Sylvain Ploux

Outcome After Implantation of a Cardioverter-Defibrillator in Patients With Brugada Syndrome A Multicenter Study

Background— Implantable cardioverter-defibrillator indications in Brugada syndrome remain controversial, especially in asymptomatic patients. Previous outcome data are limited by relatively small numbers of patients or short follow-up durations. We report the outcome of patients with Brugada syndrome implanted with an implantable cardioverter-defibrillator in a large multicenter registry. Methods and Results— A total of 378 patients (310 male; age, 46±13 years) with a type 1 Brugada ECG pattern implanted with an implantable cardioverter-defibrillator (31 for aborted sudden cardiac arrest, 181 for syncope, and 166 asymptomatic) were included. Fifteen patients (4%) were lost to follow-up. During a mean follow-up of 77±42 months, 7 patients (2%) died (1 as a result of an inappropriate shock), and 46 patients (12%) had appropriate device therapy (5±5 shocks per patient). Appropriate device therapy rates at 10 years were 48% for patients whose implantable cardioverter-defibrillator indication was aborted sudden cardiac arrest, 19% for those whose indication was syncope, and 12% for the patients who were asymptomatic at implantation. At 10 years, rates of inappropriate shock and lead failure were 37% and 29%, respectively. Inappropriate shock occurred in 91 patients (24%; 4±4 shocks per patient) because of lead failure (n=38), supraventricular tachycardia (n=20), T-wave oversensing (n=14), or sinus tachycardia (n=12). Importantly, introduction of remote monitoring, programming a high single ventricular fibrillation zone (>210–220 bpm), and a long detection time were associated with a reduced risk of inappropriate shock. Conclusions— Appropriate therapies are more prevalent in symptomatic Brugada syndrome patients but are not insignificant in asymptomatic patients (1%/y). Optimal implantable cardioverter-defibrillator programming and follow-up dramatically reduce inappropriate shock. However, lead failure remains a major problem in this population.

Driver Domains in Persistent Atrial Fibrillation

Background— Specific noninvasive signal processing was applied to identify drivers in distinct categories of persistent atrial fibrillation (AF). Methods and Results— In 103 consecutive patients with persistent AF, accurate biatrial geometry relative to an array of 252 body surface electrodes was obtained from a noncontrast computed tomography scan. The reconstructed unipolar AF electrograms acquired at bedside from multiple windows (duration, 9±1 s) were signal processed to identify the drivers (focal or reentrant activity) and their cumulative density map. The driver domains were catheter ablated by using AF termination as the procedural end point in comparison with the stepwise-ablation control group. The maps showed incessantly changing beat-to-beat wave fronts and varying spatiotemporal behavior of driver activities. Reentries were not sustained (median, 2.6 rotations lasting 449±89 ms), meandered substantially but recurred repetitively in the same region. In total, 4720 drivers were identified in 103 patients: 3802 (80.5%) reentries and 918 (19.5%) focal breakthroughs; most of them colocalized. Of these, 69% reentries and 71% foci were in the left atrium. Driver ablation alone terminated 75% and 15% of persistent and long-lasting AF, respectively. The number of targeted driver regions increased with the duration of continuous AF: 2 in patients presenting in sinus rhythm, 3 in AF lasting 1 to 3 months, 4 in AF lasting 4 to 6 months, and 6 in AF lasting longer. The termination rate sharply declined after 6 months. The mean radiofrequency delivery to AF termination was 28±17 minutes versus 65±33 minutes in the control group (P<0.0001). At 12 months, 85% patients with AF termination were free from AF, similar to the control population (87%,); P=not significant. Conclusions— Persistent AF in early months is maintained predominantly by drivers clustered in a few regions, most of them being unstable reentries.

Optimizing Hemodynamics in Heart Failure Patients by Systematic Screening of Left Ventricular Pacing Sites : The Lateral Left Ventricular Wall and the Coronary Sinus Are Rarely the Best Sites

OBJECTIVES We sought to evaluate the impact of the left ventricular (LV) pacing site on hemodynamic response to cardiac resynchronization therapy (CRT). BACKGROUND CRT reduces morbidity and mortality in heart failure patients. However, 20% to 40% of eligible patients may not fully benefit from CRT device implantation. We hypothesized that selecting the optimal LV pacing site could be critical in this issue. METHODS Thirty-five patients with nonischemic dilated cardiomyopathy referred for CRT device implantation were studied. Intraventricular dyssynchrony and latest activated LV wall were defined by tissue Doppler imaging analysis before the study. Eleven predetermined LV pacing sites were systematically assessed in random order: basal and mid-cavity (septal, anterior, lateral, inferior), apex, coronary sinus (CS), and the endocardial site facing the CS pacing site. For each patient, +dP/dT(max), -dP/dT(min), pulse pressure, and end-systolic pressure during baseline (AAI) and DDD LV pacing were compared. Two atrioventricular delays were tested. RESULTS Major interindividual and intraindividual variations of hemodynamic response depending on the LV pacing site were observed. Compared with baseline, LV DDD pacing at the best LV position significantly improved +dP/dT(max) (+31 +/- 26%, p < 0.001) and was superior to pacing the CS (+15 +/- 23%, p < 0.001), the lateral LV wall (+18 +/- 22%, p < 0.001), or the latest activated LV wall (+11 +/- 17%, p < 0.001). CONCLUSIONS The pacing site is a primary determinant of the hemodynamic response to LV pacing in patients with nonischemic dilated cardiomyopathy. Pacing at the best LV site is associated acutely with fewer nonresponders and twice the improvement in +dP/dT(max) observed with CS pacing.

Outcome After Implantation of a Cardioverter-Defibrillator in Patients With Brugada Syndrome

Background— Brugada syndrome is an arrhythmogenic disease characterized by an increased risk of sudden cardiac death (SCD) by ventricular fibrillation. At present, an implantable cardioverter-defibrillator (ICD) is the recommended therapy in high-risk patients. This multicenter study reports the outcome of a large series of patients implanted with an ICD for Brugada syndrome. Methods and Results— All patients (n=220, 46±12 years, 183 male) with a type 1 Brugada ECG pattern implanted with an ICD in 14 centers between 1993 and 2005 were investigated. ICD indication was based on resuscitated SCD (18 patients, 8%), syncope (88 patients, 40%), or positive electrophysiological study in asymptomatic patients (99 patients, 45%). The remaining 15 patients received an ICD because of a family history of SCD or nonsustained ventricular arrhythmia. During a mean follow-up of 38±27 months, no patient died and 18 patients (8%) had appropriate device therapy (10±15 shocks/patient, 26±33 months after implantation). The complication rate was 28%, including inappropriate shocks, which occurred in 45 patients (20%, 4±3 shocks/patient, 21±20 months after implantation). The reasons for inappropriate therapy were lead failure (19 patients), T-wave oversensing (10 patients), sinus tachycardia (10 patients), and supraventricular tachycardia (9 patients). Among implantation parameters, high defibrillation threshold, high pacing threshold, and low R-wave amplitude occurred, respectively, in 12%, 27%, and 15% of cases. Conclusion— In this large Brugada syndrome population, a low incidence of arrhythmic events was found, with an annual event rate of 2.6% during a follow-up of >3 years, in addition to a significant risk of device-related complications (8.9%/year). Inappropriate shocks were 2.5 times more frequent than appropriate ones.

Outcome After Implantation of a Cardioverter-Defibrillator in Patients With Brugada SyndromeClinical Perspective: A Multicenter Study–Part 2

Background— Implantable cardioverter-defibrillator indications in Brugada syndrome remain controversial, especially in asymptomatic patients. Previous outcome data are limited by relatively small numbers of patients or short follow-up durations. We report the outcome of patients with Brugada syndrome implanted with an implantable cardioverter-defibrillator in a large multicenter registry. Methods and Results— A total of 378 patients (310 male; age, 46±13 years) with a type 1 Brugada ECG pattern implanted with an implantable cardioverter-defibrillator (31 for aborted sudden cardiac arrest, 181 for syncope, and 166 asymptomatic) were included. Fifteen patients (4%) were lost to follow-up. During a mean follow-up of 77±42 months, 7 patients (2%) died (1 as a result of an inappropriate shock), and 46 patients (12%) had appropriate device therapy (5±5 shocks per patient). Appropriate device therapy rates at 10 years were 48% for patients whose implantable cardioverter-defibrillator indication was aborted sudden cardiac arrest, 19% for those whose indication was syncope, and 12% for the patients who were asymptomatic at implantation. At 10 years, rates of inappropriate shock and lead failure were 37% and 29%, respectively. Inappropriate shock occurred in 91 patients (24%; 4±4 shocks per patient) because of lead failure (n=38), supraventricular tachycardia (n=20), T-wave oversensing (n=14), or sinus tachycardia (n=12). Importantly, introduction of remote monitoring, programming a high single ventricular fibrillation zone (>210–220 bpm), and a long detection time were associated with a reduced risk of inappropriate shock. Conclusions— Appropriate therapies are more prevalent in symptomatic Brugada syndrome patients but are not insignificant in asymptomatic patients (1%/y). Optimal implantable cardioverter-defibrillator programming and follow-up dramatically reduce inappropriate shock. However, lead failure remains a major problem in this population.

Positron emission tomography in patients with suspected pacing system infections may play a critical role in difficult cases

BACKGROUND A pacemaker recipient may be hospitalized recurrently with an infection of unknown origin despite detailed investigations. OBJECTIVE The purpose of this study was to investigate whether (18)F-fluorodeoxyglucose positron emission tomography/computerized tomography (FDG-PET/CT) scanning has a role in identifying pacing material infection in these difficult cases. METHODS Ten patients who presented with fever of unknown origin despite detailed investigations including transesophageal echocardiography underwent FDG-PET/CT scanning. Identification of increased FDG uptake along a pacing lead prompted the removal of the entire pacing system, whereas in the absence of increased FDG uptake the pacing material was left in place. Forty control pacemaker recipients underwent FDG-PET/CT scanning as part of investigation of malignancy. RESULTS Among the 40 patients in the control group, FDG-PET/CT scanning was normal in 37 (92.5%) patients. Among the 10 patients who presented with suspected pacing system infections, FDG-PET/CT scanning showed increased FDG uptake along a lead in six patients; as a result of this finding, these patients subsequently underwent complete removal of the implanted material. Cultures of the leads were positive in all six patients, confirming involvement of the leads in the infectious process. In the other four patients, the pacing system was left in place without objective signs of active lead endocarditis during follow-up. CONCLUSION This study demonstrates the potential value of FDG-PET/CT scanning in the diagnosis of pacing lead endocarditis in difficult cases. Increased FDG uptake along a lead in this clinical context appears to be a reliable sign of active infection.

Comparative Electromechanical and Hemodynamic Effects of Left Ventricular and Biventricular Pacing in Dyssynchronous Heart Failure: Electrical Resynchronization Versus Left–Right Ventricular Interaction

OBJECTIVES The purpose of this study was to enhance understanding of the working mechanism of cardiac resynchronization therapy by comparing animal experimental, clinical, and computational data on the hemodynamic and electromechanical consequences of left ventricular pacing (LVP) and biventricular pacing (BiVP). BACKGROUND It is unclear why LVP and BiVP have comparative positive effects on hemodynamic function of patients with dyssynchronous heart failure. METHODS Hemodynamic response to LVP and BiVP (% change in maximal rate of left ventricular pressure rise [LVdP/dtmax]) was measured in 6 dogs and 24 patients with heart failure and left bundle branch block followed by computer simulations of local myofiber mechanics during LVP and BiVP in the failing heart with left bundle branch block. Pacing-induced changes of electrical activation were measured in dogs using contact mapping and in patients using a noninvasive multielectrode electrocardiographic mapping technique. RESULTS LVP and BiVP similarly increased LVdP/dtmax in dogs and in patients, but only BiVP significantly decreased electrical dyssynchrony. In the simulations, LVP and BiVP increased total ventricular myofiber work to the same extent. While the LVP-induced increase was entirely due to enhanced right ventricular (RV) myofiber work, the BiVP-induced increase was due to enhanced myofiber work of both the left ventricle (LV) and RV. Overall, LVdP/dtmax correlated better with total ventricular myofiber work than with LV or RV myofiber work alone. CONCLUSIONS Animal experimental, clinical, and computational data support the similarity of hemodynamic response to LVP and BiVP, despite differences in electrical dyssynchrony. The simulations provide the novel insight that, through ventricular interaction, the RV myocardium importantly contributes to the improvement in LV pump function induced by cardiac resynchronization therapy.

Biventricular stimulation improves right and left ventricular function after tetralogy of Fallot repair: acute animal and clinical studies.

BACKGROUND Optimal treatment of right ventricular (RV) dysfunction observed in patients after tetralogy of Fallot (TOF) repair is unclear. Studies of biventricular (BiV) stimulation in patients with congenital heart disease have been retrospective or have included patients with heterogeneous disorders. OBJECTIVE The purpose of this study was to determine the effects on cardiac function of stimulating at various cardiac sites in an animal model of RV dysfunction and dyssynchrony and in eight symptomatic adults with repaired TOF. METHODS Pulmonary stenosis and regurgitation as well as RV scars were induced in 15 piglets to mimic repaired TOF. The hemodynamic effects of various configurations of RV and BiV stimulation were compared with sinus rhythm (SR) 4 months after surgery. In eight adults with repaired TOF, RV and left ventricular (LV) dP/dt(max) were measured invasively during SR, apical RV stimulation, and BiV stimulation. RESULTS At 4 months, RV dilation, dysfunction, and dyssynchrony were present in all piglets. RV stimulation caused a decrease in LV function but no change in RV function. In contrast, BiV stimulation significantly improved LV and RV function (P < .05). Echocardiography and epicardial electrical mapping showed activation consistent with right bundle branch block during SR and marked resynchronization during BiV stimulation. In patients with repaired TOF, BiV stimulation increased significantly RV and LV dP/dt(max) (P < .05). CONCLUSION In this swine model of RV dysfunction and in adults with repaired TOF, BiV stimulation significantly improved RV and LV function by alleviating electromechanical dyssynchrony.

Left Ventricular Endocardial Stimulation for Severe Heart Failure

Biventricular resynchronization, a therapy recommended for patients presenting with left ventricular (LV) dysfunction and ventricular dyssynchrony, requires the implantation of an LV lead, usually placed in a lateral or posterolateral tributary of the coronary sinus. Despite important progress made in the development of dedicated instrumentation, the procedure remains sometimes challenging and unsuccessful in a minority of patients. In the rare instances of unsuccessful transvenous implantations occurring in the presence of major surgical contraindications, a few operators have implanted the LV lead transseptally, an approach limited by technical difficulties and by the thromboembolic risk associated with the presence of a lead inside the LV cavity. The interest in this approach was recently renewed by 2 studies in an animal model and in humans, respectively, which both found a distinctly superior hemodynamic performance associated with endocardial compared with epicardial stimulation. This review discusses the advantages and disadvantages of LV endocardial stimulation, examines the various techniques of LV endocardial stimulation, and projects their future applications in light of these highly promising recent results. The implementation of endocardial stimulation will ultimately depend on: 1) the development of safe, effective, and durable instrumentation, and reliable and reproducible intraprocedural methods to identify the optimal site of stimulation; and 2) the completion of controlled trials confirming the superiority of this technique compared with standard cardiac resynchronization therapy.

Management of subacute and delayed right ventricular perforation with a pacing or an implantable cardioverter-defibrillator lead.

The development of small-diameter active fixation pacing and implantable cardioverter-defibrillator leads may be associated with increased risk for delayed right ventricular perforation. The management of this unforeseen complication has been poorly described. Eleven successive patients referred for right ventricular subacute or delayed perforation (no evidence of lead perforation at the time of the procedure, perforation of the right ventricle diagnosed > or =5 days after implantation) were reviewed. The perforation was related to a pacing (n = 7) or an implantable cardioverter-defibrillator (n = 4) lead. The main symptoms were major dyspnea with pericardial effusion requiring emergency pericardial drainage (n = 3), inappropriate implantable cardioverter-defibrillator shock (n = 1), syncope (n = 2), abdominal pain (n = 1), mammary hematoma (n = 1), diaphragm stimulation (n = 1), and chest pain (n = 1). One patient was strictly asymptomatic. Signs of lead dysfunction were observed in all 11 patients. The diagnosis of lead perforation was confirmed by chest x-ray, echocardiography, or computed tomography. Surgery was directly performed in 1 patient with suspicion of digestive perforation. In the remaining 10 patients, the leads were removed by simple traction under fluoroscopic guidance in the operating room, with surgical backup support. The need for close monitoring was highlighted by the occurrence in 1 patient of tamponade requiring percutaneous pericardiocentesis and urgent surgical revision. The postoperative course of these patients was unremarkable. In conclusion, subacute ventricular perforation is a rare but potentially life threatening complication of lead implantation. In most patients, the leads can safely be removed under fluoroscopic guidance, with surgical backup support and close monitoring.