Muscle sympathetic nerve activity is reduced in IDDM before overt autonomic neuropathy.

Studies of heart-rate variability have demonstrated that abnormal cardiac parasympathetic activity in individuals with IDDM precedes the development of other signs or symptoms of diabetic autonomic neuropathy. To determine whether IDDM patients have impaired sympathetic activity compared with normal control subjects before the onset of overt neuropathy, we directly recorded MSNA. We also examined the effects of changes in plasma glucose and insulin on sympathetic function in each group. MSNA was recorded by using microneurographic techniques in 10 IDDM patients without clinically evident diabetic complications and 10 control subjects. MSNA was compared during a 15-min fasting baseline period and during insulin infusion (120 mU.m-2.min-1) with 30 min of euglycemia. A cold pressor test was performed at the end of euglycemia. Power spectral analysis of 24-h RR variability was used to assess cardiac autonomic function. IDDM patients had lower MSNA than control subjects at baseline (8 +/- 1 vs. 18 +/- 3 burst/min, P < 0.02). MSNA increased in both groups with insulin infusion (P < 0.01) but remained lower in IDDM patients (20 +/- 3 vs. 28 +/- 3 burst/min, P < 0.01). In the IDDM group, we found no relationships between MSNA and plasma glucose, insulin, or HbA1c concentrations. BP levels did not differ at rest or during insulin. Heart-rate variability and the MSNA response to cold pressor testing in IDDM patients did not differ from those in healthy control subjects. IDDM patients had reduced MSNA at rest and in response to insulin. The lower MSNA is not attributable to differences in plasma glucose or insulin, but, rather, is most likely an early manifestation of diabetic autonomic neuropathy that precedes impaired cardiac parasympathetic control.

Propranolol blocks ventricular refractory period changes with orthostatic stress in humans.

The purpose of this study was to test the hypothesis that orthostatic stress shortens the right ventricular effective refractory period by reflex activation of beta-adrenergic receptors. Twelve patients undergoing electrophysiologic testing for standard clinical indications were studied. After a full electrophysiologic study, patients underwent graded lower body negative pressure before and after administration of either propranolol (0.2 mg/kg intravenously) in Group I or atropine (0.035 mg/kg intravenously) in Group II. Before the addition of drugs, lower body negative pressure produced decreases in systolic blood pressure and significant increases in sinus rate. The effective refractory period shortened from 214 +/- 8 (mean +/- SEM) to 206 +/- 7 ms at -40 cm H2O and to 197 +/- 4 ms at -60 cm H2O lower body negative pressure. After propranolol, Group I patients had no change in right ventricular effective refractory period despite similar changes in sinus rate and systolic blood pressure. In group II patients, atropine did not alter effective refractory period responses to lower body negative pressure. Thus, reflex adjustments to orthostatic stress result in shortening of right ventricular effective refractory period mediated by way of beta-adrenergic mechanisms. These findings constitute the first evidence that sympathetic influences mobilized by the body can directly modulate ventricular electrophysiologic changes.

Morphologically distinct sustained ventricular tachycardias in coronary artery disease: significance and surgical results.

One hundred patients with drug-refractory recurrent sustained ventricular tachycardia associated with coronary artery disease who underwent mapping-directed subendocardial resection for ventricular tachycardia were retrospectively evaluated with respect to a number of morphologically distinct tachycardias on a 12 lead electrocardiogram. Of 91 operative survivors, 18 patients had only one configuration of tachycardia, whereas 73 (81%) had multiple distinct tachycardia configurations; 36 had multiple configurations clinically. Patients with multiple clinical configurations had a longer mean HV interval (65 +/- 11 versus 53 +/- 10 ms, p less than 0.005) and a higher failure rate of surgery alone (47 versus 25% for single clinical tachycardia, p less than 0.05). The 13 patients whose multiple clinical tachycardias originated in disparate sites in the heart (greater than 5 cm between sites of origin) were less often cured by surgery alone than were those whose multiple tachycardias originated in the same or adjacent sites (83 versus 38% failure rate of surgery alone, p less than 0.05). On the basis of mapping data, multiple configurations of ventricular tachycardia appear to originate in the same or adjacent sites in the majority of patients, although in 16% of patients with multiple tachycardias, the tachycardias originate at widely separated sites.

Polymorphous ventricular tachycardia: a side effect of intracoronary papaverine.

Polymorphous ventricular tachycardia occurred in 1.3% of patients (5 of 391) who received intracoronary papaverine over a 47 month period. The arrhythmia lasted less than 1 min in all five patients, converting spontaneously in four and requiring electrical cardioversion in one. Ventricular tachycardia occurred in 4.4% of women (4 of 90) and 0.3% of men (1 of 301) (p less than 0.0025). Only one of the patients with ventricular tachycardia had coronary artery disease. To determine whether other clinical or procedural factors predispose patients to this side effect of papaverine, these 5 patients were compared with 25 control patients who were matched for gender and extent of coronary artery disease. The following variables were analyzed: age, baseline serum potassium and calcium levels, left ventricular ejection fraction, baseline heart rate, mean arterial pressure, corrected QT interval, the change in corrected QT interval produced by papaverine and the maximal dose of the drug per kilogram of body weight. Of these variables, only baseline heart rate differed significantly in the two groups of patients. Thus, polymorphous ventricular tachycardia is an infrequent, but important, side effect of papaverine that is usually self-limited. Women with a relatively slow heart rate appear to be predisposed to this side effect.

Subendocardial resection for refractory ventricular tachycardia: effects on ambulatory electrocardiogram, programmed stimulation and ejection fraction, and relation to outcome.

The inducibility of ventricular tachycardia by programmed stimulation was correlated with ventricular ectopic activity on ambulatory electrocardiogram, ejection fraction and clinical outcome in 36 patients after endocardial resection for medically refractory ventricular tachycardia. Ventricular tachycardia was noninducible postoperatively in 25 patients and was inducible in 11. After administration of antiarrhythmic drugs, ventricular tachycardia could no longer be induced in four patients and remained inducible in the other seven patients. All 36 patients had postoperative and 20 had preoperative ambulatory electrocardiograms obtained while they were not receiving drug therapy. Pre- and postoperative ambulatory electrocardiograms did not differ in mean hourly ventricular premature depolarization frequency, Lown arrhythmia grade or change in grade (pre- vs. postoperative). The majority of postoperative patients had repetitive forms of ventricular arrhythmia postoperatively and there was no difference between patients with inducible and noninducible ventricular tachycardia in regard to Holter monitoring characteristics. There was no significant difference in postoperative ejection fraction between patients with inducible and noninducible ventricular tachycardia postoperatively. Ventricular tachycardia has recurred in 2 of 29 patients who had no inducible tachycardia at the time of hospital discharge and were followed up for a mean of 1 year; it has recurred in one of seven patients in whom it was still inducible at the time of hospital discharge and who were followed up for a mean of 7 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Limited role of intravenous propafenone hydrochloride in the treatment of sustained ventricular tachycardia: electrophysiologic effects and results of programmed ventricular stimulation.

The electrophysiologic effects and response to programmed ventricular stimulation of intravenous propafenone, an experimental antiarrhythmic agent, were studied in a group of 14 patients with both clinical and induced sustained ventricular tachycardia. Twelve of the 14 patients had not responded to conventional antiarrhythmic drug therapy. Propafenone had no significant effect on sinus cycle length (836 +/- 170 ms before and 750 +/- 124 ms after propafenone), P wave duration (108 +/- 24 ms before and 106 +/- 23 ms after propafenone) or PR interval (181 +/- 45 ms before and 194 +/- 53 ms after propafenone). QRS duration and ventricular effective refractory periods increased significantly (109 +/- 20 to 130 +/- 21 ms and 235 +/- 24 to 256 +/- 19 ms, respectively). Ventricular tachycardia remained inducible or occurred spontaneously in 13 of 14 patients after propafenone administration. Neither mode of initiation nor mode of termination of ventricular tachycardia was predictably altered. Additional forms of ventricular tachycardia were seen in six patients. Cycle length of ventricular tachycardia was 303 +/- 73 ms before and 346 +/- 143 ms after propafenone (p = NS). In conclusion, intravenous propafenone does not significantly affect sinus rate, intraatrial conduction or atrioventricular conduction. Ventricular refractoriness and intraventricular conduction are prolonged. The mode of initiation, mode of termination and ventricular tachycardia cycle length are not predictably altered, but ventricular tachycardia occasionally occurs spontaneously after propafenone. Intravenous propafenone rarely prevents induction of ventricular tachycardia in patients with sustained ventricular tachycardia refractory to conventional antiarrhythmic agents.

Optimizing utilization of pediatric echocardiography and implications for telemedicine.

Telemedicine can deliver tertiary level services to remote communities where subspecialty care is limited. Locally performed echocardiography has been initiated at several locations around Iowa. The goal of this study was to examine utilization and diagnostic yield of community-based echocardiographic services. Community physicians selected patients for remote echocardiograms (echoes), and studies were performed locally by sonographers trained in recording pediatric echoes. Echoes were sent to the pediatric echocardiography laboratory by mail or via telemedicine systems. Echoes were also ordered locally by pediatric cardiologists during outreach clinics in the same communities. Numbers of normal and abnormal echoes ordered by community physicions and pediatric cardiologists were compared by chi-square analysis. Since January 1996, community physicians ordered 378 echoes, whereas 154 echoes were ordered by pediatric cardiologists at outreach clinics. Stratifying echoes by patient age found that the percentage of normal studies in patients < 1 year of age was no different between groups (27% normal by community physicians vs 15%; chi-square 0.92; p = 0.34). The percentage of normal studies ordered by community physicians was significantly greater in patients > 1 year of age (83% normal by community physicians vs 25%; chi-square 80.2; p <0.0001). Thus, (1) community physicians effectively identified patients < 1 year of age with abnormal echoes, (2) significantly fewer echoes may be required in patients > 1 year of age if patients are first evaluated by a pediatric cardiologist, and (3) patient selection will impact cost effectiveness of remotely obtained echoes.

Alterations in the initial portion of the signal-averaged QRS complex in acute myocardial infarction with ventricular tachycardia.

This study was designed to examine 2 hypotheses: that acute myocardial infarction (AMI) alters early cardiac activation measured by signal-averaging; and that the magnitude of abnormality of early activation may be greater in patients with post-AMI ventricular tachycardia (VT). We examined the root-mean square voltage amplitude in 10-ms intervals over the first 80-ms of the signal-averaged QRS complex. Data from 42 healthy volunteers were compared with those from 52 patients with previous AMI (24 anterior) but no VT and 46 post-AMI patients (33 anterior AMI) with recurrent sustained VT. Patients with VT differed from other post-AMI patients because of lower left ventricular ejection fraction, more frequent aneurysm formation and higher levels of ventricular ectopic activity. A significant decrease in initial voltage amplitude occurred at 30 to 40 ms after the beginning of the QRS in both anterior and inferior AMI patients compared with the normal group. A further significant decrease in initial amplitude occurred in VT patients both after anterior and inferior AMI. These differences persisted for the remainder of the 80-ms interval. These changes were weakly related to QRS duration (r = 0.45), ejection fraction (r = 0.50) and poorly correlated with the presence of Q waves on 12-lead electrocardiogram (r = 0.21). Direct endocardial catheter recordings performed in VT patients confirmed abnormalities of local septal activation after anterior and inferior AMI.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of direct, reflex and exercise-provoked increases in sympathetic tone on idiopathic ventricular tachycardia.

Exercise treadmill testing and direct enhancement of sympathetic influence with agents such as isoproterenol are often used to reproduce ventricular tachycardia (VT). The cardiac effects of, and arrhythmia responses to, graded exercise, isoproterenol infusion and lower body negative pressure (the latter 2 with and without atrial and ventricular stimulation) were studied in 11 patients with idiopathic VT. During maximal exercise, substantial increases in heart rate and blood pressure occurred, but only 2 of 9 exercised patients had VT (during recovery in both). During programmed stimulation alone, VT was initiated in 6 patients. During maximum levels of lower body negative pressure (-60 cm of water in most), mean systolic blood pressure decreased by 10 mm Hg, heart rate increased by 15 beats/min, and ventricular refractory period decreased by 10 ms. In 4 patients VT occurred spontaneously during lower body negative pressure; in 2, lower body negative pressure was the only intervention producing VT. During isoproterenol infusion VT occurred spontaneously in 2 patients; both had VT initiated during other interventions. Lower body negative pressure and isoproterenol increased VT rate, but did not prolong it. It is concluded that there is significant variability in arrhythmia responses to sympathetic augmentation, suggesting that additional covariables such as parasympathetic input and ventricular volume may also have a role in arrhythmia occurrence.

Enhanced efficacy of oral sotalol for sustained ventricular tachycardia refractory to type I antiarrhythmic drugs.

Sotalol is a nonselective beta-adrenergic blocking agent with Vaughn-Williams class III activity. Its efficacy was tested in 9 patients with sustained ventricular tachycardia (VT) that had previously remained inducible during electrophysiologic testing of type I drugs (procainamide or quinidine). Eight patients had coronary artery disease with remote myocardial infarction and 1 had cardiomyopathy (ejection fraction 0.34 +/- 0.08, mean +/- standard deviation). Type I drugs prolonged the effective refractory period of the right ventricle 12 +/- 14% and prolonged the VT cycle length 41 +/- 24%. In contrast, despite an equivalent effect on the effective refractory period, a sustained VT could no longer be initiated in any of the 8 patients ultimately tested while taking oral sotalol. Daily doses averaged 600 +/- 103 mg and blood levels associated with VT suppression in electrophysiologic studies were generally greater than 3,000 ng/ml. In addition, sotalol was moderately effective at reducing ventricular ectopic activity measured by ambulatory electrocardiography. Over a mean follow-up of 23 months (range 1 to 37), mild heart failure (3 patients), symptomatic brady-cardia requiring pacemaker (1) and drug-related polymorphous VT (1) have occurred. Sudden death occurred in 1 patient and nonfatal VT recurrence was noted in 2. Five of 8 chronically treated patients currently are successfully treated with minimal side effects. Sotalol appears to be a promising antiarrhythmic drug in the treatment of serious ventricular arrhythmias, even in patients refractory to type I antiarrhythmic agents.

Noninvasive prediction of efficacy of type IA antiarrhythmic drugs by the signal-averaged electrocardiogram in patients with coronary artery disease and sustained ventricular tachycardia.

This study attempted to determine if specific changes on the signal-averaged electrocardiogram (ECG) after type IA antiarrhythmic therapy are predictive of efficacy in the treatment of ventricular tachycardia (VT). Scalar and signal-averaged ECGs were obtained at baseline and after type IA drug therapy in 15 patients with coronary artery disease and inducible VT at baseline electrophysiologic testing. Signal-averaged QRS duration, root-mean-square amplitude in the last 40 ms of signal-averaged QRS, and the duration under 40 mu v of the signal-averaged QRS (low-amplitude signal), as well as ventricular effective refractory period at electrophysiologic study, and QTc on the scalar ECG were compared. At drug study, 6 patients (group A) had persistent but slower VT, whereas 9 (group B) had VT rendered noninducible. The baseline signal-averaged QRS duration was longer in group A than in B (136 +/- 10 vs 115 +/- 13 ms; p < 0.05), as was the scalar QRS (115 +/- 19 vs 98 +/- 11 ms; p < 0.05). After antiarrhythmic therapy, group A had a greater prolongation of both signal-averaged QRS (24 +/- 10 vs 8 +/- 3 ms; p < 0.05) and low-amplitude signal (31 +/- 13 vs 3 +/- 7 ms; p < 0.05), whereas group B had a greater increase in ventricular effective refractory period (49 +/- 20 vs 20 +/- 13 ms; p < 0.05) and corrected QT interval (100 +/- 39 vs 43 +/- 23 ms; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Usefulness of isoproterenol in facilitating atrioventricular nodal reentry tachycardia during electrophysiologic testing.

In some patients with documented atrioventricular (AV) nodal supraventricular tachycardia (SVT), the arrhythmia is not inducible during a standard stimulation protocol. In these patients the level of sympathetic activity may be an important factor. This study evaluates the influence of isoproterenol on anterograde and retrograde pathway properties in patients with AV nodal SVT and the mechanism by which this SVT is facilitated. Group 1 consisted of 8 consecutive patients, ages 23 to 85 years (mean +/- standard error, 57 +/- 8) who had no inducible AV nodal SVT during electrophysiologic testing until isoproterenol (0.5 to 3.0 micrograms/min) was infused. These patients were compared with 6 patients in the same age range (45 to 78 years, mean +/- standard error, 64 +/- 5) who had inducible AV nodal SVT without isoproterenol and who comprised group 2. In comparing group 1 (before isoproterenol) with group 2, there was no significant difference in the refractory periods of the anterograde slow and fast pathways, although the anterograde block cycle length was longer in group 1 patients (421 +/- 18 vs 362 +/- 14 ms, p less than 0.05). The retrograde block cycle length was also longer in 7 of the 8 group 1 (before isoproterenol) patients in whom it could be measured versus those in group 2 (411 +/- 14 vs 318 +/- 27 ms, p less than 0.05). During isoproterenol, the anterograde and retrograde block cycle lengths in group 1 were not different from group 2. Therefore, AV nodal SVT may not be inducible in some patients during routine electrophysiologic testing.(ABSTRACT TRUNCATED AT 250 WORDS)

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 0.005) and amplitude lower (3.9 +/- 2.1 vs 6.1 +/- 2.0 mV, p less than 0.05). Comparisons of infarcted and noninfarcted regions in MI patients revealed an increased threshold of excitability at infarct sites (e.g., 1.9 +/- 1.0 vs 0.7 +/- 0.4 mA, p less than 0.05) and prolongation of refractory periods (375 +/- 118 vs 275 +/- 13 ms, p less than 0.05) at the lowest level of stimulating current. Shortening of refractory period as a result of change in pacing cycle length was not affected by infarction. The local electrographic duration (95 +/- 17 ms) was significantly longer in infarcted regions than at noninfarcted sites (p less than 0.005), but the electrographic amplitude (3.4 +/- 3.0 mV) differed significantly only in noninfarct patients. It is concluded that considerable electrophysiologic disparity exists between infarcted and noninfarcted myocardium. Whether or not arrhythmogenic tissue possesses unique alterations in electrophysiologic characteristics remains to be established.

Clinical, hemodynamic and sympathetic neural correlates of heart rate variability in congestive heart failure.

Heart rate (HR) variability has long been recognized as a sign of cardiac health. In the presence of heart disease, HR variability decreases, an observation that has been associated with poor prognosis in a number of recent studies. HR variability is particularly altered in congestive heart failure (CHF), a condition associated with a number of typical functional hemodynamic and neurohumoral alterations. The relation of measurements of HR variability to these abnormalities in patients with heart failure has not been carefully examined. Twenty-three patients (19 men, 4 women, mean age 49 years) with New York Heart Association class II to IV CHF were studied prospectively without cardiac medications; radionuclide ventriculography, right-sided heart catheterization, peroneal microneurography, plasma norepinephrine and 24- to 48-hour ambulatory electrocardiography were performed. Average RR interval and its standard deviation, and HR power spectrum (0 to 0.5, 0.05 to 0.15 and 0.2 to 0.5 Hz) were derived from the ambulatory electrocardiographic recordings and compared with left ventricular ejection fraction, thermodilution cardiac output, pulmonary arterial wedge pressure, New York Heart Association class, age, muscle sympathetic nerve activity (peroneal nerve) and norepinephrine level by linear regression. None of the measures of HR variability were significantly related to age, left ventricular ejection fraction, cardiac output or functional classification, whereas the 0.05 to 0.15 and 0.20 to 0.50 Hz components were weakly but significantly related to cardiac output (r = 0.49 and 0.42, p = 0.02 and 0.045, respectively). In contrast, a generally stronger and negative relation was demonstrated between spectral and nonspectral measurements of HR variability, and indicators of sympathoexcitation, muscle sympathetic nerve activity and plasma norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Establishment of signal-averaged electrocardiographic criteria with Frank XYZ leads and spectral filter used alone and in combination with ejection fraction to predict inducible ventricular tachycardia in coronary artery disease.

Signal-averaged electrocardiographic criteria are reported for corrected Frank XYZ leads and a spectral filter. The new criteria were used alone and in combination with ejection fraction to predict inducibility of ventricular tachycardia (VT) at electrophysiologic testing. Signal-averaged electrocardiographic criteria were developed in 87 control subjects and validated in 182 patients (aged 63 +/- 10 years) with coronary artery disease and QRS duration less than 118 ms. Patients underwent electrophysiologic testing in which up to 3 extra-stimuli were used during 2 paced drives from 2 right ventricular sites. A positive finding was monomorphic VT lasting 30 seconds or needing intervention. An ejection fraction less than 40% was considered abnormal. Signal-averaged electrocardiographic variables that best characterized control subjects and separated patients with and without inducible VT were filtered QRS duration less than 120 ms, low-amplitude signal duration less than 38 ms and root-mean-square voltage greater than 20 muv. With these criteria, signal-averaged electrocardiographic and ejection fraction sensitivities were 87 and 45%, respectively, and specificities were 65 and 77%, respectively. Combining signal-averaged electrocardiography with ejection fraction improved the predictive accuracy. In conclusion, diagnostic criteria for signal-averaged electrocardiography with use of Frank XYZ leads and a spectral filter produced results similar to those reported for use of bipolar XYZ leads and a Butterworth filter. Signal-averaged electrocardiography was a better predictor of VT than was ejection fraction.

Safety and utility of flecainide acetate in the routine care of patients with supraventricular tachyarrhythmias: results of a multicenter trial. The Flecainide Supraventricular Tachycardia Study Group.

Patients with supraventricular arrhythmias have been safely and effectively treated with flecainide. We conducted an open-label, 20-center trial to define further the safety and efficacy profile of oral flecainide in patients with supraventricular arrhythmias, including atrial tachycardias (ectopic or multifocal), atrial-ventricular tachycardias (reentrant), paroxysmal atrial fibrillation/flutter (PAF), and chronic atrial fibrillation (CAF). Our study population of 151 patients with documented supraventricular arrhythmias requiring treatment included 67 with paroxysmal supraventricular tachycardia (PSVT), 67 with PAF (symptoms < 15 days), and 17 with CAF (symptoms > of = 15 days)> The initial flecainide dose of 100 mg twice daily could be increased by 50 mg bid every 4 days to a maximum of 200 mg twice daily. Patients who were effectively treated could receive flecainide for 1 year. The study was terminated April 26, 1989, in response to interim results reported by the Cardiac Arrhythmia Suppression Trial (CAST). All patients were removed from the study by August 1989. At study termination 87% of PSVT, 73% of PAF, and 56% of CAF patients had improved symptomatically while on flecainide therapy. Eleven patients experienced cardiac adverse experiences: proarrhythmic events (3 patients), new or worsened congestive heart failure (7 patients), sinus pauses (1 patient). Cardiac side effects appeared to be more frequent in patients in the CAF group (5/17 patients), all of whom had structural heart disease. Overall, 45 (67%) PSVT, 43 (64%) PAF, and 9 (56%) CAF patients reported at least 1 noncardiac adverse experience; the most common were abnormal vision, dizziness, and headaches. One patient from the CAF group died; the death was considered to be unrelated to flecainide. Flecainide appears to be safe and effective treatment for patients with supraventricular arrhythmias of a variety of mechanisms and appears particularly effective for patients with PSVT. The efficacy is lowest and side effects most frequent in patients with CAF, as seen with other trials of antiarrhythmic medication in these patients. In the context of the CAST experience and other trials of antiarrhythmic drugs in patients with CAF, the balance of risk and benefit of therapy should be considered carefully before initiating treatment.

Relation of mode of induction and cycle length of ventricular tachycardia: analysis of 104 patients.

One hundred four consecutive patients with ventricular tachycardia (VT) were examined to correlate the cycle length with the mode of initiation of VT (single, double, and triple extrastimuli and rapid pacing). Tachycardias induced with a single extrastimulus were slower (342 +/- 72 ms, mean cycle length) than those induced with double (295 +/- 60 ms) or triple (282 +/- 56 ms) extrastimuli or rapid pacing (293 +/- 40 ms). There were no differences among the last 3 groups. In 38 patients who had endocardial catheter mapping to determine the site of origin of VT, distance from stimulation site to the site of origin was estimated and correlated with mode of initiation. There was no difference in mode of initiation when the stimulation site was close (less than 3 cm), intermediate (3 to 5 cm), or distant (greater than 8 cm) from the site of origin. To address the issue of distance from stimulation site to the site of origin somewhat differently, mode of initiation was correlated with site of previous myocardial infarction in 69 patients with VT initiated from the right ventricular apex. Again, mode of initiation did not differ among patients with septal, inferior, lateral, or multiple myocardial infarctions. Thus, cycle length of VT initiated with a single extrastimulus was slower than that initiated with double or triple extrastimuli or rapid pacing and the mode of initiation of VT was unrelated to site of myocardial infarction or distance between stimulation site and site of origin of VT.

Clinical characteristics and long-term follow-up in 119 survivors of cardiac arrest: relation to inducibility at electrophysiologic testing.

Electrophysiologic studies were performed in 119 survivors of cardiac arrest. Sustained ventricular arrhythmias were initiated by programmed ventricular stimulation in 72 patients (61%). Coronary artery disease patients with induced sustained ventricular arrhythmias had a higher incidence of prior myocardial infarction (95 versus 72%) and ventricular aneurysm (59 versus 28%) and a lower ejection fraction (37 versus 50%) than those with no inducible sustained ventricular arrhythmias. Of the 72 patients with inducible ventricular arrhythmias, 11 (15%) died suddenly during a mean follow-up of 18 months (range 15 days to 58 months). In this group, 6 of 41 patients (15%) discharged on a successful antiarrhythmic regimen and 5 of 27 patients (19%) discharged on an unsuccessful regimen or without a predischarge study have died suddenly. Of these 27 patients, 1 of 12 patients treated with amiodarone and 4 of 15 (27%) with conventional antiarrhythmic therapy died suddenly. The remaining 4 patients died of nonarrhythmic causes in the postoperative period. Of 47 patients without inducible sustained ventricular arrhythmias, 15 (32%) died suddenly at a mean follow-up of 20 months, 10 (34%) with and 15 (28%) without empiric therapy. It is concluded that sustained ventricular arrhythmias can be initiated in most patients resuscitated from cardiac arrest. Patients with inducible arrhythmias have greater left ventricular dysfunction than those without inducible arrhythmias. Medical or surgical therapy that prevented the induction of sustained ventricular arrhythmias was predictive of a successful outcome in 85% of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Programmed ventricular stimulation at a second right ventricular site: an analysis of 100 patients, with special reference to sensitivity, specificity and characteristics of patients with induced ventricular tachycardia.

One hundred patients without ventricular tachycardia (VT) initiated from the right ventricular (RV) apex were subjected to stimulation at the RV outflow tract. Sixty-two patients had no clinical arrhythmias, and 38 had sustained VT, ventricular fibrillation (VF) or cardiac arrest. Of the 38 patients with clinical arrhythmias, 22 (58%) had VT or VF induced from the RV outflow tract. Among the 62 patients without arrhythmias, 5 (13%) had polymorphic nonsustained VT or VF induced, which occurred with triple extrastimuli in all 5 patients. The 22 patients with VT initiated at the RV outflow tract were a heterogeneous group; 10 (45%) patients had cardiac diagnoses other than coronary artery disease (CAD). In contrast were patients whose VT was initiated at the RV apex (n = 84); in this group, 20 patients (22%) had diagnoses other than CAD (p less than 0.05). These 22 patients also were younger (mean age 46 years) than patients whose VT was initiated at the RV apex (mean age 58; p less than 0.01). Of the 16 patients with clinical VT and no induced arrhythmia from either RV site, 7 had CAD (4 with cardiac arrest), 5 had the long QT syndrome, 3 had dilated cardiomyopathy and 1 had valvular heart disease. In conclusion, stimulation at a second RV site increases the sensitivity of RV stimulation in patients with known VT and seldom initiates VT in patients without clinical VT.

Discordant results of programmed ventricular stimulation at different right ventricular sites in patients with and without spontaneous sustained ventricular tachycardia: a prospective study of 56 patients.

Programmed ventricular stimulation (PVS) was prospectively performed in 56 consecutive patients from both the right ventricular (RV) apex and the RV outflow tract. Thirty-seven patients had documented clinical sustained ventricular tachycardia (VT) and 19 patients had no sustained spontaneous VT in the absence of antiarrhythmic drugs. The sensitivity of VT induction was 65% from the RV apex, 76% from the RV outflow tract and was 89% with combined stimulation at both RV sites. The specificity from the RV apex, the RV outflow tract and both sites combined was 100%. When sustained VT was induced from both sites (51%), it was usually of the same morphologic characteristics, axis and cycle length. When sustained VT was induced at 1 site and nonsustained VT at the second site, the morphologic characteristics or axis usually differed. Of patients who had VT induced at both RV sites during the baseline study 37% had VT rendered noninducible during treatment with conventional antiarrhythmic agents. No patients whose VT was induced at only 1 RV site responded to conventional drugs. We conclude that programmed ventricular stimulation at a second RV site is frequently helpful in the evaluation of VT. Inducibility at only 1 of 2 RV sites predicts a poor response to conventional antiarrhythmic drugs.