Efficacy and Safety of ICD Therapy in a Population of Elderly Patients Treated with Optimal Background Medication

Introduction: Implantable cardioverter-defibrillator (ICD) therapy has been shown to improve survival in patients with structural heart disease and at high risk for life threatening ventricular arrhythmias. Whether elderly patients benefit from device therapy in a similar way as younger patients is largely unknown. Methods: We retrospectively analyzed data from 375 consecutive ICD recipients with structural heart disease. Patients were divided into two groups, younger than 70 years at time of ICD implantation (group 1) or 70 years or older (group 2). Main outcome measures were time to death from any cause and time from first appropriate ICD therapy to death. Results: Group 1 and 2 patients were comparable with respect to clinical presentation and average follow-up duration. In the elderly patient group, 78% received an ICD for secondary prevention versus 63% in group 1 (p = 0.007). During a mean follow-up period of 26.5 ± 18.1 months, there was no significant difference in overall mortality among the two groups: 47 patients died, 34 (12.5%) of group 1 versus 13 (12.7%) of group 2. The average time to death was 28.4 ± 16.7 vs 30.4 ± 22.1 months after device implantation, respectively (p = ns). There was no difference in time from device implantation to first adequate ICD therapy and time from first appropriate ICD therapy to death among the two groups (p = ns). Device associated complications were comparable in both groups. Conclusions: Elderly ICD recipients had comparable survival rates and appropriate use of the ICD compared to younger individuals. There was no external financial support of this study.     

ICD-Antiarrhythmic Drug and ICD-Pacemaker Interactions

Implantable Cardioverter Defibrillators. Antiarrhythmic drugs and separate bradycardia pacing systems are prescribed commonly in patients with implantable cardioverter defibrillators (ICDs). Adverse effects of antiarrhythmic drugs on ICD function and adverse interactions between ICDs and pacemakers have been documented. The effect of antiarrhythmic drugs on the defibrillation threshold (DFT) in patients has not been well assessed. Most studies have been performed in animal models in which cardiac function was normal and drug doses were supraphysiologic. In addition, most studies have utilized monophasic defibrillation shock waveforms and epicardial lead systems. Despite the lack of clinical data applicable to current defibrillation systems, it appears that chronic amiodarone administration causes a significant DFT increase. In addition, antiarrhythmic drugs can influence antitachycardia pacing and tachycardia sensing. Defibrillation shocks can cause transient failure of pacemaker sensing and pacing, and cause spurious pacemaker reprogramming. Pacemaker function can result in ICD oversensing, leading to inappropriate therapy, or cause ICD undersensing, potentially resulting in failure to deliver therapy during ventricular fibrillation. The susceptibility of an ICD to undersensing appears related to the amplitude of the pacing stimulus artifact recorded by the ICD rate-sensing circuit and to the characteristics of the fibrillation electrogram. Preliminary data suggest that undersensing of ventricular fibrillation by current ICDs is an unlikely event.     

Effect of an active abdominal pulse generator on defibrillation thresholds with a dual-coil, transvenous ICD lead system

INTRODUCTION: Many patients with implantable cardioverter defibrillators (ICDs) have older lead systems, which are usually not replaced at the time of pulse generator replacement unless a malfunction is noted. Therefore, optimization of defibrillation with these lead systems is clinically important. The objective of this prospective study was to determine if an active abdominal pulse generator (Can) affects chronic defibrillation thresholds (DFTs) with a dual-coil, transvenous ICD lead system. METHODS AND RESULTS: The study population consisted of 39 patients who presented for routine abdominal pulse generator replacement. Each patient underwent two assessments of DFT using a step-down protocol, with the order of testing randomized. The distal right ventricular (RV) coil was the anode for the first phase of the biphasic shocks. The proximal superior vena cava (SVC) coil was the cathode for the Lead Alone configuration (RV --> SVC). For the Active Can configuration, the SVC coil and Can were connected electrically as the cathode (RV --> SVC + Can). The Active Can configuration was associated with a significant decrease in shock impedance (39.5 +/- 5.8 Omega vs. 50.0 +/- 7.6 Omega, P < 0.01) and a significant increase in peak current (8.3 +/- 2.6 A vs. 7.2 +/- 2.4 A, P < 0.01). There was no significant difference in DFT energy (9.0 +/- 4.6 J vs. 9.8 +/- 5.2 J) or leading edge voltage (319 +/- 86 V vs. 315 +/- 83 V). An adequate safety margin for defibrillation (> or =10 J) was present in all patients with both shocking configurations. CONCLUSION: DFTs are similar with the Active Can and Lead Alone configurations when a dual-coil, transvenous lead is used with a left abdominal pulse generator. Since most commercially available ICDs are only available with an active can, our data support the use of an active can device with this lead system for patients who present for routine pulse generator replacement.     

Frequent ICD Shocks due to Double Sensing in Patients with Bi-Ventricular Implantable Cardioverter Defibrillators

Biventricular pacing has emerged as a modality for treatment of patients with heart failure. Combined biventricular pacers and implantable cardioverter defibrillators offer treatment of heart failure as well as protection from sudden cardiac death. However, inappropriate ICD shocks as a result of double sensing due to widely spaced ventricular bipoles may pose a significant problem in these patients.We examined the ICD records of twenty-three patients with biventricular ICDs, and evaluated all episodes of double sensing that resulted in aborted or delivered therapy.In follow-up of 3.7 ± 2.6 months, thirty-three shocks in fifteen episodes occurred in five patients (21.7%) due to double sensing. Four patients (17.4%) had aborted shocks due to double sensing. All episodes resulting in shock occurred because of sinus tachycardia or supraventricular tachycardia above the upper programmed pacing rate of the device with resultant AV conduction and double sensing of the nonpaced ventricular depolarization.In conclusion, double sensing of the R-wave is a common and clinically important cause of inappropriate ICD detection and shock in patients with biventricular ICDs. Appropriate programming of the ICD can prevent episodes of inappropriate shocks.     

Two different therapeutic strategies in ICD lead defects: additional combined lead versus replacement of the lead

Objectives: Implantation of an additional HV-P/S lead versus extraction of the defective HV-P/S lead and implantation of a new one is one possible therapeutic approach in cases of a defective high-voltage pace/sense lead (HV-P/S). No information is available on potential differences in clinical outcome in these different approaches.
Methods: Between January 2000 and February 2006, 86 patients with HV-P/S lead defect received either an additional transvenous HV-P/S lead (n = 33, group 1) or the HV-P/S lead was replaced (n = 53, group 2). The duration of the initially implanted leads was significantly different in the two groups (7.4 ± 2.9; group 1 and 4.1 ± 3.4 years; group 2).The outcome of these two groups of patients was retrospectively analyzed.
Results: Seventy-three patients [85%] survived until the end of follow-up of 29 ± 15 (group 1) and 33 ± 21 (group 2) months (P = ns), respectively. Thirteen patients died: six in group 1 and seven in group 2 (P = ns). Fourteen patients experienced perioperative complications (group 1: six; group 2: eight; P = ns). ICD system-related complications occurred in 22 patients (group 1: seven; group two: 15; P = ns). The event-free cumulative survival of patients with additional and replaced HV-P/S lead for postoperative events (including death) after 1, 2, and 3 years was 82%, 70%, 70%, and 86%, 81%, 66%, respectively (P = 0.93).
Conclusions: Implantation of an additional HV-P/S lead or replacement of the HV-P/S lead in case of HV-P/S lead failure is statistically not different concerning mortality and morbidity. There are no predictors for further lead defects. Implantation of an additional HV-P/S lead should not be recommended in young patients or patients with greater likelihood of living many years. Predictors for death were an age over 70 years and renal insufficiency.     

Have all the ICD primary prevention trials excluded an important group of patients?

Primary prevention trials of implantable cardioverter defibrillator (ICD) therapy have generally excluded patients early after revascularization. Clinicians are commonly faced with patients who have ventricular dysfunction and nonsustained ventricular tachyarrhythmia developing shortly after revascularization. Since there are no evidence-based guidelines, management is currently at the discretion of the treating clinician. Recently, evidence has emerged that this patient population is at increased risk of development of life-threatening ventricular tachyarrhythmia and, pending prospective trials, we suggest that ICD therapy should be used in appropriately selected patients with perioperative ventricular arrhythmia.     

Pregnancy with an ICD and a documented ICD discharge.

We report a successful pregnancy in a patient affected by idiopathic ventricular fibrillation 3 years after insertion of an ICD, with a documented defibrillator discharge.     

Arrhythmias in heart failure: current concepts of mechanisms and therapy

About one half of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT) degenerating to ventricular fibrillation or immediate ventricular fibrillation. In severe heart failure, sudden cardiac death also may occur due to bradyarrhythmias. Other dysrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation (AF), and sustained and nonsustained ventricular tachyarrhythmias. The exact mechanism of the increased vulnerability to arrhythmias is not known. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations such as fibrosis or myocardial scarring, may be prominent. Reentrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. Furthermore, alterations in potassium currents leading to action potential prolongation and an increase in dispersion of repolarization play a significant role. Treatment of arrhythmias is necessary either because patients are symptomatic or to reduce the risk for sudden cardiac death. The individual history, left ventricular function, electrophysiologic testing, and the signal-averaged ECG give useful information for identifying patients at risk for sudden cardiac death. The implantable cardioverter defibrillator (ICD) has evolved as a promising therapy for life-threatening arrhythmias. A potential role may exist for antiarrhythmic drugs, mainly amiodarone. There is growing evidence that patients with sustained VT or a history of resuscitation have the best outcome with ICD therapy regardless of the degree of heart failure. Many of these patients require additional antiarrhythmic therapy because of AF or nonsustained VTs that may activate the device. Catheter ablation or map-guided endocardial resection are additional options in selected patients but seldom represent the only therapeutic strategy.     

Management of Ventricular Fibrillation with Transvenous Defibrillators Without Baseline Electrophysiologic Testing or Antiarrhythmic Drugs

Tranvenous Defibrillators Without EP Testing. Introduction : Baseline electrophysiologic study (EPS) is routinely performed in patients resuscitated from ventricular fibrillation (VF) to risk stratify and select patients for chronic antiarrhythmic drug therapy. The role of EP testing prior to insertion of a multiprogrammable implantable cardioverter defibrillator (ICD), however, is unclear.
Methods and Results: This study was a retrospective review of outcome in 66 survivors of an initial episode of out-of-hospital VF not associated with a Q wave myocardial infarction or reversible causes, treated with transvenous ICDs as first-line therapy. Patients were excluded from the study if they had a previous history of monomorphic ventricular tachycardia (VT), a clinical history suggestive of supraventricular tachycardia, or had undergone preoperative EP testing. Fifty-two of the patients (79%) were male with an average age of 58 ± 11 years. Coronary artery disease was present in 43 patients (66%), cardiomyopathy in 15 patients (23%), and valvular heart disease in 1 patient (1.5%). Seven patients (11%) had no detectable structural heart disease. The mean left ventricular ejection fraction was 0.40 ± 0.16. With an average follow-up of 25 ± 12 months, survival free of death from any cause was 100%. Twenty-three patients (35%) experienced 48 episodes of recurrent rapid VT or VF (average cycle length: 236 ± 47 msec) treated by their device. The mean time to first therapy was 223 ± 200 days. Only one of these patients also received antitachycardia pacing for two episodes of VT. One patient (1. 5%) temporarily received amiodarone after removal of an infected device that was subsequently replaced. No other patient received antiarrhythmic drug therapy.
Conclusion : After a cardiac arrest due to primary VF, select patients treated with multiprogrammable ICDs can be managed successfully without baseline EPS or antiarrhythmic drug therapy.     

Outcome Studies with Device Therapy in Patients with Heart Failure

Device Therapy for Heart Failure. Heart failure is a common debilitating condition for which pharmacologic therapy thus far has provided only partial relief. Despite, and sometimes because of, medical therapy, the overall prognosis remains poor, with high rates of sudden death and death from progressive heart failure. Device‐based therapies offer considerable promise for relief of symptoms and for improving prognosis. It is clear that implantable defibrillators should be considered for patients with heart failure who have been resuscitated from ventricular fibrillation or sustained ventricular tachycardia. Several large studies currently are investigating the effects of implantable defibrillators on total mortality in patients with major left ventricular systolic dysfunction but without other risk factors for sudden death. Cardiac resynchronization is a promising new therapy that may relieve the symptoms of heart failure in appropriately selected patients resistant to optimal pharmacologic therapy. Two large trials (CARE‐HF and COMPANION) currently are investigating the effects of cardiac resynchronization therapy (CRT) on morbidity and mortality. It is important that those involved in these trials enroll patients quickly and minimize device implantation into patients who have not been assigned this therapy (cross‐overs). Overenthusiasm for the benefits that doctors believe devices might bring could destroy the future basis for our clinical practice, denying future generations of patients and the doctors themselves access to what they believe to be effective treatments.     

What is the "optimal" follow-up schedule for ICD patients?

BACKGROUND: In the absence of comparative studies, recommended routine follow-up (FU) intervals for implantable cardioverter defibrillator (ICD) patients range from 1 to 6 months; most patients are followed at 3 month intervals. METHODS: Six hundred and eighteen ICD patients were routinely seen 4 weeks after implant and then every 3 months. Unplanned visits (UPV) were either patient initiated or due to manufacturer recalls. FU visits included patient history/examination, ICD interrogation, pacing/sensing threshold and pacing/shock impedance. Chest X-rays were performed every 6 months. To validate FU interval recommendations, a comparative analysis on the detection of complications was performed, relying either on the information of every, or of every other FU visit, i.e., on 3 or 6 month intervals. RESULTS: During 3.3+/-2.8 years, 137 complications occurred in 110 patients (17%). However, identification of only 34% was dependent on the FU schedule, since the mode of detection was ICD interrogation in 38 and history/physical examination in nine patients. The remainder was diagnosed by UPV in 47, manufacturer recall in seven, accidental discovery during device replacement in two, and routine X-ray in 34 patients. Complication free survival at 2 years was 86.4% for patients implanted before 1999, and 89.2% thereafter (P=0.003). Regarding 6 rather than 3 month FU intervals, a theoretical maximum delay of 3 months in the detection of potentially life-threatening complications would have occurred in 1.7% of all patients. For those implanted after 1999, this related to only 0.9%. CONCLUSIONS: ICD-related complications detected during routine FU visits are relatively rare, particularly with newer generation ICD systems. Thus, 6 month FU intervals appear to be safe. With new developments such as patient alert features and telemedical data transmission, FU intervals in ICD clinics might even be further extended.     

植入型心律转复除颤器抗心动过速起搏治疗室性心动过速疗效评价

目的恶性室性心律失常（室性心动过速,心室颤动）是心脏性猝死的主要直接原因.而大部分患者先发生室性心动过速（室速）,继而蜕变为心室颤动（室颤）.研究表明,抗心动过速起搏（ATP）可有效终止室速.本文观察了172例植人植入型心律转复除颤器（ICD）的患者应用ATP终止室速的效果.方法172例植入ICD的患者,男性137例,女性35例,平均年龄52.8岁.103例患者术前有阿-斯综合征发作史,其中75例有电击除颤史.137例术前记录到室速或室颤心电图.植入ICD患者定期随访,随访时应用体外程控仪调出ICD储存记录,分析ICD治疗中ATP治疗室速的效果.结果在平均随访37个月中,ICD共记录室速l 789阵.其中,316阵为短阵室速,在ICD治疗前自行终止;1 473阵室速接受了ICD有效治疗.其中ATP治疗成功981阵（成功率66.6%）,余492阵室速由低能量转复终止.在981阵ATP治疗成功的事件中,ICD第一次发放ATP成功终止室速513阵（成功率52.3%）.结论ICD抗室速起搏功能可有效终止大多数室速,对于植入ICD前有明确室速史的患者,ICD治疗应尽量先采用ATP治疗,以减少ICD放电,延长ICD使用寿命及避免电击时的痛苦,即所谓的＂无痛性ICD治疗＂.     

Right ventricular pressure changes during induced ventricular tachycardias predict clinical symptoms of cerebral hypoperfusion: implications for a reduction of unnecessary, painful ICD shocks

Background : ICD shocks occurring in conscious patients (as in the case of well-tolerated arrhythmias, electromagnetic interference, or oversensing) have a deleterious impact on the quality of life. We evaluated if a hemodynamic parameter, calculated from the right ventricular pressure (RVP) or systemic arterial pressure (AP) signals, could predict early clinical symptoms of cerebral hypoperfusion during induced ventricular tachycardias (VTs).
Methods and results: We analyzed 42 tolerated (no symptoms) and 30 untolerated (syncope or severe symptoms within 30 seconds from the onset) VTs, induced during electrophysiological study. The cycle length (CL) and the hemodynamic data (mean AP and RVP, arterial pulse pressure and RV pulse pressure, and maximum AP and RVP dP/dT) were automatically sampled in two VT epochs: the "detection" window, from beat 24 to 32, and the "preintervention" window, immediately before the first therapeutic attempt. Although the CL and all the hemodynamic parameters (expressed as % change versus pre-VT values) were significantly lower in untolerated versus tolerated VTs both at detection and preintervention (with the exception of the mean RVP which progressively increased in both groups), ROC analysis demonstrated that only the preintervention RV pulse pressure showed no overlap between groups, providing 100% sensitivity and positive predictive value.
Conclusions: The reduction of the RV pulse pressure is a better predictor of early cerebral symptoms than CL or other hemodynamic indexes during induced VTs. Since long-term RVP monitoring is feasible, this parameter could be incorporated into ICDs decisional path, in the perspective of reducing unnecessary, painful shocks.     

Fatal inappropriate ICD shock

Introduction: Inappropriate implantable cardioverter defibrillator (ICD) therapy carries a low but relevant risk of ventricular proarrhythmia. In the present case, the extremely rare event of a fatal arrhythmia caused by inappropriate therapy is reported. Dislodgement of the ventricular lead to the level of the tricuspid annulus led to additional sensing of the atrial signal during sinus tachycardia. Spuriously, ventricular fibrillation was sensed and induced inappropriate ICD shocks. The fourth inappropriate shock caused ventricular fibrillation, which was subsequently undersensed by the dislodged lead due to low ventricular amplitudes. The ICD started antibradycardic pacing during ventricular fibrillation. After initial successful resuscitation, the patient died 1 week later due to severe hypoxic brain damage. Although not preventable in the present case, it underlines the necessity of immediate interrogation of the ICD after ICD therapy and deactivation of the ICD in the setting of a dislodged endocardial lead and intensive care monitoring of the patient until revision.