation group. Comparison of the initial and recent series of radiofrequency catheter ablated patients showed an increased initial success rate with fewer applications. In the radiofrequency catheter ablation group, a second- or third-degree block developed in three patients (2%), requiring permanent pacing, whereas in the surgical group no complete atrioventricular block was observed. Inappropriate sinus tachycardia needing drug treatment was observed in 13 patients (11%), mostly after fast pathway ablation, but was never observed after surgery. New and different supraventricular tachyarrhythmias arose in 27% of the patients in the surgical group and in 11% of the radiofrequency catheter ablation group, but did not clearly differ. Conclusion This one-institutional follow-up study demonstrated comparable initial and late success rates as well as incidence of new and different supraventricular arrhythmias following arrhythmia surgery and radiofrequency catheter ablation for atrioventricular nodal reentrant tachycardia. Today radiofrequency catheter ablation has replaced arrhythmia surgery for various reasons, but the late arrhythmic side-effects warrant refinement of technique.

In this issue of the Netherlands Heart Journal, the results of a substudy of the PREVEND trial are published.1 This prospective registry of presumably healthy citizens of Groningen aims to establish the association between microalbuminuria and the emergence of renal and cardiovascular diseases.2 This general population based long-term study extends the series of previous large-scale epidemiological trials conducted in the Netherlands. We recall among them the 1970 Vlagtwedde study for epidemiological cardiology and ischaemic heart disease, the 1982 Zutphen study of diet and cardiovascular diseases, the 1997 Maastricht study of circulatory arrest and sudden death, the 1998 Amsterdam study of out-of-hospital cardiac arrest and the 1999 Rotterdam study of prolonged QT interval and mortality.

Background It is still unknown whether a fast heart rate or an irregular ventricular response in atrial fibrillation causes tachycardiomyopathy. Reduction in the variability of RR intervals without an increase in heart rate might be an alternative treatment when antiarrhythmic drugs fail to control the irregularity accompanying atrial fibrillation. Subjects and methods Eight patients underwent temporary right ventricular pacing, using a novel rate-smoothing algorithm prior to DC cardioversion or His bundle ablation. A rate-smoothing algorithm was utilized by right ventricular apical stimulation. Spontaneous and paced RR intervals during atrial fibrillation were quantified and processed for statistical analysis. Results The rate-smoothing algorithm resulted in a substantial reduction in the variance of the RR intervals (slow mode 73·1%, fast mode 40·0%) and RR range (slow mode 49·3%, fast mode 34·3%). In contrast to previous algorithms, the mean heart rate during pacing intervention in atrial fibrillation did not change significantly to the heart rate directly preceding the pacemaker intervention (+2%). Conclusions This initial study of the novel rate-smoothing algorithm shows that pacing intervention is a relatively safe, rapid and reliable alternative therapy for controlling irregular ventricular rhythms due to atrial fibrillation. Incorporation of the algorithm in implantable pacemakers appears justified, but demands further prospective studies in patients to evaluate relief of symptoms and reduction of tachycardiomyopathy due to atrial fibrillation.

In two patients with a symptomatic posteroseptally localized accessory atrioventricular pathway, but with distinct electrocardiographic patterns, a coronary sinus diverticulum appeared to be the site of this connection. Radiofrequency catheter ablation in the diverticulum was implemented to interrupt the pathway in both cases. This study demonstrates the necessity to perform coronary sinus angiography when ablation attempts in the posteroseptal region are not immediately successful, or optimal signals are not detected.

OBJECTIVE--To investigate the long-term results of the corridor operation in the treatment of symptomatic atrial fibrillation refractory to drug treatment. BACKGROUND--The corridor operation is designed to isolate from the left and right atrium a conduit of atrial tissue connecting the sinus node area with the atrioventricular node region in order to preserve physiological ventricular drive. The excluded atria can fibrillate without affecting the ventricular rhythm. This surgical method offers an alternative treatment when atrial fibrillation becomes refractory to drug treatment. PATIENTS--From 1987 to 1993, 36 patients with drug refractory symptomatic paroxysmal atrial fibrillation underwent surgery. The in hospital rhythm was followed thereafter by continuous rhythm monitoring and with epicardial electrograms. After discharge Holter recording and stress testing were regularly carried out to evaluate the sinus node function and to detect arrhythmias; whereas Doppler echocardiography was used to measure atrial contraction and size. MAIN OUTCOME MEASURES--Maintained absence of atrial fibrillation without drug treatment after operation; preservation of normal chronotropic response in the sinus node. RESULTS--The corridor procedure was successful in 31 (86%) of the 36 patients. After a mean (SD) follow up of 41 (16) months 25 (69%) of the 36 patients were free of arrhythmias without taking drugs (mean (SE) actuarial freedom at four years 72 (9)%)). Paroxysmal atrial fibrillation recurred in three patients; paroxysmal atrial flutter (two patients) and atrial tachycardia (one patient) developed in the corridor in three others. Among the 31 patients in whom the operation was successful sinus node function at rest and during exercise remained undisturbed in 26 and 25 patients respectively (mean (SE) actuarial freedom of sinus node dysfunction at four years (81(7)%)). Pacemakers were needed in five (16%) of the 31 patients for insufficient sinus node rhythm at rest only. Doppler echocardiography showed maintenance of right atrial contribution to right ventricle filling in 26 of the 31 patients after operation in contrast to the left atrium, which never showed such contribution. His bundle ablation was performed and a pacemaker implanted in the five patients in whom the corridor operation was unsuccessful. CONCLUSION--These results substantiate the idea of this surgical procedure. Modification of the technique is, however, needed to achieve a reliable isolation between left atrium and corridor, which would make this experimental surgery widely applicable in the treatment of drug refractory atrial fibrillation.

In animal studies reperfusion of coronary arteries is commonly accompanied by ventricular arrhythmias. It is not certain, however, whether ventricular arrhythmias can be used as a reliable non-invasive marker of reperfusion in humans. Two-channel Holter recordings were obtained from the start of an intravenous infusion of streptokinase until coronary angiography (2.8 (2.7) hours (mean SD)) afterwards) in 57 patients with acute myocardial infarction of less than four hours who were generally not treated with antiarrhythmic drugs. Ventricular arrhythmias occurred in 21 (37%) of the 57 patients: accelerated idioventricular rhythm in 13 patients and non-sustained ventricular tachycardia in 15 patients. Seven patients had both accelerated idioventricular rhythm and non-sustained ventricular tachycardia. Coronary angiography showed a patent infarct-related vessel in 12 (92%) of the 13 patients with accelerated idioventricular rhythm (95% confidence interval 66 to 99%), in 22 (50%) of the 44 patients without accelerated idioventricular rhythm (95% CI 34 to 66%), in 11 (73%) of the 15 patients with non-sustained ventricular tachycardia (95% CI 45 to 92%), and in 23 (55%) (95% CI 39 to 71%) of the 42 patients who did not have non-sustained ventricular tachycardia. Seventeen (81%) of the 21 patients with accelerated idioventricular rhythm, or non-sustained ventricular tachycardia, or both, had a patent infarct-related vessel (95% CI 58 to 94%) as did 17 (47%) of the 36 patients with no ventricular arrhythmia (95% CI 29 to 65%). In patients with accelerated idioventricular rhythm after thrombolysis the infarct-related vessel is almost certain to be patent; but the infarct-related coronary artery can still be patent when no arrhythmia is seen.

The value of simultaneous 62-lead electrocardiographic recordings in localizing the site of origin of ectopic ventricular activation in a structurally normal heart was assessed by examining body surface QRS integral maps in 12 patients during left and right ventricular (LV and RV) pacing at 182 distinct endocardial sites. A data base of 38 characteristic mean integral maps was composed after visually selecting subgroups with nearly identical total QRS integral morphology and numerically evaluating intrasubgroup pattern uniformity and intersubgroup pattern variability. Corresponding endocardial pacing site locations were computed by a biplane cineradiographic method and outlined as segments on a standardized LV and RV polar projection. LV pacing resulted in 25 markedly different mean total QRS integral patterns, showing higher electrocardiographic sensitivity for anteroseptal (18 patterns) compared with posterolateral regions (seven patterns). RV pacing demonstrated 13 mean total QRS integral patterns, exhibiting less intersubgroup variation and comparatively low electrocardiographic sensitivity for the basal anterior and outflow regions. Comparison of LV with RV pacing revealed that QRS configurations produced at LV apical and LV midseptal sites closely resembled QRS configurations generated at RV apical, RV septal, and RV anterior sites, respectively. Total QRS time integral amplitudes showed considerable intrasubgroup variation but permitted global differentiation of spatially similar QRS patterns obtained during pacing at LV and RV sites. This study demonstrates that the QRS pattern of the total body surface electrocardiogram allows discrimination among 38 different LV and RV segments of ectopic endocardial impulse formation in patients with normal cardiac anatomy.

BACKGROUND Asynchronous activation resulting from right ventricular apical (RVA) pacing can adversely affect left ventricular function and myocardial perfusion despite normal coronary arteries. This situation makes detection of coronary heart disease in paced patients difficult. OBJECTIVES The purpose of this study was to assess the distribution, extent, and severity of myocardial perfusion defects with RVA pacing at low and high rates and increased coronary blood flow with adenosine. METHODS Fourteen patients with permanent RVA pacing and angiographically normal coronary arteries underwent myocardial perfusion single-photon emission computed tomography at rest at low and high pacing rates and with pacing at low rates with adenosine. Data were analyzed semiquantitatively using a 20-segment scoring model and coded using a four-point scoring system. RESULTS At rest, 23 (55%) of 42 coronary flow territories showed abnormal perfusion and 52 (19%) of 280 corresponding segments demonstrated abnormal perfusion; mean perfusion score was 0.22. After high-rate pacing, perfusion was abnormal in 31 (74%) of 42 flow territories and 122 (44%) of 280 segments; mean perfusion score was 0.67. Adenosine infusion resulted in 28 (67%) of 42 abnormal flow territories and 90 (32%) of 280 abnormal segments; mean perfusion score was 0.44. Perfusion defects were observed most often in close proximity to the origin of the pacing site. CONCLUSION RVA pacing results in myocardial perfusion defects. The false-positive findings are present at rest and more obvious with high-rate pacing than during adenosine infusion. Detection of coronary artery disease should be performed with caution in RVA paced patients because of the high number of perfusion defects observed in the absence of coronary artery disease.

In this report we describe electrophysiologic and histologic findings in hearts and endocardially resected preparations from patients with sustained ventricular tachycardias in the chronic phase of myocardial infarction. We recorded simultaneously from 64 endocardial sites during tachycardia in 72 patients that were operated on for medically intractable ventricular tachycardias. Two other patients underwent heart transplantation, and mapping was performed on the explanted isolated heart connected to a Langendorff perfusion set-up. During operation 139 tachycardias with different morphologies could be induced. Although the majority of evidence supports the concept of a reentrant mechanism for these tachycardias, we found that 105 tachycardias appeared to arise at a focal area of less than 1.4 cm2. In only three cases macroreentry around the infarction scar could be detected. Of 21 tachycardias in which the "origin" appeared to be focal, earliest subendocardial activation was preceded by discrete electrograms of low amplitude (presystolic activity). In three tachycardias presystolic activity was detected at several sites, permitting reconstruction of its route. Histology of the endocardial resected preparation in one of these cases revealed separate zones of viable myocardial fibers in areas in which presystolic activity was recorded. These zones were located intramurally and subendocardially, supporting the concept that reentry occurred via isolated bundles of surviving myocytes at the border of the infarct and the larger subendocardial muscle mass. Conduction velocity through the isolated tracts was on the order of 25 cm/sec. Similar reentrant pathways were found in the two isolated hearts. Extracellular and intracellular recordings were made from 20 endocardial preparations that were excised from areas in which tachycardia originated. Preparations were superfused in a tissue bath. These experiments showed that action potentials were usually close to normal, but occasionally action potentials with reduced amplitude and slow upstrokes were found. In addition, there were cells that exhibited both fast and slow upstrokes, depending on the direction of the wavefront. Histology of seven resected preparations and the isolated hearts showed subendocardially as well as intramurally located zones of viable myocardium. Fractionation of extracellular electrograms and slow conduction were found in areas where surviving muscle fibers and strands of fibrous tissue were interwoven, and in zones where muscle fibers were oriented in parallel but isolated by strands of connective tissue.(ABSTRACT TRUNCATED AT 400 WORDS)

A syndrome of slowly progressive muscle weakness with scapulo-ilio-peroneal distribution and cardiopathy was identified in 26 members of two families. Inheritance was autosomal dominant. Onset of the disease was between 17 and 42 years. Cardiopathy did not antedate skeletal muscle disease and patients had no symptoms of cardiopathy until a late phase of the disease. Initial ECG changes were non-specific, disturbances of conduction and impulse formation developed subsequently. Skeletal muscle biopsies showed neurogenic and myopathic changes with inflammatory cell reaction and perivascular cuffing. The combination of myopathy with neurogenic-like changes is characteristic of many cases of SPA. The inflammatory cell reaction is considered as part of a secondary polymyositis which is at leart partly responsible for muscle pathology.

101 patients suffering from acute myocardial infarction during less than 4 hours were immediately treated with intravenous (i.v.) streptokinase (SK), infused in 1 hour. No concomitant medications like steroids, salicylates or anti-arrhythmic drugs were routinely given.Patients were blindly allocated to one of four dosages of SK (see below). Coronary angiography was performed within 3 hours after SK infusion in 90% of all patients . The infarct-related vessel was open in 59% of 91 patients. The results in the four dosage groups were as follows:Haematomas at the puncture site were common complications in all groups. No strokes occurred, nor life-threatening bleeding complications. Blood transfusion was needed in only one parient, who had an important bleeding and formation of a large haematoma at the puncture site.It is concluded that there is a trend to better results of higher doses of i.v. SK in patients suffering from acute myocardial infarction without an evident rise of the rate of complications. The efficacy and safety of recently developed fibrinolytic drugs and streptokinase should be compared at optimal dosages.

Dr. Maseri, Dr. Laurent, ladies and gentlemen. I think it is very appropriate that the first session should be related to arrhythmia monitoring in the coronary care unit because the coronary care unit at its initiation was essentially an arrhythmia monitoring unit although it has expanded into many other fields subsequently. I hope you will forgive me if I start talking a little bit about history of the CCU. Now history is something that the older members of the profession, like myself, like to use to impress our younger colleagues, and it usually succeeds in boring them. But it’s important because our current practices are rooted in history rather than in reason or experience.

A patient free of symptoms, with a pseudoaneurysm of the left ventricle after inferoposterolateral myocardial infarction, is reported. The diagnosis was established by nuclear cardiography and echocardiography of the left ventricle.

Mechanisms of ventricular arrhythmias were assessed by the application of ECG criteria derived from experimental electrophysiology. These interval criteria describe for ideal and modulated parasystole, resettable spontaneous automaticity, early and delayed after depolarizations and reentry, how QRS complexes of ectopic ventricular origin relate to those of supraventricular origin. Ventricular arrhythmias were studied in: (a) longterm, 1-lead ECG recordings of 85 patients with uncomplicated and untreated acute myocardial infarction (AMI) (group I); (b) one-hour, 4-lead ECG recordings of 23 comparable patients with AMI (group 2), and (c) one-hour, 4-lead ECG recordings of 10 patients with chronic ventricular arrhythmias (group 3). All QRS complexes of ectopic ventricular origin having identical morphology (V type) were assumed to be the manifestation of a single site in the ventricle. The supraventricular rhythm in groups 2 and 3 was varied by programmed atrial stimulation to increase the range of intervals and patterns of the V types in the ECG. Positive evidence for a particular mechanism was obtained by applying tested criteria in 38% of 263 V types in group I (mainly reentry, but also early and delayed afterdepolarizations). In group 2, there was positive evidence in 67% of 84 V types (mainly reentry, but also early and delayed afterdepolarizations) and also in 67% of 18 V types in group 3, (mainly reentry). The application of these ECG criteria to ventricular arrhythmias identifies mechanisms in a satisfactory proportion. The yield can be increased by artificial variation of the heart rate.

Disabling monomorphic ventricular bigeminy has not been described as an indication for surgery. Three young patients with this arrhythmia sometimes deteriorating into ventricular tachyarrhythmias and in whom drug therapy failed completely were accepted for surgical ablation of the arrhythmogenic area. The earliest endocardial site of origin was located preoperatively by catheter mapping of the spontaneously occurring ventricular bigeminy in the left and right ventricles. For maximum preservation of myocardial muscle and function, the preoperative mapping and surgical procedure were performed through the aortic root; mapping by transaortic multipolar balloon was done during normothermic coronary perfusion and cryocoagulation was done during cardioplegic arrest. Cryocoagulation of the endocardial site was performed using the transaortic approach and epicardial cryocoagulation at the opposite site was done afterwards. In the two patients in whom the preoperative mapping results were consistent with those of preoperative catheter mapping, the arrhythmia could be abolished, as documented during long-term follow-up. In the only patient in whom the mapping results were not in agreement, the ventricular arrhythmia reoccurred and was the cause of death at five months after surgery. Postoperative wall-motion studies performed in the two surviving patients showed limited scars in the area of cryocoagulation and minor damage to the coronary arteries in that area. The transaortic approach can be considered as a new and important surgical option for endocardial mapping and cryocoagulation which prevents the damaging effects of a left ventriculotomy.

In the years before direct revascularisation for drug-refractory angina pectoris, some indirect methods were explored to improve myocardial ischaemia. Carotid nerve stimulation activated by the patient when angina emerged and Vineberg surgery [1] with implantation of the free end of the mammary artery (started about 1963) are examples of desperate attempts to suppress untreatable symptoms. Both were abandoned because of non-proven effects in contrast to direct revascularisation, which arrived around 1967. The favourable effects and safety of the current percutaneous coronary intervention and bypass surgery permit direct revascularisation in almost all categories of patients with myocardial ischaemia. However, for some patients direct revascularisation or redo procedures are not feasible because of the poor condition of the coronary arteries, age or major comorbidity; the number of these patients is gradually increasing. This observation initiates new experimental, non-invasive methods to improve coronary circulation and myocardial perfusion with the option of relief of untreatable angina. These attempts vary from nerve stimulation to gene therapy [2]. Acoustic pulse waves are used in an experimental attempt to eradicate drug-refractory angina because it initiates angiogenesis in experimental conditions [3]. With an amount of energy about 10 % of that usually applied to crush kidney stones, several favourable bio-effects have been documented. An increase of vascular endothelial growth factor and of capillary density resulting in a better left ventricular ejection fraction, wall thickening fraction and myocardial blood flow of the ‘treated’ area could be documented. Several preliminary studies in patients with severe angina pectoris without other therapeutic options could show promising results in qualitative terms. However, as Slikkeveer and coworkers [4] stated, quantitative observations of changes of myocardial blood flow in the target ischaemic area after application of acoustic pulse waves have not been published until now. In their small pilot study of patients with severe angina pectoris and major coronary disease, these authors could not observe an obvious improvement of the blood flow four weeks after the last application of acoustic pulse waves by measuring myocardial blood flow with cardiac magnetic resonance imaging (CMR) [5]. Nevertheless, despite an unchanged frequency of angina attacks, some improvement in the physical condition and less use of nitroglycerin were noted. The authors concluded that this negative outcome requires more scientific insight into the bio-effects of acoustic pulse waves before further clinical exploration can be justified. With full appreciation for the efforts of the investigators, some elements of this clinical pilot study that might affect the reported results should be pointed out. The course of patient symptoms, timing and methods of measurement of myocardial blood flow after acoustic pulse waves, and ‘collateral damage’ of tissue beyond the target zone are questionable. The unchanged frequency of attacks conflicts with a better perceived physical condition according to New York Heart Association class, and less daily use of nitroglycerin, respectively. Despite use of a disease-specific quality of life questionnaire, one can safely assume that the small cohort of patients, as well as a placebo effect resulting from frequent and intensive attention and care of the study patients, affect the documented changes of health perception and symptoms. Therefore this part of the outcome of the pilot study can be classified as arbitrary. The follow-up time after application of the acoustic pulse waves needs to be questioned. At three months after the last application, quality of life was again determined whereas the time of the second CMR was not precisely presented, presumably in conjunction with filling out the questionnaire, in total about 5 months after the last application. This interval appears too short to permit a reliable quantification of new angiogenesis and presumably other bio-effects. In the past, at least 6 months of follow-up after Vineberg surgery was required to determine any contribution of the implanted artery to myocardial perfusion. A longer follow-up and an additional CMT, e. g. after a further six months, could have shown a different picture. The acoustic pulse waves were applied towards previously mapped ischaemic zones. To catch the entire zone, the application area was extended including ‘treatment of healthy segments’ [4]. This approach can elicit negative effects because the bio-effects on ‘normal’ human myocardial tissue with a fixed dosage are uncertain. More importantly, the so-called ischaemic zone in the end stage of coronary heart disease is a conceptual area rather than a well-described entity. Pathology of these hearts shows unclear border zones intermingled with fibrosis, scar tissue and surviving myocytes [6]. That mixture excludes a sharp anatomical separation of the target zone and healthy neighbours without ischaemia and complicates the direction and penetration of the ‘beam’ of the acoustic pulse waves. One can consider whether application of pulsed acoustic waves in this specific patient group brought more harm as possible ‘collateral damage’ of tissue beyond the target area than benefit. CMR is well established for assessing myocardial volumes and function, and for myocardial fibrosis and (non)ischaemic heart diseases. In regions with reduced perfusion, concentrations of Gadolinium are decreased, resulting in lower signal intensity. Recently, different techniques have been developed to improve quantification, aiming to determine a reliable tissue function. None of these techniques were employed in this study. The accuracy of the employed quantification technique is insufficient to calculate absolute flow in these difficult areas [7]. We agree with the authors that our knowledge of the bio-effects of pulsed acoustic wave shocks applied to specific myocardial targets is so limited that more knowledge is strongly needed. Consequently one cannot explore this ‘treatment’ in new patients before we know more about the precise individual dosages, the optimal timing and the best method to measure positive and side effects of acoustic pulse waves. Until now, this indirect treatment has not proven to constitute a beneficial and harmless “weapon” against drug-refractory angina. Whether other treatment indications in cardiology can profit from acoustic pulse waves, also remains questionable.