Biomedical subjects

D L Ross

Publications and source records attributed to D L Ross.

At least 73 records · Page 4Linked to original sources

PubMed1991

Permanent junctional reciprocating tachycardia misdiagnosed as 'cardiomyopathy'.

In a nine-year-old female, cardiac failure was erroneously attributed to idiopathic cardiomyopathy and cardiac transplantation was planned. The actual cause of cardiac failure was permanent junctional reciprocating tachycardia (PJRT), a rare form of supraventricular tachycardia. The diagnostic error was discovered before transplantation was performed and the arrhythmia was treated surgically. This resulted in return of near normal cardiac function.

Cardiomyopathies↗

PubMed1991

What is the best method for assessing the long-term outcome of surgery for accessory pathways and atrioventricular junctional reentrant tachycardias?

The success of surgery for supraventricular tachycardia (SVT) is evaluated by a variety of methods in different hospitals. Unfortunately, the predictive values of these methods are not known. We therefore compared the various methods in 261 patients undergoing surgery for SVT at Westmead Hospital since 1981. Surgical outcome was assessed by early tests during the first week after surgery (serial 12-lead electrocardiograms, telemetric monitoring of the electrocardiogram, and electrophysiological study performed using epicardial wires); later tests at 6 months after surgery (12-lead electrocardiograms and electrophysiological study); and symptomatic review done by telephone interview at a median of 34 months after surgery. Early tests were obtained in 97%, later tests were obtained in 76%, and symptomatic review was obtained in 98% of patients. All of the examined tests were inaccurate methods of surgical assessment compared with the late electrophysiological study. A large proportion of the patients proven to be surgical failures at the late electrophysiological study were not detected by early tests (83%), by later electrocardiograms (66%), or by symptomatic assessment (41%). Accurate assessment of surgical outcome requires a late electrophysiological study to permit comparison of surgical techniques. Late electrophysiological study also provides accurate information on the current risks and benefits of proposed surgery for communication to patients to enable them to make an informed decision on future treatment. Most patients are willing to have a late electrophysiological study and usually benefit from clarification of their true surgical outcome.

Cardiac Pacing, Artificial↗

PubMed1991

What is the best predictor of spontaneous ventricular tachycardia and sudden death after myocardial infarction?

BACKGROUND: Death during the first year after myocardial infarction is most commonly due to spontaneous ventricular tachycardia (VT) or fibrillation (VF). The purpose of this study was to compare, in a single cohort of patients, the values of inducible VT, delayed ventricular activation, low left ventricular ejection fraction, high-grade ventricular ectopy, and ST segment displacement on exercise in predicting electrical events (witnessed instantaneous death and spontaneous VT or VF) during the first year after myocardial infarction. METHODS AND RESULTS: Three hundred sixty one patients aged less than 71 years underwent electrophysiological study, signal-averaged electrocardiogram, gated blood-pool scan, 24 hour ambulatory electrocardiographic monitoring, and exercise testing 1-2 weeks after myocardial infarction and were then followed up for at least 1 year. There were 34 deaths (eight witnessed instantaneous, 26 other), and nine patients survived one or more episodes of spontaneous VF or VT. Patients with inducible VT were 15.2 times more likely to suffer electrical events than patients without inducible VT. No proportional-hazards model excluding inducible VT was as good a predictor of electrical events as was inducible VT alone. CONCLUSIONS: Inducible VT at electrophysiological study was the single best predictor of spontaneous VT and sudden death after myocardial infarction.

Aged↗

PubMed1991

Patients with two types of atrioventricular junctional (AV nodal) reentrant tachycardia. Evidence that a common pathway of nodal tissue is not present above the reentrant circuit.

BACKGROUND: The site of the reentrant circuit in atrioventricular (AV) junctional reentrant tachycardia has not been defined; in particular, the existence of a common pathway of AV nodal tissue above the reentrant circuit is controversial. METHODS AND RESULTS: Two types of AV junctional reentrant tachycardia were induced in each of three patients at electrophysiological study. In one type of tachycardia (anterior), the onset of atrial activity occurred from 0 to 12 msec before the onset of ventricular activation, and earliest atrial activity was recorded near the His bundle. In the second type of tachycardia (posterior), the ventriculoatrial intervals were longer (76-168 msec), and earliest atrial activity was recorded near the mouth of the coronary sinus. In individual patients, the two types of tachycardia had different cycle lengths. Posterior AV junctional reentrant tachycardia was not a fast-slow form of AV junctional reentry in at least two of the three patients. Surgical cure was attempted in two patients. In one patient, anterior AV junctional reentrant tachycardia was abolished by dissection of the anterior perinodal atrium, but posterior AV junctional reentrant tachycardia could still be induced. At reoperation 4 months later, dissection of the posterior perinodal atrium abolished posterior AV junctional reentrant tachycardia while preserving AV conduction. CONCLUSION: Differences in ventriculoatrial intervals and cycle lengths and the results of selective surgery suggest that the two types of AV junctional reentrant tachycardia used different reentrant circuits. These observations imply that a common pathway of AV nodal tissue is not present above the reentrant circuit and suggest that perinodal atrium is part of these circuits.

Adolescent↗

PubMed1990

Proarrhythmic effects of antiarrhythmic drugs.

Drugs that are described as antiarrhythmic drugs may actually aggravate arrhythmia in several ways and these are termed proarrhythmic effects. The most common type of proarrhythmia is a paradoxical increase in the frequency of episodes of the target arrhythmia. This type of effect had not been suspected until recently and has not been widely publicized. It is a phenomenon common to all antiarrhythmic drugs when they are used to treat arrhythmias based on a re-entrant mechanism (the most common mechanism of clinical arrhythmias). Different drugs vary in their tendency to produce this type of proarrhythmic response. These differences are explicable in terms of the relative effects of the drugs on refractoriness and conduction times in the re-entrant circuit. Proarrhythmic effects are most important in the treatment of ventricular tachycardias because recurrences are often fatal. Proarrhythmic effects on ventricular tachycardia can now be predicted at electrophysiological study before commencement of long-term therapy, and potentially dangerous treatment can be avoided. The key to proper treatment to proarrhythmia is to recognize that it is a drug-induced problem and to withdraw the offending drug.

Aged↗

PubMed1990

Effect of isoproterenol on induction of ventricular tachyarrhythmias in the normal and infarcted canine heart.

The influence of isoproterenol on induction of ventricular arrhythmias was evaluated in 10 normal dogs and 17 dogs with experimentally induced myocardial infarction. Programmed stimulation (using up to 6 extrastimuli) was performed before and then during infusion of isoproterenol (2 micrograms/minute followed by 4 micrograms/minute). Isoproterenol facilitated induction of sustained monomorphic ventricular tachycardia (cycle length 163 +/- 26 msec) in 5 of the 10 animals with no inducible baseline arrhythmia (P less than 0.05). Isoproterenol did not affect cycle length or the number of extrastimuli required in animals with baseline ventricular tachycardia (cycle length 158 +/- 15 msec before versus 163 +/- 17 msec during isoproterenol, P = 0.3; extrastimuli 3.8 +/- 0.6 before versus 3.8 +/- 0.4 during isoproterenol infusion, P = 0.3). Isoproterenol did not significantly facilitate induction of ventricular fibrillation in either normal dogs or those studied after production of myocardial infarction. We conclude that infusion of isoproterenol increases the incidence of inducible ventricular tachycardia in the infarcted heart, but does not facilitate the induction of ventricular fibrillation in infarcted or normal hearts, despite the use of an aggressive protocol for programmed stimulation. Isoproterenol is, therefore, a safe and useful adjunct to programmed stimulation in this setting.

Animals↗

PubMed1990

Right versus left ventricular stimulation: influence on induction of ventricular tachyarrhythmias in dogs.

The contribution of left (versus right) ventricular stimulation to the induction of ventricular tachyarrhythmias was studied in 37 dogs with chronic experimental myocardial infarction, and 17 dogs with normal hearts. Programmed stimulation of the endocardium at both ventricular apices employed an aggressive protocol of up to 7 extrastimuli. The right ventricle was the most successful site for induction of ventricular tachycardia after myocardial infarction (74% of dogs with ventricular tachycardia). Ten of 11 animals with slow ventricular tachycardia (greater than or equal to 140 msec) were inducible from the right ventricle. In contrast, left ventricular stimulation was required to induce rapid ventricular tachycardia (cycle length less than 140 msec) in 5 of 10 dogs (P less than 0.05). No animal required more than five extrastimuli from any site for induction of ventricular tachycardia. In the normal heart, ventricular fibrillation was induced most often from the right ventricle (77% of dogs) when compared with the left ventricle (47%, P less than 0.05). Ventricular tachycardia was never induced in normal animals. These results show that the right ventricular apex is the most successful site for induction of "slow" ventricular tachycardia in this canine model when using five extrastimuli. Rapid ventricular tachycardia is frequently induced from the infarcted left ventricle, but this arrhythmia may not be clinically significant. The normal right ventricle is significantly more susceptible to ventricular fibrillation than is the left ventricle, but this does not interfere with induction of ventricular tachycardia in the infarcted heart.

Animals↗

PubMed1990

Incessant ventricular tachycardia in infancy.

Two infants with incessant tachycardia uncontrolled by multiple drug treatment were thought initially to have supraventricular tachycardia. Careful examination of the 12-lead electrocardiogram suggested ventricular tachycardia, which was confirmed by electrophysiological studies. Intra-operative mapping showed that the arrhythmia arose from the posterior left ventricular free wall in one infant and at the left ventricular apex in the other. Cryoablation of these foci led to cessation of ventricular tachycardia. Myocardial biopsy showed hamartomatous involvement in the first infant and normal tissue in the other. In the first infant the incessant arrhythmia was cured but in the other it recurred 4 months later. The origin of the recurrent tachycardia was adjacent to the previously cryoablated arrhythmogenic area. This area was also cryoablated, leading to disappearance of the ventricular tachycardia. Both patients are free of arrhythmia 10 months and 3 months after their surgery. Surgically ablatable lesions are common in infants with incessant ventricular tachycardia. Early diagnosis and prompt surgical treatment usually can effect 'cure' of this potentially fatal problem in childhood.

Cryosurgery↗

PubMed1990

Promotion of ventricular tachycardia induction by procainamide in dogs with inducible ventricular fibrillation late after myocardial infarction.

UNLABELLED: The influence of procainamide on inducible ventricular tachyarrhythmias was evaluated in 35 dogs with experimental myocardial infarction, and 9 normal dogs. Programmed stimulation was performed from the right ventricular apex via a percutaneously positioned electrode catheter, using up to five extrastimuli before and after intravenous administration of procainamide (15 mg/kg). Procainamide levels in postinfarct dogs were 8.5 +/- 0.7 micrograms/mL (range 5.3-13.6 micrograms/mL). Procainamide exerted its greatest effect in postinfarct dogs with reproducible baseline ventricular fibrillation. Six of nine dogs (P less than 0.05) with ventricular fibrillation had sustained monomorphic ventricular tachycardia (cycle length: 147 +/- 4 msec) induced after procainamide administration. This ventricular tachycardia required significantly more extrastimuli than baseline ventricular fibrillation (3 +/- 0.3 extrastimuli before vs 4 +/- 0.3 extrastimuli after procainamide). Procainamide never converted ventricular fibrillation to ventricular tachycardia in normal dogs. Procainamide had minimal effect on inducible ventricular tachycardia after myocardial infarction. Ventricular tachycardia induction was abolished in only 2 of 17 dogs despite significant prolongation of electrophysiological parameters. Ventricular tachycardia cycle length, and the number of extrastimuli required were unchanged by procainamide in this subgroup. CONCLUSION: Ventricular tachycardia is insensitive to the antiarrhythmic properties of procainamide in this model. In contrast, procainamide is able to convert postinfarction ventricular fibrillation to ventricular tachycardia, presumably by promoting sustained, organized reentry. This previously undescribed action is an unusual form of proarrhythmic effect, and suggests that this drug should be used cautiously in patients after myocardial infarction.

Animals↗

PubMed1990

Electrophysiological study in supraventricular tachycardia.

Supraventricular tachycardia is a common clinical problem. Although its primary mortality is usually low, it often causes significant life long symptoms. It can be life threatening when associated with rapidly conducting accessory atrioventricular connections or nodo-ventricular fibres. Electrophysiological study is now the "gold standard" investigation for diagnosis of this problem. It is also an essential tool for choosing therapeutic options. It is safe and cost effective and should be available in all major hospitals. Since surgical cure is currently feasible for almost all forms of supraventricular tachycardia with a high success rate and a low mortality, electrophysiological study and arrhythmia surgery should be offered to symptomatic patients early in the course of disease. Catheter ablation of supraventricular tachycardia is presently investigational but may in the future become the standard treatment for some forms of supraventricular tachycardia if the cure rate and risk of the procedure can be improved so that they are superior to surgery.

Cardiac Pacing, Artificial↗

PubMed1989

Surgical therapy for atrial tachycardia in adults.

Eighteen adult patients with atrial tachycardia refractory to treatment with a mean of four drugs underwent attempted surgical cure. Atrial tachycardia originated in the right atrium in 17 patients and the left atrium in 1 patient. Tachycardia could be reproducibly induced and terminated by atrial extrastimuli or atrial pacing in 8 patients (44%). Resection of the arrhythmogenic area was performed in 16 patients (89%), and an isolation procedure was performed in 1 patient. In seven cases (39%), the area of isolation or excision included the sinoatrial node. One patient underwent His bundle section because the arrhythmogenic region was too close to the atrioventricular (AV) conduction system to enable resection. The mean duration of clinical follow-up was 56 +/- 34 months. Clinical tachycardia recurred in five patients (28%), but in two patients it did not recur until greater than 1 year after surgery. A permanent pacemaker was implanted in 3 (18%) of the 17 patients whose His-Purkinje system was left intact. One other patient had required permanent pacing before surgery. Only one of the seven patients undergoing sinoatrial node resection or isolation required permanent pacing for symptomatic bradycardia. Apart from the requirement for permanent pacing, no significant complications occurred. Surgical therapy for atrial tachycardia is a safe procedure, but the rate of cure appears to be less than that of supraventricular tachycardias associated with accessory AV connections. Excision or isolation of the sinoatrial node does not necessitate permanent pacing in most patients.

Adolescent↗

PubMed1989

Influence of infarct age on reproducibility of ventricular tachycardia induction in a canine model.

The inducibility and reproducibility of ventricular tachycardia were evaluated in 97 dogs after myocardial infarction produced by single stage coronary artery ligation. Arrhythmia induction was performed with use of an endocardial electrode catheter positioned at the right ventricular apex before each study. An aggressive protocol of programmed stimulation was used, employing up to seven extrastimuli and three attempts at arrhythmia induction in each study. Electrophysiologic study was performed in individual dogs at the following times after infarction: 1) 7.7 +/- 0.3 and 15 +/- 0.2 days (34 consecutive dogs); 2) 14 +/- 0.6 and 26 +/- 1.7 days (24 selected dogs); 19 +/- 2 and 43 +/- 3 days (12 selected dogs); 4) 36 +/- 2 and 60 +/- 6 days (8 selected dogs); and 5) 59 +/- 12 and 130 +/- 10 days (3 selected dogs). Inducibility of ventricular tachycardia decreased significantly from 74% 1 week after infarction to 41% 2 weeks after infarction. Thus, early reproducibility was low (48%). Reproducibility increased thereafter, with 88% of the dogs having reproducible ventricular tachycardia between 2 and 4 weeks (p less than 0.025) and 100% having reproducibly inducible ventricular tachycardia between 4 weeks and 4 months after infarction. Dogs with no inducible arrhythmia early after infarction did not develop inducible ventricular tachycardia or fibrillation at later studies. Twelve dogs developed spontaneous ventricular tachycardia or sudden arrhythmic death late after infarction. Overall, 22% of dogs with inducible ventricular tachycardia with a cycle length greater than 140 ms developed spontaneous ventricular tachycardia or sudden death. Arrhythmia induction decreases significantly during the 1st 2 weeks after myocardial infarction, but long-term reproducibility of ventricular tachycardia induced greater than or equal to 2 weeks after infarction is very high. This canine model of long-term, reliably inducible ventricular tachycardia is suitable for investigation of antiarrhythmic drugs, surgery and other interventions.

Animals↗

PubMed1989

Comparison of immediate versus day to day variability of ventricular tachycardia induction by programmed stimulation.

The use of programmed stimulation to assess long-term oral antiarrhythmic drug efficacy for ventricular tachycardia is complicated by the fact that mode of ventricular tachycardia induction varies from day to day in the absence of drug therapy. The purpose of this prospective study was to assess whether mode of ventricular tachycardia induction is more reproducible within one study than from day to day. Thirty-nine consecutive patients with documented sustained ventricular tachyarrhythmias secondary to coronary artery disease underwent three inductions of ventricular tachycardia at 15 min intervals in the absence of drug therapy. A stimulation protocol in which the only major variable was the number of extrastimuli required for tachycardia induction was used. Subsequent day to day variability in mode of tachycardia induction was also assessed in the same patients at two further drug-free inductions at intervals of 5 +/- 2 days. The number of extrastimuli required for tachycardia induction was significantly more reproducible at the immediate repeat studies than from day to day (69% of patients versus 31%, p less than 0.01). From these data, probability tables were derived that show the likelihood that changes in inducibility at subsequent tachycardia inductions are due to chance. The QRS configuration of induced ventricular tachycardia was also more reproducible at the immediate studies (64% versus 26%, p less than 0.01). Basic electrophysiologic and stimulation variables differed over a significantly wider range from day to day than at the immediate studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Efficacy of exercise for end-stage renal disease patients immediately following high-efficiency hemodialysis: a pilot study.

Nine patients receiving maintenance high-efficiency hemodialysis were studied before and after a 12-week conditioning program to determine the efficacy of exercise immediately following hemodialysis. Each patient performed a combination of bicycle ergometry on the Schwinn Air-Dyne ergometer (SAE) and treadmill walking three times a week for a total exercise time of 15-35 min per session. A low-level Bruce treadmill test and an exercise test on the SAE were administered before and after training. Hematological, serum electrolyte, and serum lipid profiles were also determined before and after training. Following training, there were improvements in exercise capacities for both treadmill walking and ergometry on the SAE. Although a significant increase in serum apolipoprotein A1 was seen following exercise, no significant changes were observed for total cholesterol, low-density-lipoprotein cholesterol, high-density-lipoprotein cholesterol or apolipoprotein B. Additionally, no significant changes were seen in hematological parameters and serum electrolyte profiles following the exercise program. The 9 patients demonstrated an average compliance record of 74%. This study demonstrated that patients on high-efficiency hemodialysis can safely engage in an exercise program immediately following dialysis at intensities and frequencies that can improve their physical work capacities.

Aged↗

PubMed1989

Electrophysiological and anatomic differences between canine hearts with inducible ventricular tachycardia and fibrillation associated with chronic myocardial infarction.

This study examined electrophysiological and anatomic differences between dogs with ventricular tachycardia (VT) and fibrillation (VF) inducible by programmed ventricular stimulation 7-21 days after left anterior descending coronary artery ligation. Of 106 dogs studied, 40 had inducible VT, 19 had inducible VF, and 47 had no inducible arrhythmias. Differences between these three groups of animals were examined with cardiac mapping (to determine ventricular activation time in sinus rhythm) and post-mortem pathology (to measure infarct size and to reconstruct the anatomy at the infarct edge). Animals with inducible VT had longer maximal epicardial activation time (127 +/- 8 msec) than did animals with inducible VF (91 +/- 8 msec, p less than 0.05) or animals with no inducible arrhythmias (75 +/- 2 msec, p less than 0.001). Delayed epicardial activation occurred in 90% of animals with VT, 42% of animals with VF, and in only 6% of animals with no inducible arrhythmias. Endocardial and myocardial activation times were similar for the VT and VF groups. Infarct size was 18 +/- 2% of the ventricles for the VT group, much higher than for the VF group (11 +/- 2%, p less than 0.001) or for the group with no inducible arrhythmias (9 +/- 1%, p less than 0.001). The maximum diameter of viable muscle bundles interdigitating with scar tissue at the infarct edge was much larger in animals with VT (2.4 +/- 0.2 mm) than in animals with VF (1.8 +/- 0.2 mm, p less than 0.05) or animals with no inducible arrhythmias (1.7 +/- 0.1 mm, p less than 0.01). Thus, when compared with animals with inducible VF, animals with inducible VT had longer epicardial activation time, larger infarct size and viable muscle bundles of larger diameter at the infarct edge.

Animals↗

PubMed1989

Comparison of early and late dimensions and arrhythmogenicity of cryolesions in the normothermic canine heart.

Little is known about myocardial cryoablation at normothermia and the effect of cryoprobe head size and duration of freeze on final lesion volume. In the present study, cryolesions were created with a carbon dioxide cryoprobe with two head sizes (cylindrical head 6 mm diameter and large circular head 18 mm diameter) in the normothermic canine heart during cardiopulmonary bypass. The duration of freeze (exposure time) varied from 2 to 3 or 4 minutes and the effects on immediate and chronic lesion size were evaluated. Lesions produced by epicardial exposures were compared with intramyocardial lesions created by placing the cylindrical head in a 6 mm stab incision. A minimum of four lesions were created in each dog. Lesion size was evaluated at 0 minutes (iceball) and 24 hours (two dogs), 7 days (one dog), or 4 weeks (five dogs). Iceball diameter was approximately 5 mm larger than chronic lesion diameter regardless of head size or exposure time. Prolongation of exposure time from 2 to 3 minutes resulted in significant increases in the volume of epicardial lesions (cylindrical head: 280 +/- 100 mm3 versus 740 +/- 200 mm3, p = 0.001; circular head: 1200 +/- 100 mm3 versus 2300 +/- 500 mm3, p = 0.007) because of increases in diameter and depth. No further increase in lesion size was observed when exposure time was prolonged from 3 to 4 minutes. A 3-minute intramyocardial exposure with the cylindrical head placed in a stab incision enabled production of transmural lesions (16 +/- 2 mm deep). Two and 4 weeks postoperatively, dogs underwent electrophysiologic study from the right and left ventricular apices. No animals had inducible ventricular tachycardia despite the heterogeneous configuration of the multiple cryolesions. In conclusion, it is possible to produce rapid and predictable ablation of clinically useful volumes of myocardium during normothermic bypass with the use of currently available equipment. Under these conditions, an exposure time of 3 minutes is optimal for a liquid carbon dioxide cryoprobe. Cryolesions should be overlapped by at least 2.5 mm to produce continuous areas of ablation. Multiple cryolesions do not form a chronic substrate for ventricular tachycardia.

Animals↗

PubMed1988

Cerebrospinal fluid indoleacetic acid in autistic subjects.

Cerebrospinal fluid (CSF) levels of the tryptamine metabolite, indoleacetic acid (IAA), have been measured in groups of autistic and control subjects. No significant difference was seen in group mean (+/- SEM) levels of CSF IAA (autistics 5.53 +/- 0.47 ng/ml, N = 10). The finding indicates that central metabolism of the behaviorally active trace amine tryptamine is probably normal in autism.

Adolescent↗

PubMed1988

Differences between patients with ventricular tachycardia and ventricular fibrillation as assessed by signal-averaged electrocardiogram, radionuclide ventriculography and cardiac mapping.

This study examined 65 patients with ventricular tachycardia or fibrillation late after myocardial infarction to determine whether they differed with respect to duration of ventricular activation in sinus rhythm and left ventricular ejection fraction. Patients with spontaneous ventricular tachycardia had a longer ventricular activation time in sinus rhythm than did patients with spontaneous ventricular fibrillation. This difference was detected with the signal-averaged electrocardiogram (ECG) (tachycardia 181 +/- 33 ms, fibrillation 152 +/- 23 ms, p less than 0.001) and at epicardial mapping (tachycardia 210 +/- 17 ms, fibrillation 192 +/- 17 ms, p less than 0.02). Left ventricular ejection fraction was lower in patients with spontaneous ventricular tachycardia (0.22 +/- 0.09) than in patients with spontaneous ventricular fibrillation (0.27 +/- 0.09) (p less than 0.05). The patients with both spontaneous and inducible ventricular fibrillation had a shorter ventricular activation time on the signal-averaged ECG (129 +/- 17 ms) and a higher ejection fraction (0.36 +/- 0.05) than did either patients with spontaneous ventricular fibrillation and inducible ventricular tachycardia (158 +/- 21 ms and 0.25 +/- 0.08, respectively, each p less than 0.01) or patients with both spontaneous and inducible ventricular tachycardia (181 +/- 33 ms and 0.22 +/- 0.09, respectively, each p less than 0.001). Of the patients with inducible ventricular tachycardia, presentation with tachycardia rather than fibrillation was associated with a longer ventricular activation time on the signal-averaged ECG (181 +/- 33 versus 158 +/- 21 ms, p less than 0.02) and a longer cycle length of inducible ventricular tachycardia (290 +/- 61 versus 259 +/- 44 ms, p = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗