Implantable cardioverter defibrillators in heart failure.

Implantable cardioverter defibrillators provide effective and reliable treatment of spontaneous VT and VF. These devices can be expected to decrease the risk for arrhythmic death in patients with heart failure but do not improve overall survival when death from severe pump dysfunction is imminent. Appropriate patient selection is a major aspect of arrhythmia management. Future devices will incorporate features that have the potential to reduce atrial arrhythmias, improve ventricular function, monitor hemodynamics, and prevent sudden arrhythmic death.

Shock reduction using antitachycardia pacing for spontaneous rapid ventricular tachycardia in patients with coronary artery disease.

BACKGROUND: Implantable cardioverter-defibrillators (ICDs) can terminate some ventricular tachycardias (VTs) painlessly with antitachycardia pacing (ATP). ATP has not routinely been applied for VT >188 bpm because of concerns about efficacy, risk of acceleration, and delay of definitive shock therapy. This prospective, multicenter study evaluated the efficacy of empirical ATP to terminate fast VT (FVT; >188 bpm). METHODS AND RESULTS: Two hundred twenty coronary artery disease patients received ICDs for standard indications. Empirical, standardized therapy was programmed so that all FVT episodes (average cycle length [CL] 240 to 320 ms, 250 to 188 bpm) were treated with 2 ATP sequences (8-pulse burst pacing train at 88% of the FVT CL) before shock delivery. A total of 1100 episodes of spontaneous ventricular tachyarrhythmias occurred during a mean of 6.9+/-3.6 months of follow-up. Fifty-seven percent were classified as slow VT (CL>/=320 ms), 40% as FVT (240 ms

Recalls and safety alerts involving pacemakers and implantable cardioverter-defibrillator generators.

CONTEXT: Unanticipated pacemaker and implantable cardioverter-defibrillator (ICD) generator malfunctions sometimes warrant recall by the US Food and Drug Administration (FDA). Despite increasingly frequent device implantation, pacemaker and ICD recalls and safety alerts (advisories) remain poorly characterized. OBJECTIVES: To determine pacemaker and ICD generator advisory rates in the United States, to identify trends in these rates, and to examine their clinical and financial implications. DESIGN AND SETTING: Analysis of weekly FDA Enforcement Reports issued between January 1990 and December 2000 to identify all advisories involving pacemaker or ICD generators in the United States. Recalls and safety alerts involving lead malfunctions were not included. MAIN OUTCOME MEASURES: Number of pacemakers and ICD generators in the United States subject to FDA recall or safety alert in 1990-2000; annual pacemaker and ICD advisory rates in the United States in 1990-2000; and estimated cost of device advisories. RESULTS: During the study period, 52 advisories (median [25th and 75th percentiles], 4 [4 and 7] per year) involving 408 500 pacemakers and 114 645 ICDs (523 145 total devices) were issued. Hardware malfunctions (35 advisories affecting 280 641 devices) and computer errors (10 advisories affecting 216 533 devices) accounted for 95% of device recalls. Implantable cardioverter-defibrillators were recalled more frequently than pacemakers (mean [SD], 16.4 [1.6] vs 6.7 [0.8] advisories per 100 person-years; P<.001). Between 1995 and 2000, the annual advisory rate increased for both pacemakers (P for trend <.001) and ICDs (P for trend =.02). An estimated 1.3 million device checks and analyses and 36 187 device replacements resulted from the advisories and cost approximately $870 million. CONCLUSIONS: Pacemaker and ICD recalls and safety alerts occur frequently, affect many patients, and appear to be increasing in number and rate. With the growing number of device implants and expanding indications for device therapy, the number of patients affected by device advisories will likely continue to increase.

Provoked and spontaneous high-frequency, low-amplitude, respirophasic noise transients in patients with implantable cardioverter defibrillators.

INTRODUCTION: Ventricular oversensing (OS) of respirophasic noise transients may cause spurious detections and therapies and pacing inhibition among patients with implantable cardioverter defibrillators (ICDs). The incidence of OS and its relationship to clinical variables and ICD system design are unknown. METHODS AND RESULTS: Three hundred twenty-nine patients performed provocative respiratory maneuvers at rest during intrinsic rhythm and continuous ventricular pacing. OS resulting in spurious ventricular detections was provoked in 3 (0.9%) of 329 patients during intrinsic rhythm and 34 (10.3%) of 329 during pacing. Noise transients not recognized and marked as sensed events, but visually evident on the local endocardial ventricular electrogram, were provoked in an additional 23 (7.0%) of 329 patients. Multivariate logistic regression identified history of spontaneous OS (P < 0.0005, odds ratio 9.7, 95% confidence interval [CI] 1.9 to 50.0), automatic gain control device (P < 0.0005, odds ratio 5.3, 95% CI 2.6 to 10.8) or integrated bipolar lead (P = 0.05, odds ratio 2.6, 95% CI 1.0 to 7.25), and male gender (P = 0.008, odds ratio 3.7, 95% CI 1.2 to 11.1) as predictive of provocable OS. Spontaneous OS resulting in spurious ventricular detections and therapies occurred in 12 (3.6%) patients during follow-up. Eleven of 12 spontaneous episodes occurred in male patients during ventricular pacing; 11 of 12 patients had automatic gain control devices and integrated bipolar leads. CONCLUSION: OS is commonly provoked in ICD patients during ventricular pacing and may occur spontaneously, causing spurious tachyarrhythmia therapies and pacing inhibition. Differences in the incidence of spontaneous and provoked OS between ICD systems can be explained on the basis of unique features of automatic sensing systems and sensing lead design.

Prospective randomized comparison of 50%/50% versus 65%/65% tilt biphasic waveform on defibrillation in humans.

It is unknown if there is a single optimal biphasic waveform for defibrillation. Biphasic waveform tilt may be an important determinant of defibrillation efficacy. The purpose of this study was to compare acute defibrillation success with a three-electrode configuration in humans using 50%/50% versus 65%/65% tilt truncated exponential, biphasic waveforms delivered through a 110-microF capacitor. Acute DFTs for biphasic waveforms with 50%/50% versus 65%/65% tilt were measured in random order in 60 patients using a binary search method. The electrode configuration consisted of a RV coil as the cathode, and a SVC coil plus a pectoral active can emulator (CAN) as the anode. The waveforms were derived from an external voltage source with 110-microF capacitance, and the leading edge voltage of phase 2 was equal to the trailing edge voltage of phase 1. Stored energy DFT (9.2 +/- 5.7 [50%/50%] vs 10.8 +/- 6.4 [65%/65%] J, P = 0.007), current DFT (10.9 +/- 4.0 [50%/50%] vs 12.0 +/- 4.4 [65%/65%] A, P = 0.002) and voltage DFT (391 +/- 118 [50%/50%] vs 424 +/- 128 [65%/65%] V, P = 0.004) were significantly lower for the 50%/50% tilt waveform versus the 65%/65% tilt waveform using this three-electrode configuration and a 110-microF capacitor. For an RV(-)/SVC plus CAN(+) electrode configuration and a 110-microF capacitor, a 50%/50% tilt biphasic waveform results in a 15% reduction in energy DFT, 9% reduction in current DFT, and 8% reduction in voltage DFT versus a 65%/65% tilt biphasic waveform.

Exploding implantable cardioverter defibrillator.

A 79-year-old man with a pectoral implantable cardioverter defibrillator (ICD) system underwent periodic defibrillation threshold testing 18 months after implant. Attempted delivery of a 15-J shock caused a light flash above the pocket and a loud "pop." High-voltage lead impedance was <20 ohms. Pocket exploration revealed insulation abrasion of the high-voltage portion of the single-coil right ventricular lead. The outer shield of the active can pulse was perforated and scorched due to arcing. Device analysis confirmed a shorted transistor in the high-voltage output circuit. Unsuspected physical contact between high-voltage electrodes of opposite polarity within the pocket can cause catastrophic ICD system failure.

Catheter ablation for hemodynamically unstable monomorphic ventricular tachycardia.

INTRODUCTION: Hemodynamic collapse precludes extensive catheter mapping to identify focal target regions in many patients with ventricular tachycardia (VT) associated with heart disease. This study tested the feasibility of catheter ablation of poorly tolerated VTs by targeting a region identified during sinus rhythm. METHODS AND RESULTS: Ablation was attempted in five patients, ages 44 to 59 years, with left ventricular ejection fractions of 0.15 to 0.20 and poorly tolerated VT causing multiple implantable defibrillator therapies (6 to 30 episodes/month). VT was due to prior infarction in three patients and nonischemic cardiomyopathy in two. Target regions were sought that met the following criteria: (1) evidence of slow conduction from fractionated sinus rhythm electrograms and stimulus-QRS delays during pace mapping, and (2) evidence that the region contains the reentrant circuit exit from pace mapping. In 4 of 5 patients, a target region was identified and radiofrequency lesions applied. Ablation abolished all recurrences of VT in 3 of 4 patients during follow-up of 14 to 22 months. There were no complications. CONCLUSION: Ablation of poorly tolerated VT is feasible in some patients by mapping during sinus rhythm and performing ablation over a region of identifiable scar that contains abnormal conduction and a presumptive VT exit.

Arrhythmias and sudden death in heart failure.

Survival of patients with heart failure has improved over the past decade due to advances in medical therapy. Sudden death continues to cause 20 to 50% of deaths. Ventricular arrhythmias are common in patients with heart failure. Ventricular hypertrophy, scars from prior myocardial infarction, sympathetic activation, and electrolyte abnormalities contribute. Some sudden deaths are due to bradyarrhythmias and electromechanical dissociation rather than ventricular arrhythmias. The risks and benefits of antiarrhythmic therapies continue to be defined. Class I antiarrhythmic drugs should be avoided due to proarrhythmic and negative inotropic effects that may increase mortality. For patients resuscitated from sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) amiodarone or an implantable cardioverter defibrillator (ICD) should be considered. ICDs markedly reduce sudden death in VT/VF survivors, but in advanced heart failure, this may not markedly extend survival. Catheter or surgical ablation can be considered for selected patients with bundle branch reentry VT or difficult to control monomorphic VT. For patients who have not had sustained VT/VF antiarrhythmic therapy should generally be avoided, but may benefit some high risk patients. Amiodarone may be beneficial in patients with advanced heart failure and rapid resting heart rates. ICDs may improve survival in selected survivors of myocardial infarction who have inducible VT.

Simulated internal defibrillation in humans using an anatomically realistic three-dimensional finite element model of the thorax.

INTRODUCTION: Determination of the optimal electrode configuration during implantable cardioverter defibrillator (ICD) implantation remains largely an empirical process. This study investigated the feasibility of using a finite element model of the thorax to predict clinical defibrillation metrics for internal defibrillation in humans. Computed defibrillation metrics from simulations of three common electrode configurations with a monophasic waveform were compared to pooled metrics for similar electrode and waveform configurations reported in humans. METHODS AND RESULTS: A three-dimensional finite element model was constructed from CT cross-sections of a human thorax. Myocardial current density distributions for three electrode configurations (epicardial patches, right ventricular [RV] coil/superior vena cava [SVC] coil, RV coil/SVC coil/subcutaneous patch) and a truncated monophasic pulse with a 65% tilt were simulated. Assuming an inexcitability threshold of 25 mA/cm2 (10 V/cm) and a 75% critical mass criterion for successful defibrillation, defibrillation metrics (interelectrode impedance, defibrillation threshold current, voltage, and energy) were calculated for each electrode simulation. Values of these metrics were within 1 SD of sample-size weighted means for the corresponding metrics determined for similar electrode configurations and waveforms reported in human clinical studies. Simulated myocardial current density distributions suggest that variations in current distribution and uniformity partially explain differences in defibrillation energy requirements between electrode configurations. CONCLUSION: Anatomically realistic three-dimensional finite element modeling can closely simulate internal defibrillation in humans. This may prove useful for characterizing patient-specific factors that influence clinically relevant properties of current density distributions and defibrillation energy requirements of various ICD electrode configurations.

Pharmacologic and nonpharmacologic treatment of ventricular arrhythmias in heart failure.

Ventricular arrhythmias are common in patients with heart failure. The risk and benefits of antiarrhythmic therapies continue to be defined. Class I antiarrhythmic drugs should be avoided due to proarrhythmic and negative inotropic effects that may be responsible for increased mortality in some trials. For patients resuscitated from sustained ventricular tachycardia or ventricular fibrillation, amiodarone or an implantable cardioverter-defibrillator should be considered. Implantable cardioverter-defibrillators markedly reduce sudden death in ventricular tachycardia and ventricular fibrillation survivors, but in advanced heart failure, this may not markedly extend survival. Catheter or surgical ablation can be considered for selected patients with bundle branch reentry ventricular tachycardia or difficult to control monomorphic ventricular tachycardia. For patients who have not had sustained ventricular tachycardia or ventricular fibrillation antiarrhythmic therapy should generally be avoided, but may benefit some high risk patients. Amiodarone may be beneficial in patients with advanced heart failure and rapid resting heart rates. Implantable cardioverter-defibrillators may improve survival in selected patients with depressed ventricular function after myocardial infarction, who also have nonsustained and inducible ventricular tachycardia.

Influence of the implantable cardioverter/defibrillator on sudden death and total mortality in patients evaluated for cardiac transplantation.

BACKGROUND: Implantable cardioverter/defibrillators (ICDs) may reduce sudden tachyarrhythmic death in patients with severe left ventricular dysfunction. It is uncertain whether this improves survival, particularly in patients awaiting cardiac transplantation. METHODS AND RESULTS: The effect of treatment for spontaneous ventricular arrhythmias (ICD [n = 59], antiarrhythmic drugs [n = 53], or no antiarrhythmic treatment [n = 179]) on total mortality and mode of cardiac death was analyzed in 291 consecutive patients evaluated for cardiac transplantation between January 1986 and January 1995. There were 109 deaths (37.4%) (63 [21.6%] sudden, 40 [13.7%] nonsudden, and 6 [2.1%] noncardiac) during mean follow-up of 15 months (range, 1 to 118 months). Baseline clinical variables, medical therapies for heart failure, and actuarial rates of transplantation were similar between treatment groups. Kaplan-Meier sudden death rates were lowest in the ICD group, intermediate in the no antiarrhythmic treatment group, and highest in the drug treatment group throughout follow-up (12-month sudden death rates, 9.2%, 16.0%, and 34.7%, respectively; P = .004). Total mortality and nonsudden death rates did not differ. Cox proportional-hazards model revealed that antiarrhythmic drug treatment was associated with sudden death (relative risk, 2.1; 95% CI, 1.04 to 3.39; P = .04) and ICD was associated with nonsudden death (relative risk, 2.26; 95% CI, 1.12 to 4.62; P = .02). CONCLUSIONS: Sudden death rates were lowest in patients treated with ICDs compared with drug treatment or no antiarrhythmic treatment. However, although ICDs reduced sudden death in selected high-risk patients with severe left ventricular dysfunction, the effect on long-term survival was limited, principally by high nonsudden death rates.

Malfunction of implantable cardioverter defibrillators placed by a nonthoracotomy approach: frequency of malfunction and value of chest radiography in determining cause.

OBJECTIVE: The purpose of this study was to determine the frequency of system malfunction in patients with nonthoracotomy implantable cardioverter defibrillators and to assess the role of chest radiography in detecting and determining the cause of malfunction. MATERIALS AND METHODS: The study population consisted of 300 consecutive patients in whom implantable cardioverter defibrillators were implanted using an initial nonthoracotomy approach between September 1990 and October 1994. Transvenous electrodes were placed via the subclavian or cephalic vein under local anesthetic. Intraoperative testing, pulse generator implantation, and, if necessary, subcutaneous patch or extrapericardial patch placement via thoracotomy were done in the operating room under general anesthetic. Follow-up consisted of routine device interrogation every 2-3 months and annual chest radiography. Chest radiographs were obtained more often if patients were symptomatic or if results of device interrogation were abnormal. RESULTS: Patients were followed up for a mean +/- SD of 19 +/- 14 months following implantation. Implantable cardioverter-defibrillator malfunction occurred in 17 patients (6%) during the follow-up period. Of these, 12 (71%) had component abnormalities on chest radiographs. Patients with radiographically apparent implantable cardioverter-defibrillator abnormalities presented in two discrete time periods after device implantation, early (mean, 35 +/- 14 days) and late (mean, 18 +/- 5 months). CONCLUSION: Malfunction of nonthoracotomy implantable cardioverter-defibrillator systems develops infrequently after device implantation. In most cases, the cause can be identified on chest radiographs.

Mortality benefits and the implantable cardioverter-defibrillator.

The automatic implantable cardioverter-defibrillator (ICD) is highly effective in reducing sudden death rates in patients with life-threatening ventricular tachyarrhythmias. However, the magnitude of the ability of the ICD to improve overall survival is less certain. Data supporting the contention that the ICD prolongs survival are reviewed. It is evident that the mortality benefit consequent to the marked reduction in sudden death varies widely across subpopulations in a predictable manner. This observation reflects the powerful influence of other clinical factors that constrain survival in typical ICD patients. The implications for future studies on the ICD are discussed.

Instantaneous cardiac death in the posthospital period after acute myocardial infarction.

Sudden arrhythmic cardiac death is a major unresolved health problem, yet there is no agreement on the chronologic definition of sudden death. This retrospective study investigates the frequency distribution of the chronology of the terminal cardiac event in a large postinfarction population and identifies factors associated with instantaneous (< 1 minute) cardiac death. This study involved 229 patients enrolled in the Multicenter Diltiazem Post-infarction Trial who died during 2-year follow-up and had quantitative information on the chronology of the terminal event. Thirty-two percent of the cardiac deaths occurred instantaneously. Patients who died instantaneously were more likely (p < 0.05) to be men, to have a baseline ejection fraction < 0.40, and to have frequent (> or = 10/hour) and repetitive (> or = 3 in a row) ventricular ectopic complexes (VECs) on an ambulatory electrocardiogram than those who did not die instantaneously. Patients who died instantaneously received more digitalis and class IA antiarrhythmic agents and less beta blockers in the week before death than those dying noninstantaneously. Logistic regression analysis identified 3 independent factors that differentiated instantaneous from noninstantaneous death (relative risk; 95% confidence interval): frequent VECs (2.15; 1.11 to 4.17); digitalis (2.57; 1.31 to 5.06); and no beta blocker medication (2.90; 1.09 to 7.75). Instantaneous death (within 1 minute) was responsible for almost one third of the cardiac deaths that occurred in this postinfarction population. Frequent VECs, digitalis, and absence of beta-blocker therapy distinguished patients who died instantaneously from those who died noninstantaneously.

Effects of oral labetalol on forearm and hepatic circulations in normotensive humans.

The effects of single oral labetalol doses (100, 200, and 400 mg) on forearm and hepatic circulations were studied over a 2-hour period in 27 normotensive human subjects by using a double-blind, placebo-controlled design. Labetalol administration resulted in a dose-dependent beta-receptor blockade as determined by an isoproterenol sensitivity test. It also produced a dose-dependent decrease in mean arterial blood pressure that was of greater duration at larger doses. At the lowest dose labetalol produced a transient decrease in arterial pressure followed by a decrease in forearm blood flow and increase in forearm vascular resistance. As the dose of labetalol increased, the hypotensive response became more prolonged, but the changes in forearm blood flow and vascular resistance no longer occurred. Heart rate did not change significantly after any of these doses. Hepatic blood flow also did not change significantly after labetalol. Our results suggest that the increase in forearm vascular resistance after the lowest dose of labetalol probably was caused by unopposed alpha-receptor activation because the agent had a relatively greater beta-receptor blocking action at the low doses, but as the dose increased the alpha-receptor blocking action of the drug became more pronounced and abolished the vasoconstrictor effect in the forearm. Furthermore, our study indicates that despite the significant drop in arterial pressure at doses greater than 100 mg, blood flow is well maintained to the skeletal muscle and splanchnic circulations during labetalol therapy.