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Empirical antiarrhythmic therapy has not reduced mortality among patients with coronary artery disease and asymptomatic ventricular arrhythmias. Previous studies have suggested that antiarrhythmic therapy guided by electrophysiologic testing might reduce the risk of sudden death.We conducted a randomized, controlled trial to test the hypothesis that electrophysiologically guided antiarrhythmic therapy would reduce the risk of sudden death among patients with coronary artery disease, a left ventricular ejection fraction of 40 percent or less, and asymptomatic, unsustained ventricular tachycardia. Patients in whom sustained ventricular tachyarrhythmias were induced by programmed stimulation were randomly assigned to receive either antiarrhythmic therapy, including drugs and implantable defibrillators, as indicated by the results of electrophysiologic testing, or no antiarrhythmic therapy. Angiotensin-converting-enzyme inhibitors and beta-adrenergic-blocking agents were administered if the patients could tolerate them.A total of 704 patients with inducible, sustained ventricular tachyarrhythmias were randomly assigned to treatment groups. Five-year Kaplan-Meier estimates of the incidence of the primary end point of cardiac arrest or death from arrhythmia were 25 percent among those receiving electrophysiologically guided therapy and 32 percent among the patients assigned to no antiarrhythmic therapy (relative risk, 0.73; 95 percent confidence interval, 0.53 to 0.99), representing a reduction in risk of 27 percent). The five-year estimates of overall mortality were 42 percent and 48 percent, respectively (relative risk, 0.80; 95 percent confidence interval, 0.64 to 1.01). The risk of cardiac arrest or death from arrhythmia among the patients who received treatment with defibrillators was significantly lower than that among the patients discharged without receiving defibrillator treatment (relative risk, 0.24; 95 percent confidence interval, 0.13 to 0.45; P0.001). Neither the rate of cardiac arrest or death from arrhythmia nor the overall mortality rate was lower among the patients assigned to electrophysiologically guided therapy and treated with antiarrhythmic drugs than among the patients assigned to no antiarrhythmic therapy.Electrophysiologically guided antiarrhythmic therapy with implantable defibrillators, but not with antiarrhythmic drugs, reduces the risk of sudden death in high-risk patients with coronary disease.

Sustained ventricular tachycardia with left ventricular aneurysm formation is a rare complication following penetrating cardiac trauma. We present an unusual case of serious ventricular tachycardia which developed 35 years after a World War II injury and was successfully treated with aneurysmectomy, map-guided subendocardial resection, and cryoablation.

Electrocardiographic signal averaging techniques have demonstrated a low-amplitude late potential and a long filtered QRS complex in patients with ventricular tachycardia (VT) after myocardial infarction. Complex ventricular ectopy and left ventricular aneurysms have also been associated with VT. The purposes of this study were (1) to determine whether the findings from the signal-averaged electrocardiogram (ECG) were independent of those from Holter monitoring and cardiac catheterization and (2) to determine the combination of findings from the signal-averaged ECG, cardiac catheterization, and Holter monitoring that best characterize patients with VT after myocardial infarction. We studied 174 patients after myocardial infarction, 98 of whom had recurrent sustained VT. By multivariate logistic regression only three parameters were found to be independently significant, listed in order of power: positive signal-averaged ECG (presence of a late potential or a long filtered QRS duration), peak premature ventricular contraction greater than 100/hr, and presence of a left ventricular aneurysm (p less than .001). The signal-averaged ECG provides independent information in identifying patients with VT after myocardial infarction.

Seventy-eight patients with ventricular tachycardia associated with coronary artery disease underwent intraoperative mapping while in sinus rhythm to evaluate the frequency and significant of late potentials. In 30 of these patients, the surface ECG was subjected to signal averaging to correlate the incidence and duration of low-amplitude, delayed electrograms with the presence of late potentials recorded during epicardial mapping. One to four epicardial late potentials were observed in nine patients (11.5%). These nine patients did not differ hemodynamically from patients without late potentials. In four patients, the site of epicardial breakthrough during ventricular tachycardia bore no relationship (i.e., greater than 3 cm away) to the late potential or the site of origin of the tachycardia. In the five other patients with late potentials, epicardial breakthrough and site of origin of ventricular tachycardia were closely related to the free wall of an apical aneurysm. However, three of these patients had additional tachycardias from disparate sites. Twenty-seven of 30 patients in whom signal averaging was used had a low-amplitude signal in the terminal 40 msec of the amplified QRS complex. In 24 of these 27 patients (89%), the low-amplitude tail was demonstrated in the absence of epicardial late potentials. We conclude that epicardial late potentials are found infrequently in patients with ventricular tachycardia associated with coronary artery disease; epicardial late potentials cannot be used to localize ventricular tachycardia; and the specific low-amplitude tail on the signal-averaged electrogram is unrelated to epicardial events.

Mapping-guided endocardial resection has proved to be an effective therapy for recurrent sustained ventricular tachycardia. However, some patients cannot be mapped during ventricular tachycardia, so that guidance from findings during normal sinus rhythm would be highly desirable. We examined the frequency, timing, and duration of several abnormal types of electrograms recorded endocardially during sinus rhythm and related these findings to activation mapping during sustained ventricular tachycardia. Thirteen patients with extensive myocardial infarction complicated by recurrent sustained ventricular tachycardia were studied intraoperatively during sinus rhythm and induced ventricular tachycardia with a standardized mapping scheme involving the entire endocardial surface. Fractionated electrograms (multicomponent with amplitude less than 1 mV and duration greater than 50 msec) were recorded in all patients. This type of electrogram could be recorded at up to 36% of mapped sites. Split electrograms (two components separated by isoelectric period) were also frequently seen but involved only a mean of 5.8% of mapped sites. Late electrograms (inscribed entirely after the QRS complex) were only recorded in four of 13 patients at a mean of 5% of mapped sites. The location of these electrograms was related to an arbitrary 8 cm2 zone around the earliest site of endocardial activation recorded during ventricular tachycardia. The longest fractionated electrogram was closely related to nine of 22 morphologies of induced ventricular tachycardia, split electrograms were related to seven of 16 morphologies, and late electrograms to two of four morphologies. We have concluded that extremely abnormal electrograms recorded endocardially during sinus rhythm are widespread in patients with extensive myocardial infarction complicated by ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Whether or not the atrium plays an essential role in initiating and/or sustaining atrioventricular (A-V) nodal re-entrant tachycardia was evaluated in eight patients. In all eight patients, the atrium could be rendered refractory to retrograde atrial echoes during the tachycardia without interrupting the arrhythmia. This was accomplished by introducing atrial premature depolarizations prior to the time the atrium would normally be retrogradely depolarized by atrial echoes. In one patient, two atrial premature depolarizations could be introduced, producing A-V dissociation, without terminating the tachycardia. In another patient, the tachycardia could be initiated without an atrial echo. Our data suggest that most, if not all of the atrium is unnecessary for the initiation and maintenance of A-V nodal re-entrant supraventricular tachycardia.

To determine whether high current strength pacing at the site of origin of ventricular tachycardia (VT) could prevent induction of VT, we studied 11 VTs in 10 patients with chronic coronary artery disease. The left ventricular site of origin of all VT was determined by endocardial catheter mapping. Reproducible VT induction from the right ventricular apex or outflow tract was demonstrated with a pacing current strength equal to twice diastolic threshold (less than or equal to 2.0 mA) with single (two VTs), double (eight VTs), or triple (one VT) extrastimuli following 8 beats of a drive cycle length of 400 to 600 msec. After determination of the baseline VT induction zone (range 10 to 80 msec), repeat induction was attempted while simultaneous pacing was performed during the 8 beat drive train from the left ventricular site of origin with the use of a high current strength (10 mA [two VTs] or 20 mA [nine VTs]) and from the baseline right ventricular site with a current strength equal to twice diastolic threshold. Extrastimuli were introduced only from the right ventricular site over the same range of coupling intervals that resulted in VT initiation during the baseline state. In five of the 11 trials, no VT could be initiated; in one trial, the VT induction zone was decreased from 80 to 10 msec; in three trials, only VT of a different morphology and a distinct (greater than 4 cm distant) site of origin was initiated; and in two trials, VT of the same morphology was initiated. In four of the five trials in which all VT was prevented by simultaneous pacing with a high current strength at the site of origin, simultaneous pacing at a lower current strength (twice diastolic threshold) at the site of origin (three VTs) or with equally increased current strength (10 to 20 mA) at nonsites of origin (two VTs) did not prevent initiation. We conclude that: high current strength pacing at the site of origin during the drive train can inhibit VT induction with extrastimuli and, successful prevention of VT may depend on the pacing site being the site of origin and the current strength used during pacing.

Catheter mapping during sinus rhythm was performed in 132 patients with coronary artery disease and 26 patients with congestive noncoronary cardiomyopathy. Each of the patients had a clinical history of one of the following: no ventricular arrhythmia, nonsustained ventricular tachycardia, cardiac arrest, or sustained ventricular tachycardia. The characteristics of the endocardial electrogram and other measured indexes of slow endocardial conduction were compared between patients with different types of disease and in different arrhythmia groups to determine if differences existed. The cardiomyopathic group had a higher percent of normal endocardial electrograms than the coronary artery disease group, with no evidence of slow endocardial conduction. The sustained ventricular tachycardia group exhibited a greater percent of abnormal endocardial electrograms and more evidence of slow endocardial conduction, distinguishing this group from the three other arrhythmia groups. We conclude the following: The underlying electrophysiologic substrate varies in patients with different ventricular arrhythmias. It is therefore inappropriate to analyze all patients with ventricular arrhythmias as a single group. Patients with congestive noncoronary cardiomyopathy, regardless of the type of their arrhythmia, have a relatively normal endocardium. Those patients with serious ventricular arrhythmias should not be considered candidates for surgery directed at removing abnormal endocardium.

Temporary epicardial pacing leads are routinely placed in patients after cardiac surgery, but the positioning of ventricular leads and the use of atrial leads is not uniform. We examined the effect of the epicardial pacing site on ventricular function in 18 patients undergoing coronary surgery. Pacing wires were sutured in the right atrium, left ventricular apex, right ventricular apex, and right ventricular outflow tract before cardiopulmonary bypass. After atrial pacing, eight patients were ventricularly paced (group I) and 10 were atrioventricular (AV) sequentially (PR = 0.12 sec) paced (group II) at 100/minute from the three ventricular sites. Comparison of the groups showed that the addition of atrial activation during ventricular pacing resulted in higher cardiac indexes (2.54 +/- 0.61 vs 1.67 +/- 0.45 liters/min/m2;p less than .00005), higher systolic blood pressures (121 +/- 24 vs 89 +/- 26 mm Hg; p = .006), lower central venous pressures (5.5 +/- 3.2 vs 10.2 +/- 2.2 mm Hg; p = .048), and similar pulmonary arterial pressures (19.5 +/- 7.6/10.8 +/- 6.7 vs 24.7 +/- 3.5/15.4 +/- 3.4 mm Hg; p = NS). Cardiac index did not differ among group I patients during pacing from the different ventricular sites. In group II, cardiac index during pacing from the right ventricular apex was higher than during pacing from the right ventricular outflow tract or the left ventricular apex (2.62 +/- 0.57 vs 2.49 +/- 0.54 and 2.51 +/- 0.76 liters/min/m2, respectively; p = .03). Right ventricular outflow tract pacing resulted in higher cardiac indexes than left ventricular apical pacing in patients with stenosis of the left anterior descending coronary artery of 90% or more, while left ventricular apical pacing produced higher cardiac indexes in the absence of such lesions (p = .006).(ABSTRACT TRUNCATED AT 250 WORDS)

A family with adult onset heart block (AOHB) and sinus bradycardia (SB) was investigated 5 yr after previous study. A 44-yr-old female previously 'normal' presented ECG evidence of 1st-degree and 2nd-degree atrioventricular block (AVB) with normal intraventricular conduction and episodic 3rd-degree AVB. His bundle electrocardiography (HBE) demonstrated A--H prolongation (245msec) with normal H--V time during sinus rhythm and 3rd-degree AV nodal block with a His bundle escape rhythm. Sinus node function served in first-order relatives. HBE and sinus node function were normal in a 38-yr-old sister with new SB. 37 families with familial 3rd-degree AVB were reviewed with attention to prognostic indices and electrophysiologic-pathologic correlates. The incidence of conduction abnormalities supported an autosomal dominant transmission with variable penetrance. Subsidiary pacemaker rate and QRS morphology showed no discriminative value with respect to prognosis. HBS identified A--H prolongation in 2 patients with AOHB and 2 with AOHB and SB, with coexistent H--V conduction delay in 2 cases of AOHB and SB with abnormal QRS morphology. Histopathology was variable, but the finding of multiple lesions in 2 of 5 patients with congenital heart block and each of 2 with AOHB and SB suggests that mixed conduction system disease is prevalent in familial heart block.

For half a century the systolic click and late systolic murmur lay dormant as innocent auscultatory curiosities. The thirteen years since Barlow related these phenomena to mitral leaflet prolapse have witnessed an astonishing information explosion. We have sought to bring together the accumulated data in this review. An Historical Perspective traces the evolution from the now abandoned "pericardial" or "extracardiac" phases, through the leafletchordal phase (redundancy), the myocardial phase (segmental left ventricular contraction abnormalities), to the anular phase (dilatation and faulty systolic contraction). Functional Anatomy is dealt with in terms of pathology, pathophysiology, hemodynamics, angiocardiography, echocardiography, and physical and pharmacological interventions. Clinical Manifestations are concerned with prevalence, natural history, symptoms, physical signs, electrocardiographic abnormalities and roentgen fingings. The four Major Complications- sudden death, infective endocarditis, spontaneous rupture of chordae tendineae, and progressive mitral regurgitation- are examined. Associated Cardiac Diseases, i.e., Marfan's syndrome, ostium secundum atrial septal defect and atherosclerotic coronary artery disease, are discussed, and a section on Treatment deals chiefly with prophylaxis for infective endocarditis and the management of arrhythmias and chest pain. A final section on Evolving Information considers etiologic concepts, the nature of left ventricular contration abnormalities, the cause of chest pain, the relationship to Marfan's syndrome and ostium secundum atrial septal defect, and the effect of aging and sex differences on leaflet chordal redundancy.

We studied 37 patients undergoing endocardial resection for medically refractory ventricular tachycardia (VT). Each was studied before and after surgery by programmed ventricular stimulation and signal-averaged electrocardiography. Low-amplitude late potentials were identified preoperatively in 76% of patients. In the 24 patients without postoperative VT the effect of surgery was to shorten the filtered QRS duration (137 +/- 27 to 121 +/- 26 msec; p = .003), increase the voltage in the last 40 msec of the filtered QRS (16.5 +/- 16.1 to 39.0 +/- 29.4 microV; p = .003), and decrease the incidence of late potentials (71% to 33%; p = .03). The filtered QRS complex was unchanged in 13 patients whose VT persisted after surgery. No preoperative variable predicted which patients would not have inducible VT after surgery. However, loss of a late potential after surgery in nine of 10 patients was associated with absence of inducible VT (p less than .02). Loss of a late potential was not necessary for surgical success. Eight of 18 patients with a persistent late potential did not have inducible VT. The signal-averaged electrocardiogram predicted a successful outcome after endocardial resection if the late potential was no longer present.

Nineteen patients undergoing a standard aneurysmectomy for recurrent ventricular tachycardia are compared with 30 patients unergoing electrophysiologically directed endocardial excision and aneurysmectomy. The electrophysiologically nondirected and electrophysiologically directed groups were aneurysmectomy. The electrophysiologically nondirected and electrophysiologically directed groups were similar for age (56.8 versus 57.5 years), interval after myocardial infarction (26.2 versus 28.3 months), preoperative episodes of ventricular tachycardia (13.2 versus 19.7), cardiac index (2.95 versus 2.79 L/min/m2), left ventricular end-diastolic pressure (15.5 versus 18.2 torr), and ejection fraction (34 versus 28%). Operative mortality rate in the nondirected group was 42%, with all but one of the deaths resulting from uncontrolled postoperative ventricular tachycardia. In the nondirected group 78.9% (15/19) of patients had recurrent ventricular tachycardia postoperatively. The operative mortality rate in the electrophysiologically directed group was 6.7% (2/30), and both patients died of left ventricular failure. Three patients (10%) have ventricular tachycardia inducible with programmed stimulation. We conclude that standard left ventricular aneurysmectomy is not an effective operation for recurrent sustained ventricular tachycardia. Conversely, electrophysiologically directed endocardial excision characteristically controls the arrhythmia at an acceptable surgical risk.

Ventricular extrastimuli or rapid ventricular pacing used to terminate ventricular tachycardia (VT) may be ineffective or may accelerate VT. Therefore, a new method to facilitate termination of VT and decrease the incidence of acceleration was evaluated. The new method utilized rapid ventricular pacing at cycle length 10 to 100 ms shorter than VT cycle length with the introduction of 1 or 2 ventricular extrastimuli. The efficacy of this combination method in terminating VT was assessed in 25 patients in whom ventricular extrastimuli and rapid ventricular pacing at cycle lengths and coupling intervals comparable with those used in the new method were unsuccessful. This combination method successfully terminated VT in 21 of 25 patients with cycle lengths of 230 to 400 ms. VT was terminated in 6 of 8 patients receiving drugs in whom VT could not be terminated by 1 to 2 ventricular extrastimuli or rapid ventricular pacing; in 6 of 8 patients unresponsive to ventricular extrastimuli and in whom rapid ventricular pacing produced acceleration of VT; and in 9 of 9 patients in whom antiarrhythmic agents made VT unresponsive to ventricular extrastimuli or rapid ventricular pacing. A combination of rapid pacing and extrastimuli can terminate VT unresponsive to ventricular extrastimuli or rapid ventricular pacing alone and may avoid acceleration of VT using rapid ventricular pacing at very short cycle lengths for termination.

Eighty patients (69 with documented or suspected recurrent ventricular tachycardia or fibrillation, ten with left bundle-branch block, and one with the Wolff-Parkinson-White syndrome) underwent both right ventricular and left ventricular programmed electrical stimulation, including ventricular pacing and the introduction of one or two ventricular extrastimuli or electrode catheter mapping of the left ventricle (or both). Left ventricular catheters were introduced precutaneously via the femoral artery (of 61 patients, one required secondary repair) or via brachial arteriotomy (of 19 patients, two required secondary repair). All patients received an intravenously administered bolus of hep arin (5,000 units) following the insertion of the left ventricular catheter and then 1,000 units/hr after the first hour of study. No patients had cerebrovascular, systemic thromboembolic, or cardiac sequelae. In four (12 percent) of 34 patients with inductible ventricular tachycardia, programmed electrical stimulation of the left ventricle was required for initiation. Extensive left ventricular endocardial mapping was performed in 45 patients. Our experience suggests that (1) electrophysiologic study of the left ventricle can be performed safely, (2) programmed electrical stimulation of the left ventricle is indicated when a suspected ventricular tachyarrhythmia cannot be induced from the right ventricle, and (3) endocardial mapping of the left ventricle is indicated when surgery is being considered to abolish recurrent sustained ventricular tachycardia.

Surgical resection of the endocardium and subendocardium often abolishes chronic recurrent sustained ventricular tachycardia in patients with healed myocardial infarcts or ventricular aneurysms, presumably by interrupting the reentrant pathway. To define the morphologic characteristics of cells in the reentrant pathway, we studied the histology and ultrastructure of the endocardial resections of 23 patients who underwent this procedure. Bundles of apparently viable myocardial fibers embedded in dense fibrous tissue were identified throughout the endocardial resections from all patients. These bundles of cells were separated from one another by fibrous tissue but extended uninterrupted to the margins of the surgical resection. In 14 patients Purkinje fibers were identified beneath the thickened endocardium whereas the remaining bundles were composed of ventricular muscle. The Purkinje fibers appeared to have normal ultrastructure and ventricular cells with both normal and abnormal ultrastructures were present. The abnormal muscle cells were characterized by loss of contractile elements, aggregates of dilated sarcoplasmic reticulum, and osmiophilic dense bodies. The sarcolemma was intact and the nuclear chromatin was evenly dispersed suggesting that these cells were still viable. The abnormal structure and arrangement of the surviving cardiac fibers in the endocardium may cause the abnormal electrophysiologic function that results in ventricular tachycardia.

Direct measurement of the QT interval during exercise is the preferred method to assess duration of this interval with changes in heart rate. The influence of exercise induced ischemia or type I antiarrhythmic drugs on the exercise QT interval has not been well studied. Exercise electrocardiograms and thallium scintigraphy were performed in three groups-normals, patients with coronary artery disease, and patients taking type I antiarrhythmic drugs. The change in QT interval with heart rate increases during exercise was compared among the three groups. The QT interval shortened progressively in the normal group. Demonstrable myocardial ischemia (positive thallium scan) had no effect on the QT interval. Type I antiarrhythmic drugs prolong the QT interval at rest compared to normals, but the interval shortened to the same degree as in normals during exercise. Thus, normal values can be used to compare QT intervals in patients with coronary artery disease. These values do not apply to patients receiving type I antiarrhythmic drugs.

Twenty-six patients with refractory ventricular arrhythmias received the automatic implantable cardioverter-defibrillator. A patch lead only was placed during arrhythmia surgery in 7 other patients. During 13 +/- 6 (SD) months, the device discharged in 10 patients because of a sustained ventricular arrhythmia. No sudden deaths occurred. There were 31 complications in 17 patients, including postoperative refractory heart failure, coronary artery erosion, subclavian vein thrombosis, postoperative stroke after conversion of atrial fibrillation, atelectasis with pneumonia, symptomatic pleural effusions, and infection at the generator site. The cardioverter-defibrillator discharged in 9 asymptomatic patients, failed to terminate ventricular fibrillation during postoperative testing in 3 patients, and had premature battery failure in 4 patients. Tachycardia slowing during chronic amiodarone therapy and unipolar ventricular pacing during ventricular fibrillation precluded or delayed arrhythmia sensing. Thus, the cardioverter-defibrillator can be life saving, but its potential complications and interactions with antiarrhythmic drugs and pacemakers must be considered at patient selection.