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Previous work had demonstrated a reduced specificity associated with head-up tilt protocols using high-dose isoproterenol in patients between 20 and 50 years of age. We evaluated the specificity of head-up tilt testing using different isoproterenol infusion doses and administration of nitroglycerin in patients aged >60 years. In addition, whether the same protocols have impact on the sensitivity of the test was also assessed. One hundred sixty subjects were included in this study. Seventy-six were volunteers randomized to either head-up tilt test with low-dose, 3- and 5-microg/min of isoproterenol (group I) or to a protocol including 0.4 mg of sublingual nitroglycerin (group II). In addition, after an upright tilt drug-free state, 58 patients with a history of syncope underwent repeat head-up tilt with increasing doses of isoproterenol infusion, followed by sublingual nitroglycerin if the test result remained negative. The remaining 33 patients were subjected to the nitroglycerin protocol after the drug-free state phase. In the control groups, the incidence of false-positive responses was 88% and 95%, respectively. In patients with syncope after a negative test result during 5 microg of isoproterenol infusion, nitroglycerin administration increased the number of positive responses from 45% to 79%. The percentage of positive tilt in patients undergoing nitroglycerin administration after the drug-free state part of the protocol was 78%. Administration of nitroglycerin was the most significant predictor of a positive upright tilt in patients with syncope. In subjects aged >60 years, head-up tilt protocols with high-dose isoproterenol infusion and nitroglycerin maintained an adequate specificity. In this subset of patients, nitroglycerin seemed to provide a better sensitivity than isoproterenol.

The Jewel 7219D was the first non-thoracotomy implantable cardioverter-defibrillator (ICD) with biphasic shock capability small enough to be placed in the prepectoral subcutaneous position. Size reduction of ICDs is desirable, but safety and efficacy of smaller devices must be demonstrated. Outcomes of patients treated with the Jewel 7219D defibrillator (n = 1,781) and with its precursor model PCD 7217B (n = 2,637) were compared. To use PCD patients (n = 2,637) as historical (n = 2,574) and concurrent controls (n = 63), statistical adjustments using the Cox proportional-hazards regression model were made. Jewel recipients (n = 1,781) treated in 106 US and 32 non-US centers exhibited similar characteristics including a mean age of 59 years, 78% men, ejection fraction of 34%, history of aborted sudden cardiac death in 41%, and coronary artery disease in 70%. Implantation was completed in 1,777 of 1,781 (99.9%) attempts and success with the first electrode configuration and polarity was 89.5%. Kaplan-Meier cumulative first-year survivals for cardiac and all-cause mortality were 98.5% and 93.3%. Complication-free first-year survival for Jewel implants in prepectoral subcutaneous (n = 582), subpectoral submuscular (n = 366), and abdominal (n = 449) positions did not differ (p >0.05). First-year survival free of pocket-related complications exceeded 98% in all locations. Adjusted cardiac and all-cause first-year mortality, and efficacy in terminating spontaneous tachyarrhythmias did not differ between the 2 device groups. In conclusion, the safety and efficacy of Jewel model 7219D in the prepectoral subcutaneous position are at least equal to either those of Jewel models implanted in different positions or to those of the previously extensively characterized PCD 7217B.

Objectives. The objective of this study was to evaluate the feasibility, safety and efficacy of placing implantable cardioverter-defibrillators (ICDs) in the electrophysiology laboratory using conscious sedation with combined hypnotic agents and deep sedation with etomidate. Background. Implantable cardioverter-defibrillators with transvenous leads permit the use of simplified implantation techniques similar to those used for the insertion of permanent pacemakers. However, implantation of ICDs without general anesthesia has thus far gained limited acceptance. Methods. In 162 patients, conscious sedation during ICD placement was achieved with combined intravenous midazolam, morphine and promethazine (Phenergan). Intravenous etomidate was administered to induce deep sedation for defibrillation threshold testing. First-time implantations were in the prepectoral position (n = 142), but some patients with preexisting devices received abdominal implants (n = 20). The results were compared with those of concurrent patients (n = 56) who received prepectoral implants under propofol anesthesia administered by an attending anesthesiologist. Results. The anesthetic protocol was implemented without major intraoperative complications. During deep sedation with etomidate, episodes of apnea, hypoxia or arterial hypotension requiring therapeutic intervention did not occur. During a mean (±SD) follow-up period of 257 ± 140 days (median 227, range 14 to 482), there were, among the 162 patients, a total of two nonsudden cardiac deaths—one 71 days and the other 157 days after the operation. There were two nonsudden deaths in the concurrent control subjects (n = 56)—one 13 days and the other 110 days after the operation. Conclusions. Implantation of ICDs under conscious sedation with combined hypnotic agents and deep sedation with etomidate is a safe and effective procedure with low perioperative morbidity and low long-term complication rates.

To study the long-term evolution, determinants, and clinical relevance of the conduction abnormalities after orthotopic heart transplantation, 87 patients, followed for a mean of 105 +/- 72 weeks, were divided into 3 groups according to the characteristics of their electrocardiograms compared with their initial electrocardiogram recorded at study entry. The first group consisted of 24 patients whose initial electrocardiogram was normal, and subsequent electrocardiograms remained normal throughout the study. The second group included 27 patients who developed electrocardiographic evidence of progressive conduction system damage. The third group comprised 36 patients whose initial electrocardiogram was abnormal and subsequent electrocardiograms remained unchanged during follow-up. Although the hemodynamic and echocardiographic evaluation of right and left ventricular function were initially similar among the 3 groups, groups 2 and 3 demonstrated a significant deterioration of left ventricular ejection fraction (62 +/- 12% to 55 +/- 16% and 62 +/- 8% to 57 +/- 14%, respectively; p < 0.05) and cardiac index (2.7 +/- 0.6 to 2.3 +/- 0.5 and 3.0 +/- 0.9 to 2.5 +/- 0.9 L/min/m2, respectively; p < 0.05) while patients in group 1 maintained their normal baseline indices. Incidence and progression of coronary artery disease, as well as frequency of rejection episodes, were comparable among the groups. Mortality was higher in the 2 groups with evidence of conduction defects. Sudden death associated with complete heart block (2 patients) or ventricular arrhythmias (3 patients) was exclusively confined to patients with evidence of progressive electrocardiogram abnormalities. We conclude that, following orthotopic heart transplantation, stable or progressive conduction system damage on the electrocardiogram is associated with left ventricular dysfunction and increased mortality. Sudden death is not uncommon among patients demonstrating worsening cardiac conduction and, in some cases, is related to the development of potentially preventable complete heart block.

During the past 10 years numerous studies on the treatment of paroxysmal atrial fibrillation (AF) by right and left atrial ablation procedures have been published. The results of studies based on follow-up periods of a few months have been repeatedly interpreted as providing evidence for curative therapy. However, insufficient focus on the variability of the natural history of paroxysmal AF, the inadequate detection of silent arrhythmic events, the eclectic post-interventional use of antiarrhythmic drugs, and the lack of appropriate control groups make the reports unconvincing. Randomized controlled trials are needed to confirm postulated long-term cure rates for AF.

The ability of Holter monitoring to predict clinical events during amiodarone therapy was evaluated in 83 patients with coronary artery disease and inducible monomorphic ventricular tachycardia. Sixty-four patients (77%) had significant ventricular ectopy activity (> or = 10 ventricular premature complexes [VPCs]/hour) at baseline, and 19 (23%) did not; patients were similar in age (63 and 65 years, respectively; p = 0.24) and ejection fraction (31 and 32%, respectively; p = 0.75). Over a mean of 23 +/- 17 months, there was no difference in arrhythmia recurrence (33 and 26%; p = 0.89) or sudden death (16 and 20%; p = 0.94) in patients with and without significant ectopy, respectively. In patients with significant ectopy, amiodarone decreased VPC frequency from baseline to 2 weeks, but not from 2 to 6 weeks. Forty-two patients had > 85% reduction in ectopy at 2 weeks; 20 patients did not. However, this reduction of simple VPCs did not predict a decrease in arrhythmic recurrence (29 vs 40%; p = 0.59) nor sudden death (25 vs 11%; p = 0.56) in patients with and without VPC suppression, respectively. Forty-five patients had Holter monitoring at 6 weeks. Twenty-one patients (47%) had > 95% suppression of ectopy, and 24 did not. Neither the recurrence (38 vs 38%; p = 0.54) nor sudden death (33 vs 13%; p = 0.45) rate was predicted by the degree of VPC suppression. Amiodarone is a powerful suppressant of VPCs, but Holter suppression of this ectopic activity is not predictive of clinical outcome.

Differentiation between primary and secondary (caused by acute myocardial infarction) ventricular fibrillation has important therapeutic and prognostic implications. The diagnosis of myocardial infarction is based on clinical, ECG, and creatine kinase MB isoenzyme (MBCK) activity. Enzymatic criteria might not be able to confirm the diagnosis of myocardial infarction after recent cardioversion. The routine use of electrophysiologic studies involving the induction and termination of ventricular dysrhythmias provides a setting in which enzyme release as a result of cardioversion alone can be examined. Therefore a systematic investigation of the magnitude and time course of creatine kinase (CK) and MBCK release was performed after termination of ventricular dysrhythmias in 57 patlents undergoing electrophysiologic studies. Of patients requiring external cardioversion, only 50% had an elevation in CK and MBCK activity. Elevation when present correlated with the number of shocks and cumulative energy delivered. The magnitude of MBCK release exceeded 10% of the total CK activity in 9% of observations. Pace-termination of ventricular tachycardia did not result in enzyme release. Arrhythmia characteriatics, coronary artery disease, and left ventricular function did not affect the magnitude of the time course of enzyme release. These data suggest that cardioversion with multipile shocks may result in a component of MBCK release, and thus a false positive diagnosis of primary acute myocardial infarction may be made by relying exclusively on the enzyme release pattern.

Heterotopic heart transplantation has been said to be contraindicated in patients with serious native heart arrhythmias that produce hemodynamic instability. Placement of heterotopic allografts, however, can theoretically act as a biological biventricular assist device to provide hemodynamic support during these unstable rhythms. Further, this operation might beneficially alter the hemodynamic milieu of heart failure such that the arrhythmias are ameliorated. Described is our experience with 4 patients with heart failure receiving heterotopic cardiac allografts, documenting changes in native heart arrhythmia that occurred. These cases demonstrate that heterotopic grafts can adequately sustain hemodynamics during malignant native heart dysrhythmia. We believe native heart ventricular arrhythmias are not a contraindication to heterotopic heart transplantation.

An automatic implantable cardioverter-defibrillator (AICD) was implanted in 40 patients with sudden cardiac arrest (n = 29), sustained monomorphic ventricular tachycardia (n = 10) or recurrent syncope (n = 1) who were unsuitable for direct ablative surgery or had had unsuccessful medical therapy. The effect of patch electrode polarity on the defibrillation threshold was prospectively evaluated. Two large epicardial patches were used. Initial polarity was selected at random. Ventricular fibrillation was induced by direct current and a preestablished defibrillation protocol employed to assess the minimal energy that would reproducibly defibrillate the heart. Nineteen patients had a lower defibrillation threshold with the inferior left ventricular patch as an anode and nine patients had a lower defibrillation threshold with this patch as a cathode. In general, the defibrillation threshold was lower when this patch was used as an anode than when it was used as a cathode (18 +/- 10 versus 22.6 +/- 12.2 J; p less than 0.01). No preoperative variable predicted optimal polarity. Therefore, the effect of patch polarity on defibrillation threshold should be assessed in each patient at the time of AICD implantation so that the safety margin for satisfactory device function can be maximized.

During a 9-year period 80 patients with drug-resistant sustained ventricular tachycardia underwent direct surgical ablation of arrhythmogenic myocardium. Sixty-nine were male (86%) and 11 female (14%), with 1.9 +/- 1.1 (standard deviation) ventricular tachycardia morphologies per patient. The mean number of drugs failed was 3.7 +/- 1.6 per patient. The preoperative left ventricular ejection fraction was 36.4% +/- 14.4%. Complete preoperative endocardial mapping data (greater than 4 endocardial sites in each ventricular tachycardia) were available for 60 of the 80 patients (75%) and intraoperative endocardial data in the clinical ventricular tachycardia was obtained in 37 (46.3%) of the patients. In 17 patients mapped intraoperatively by computer-assisted techniques, complete epicardial and endocardial data in the clinical ventricular tachycardia were obtained in 14 patients (82.4%). Overall, 73 of 80 (91.3%) had some mapping data available. Hospital mortality occurred in 10 patients (12.5%) at a mean interval of 13.5 days, range 0 to 62 days. Postoperatively the clinical ventricular tachycardia has not recurred in 65 of 70 surviving patients (92.9%). Nonclinical ventricular tachycardia occurred in another four patients. All nine patients with postoperative ventricular tachycardia responded to drugs. The major factors predictive of hospital mortality were prolonged cardiopulmonary bypass (greater than 150 minutes), preoperative ejection fraction less than 31%, and incomplete preoperative mapping. Hospital mortality in patients with an ejection fraction below 31% was significantly associated with a history of amiodarone usage. At 3 years of follow-up, freedom from sudden cardiac death was 95.7%, and 86.7% of patients were free of ventricular tachycardia on no antiarrhythmic drugs. These results suggest that direct ventricular tachycardia operations are an effective form of therapy for patients with sustained monomorphic ventricular tachycardia.

Summary Trials of drug treatment for prevention of sudden arrhythmic death have been disappointing, perhaps because suppressive therapy with arrhythmic agents fails to address the mechanisms leading to electrophysiological failure. We propose that preventive treatment should pay more attention to molecular mechanisms responsible for the progression of cardiac disease to electrophysiological failure. Most sudden cardiac deaths occur in people with atherogenic dyslipidaemias. Our hypothesis is that the pathogenic molecular mechanisms of dyslipidaemias contribute directly to arrhythmogenesis. Proinflammatory-prothrombotic lipid-derived mediators that may play a part in arrhythmogenesis include phospholipids and leucotrienes acting through the platelet-activating-factor and peroxisome proliferator-activated-receptor pathways. There are drugs available to test the hypothesis of dyslipidaemias-specific prevention of electrophysiological failure.

The database of the registry for an implantable cardioverter defibrillator was analyzed to determine the efficacy and safety of antitachycardia pacing for the termination of ventricular tachycardia. In 22,339 episodes treated, termination occurred in 94% and acceleration in only 1.4%.

A 23-year-old woman presented with sustained ventricular tachycardia and was found to have an endocardial mass by echocardiography and by magnetic resonance imaging. The diagnosis of cardiac endocardial tuberculoma was made, and she was treated with antituberculous therapy and an antiarrhythmic drug for one year. After a year, the mass was no longer present, and with all antiarrhythmic medications stopped, ventricular tachycardia could no longer be induced by electrophysiologic study. There has been no clinical recurrence.

The question is addressed whether patients with thoracotomy defibrillators and failing epicardial electrodes can be effectively treated with the implantation of prepectoral unipolar ("active can") defibrillators. Results indicate that abandoned epicardial patches in the pathway of unipolar defibrillation currents do not affect defibrillation thresholds and active can efficacy.

We analyzed the clinical characteristics of 10 patients with pneumococcal endocarditis hospitalized between 1974 and 1984. Patients with pneumococcal endocarditis were typically middle-aged men. Forty percent were alcoholic. They sought medical attention early in the course of their illness and were given appropriate antibiotics promptly. The aortic valve was involved in seven patients. Five patients developed signs of severe valvular insufficiency, and congestive heart failure was present at the time of admission in four patients. Only three patients were recognized to have endocarditis prior to death or to the occurrence of a major complication of their infection. The total in-hospital mortality rate among these patients was 50%. Thus pneumococcal endocarditis is generally an acute, left-sided endocarditis that is associated with rapid valvular destruction and a high mortality rate. Unfortunately, recent advances in diagnosis and treatment of bacterial endocarditis have not substantially improved the outcome of this devastating infection.

Intraoperative mapping and cryoablation of ventricular tachycardia was achieved without ventriculotomy in seven patients, who are a subgroup of the 80 patients undergoing map-directed ablation of ventricular tachycardia over a 9-year period. There were four male and three female patients. Their mean age was 53.6 ± 24.1 years. Coronary artery disease was present in five patients, and two patients had idiopathic ventricular tachycardia. The mean preoperative ejection fraction was 42.4% ± 13.6%. The mean number of ventricular tachycardia morphologies was 1.7 (range 1 to 3). Epicardial mapping was obtained intraoperatively in all seven patients and endocardial data in five of seven patients (71.4%). There were no hospital deaths and no early or late spontaneous recurrence of clinical monomorphic ventricular tachycardia. Nonclinical monomorphic ventricular tachycardia was inducible in two patients postoperatively and both were treated with procainamide. Death occurred late after operation in two patients: One death was related to recurrent nonclinical VT at 8 months and one at 3 months was due to carcinoma of the stomach. These results suggest that the transannular approach is feasible in selected cases, especially when computerized mapping systems with endocardial balloon electrode arrays can be used.

High defibrillation thresholds are encountered in some patients during implantation of the automatic implantable cardioverter defibrillator (AICD). In a consecutive series of 52 patients with AICD implants, 46 had allepicardial implants by left subcostal thoracotomy, and 8 of these patients had thresholds greater than 30 J. Placement of an apicolateral large left ventricular patch and an extrapericardial large right atrial patch electrode through a limited right thoracotomy produced substantial reduction in their thresholds. Especially in patients who have had previous intrapericardial operations, this technique provides a simple solution to the problem of high thresholds.