Intradevice interaction in a dual chamber implantable cardioverter defibrillator preventing ventricular tachyarrhythmia detection.

Failure to detect ventricular tachycardia and/or ventricular fibrillation by implantable cardioverter defibrillators (ICDs) is a rare but serious problem. We report a case of failure to detect an episode of induced ventricular tachycardia by a dual chamber ICD, due to abbreviation of ventricular detection window secondary to programmed pacing parameters and a rate-smoothing algorithm. In this patient, the intradevice interaction was corrected by programming rate-smoothing off. This report highlights the potentially lethal consequences of critical timing relationships among the pacing function, arrhythmia detection, and the characteristics of the arrhythmia when using a modern dual chamber ICD. Physicians responsible for patients with ICDs must be aware of such interactions.

Improved survival in patients with nonischemic advanced heart failure and syncope treated with an implantable cardioverter-defibrillator.

The purpose of this study was to assess whether in patients with syncope and heart failure due to nonischemic cardiomyopathy, treatment with an implantable cardioverter-defibrillator (ICD) compared with conventional medical therapy is associated with a reduction in sudden death and total mortality. Patients with advanced heart failure who have syncope have been shown to be at high risk for sudden death. Further risk stratification has been difficult in patients with nonischemic cardiomyopathy in whom inducibility on electrophysiologic study is not predictive of future risk. Of 639 consecutive patients with nonischemic cardiomyopathy referred for heart transplantation, 147 patients with history of syncope and no prior history of sustained ventricular tachycardia or cardiac arrest were identified. Outcomes were compared for the 25 patients managed with an ICD and 122 patients managed with conventional medical therapy. There were no differences in the baseline variables in the 2 groups of patients, including age, ejection fraction, and medical treatments for heart failure, but patients receiving an ICD were more likely to have had nonsustained ventricular tachycardia (56% vs. 15%, p = 0.001). During a mean follow-up of 22 months, there were 31 deaths, 18 sudden, in patients treated with conventional therapy, whereas there were 2 deaths, none sudden, in patients treated with an ICD. An appropriate shock occurred in 40% of the ICD patients. Actuarial survival at 2 years was 84.9% with ICD therapy and 66.9% with conventional therapy (p = 0.04). Thus, in patients with nonischemic cardiomyopathy and syncope, therapy with an ICD is associated with a reduction in sudden death and an improvement in overall survival.

Anatomic and electrophysiologic relation between the coronary sinus and mitral annulus: implications for ablation of left-sided accessory pathways.

To determine whether precise left-sided accessory pathway localization is possible from the coronary sinus, electrocardiogram (ECG) characteristics from the coronary sinus pair demonstrating earliest activation via the accessory pathway were compared to simultaneous mitral annular ablation catheter ECGs at successful ablation sites in 48 patients. To define the coronary sinus-mitral annular relation, the coronary sinus to mitral annulus distance (D) was measured at sequential distances from the coronary sinus os in 10 cadaver hearts. Mitral annular ECGs demonstrated earliest activation via the accessory pathway more frequently than the earliest coronary sinus pair (p < 0.001), more frequent continuous electrical activity (p < 0.001), and more frequent accessory pathway potentials (p < 0.01). D was >10 mm at 20, 40, and 60 mm, respectively, from the coronary sinus os. Coronary sinus ECGs do not precisely localize left-sided accessory pathways, which may be due in part to an average anatomic separation of more than 10 mm between the coronary sinus and accessory pathways bridging the mitral annulus.

Exploring postinfarction reentrant ventricular tachycardia with entrainment mapping.

Ventricular tachycardia late after myocardial infarction is usually due to reentry in the infarct region. These reentry circuits can be large, complex and difficult to define, impeding study in the electrophysiology laboratory and making catheter ablation difficult. Pacing through the electrodes of the mapping catheter provides a new approach to mapping. When pacing stimuli capture the effects on the tachycardia depend on the location of the pacing site relative to the reentry circuit. The effects observed allow identification of various portions of the reentry circuit, without the need for locating the entire circuit. Isthmuses where relatively small lesions produced by radiofrequency catheter ablation can interrupt reentry can often be identified. A classification that divides reentry circuits into one or more functional components helps to conceptualize the reentry circuit and predicts the likelihood that heating with radiofrequency current will terminate tachycardia. These methods are helping to define human reentry circuits.

Implantable defibrillators for high-risk patients with heart failure who are awaiting cardiac transplantation.

The objective of this study was to assess the operative risk and efficacy of implantable defibrillators for preventing sudden death in patients with heart failure awaiting transplantation. The average waiting time for elective cardiac transplantation is 6 months to 1 year. Sudden cardiac death is the major source of mortality in outpatients in stable condition awaiting cardiac transplantation. The efficacy of implantable defibrillator therapy in this population is not established. We analyzed the operative risk, time to appropriate shock, and sudden death in 15 patients determined to be at high risk of sudden death who were accepted onto the outpatient cardiac transplant waiting list. Nonfatal postoperative complications occurred in two (13%) subjects with epicardial defibrillating lead systems and in none with transvenous lead systems. Defibrillation energies were 16 +/- 2 J versus 24 +/- 2 J with epicardial and transvenous lead systems, respectively. Sudden death free survival until transplantation was 93%. Most of the patients (60%) had an appropriate shock during a mean follow-up of 11 +/- 12 months. The mean time to an appropriate shock was 3 +/- 3 months. Hospital readmission was required in three (20%) subjects to await transplantation on an urgent basis. However, two of these subjects had received appropriate shocks before readmission. In selected patients at high risk for sudden death while on the outpatient cardiac transplant waiting list, the operative risk is low and adequate defibrillation energies can be obtained to allow implantable defibrillator placement. Most subjects will have an appropriate shock as outpatients before transplantation, and sudden death free survival is excellent.(ABSTRACT TRUNCATED AT 250 WORDS)

Relation of pace mapping QRS configuration and conduction delay to ventricular tachycardia reentry circuits in human infarct scars.

OBJECTIVES: This study sought to determine the relation of the paced QRS configuration and conduction delay during pace mapping to reentry circuit sites in patients with ventricular tachycardia late after myocardial infarction. BACKGROUND: The QRS configuration produced by ventricular pacing during sinus rhythm (pace mapping) can locate focal idiopathic ventricular tachycardias during catheter mapping, but postinfarction reentry circuits may be relatively large and contain regions of slow conduction. We hypothesized that for postinfarction ventricular tachycardia, 1) pacing during sinus rhythm at reentry circuit sites distant from the exit from the scar would produce a QRS configuration different from the tachycardia; and 2) a stimulus to QRS delay during pace mapping may be a useful guide to reentry circuit slow conduction zones. METHODS: Catheter mapping and ablation were performed in 18 consecutive patients with ventricular tachycardia after myocardial infarction. At 85 endocardial sites in 13 patients, 12-lead electrocardiograms (ECGs) were recorded during pace mapping, and participation of each site in a reentry circuit was then evaluated by entrainment techniques during induced ventricular tachycardia or by application of radiofrequency current. RESULTS: Pace maps resembled tachycardia at < 30% of likely reentry circuit sites identified by entrainment criteria and at only 1 (9%) of 11 sites where radiofrequency current terminated tachycardia. Analysis of the stimulus to QRS interval during entrainment with concealed fusion showed that the conduction time from the pacing site to the exit from the scar was longer at sites where the pace map did not resemble tachycardia. Evidence of slow conduction during pace mapping, with a stimulus to QRS interval > 40 ms was observed at > or = 70% of reentry circuit sites. CONCLUSIONS: At many sites in postinfarction ventricular reentry circuits, the QRS configuration during pace mapping does not resemble the ventricular tachycardia QRS complex, consistent with relatively large reentry circuits or regions of functional conduction block during ventricular tachycardia. A stimulus to QRS delay during pace mapping is consistent with slow conduction and may aid in targeting endocardial sites for further evaluation during tachycardia.

Low-dose amiodarone for atrial fibrillation.

Concerns about proarrhythmia risk and inefficacy associated with class I antiarrhythmic drugs have revived interest in low-dose amiodarone (maintenance dose 200-400 mg/day) for suppression of atrial fibrillation. In nonrandomized trials of amiodarone for atrial fibrillation refractory to conventional agents, amiodarone has been successful in maintaining sinus rhythm in 53-79% of patients during a mean follow-up of 15-27 months. Intolerable side effects, including pulmonary toxicity, are in the range of 1-12% per year and resolve following amiodarone withdrawal in the majority of cases. Proarrhythmia risk associated with amiodarone, even in the setting of left ventricular dysfunction, is extremely low. In patients with congestive heart failure, in whom other pharmacologic options are limited by proarrhythmia risk and negative inotropism, preliminary experience with amiodarone is especially promising. Randomized trials are needed, directly comparing amiodarone to conventional antiarrhythmic therapy for atrial fibrillation suppression and comparing amiodarone to warfarin for thromboembolism prevention in patients with atrial fibrillation refractory to conventional antiarrhythmic drugs.

Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction.

BACKGROUND: Ventricular tachycardia reentry circuits in chronic infarct scars can contain slow conduction zones, which are difficult to distinguish from bystander areas adjacent to the circuit during catheter mapping. This study developed criteria for identifying reentry circuit sites using computer simulations. These criteria then were tested during catheter mapping in humans to predict sites at which radiofrequency current application terminated ventricular tachycardia. METHODS AND RESULTS: In computer simulations, effects of single stimuli and stimulus trains at sites in and adjacent to reentry circuits were analyzed. Entrainment with concealed fusion, defined as ventricular tachycardia entrainment with no change in QRS morphology, could occur during stimulation in reentry circuit common pathways and adjacent bystander sites. Pacing at reentry circuit common pathway sites, the stimulus to QRS (S-QRS) interval equals the electrogram to QRS interval (EG-QRS) during tachycardia. The postpacing interval from the last stimulus to the following electrogram equals the tachycardia cycle length. Pacing at bystander sites the S-QRS exceeds the EG-QRS interval when the conduction time from the bystander site to the circuit is short but may be less than or equal to the EG-QRS interval when the conduction time to the circuit is long. The postpacing interval, however, always exceeds the tachycardia cycle length. When conduction in the circuit slows during pacing, the S-QRS and postpacing intervals increase and the slowest stimulus train most closely reflects conduction times during tachycardia. Endocardial catheter mapping and radiofrequency ablation were performed during 31 monomorphic ventricular tachycardias in 15 patients with drug refractory ventricular tachycardia late after myocardial infarction. During ventricular tachycardia, trains of electrical stimuli or scanning single stimuli were evaluated before application of radiofrequency current at the same site. Radiofrequency current terminated ventricular tachycardia at 24 of 241 sites (10%) in 12 of 15 patients (80%). Ventricular tachycardia termination occurred more frequently at sites with entrainment with concealed fusion (odds ratio, 3.4; 95% confidence interval [CI], 1.4 to 8.3), a postpacing interval approximating the ventricular tachycardia cycle length (odds ratio, 4.6; 95% CI, 1.6 to 12.9) and an S-QRS interval during entrainment of more than 60 milliseconds and less than 70% of the ventricular tachycardia cycle length (odds ratio, 4.9; 95% CI, 1.4 to 17.1). Ventricular tachycardia termination was also predicted by the presence of isolated diastolic potentials or continuous electrical activity (odds ratio, 5.2; 95% CI, 1.8 to 15.5), but these electrograms were infrequent (8% of all sites). Combinations of entrainment with concealed fusion, postpacing interval, S-QRS intervals, and isolated diastolic potentials or continuous electrical activity predicted a more than 35% incidence of ventricular tachycardia termination during radiofrequency current application versus a 4% incidence when none suggested that the site was in the reentry circuit. Analysis of the postpacing interval and S-QRS interval suggested that 25% of the sites with entrainment with concealed fusion were in bystander areas not within the reentry circuit. At restudy 5 to 7 days later, 6 patients had no monomorphic ventricular tachycardia inducible, and inducible ventricular tachycardias were modified in 4 patients. None of these 10 patients have suffered arrhythmia recurrences during a follow-up of 316 +/- 199 days, although 4 continue to receive previously ineffective medications. CONCLUSIONS: Regions giving rise to reentry after myocardial infarction are complex and can include bystander areas, slow conduction zones, and isthmuses for impulse propagation at which radiofrequency current lesions can interrupt reentry.

Ventricular tachycardia after infarction: sources of coronary blood flow to the infarct zone.

The purpose of this study was to determine the sources of coronary blood flow to infarct scars in patients with sustained ventricular tachycardia occurring late after myocardial infarction, which is necessary for transcoronary sclerosis or embolization. Angiograms of 32 consecutive patients (age 63 +/- 8 years, ejection fraction 0.30 +/- 0.10) were reviewed. Sources of blood flow to the infarct zone were identified as coming from a recanalized infarct-related artery, side branch, collateral, or coronary bypass graft. Eighty-four percent of patients in the study had an identifiable blood supply to the area of previous infarction. More than one source of blood flow to anterior infarct locations were observed more often than to inferior infarct locations (53% vs 17%, p = 0.03). Transcoronary mapping for possible chemical ablation should be technically feasible in the majority of patients with ventricular tachycardia. Infarct zone blood flow arises from any of several sources and varies somewhat depending on infarct location.

Low-dose amiodarone for atrial fibrillation: time for a prospective study?

Because atrial fibrillation is associated with substantial morbidity, restoration of sinus rhythm is desirable. Long-term maintenance of sinus rhythm often requires chronic antiarrhythmic therapy. Class I antiarrhythmic drugs such as quinidine or propafenone maintain sinus rhythm in approximately 50% of patients at 1 year and have risks for proarrhythmia and noncardiac toxicity. Studies of low-dose amiodarone for atrial fibrillation have reported sinus rhythm maintenance in 53% to 79% of patients during a mean follow-up of 27 months. Amiodarone has a lower incidence of proarrhythmia and heart failure exacerbation compared with class I drugs. Most noncardiac side effects are dose related, and low-dose amiodarone (less than 300 mg/d) is well tolerated. The time has come for a large-scale prospective evaluation of low-dose amiodarone treatment early in the course of atrial fibrillation.

Identifying sites for catheter ablation of ventricular tachycardia.

The approach to localizing sites for catheter ablation of ventricular tachycardia foci depends on the type of tachycardia. In large reentry circuits such as those arising from infarct scars, areas of slow conduction in and around the scar should be targeted. During sinus rhythm, these can be suspected from the presence of fractionated electrograms and, at some sites, long stimulus to QRS delays during pacing. Slow conduction areas can be classified as: 1. central slow conduction zone sites, 2. exits from the slow conduction zone, 3. entrances to the slow conduction zone, and 4. bystander areas which are not involved in the tachycardia circuit. In the central slow conduction zone stimulation entrains or resets tachycardia with a long stimulus to QRS (S-QRS) delay (40 to greater than 300 ms) without altering the QRS morphology (entrainment with concealed fusion). At slow conduction zone exits, presystolic electrograms are recorded during VT, the pacemap matches the VT QRS morphology, and with pacing during VT the S-QRS interval is relatively short and VT may or may not be entrained. At entrances to the slow conduction zone electrogram timing is variable but early diastolic electrograms are expected and the pace-map QRS may differ from the VT QRS morphology. Relatively late stimuli or slow trains of stimuli entrain VT with concealed fusion with a relatively longer S-QRS interval than observed in the central slow conduction zone. Early stimuli may entrain VT while altering the QRS morphology due to propagation of the stimulated antidromic wavefront out of the scar from a site other than the tachycardia exit. At bystander sites electrogram timing, pace-mapping, and the effects of programmed stimulation are variable but may occasionally mimic reentry circuit sites. Relatively late stimuli are likely to capture the site without altering the VT. If discrete electrograms are present, analysis of these during pacing may provide further evidence that the site is not in the reentry circuit. Catheter ablation will probably be most effective at central slow conduction zone sites. When VT originates from a small focus surrounded by normal myocardium, such as is likely for idiopathic RV outflow tract and some idiopathic left ventricular tachycardias, presystolic electrical activity and pacemapping are likely to identify the tachycardia focus. For macroreentry involving the bundle branches, the right bundle branch can be easily targeted.

Cholelithiasis associated with medroxyprogesterone acetate therapy in men.

Five out of forty-five adult men, 50 years of age or less, who had received, for at least six months, medroxyprogesterone acetate (MPA, Depo Provera) IM, 200-400 mg/week, for prevention of sex-offending or genital-mutilating behavior developed symptomatic cholelithiasis. Thirty of these men were studied with gallbladder ultrasound prospectively off MPA and at six-month intervals while taking the medication and then six months off MPA. Gallstones recovered from two patients were found to have very high cholesterol content, suggesting they were formed in cholesterol supersaturated bile. These findings are consistent with the increased incidence of gallbladder disease related to high-progesterone states and suggest that MPA may be a causative agent in cholelithiasis. The physiologic studies on gallbladder contraction and cholecystokinin release in a subset of the patients failed to provide information on a mechanism for the possible increased incidence of gallbladder disease.

Treatment of catecholamine-sensitive right ventricular tachycardia by endocardial catheter ablation.

Endocardial catheter ablation with direct current high voltage shocks was performed in a patient with recurrent syncope due to a catecholamine-sensitive ventricular tachycardia that was drug refractory and occurred in the absence of identifiable heart disease. Pace mapping and catheter activation mapping of the spontaneous and isoproterenol-induced ventricular tachycardia located the tachycardia origin in the right ventricular outflow tract. Ablation dramatically reduced spontaneous ventricular tachycardia and ectopic activity (from 50,000 to less than 100 ectopic beats/24 h). The patient has remained symptom free and without ventricular tachycardia recurrence for 3 years. These observations and review of previous studies suggest that catheter mapping can easily locate the arrhythmia focus in the right ventricular outflow tract and that catheter ablation can be performed at low risk. Catheter ablation is a viable option for the treatment of right ventricular catecholamine-sensitive tachycardias that are unresponsive to antiarrhythmic drugs.

Coronary artery spasm and myocardial infarction in a patient with normal coronary arteries: temporal relationship to pseudoephedrine ingestion.

A 28 yr-old male presented with chest pain and acute ST elevation following ingestion of pseudoephedrine. The pain and electrocardiographic changes disappeared after the administration of sublingual Nitroglycerin. Myocardial enzymes did show some evidence for myocardial necrosis. A subsequent coronary arteriogram showed no occlusive lesions. Pseudoephedrine, a sympathomimetic agent, may be implicated in the initiation of coronary spasm and myocardial infarction in some patients.