Nonpharmacologic therapy of ventricular tachycardia.

Nonpharmacologic therapies for patients with sustained ventricular tachycardia have been necessitated by the low frequency of drug-responsive patients. These nonpharmacologic therapies include antitachycardia pacemakers, low-energy cardioverters, defibrillators, surgery and, for the present, catheter ablation. Antitachycardia pacing alone should never be used because of the known incidence of acceleration of ventricular tachycardia to ventricular fibrillation.

Automatic implantable defibrillator discharge resulting from routine pacemaker programming.

A middle-aged gentleman with an idiopathic dilated cardiomyopathy, drug-refractory sustained ventricular arrhythmia, and high-degree AV block was managed with an automatic implantable cardioverter-defibrillator (AICD) and a Cordis Multicor II VVI pacemaker. During a routine follow-up visit, the pacemaker threshold was determined. Seven seconds after reprogramming the Cordis pacemaker to the "stat" VVI mode, the AICD discharged.

Prevention of ventricular tachycardia induction during right ventricular programmed stimulation by high current strength pacing at the site of origin.

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.

Results of signal-averaged electrocardiography and electrophysiologic study in patients with nonsustained ventricular tachycardia after healing of acute myocardial infarction.

Programmed stimulation and signal-averaged electrocardiography were performed in 43 consecutive patients with nonsustained ventricular tachycardia (VT) after healing of inferior (29 patients) or anterior wall (14 patients) acute myocardial infarction. Twenty-two patients had inducible sustained VT. Patients with inferior infarction and inducible sustained VT had significantly longer filtered QRS durations (125 +/- 19 vs 112 +/- 15 ms, p less than 0.

Usefulness of electrophysiologic study to determine the clinical tolerance of arrhythmia recurrences during amiodarone therapy.

The relation of clinical and electrophysiologic variables to outcome was evaluated in 121 patients treated with amiodarone for sustained ventricular tachyarrhythmias. Electrophysiologic study was performed in all patients a mean of 14 days after beginning amiodarone therapy. Forty-six patients who were given oral amiodarone therapy experienced arrhythmia recurrence.

Experimental myocardial cryoinjury: local electromechanical changes, arrhythmogenicity, and methods for determining depth of injury.

To characterize the electromechanical effects of acute and 2-week-old cryoinjury, programmed stimulation and epicardial M-mode echo mapping (7.5 mHz) were performed prior to, at 15 minutes and 15 +/- 2 days after cryoinjury in 10 dogs. Epicardial and intramural bipolar and unipolar electrograms were recorded in five of the dogs.

Relationship of steady-state serum concentrations of amiodarone and desethylamiodarone to therapeutic efficacy and adverse effects.

The relationship of steady-state serum levels of amiodarone and its major metabolite, desethylamiodarone, to therapeutic and toxic effects was evaluated in 111 patients treated for supraventricular and ventricular arrhythmias. All patients were treated for more than two months (mean 10 +/- 7), and repeated serum levels determined at least two months apart were within 0.5 mg/liter of each other.

Nonsustained ventricular tachycardia in patients with coronary artery disease: role of electrophysiologic study.

Sixty-two consecutive patients with chronic coronary artery disease referred for evaluation of nonsustained ventricular tachycardia (VT) underwent electrophysiologic studies. Sustained VT was induced by one to three ventricular extrastimuli in 28 patients (45%). Therapy was guided by the results of electrophysiologic testing in 44 patients: 19 patients without inducible sustained VT received no antiarrhythmic therapy, and 25 patients with inducible sustained or symptomatic nonsustained VT received therapy guided by the results of electrophysiologic studies.

Hazards of intravenous verapamil for sustained ventricular tachycardia.

In 11 of 25 patients (44%) with sustained ventricular tachycardia (VT) who received intravenous verapamil (5 to 10 mg), acute severe hypotension or loss of consciousness developed, necessitating immediate cardioversion. Comparison of these 11 patients with the 14 who did not have adverse effects after verapamil revealed no significant difference in age, heart disease, ejection fraction, blood pressure before verapamil administration, other oral or intravenous drugs use, verapamil dose or VT characteristics (rate and morphologic pattern). Although most patients with severe adverse effects after verapamil had prior myocardial infarction, deterioration also occurred in patients without coronary disease and in patients with a normal left ventricular ejection fraction.

Characterization of oscillations in ventricular refractoriness in man after an abrupt increment in heart rate.

Oscillations in ventricular myocardial refractoriness after a change in rate have not been described in man. During 25 baseline paced cycle lengths (SB-SB) of 400 to 800 msec in 14 patients, a shorter cycle length (S'-S') was introduced that was 10 to 20 msec (mean 15 +/- 5) greater in duration than the ventricular effective refractory period (VERP) determined after 12 beats of the respective baseline cycle length (group 1 trials). In addition, during 14 of the 25 baseline cycle lengths, a second shorter cycle length was introduced that was 50 to 80 msec (mean 65 +/- 10) greater than the VERP of the respective baseline cycle length (group 2 trials).

Swallowing syncope: observations in the absence of conduction system or esophageal disease.

A patient is described with the clinical syndrome of "swallowing syncope" who reproducibly demonstrated sinus bradycardia, A-H prolongation, and intranodal atrioventricular block in response to swallowing during electrophysiologic study. Baseline electrophysiologic and esophageal manometric results were normal, as was his response to other vagal maneuvers. Demand ventricular pacing alleviated his symptoms.

Amiodarone: correlation of early and late electrophysiologic studies with outcome.

Twenty-nine patients with recurrent sustained ventricular tachycardia (VT) or cardiac arrest underwent baseline, early (after 2 weeks of therapy) and late (after 5 months, mean) electrophysiologic studies during oral amiodarone therapy. Inducible sustained VT was present in all patients at baseline study, in 21 of 22 at early and in 26 of 29 at late study. The cycle length of induced VT increased from 263 +/- 60 msec at baseline study to 305 +/- 58 msec at early follow-up study and to 318 +/- 64 msec at late study (p less than .

Usefulness of programmed stimulation in idiopathic dilated cardiomyopathy.

The response to programmed electrical stimulation and the clinical outcome was determined in 47 patients with nonischemic dilated cardiomyopathy (DC). Thirteen patients (group 1) presented with sustained uniform ventricular tachycardia (VT), 14 (group 2) presented with cardiac arrest and 20 (group 3) presented with nonsustained VT. The mean ejection fraction of the study population was 28 +/- 9%.

Influence of the site of stimulation on the resetting phenomenon in ventricular tachycardia.

Uniform, sustained ventricular tachycardia (VT) in the setting of prior myocardial infarction is believed to be due to reentry. The ability to reset VT with programmed extrastimuli requires that the premature impulse reach and enter the reentrant circuit. To evaluate the importance of the site of pacing on the ability to reset VT, single ventricular extrastimuli were delivered during 32 morphologically distinct, uniform VTs from both the right ventricular (RV) apex and RV outflow tract.

Amiodarone versus amiodarone and a type IA agent for treatment of patients with rapid ventricular tachycardia.

Induction of rapid ventricular tachycardia or fibrillation during therapy with amiodarone is associated with an increased risk of sudden death. To determine whether the addition of a type IA antiarrhythmic agent to therapy would improve outcome, 37 patients in whom ventricular tachyarrhythmia of a cycle length less than 350 msec was induced after 14 +/- 2 days of amiodarone were randomly assigned to therapy with amiodarone alone (group 1, 20 patients) or amiodarone plus type IA agent (group 2, 17 patients). Type IA therapy consisted of procainamide in 13 patients and quinidine in four procainamide-intolerant patients.

Resetting response patterns during sustained ventricular tachycardia: relationship to the excitable gap.

We analyzed the resetting response (a noncompensatory pause after electrical stimulation) during 37 hemodynamically tolerated ventricular tachycardias (VTs) induced by programmed electrical stimulation in 32 patients with chronic coronary artery disease. The mean cycle length of VT was 369 +/- 59 msec. Single extrastimuli were delivered at the right ventricular apex during all 37 VTs, and double extrastimuli were delivered at the same site during 23 VTs.

Abnormalities of endocardial activation pattern in patients with previous healed myocardial infarction and ventricular tachycardia.

Endocardial catheter mapping was performed in 27 patients with anterior wall acute myocardial infarction (AMI) and in 10 patients with inferior wall AMI. All patients had a history of ventricular tachycardia. Left ventricular breakthrough occurred at 10 +/- 4 ms after the QRS complex in inferior AMI and 11 +/- 7 ms after the QRS complex in anterior AMI.

Electrocardiographic response of digoxin-toxic fascicular tachycardia to Fab fragments: implications for tachycardia mechanism.

The electrocardiographic response of digoxin-induced fascicular tachycardia to Fab fragments was evaluated in two patients. In addition, we documented the response of the fascicular tachycardia to spontaneous premature ventricular depolarizations during different tachycardia rates, the response to a nonsustained episode of ventricular tachycardia, and the mode of spontaneous initiation and termination of short-lived episodes of the tachycardia during the treatment process. The following findings were noted: slowing of the tachycardia in response to Fab administration; change in the morphologic characteristics of the tachycardia from multiform to uniform; resetting of the tachycardia by spontaneous premature ventricular depolarization with the return cycle equal to the observed tachycardia cycle length; acceleration of the tachycardia in response to five beats of a faster nonsustained ventricular tachycardia; and initiation and termination of the tachycardia, both by spontaneously occurring premature ventricular depolarizations and in the absence of premature ventricular depolarizations.

Analysis of the resetting phenomenon in sustained uniform ventricular tachycardia: incidence and relation to termination.

Unlabelled: Although the phenomenon of resetting has been studied in several experimental and clinical rhythms, it has not been systematically analyzed in ventricular tachycardia. To define the incidence and determinants of resetting as well as its relation to ventricular tachycardia termination, the response to programmed stimulation was prospectively studied during 78 electrically induced episodes of sustained, uniform ventricular tachycardia (mean cycle length 365 +/- 59 ms) in 53 patients. Single and double ventricular extrastimuli were introduced during 78 and 39 episodes of ventricular tachycardia, respectively.

Electrophysiologic sequelae of chronic myocardial infarction: local refractoriness and electrographic characteristics of the left ventricle.

Ventricular tachycardia (VT) has been shown to arise from ischemically damaged left ventricular myocardium, which possesses heterogeneity of refractoriness and activation. Catheter techniques were used to study left ventricular refractoriness using the strength-interval relation and activation by local electrographic characteristics in 8 patients with and 6 patients without previous myocardial infarction (MI). Noninfarcted myocardium in patients with and without previous MI was similar overall with respect to refractoriness and excitability, whereas local electrographic duration in MI patients was longer (66 +/- 2 vs 52 +/- 3 ms, p less than 0.