John J. Rozanski

Body surface detection of delayed depolarizations in patients with recurrent ventricular tachycardia and left ventricular aneurysm.

In eight patients with chronic ventricular tachycardia and left ventricular aneurysms, we detected delayed ECG wave forms after the QRS complex from the body surface using a high-resolution ECG recorder, amplification and signal averaging. Delayed wave-form activity (D wave) extended a mean of 70 msec beyond the termination of the QRS complex. This delayed activity frequently extended to the limit of the recording window, and may thus continue throughout much of diastole. Antiarrhythmic agents never abolished the delayed activity; however, it was abolished by aneurysmectomy in four patients. Ventricular tachycardia did not recur after surgery in the four patients during a mean follow-up of 1 year. The D wave was not found in eight control patients who had chronic recurrent ventricular tachycardia nor in 11 of 12 who had aneurysms alone. The surface D wave can be readily and reproducibly detected by high-resolution electrocardiography and appears to be specific for patients with left ventricular aneurysms who also have chronic recurrent ventricular tachycardia. This delayed wave-form activity has been noted during catheter and surgical endocardial and epicardial mapping. It may represent persistence of the cardiac impulse in islands of myocardium and may be a manifestation of the delayed and fractionated activity, noted by previous investigators.

Lymphocytic Myocarditis Presenting as Unexplained Ventricular Arrhythmias: Diagnosis With Endomyocardial Biopsy and Response to Immunosuppression

During a period of 18 months beginning in January 1982, a total of 65 patients were referred to the Miami Heart Institute for evaluation of either aborted out of hospital sudden death, ventricular tachycardia resistant to standard clinically directed antiarrhythmic medication programs or high grade ventricular arrhythmia (Lown class greater than or equal to IV B) with or without syncope. After complete evaluation including cardiac catheterization in all but 1 patient, 17 patients were identified in whom no obvious cardiac disease could be found. Twelve of the 17 underwent right ventricular endomyocardial biopsy. Six of the 12 biopsies demonstrated clinically unsuspected lymphocytic myocarditis (Group A). Findings in three of the remaining six biopsies were consistent with an early cardiomyopathy and in three were completely normal (Group B). Retrospective review of the clinical, laboratory, electrophysiologic, hemodynamic and angiographic data failed to identify a marker that reliably separated Group A from Group B patients. In addition to antiarrhythmic therapy guided by laboratory electrophysiologic study, all Group A patients were treated with prednisone and azathioprine. After 6 months of immunosuppression, all patients with myocarditis were reevaluated in the hospital without antiarrhythmic medication. Ventricular tachycardia/fibrillation could not be provoked in the laboratory during repeat electrophysiologic testing in five of the six patients. Repeat myocardial biopsy after all immunosuppressive therapy had been discontinued revealed absence of inflammation associated with varying degrees of residual interstitial fibrosis. There were no deaths. It was concluded that a patient with an otherwise clinically silent lymphocytic myocarditis can present with potentially life-threatening ventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Alternans of the ST segment in Prinzmetal's angina.

Alternans of the elevated ST segment (STEA) was found in 8 of 21 patients (38%) with Prinzmetals variant angina. In addition to STEA, all eight patients had varying cardiac arrhythmias: multiple premature ventricular depolarizations in eight, ventricular tachycardia in five, and ventricular fibrillation in three. There was no consistent temporal relationship between the occurrence of STEA and the cardiac arrhythmias. Alternans occurred during periods when no arrhythmias were present. All eight patients underwent coronary angiography. Spontaneous coronary artery spasm was documented angiographically in three patients including two who had minimal or no coronary atherosclerotic disease. Six patients had severe, fixed, occlusive coronary artery disease. Possible mechanisms for STEA include: 1) failure of regions of myocardium to depolarize on alternate beats due to variation in conduction and refractoriness between ischemic and nonischemic zones of myocardium, and 2) electrical alternans of the transmembrane action potential during phases 2 and 3 (repolarization) caused by changes in the rate and extent of electrolyte transfer across cell membranes during ischemia. It is postulated that STEA is an electrocardiographic sign in the surface ECG of a dysequilibrium of refractory periods during ischemia and reflects an unstable electrical state of the myocardium.

Electrophysiologic effects of diltiazem hydrochloride on supraventricular tachycardia

The effects of intravenous diltiazem hydrochloride (0.25 mg/kg body weight) were studied in eight patients with nine episodes of supraventricular tachycardia. Five episodes of tachycardia were due to atrioventricular (A-V) nodal reentry (group A), two were due to retrograde utilization of a concealed A-V accessory pathway (group B) and two were episodes of atrial fibrillation (group C). Intravenous administration of diltiazem slowed the ventricular rate in eight of nine episodes of tachycardias. Supraventricular tachycardia was terminated within 2 minutes after intravenous diltiazem in four of five patients in group A, and one of two in group B. Cycle length alternation was observed before termination of the arrhythmia in two patients from group A. In group C the ventricular response slowed but also became regular during atrial fibrillation. Although diltiazem depressed both anterograde and retrograde conduction as assessed by programmed stimulation, tachycardia termination or slowing or alternation of cycle length all occurred because of the effects of diltiazem predominantly on anterograde A-V nodal properties during supraventricular tachycardia. Although no statistical conclusions can be made from this limited study, it appears that diltiazem has significant depressant electrophysiologic effects on both anterograde and retrograde A-V nodal function as assessed by programmed stimulation during sinus rhythm. Further electrophysiologic studies are needed before determining the clinical efficacy of this agent for treatment or prophylaxis of recurrent supraventricular tachycardias.

Advanced ventricular arrhythmias during bedside pulmonary artery catheterization

To determine the incidence of advanced arrhythmias and acute right bundle branch block during beside pulmonary artery catheterization, 119 critically ill patients undergoing 150 pulmonary artery catheterizations were prospectively studied using continuous electrocardiographic monitoring with permanent recordings. Ventricular arrhythmias other than isolated premature ventricular contractions, couplets or bigeminy occurred during 80 of the 150 catheterizations (53 percent). These included ventricular salvos (three to five consecutive premature ventricular contractions) in 30 percent, nonsustained ventricular tachycardia (five to 30 premature ventricular contractions) in 20 percent and sustained ventricular tachycardia (more than 30 consecutive premature ventricular contractions) in 3 percent. In two patients, ventricular fibrillation developed; in another three patients, lidocaine or precordial thump was required to terminate the episodes of ventricular tachycardia. The incidence of advanced ventricular arrhythmias was statistically correlated with either the presence of predisposing risk factors for ventricular ectopy (p less than 0.05) or prolonged catheterization time (p less than 0.01). A new right bundle branch block developed in seven patients (5 percent) and persisted for a mean of 9.5 hours.

Efficacy of procainamide on ventricular tachycardia: Relation to prolongation of refractoriness and slowing of conduction

The effect of procainamide on intraventricular conduction and refractoriness, and the prevention of induction of ventricular tachycardia (VT) were studied in 29 patients who had remote myocardial infarction and inducible sustained monomorphic VT. AFter intravenous administration of 15 mg/kg procainamide, induction of VT was suppressed in seven (24%) patients (responders), while in 22 (76%) VT was still inducible (nonresponders). The percent change in paced QRS duration at a cycle length (CL) of 400 msec produced by procainamide was significantly less in responders than in nonresponders: 29.8 +/- 3.9% versus 38.9 +/- 10.8% (p = 0.0020). The percent change in the right ventricular effective refractory period (ERP) at CLs of 600 and 400 msec was significantly greater in responders than in nonresponders: 14.6 +/- 6.9% versus 7.9 +/- 7.3% (p = 0.0414) for ERP at a CL of 600 msec and 15.1 +/- 7.0% versus 8.0 +/- 7.4% (p = 0.0386) for ERP at a CL of 400 msec. Stepwise discriminant analysis showed that greater percent increase in ERP at a CL of 400 msec and lesser percent increase in paced QRS duration at a CL of 400 msec were significantly independent markers for the responders. These findings suggest that lesser slowing of conduction and greater prolongation of refractoriness by procainamide tend to abolish reentry within the reentrant circuit. Greater slowing of conduction and lesser prolongation of refractoriness tend to stabilize a reentrant circuit, and promote the continued induction of VT.

Susceptibility of infarcted canine hearts to digitalis-toxic ventricular tachycardia

The susceptibility to the toxic arrhythmogenic effects of digitalis was studied in 10 normal dogs (group 1) and in 15 dogs with healed myocardial infarction (group 2) 26 ± 5 days after coronary artery ligation. The dose of ouabain required to cause stable digitalis-toxic ventricular tachycardia was 25% less in the group 2 dogs than in the group 1 control dogs (70 ± 21 versus 93 ± 16 μg/kg, probability [p] These findings are consistent with healed infarcted myocardium serving as a site of predilection for the origin of digitalis-toxic ventricular tachycardia. Our observations add to a growing body of information suggesting that hearts with healed myocardial infarction have an enhanced susceptibility to digitalis intoxication.

Multiple electrophysiologic manifestations and clinical implications of vagally mediated AV block

Clinical, surface ECG, and intracardiac findings were analyzed in 20 patients with spontaneous conduction disturbances in whom vagally mediated AV block could be induced by carotid sinus pressure during electrophysiologic evaluation. The latter demonstrated that the surface ECG pattern attributed to bradycardia-dependent (phase 4), and paroxysmal block within the His bundle and bundle branches could reflect vagally mediated, bradycardia-associated (rather than bradycardia-dependent), and paroxysmal AV nodal (AH) block. The decision regarding the use of pacemakers was not based on QRS duration or on patterns (or site) of block but on the underlying clinical settings and the correlation of symptoms with maximal ventricular (R-R) pauses. However, more studies are required to extend our findings, especially to other subgroups of patients (or normal individuals) in whom vagally mediated block occurs.

Left fascicular blocks during right-heart catheterization using the Swan-Ganz catheter.

During insertion of Swan-Ganz catheters, mechanical right bundle branch block occurred in association with left posterior fascicular block in two patients and with left anterior fascicular block in two. None of the four patients had acute myocardial infarction or acute (spontaneous or iatrogenic) pulmonary dis. ease. In two cases, electrophysiologic studies demonstrated the coexistence of intra- and infra-Hisian conduction delays and blocks. Although the right bundle branch block may have resulted from injury to the central or peripheral right branch, the left fascicular blocks could not be explained by direct trauma to these left-sided structures. Our findings support the recent clinical and experimental reports that show that, left fascicular block (as well as right bundle branch block) may be due to lesions involving the His bundle; presumably because of longitudinal dissociation of this structure affecting the transverse interconnections. In one patient, 2: 1 intra-Hisian block may have coexisted with bradycardia-dependent (phase 4) right bundle branch block. More studies are required to determine the implications of catheter-induced conduction disturbances in other clinical settings, such as acute myocardial infarction.

Clinical Evaluation of an Improved High Resolution ECG Cart for Recording the His Bundle Electrogram Non-Invasively

The Marquette high resolution MAC‐3 ECG cort con record the His bundle electrogram non‐invasively at the bedside. The second generation MAC‐1 has several unique features and technical advances which may now make the technique clinically applicable. In addition to amplification and signal averaging, an adjustable input filtration system excludes beats which are unacceptably “noisy” compared to a 4 beat template. Thus, extremely “clean” signals are presented for processing by the averages allowing resolution of very low amplitude signals. Clear unequivocal His bundle recordings were obtainable in 25 of 55 patients (45%). A correlation coefficient of +.97 was obtained between invasive and non‐invasive HV intervals. The 55% failure rate was attributed to prolonged atriol activity in 31%, short PR in 9%, and technically unsatisfactory recordings with excessive or overwhelming noise which did not allow appreciable signal resolution in 15%.