Biomedical subjects

D G Benditt

Publications and source records attributed to D G Benditt.

At least 127 records · Page 7Linked to original sources

PubMed1985

Kinetics of electrophysiologic changes during oral loading of amiodarone and after withdrawal of amiodarone in the unsedated dog.

We examined the temporal kinetics of onset and offset of the cardiac electrophysiologic effects of orally administered amiodarone in chronically instrumented, unsedated adult dogs (n = 8). Right atrial (RA), atrioventricular nodal (AVN), and right ventricular (RV) effective refractory period (ERP), and AVN functional refractory period (FRP), were determined daily for 21 days during amiodarone loading (24 mg/kg/day) and for 21 days after cessation of amiodarone. Left ventricular (LV) ERP was assessed in four of eight animals. Group mean RA-ERP peaked and plateaued early during amiodarone loading (time to reach one-half observed peak change [t1/2 onset] = 1.2 +/- 0.5 days) and rapidly returned toward baseline after cessation of drug (decay time to one-half peak value [t1/2 offset] = 2.0 +/- 1.7 days). Group mean RV-ERP rose in a linear manner throughout the loading period (t1/2 onset = 9.3 +/- 2.1 days) and remained elevated after cessation of drug (t1/2 offset greater than 21.0 days). Group mean AVN-ERP and FRP exhibited temporal kinetics intermediate between those of the RA-ERP and RV-ERP, both during amiodarone loading and after cessation of the drug. Group mean LV-ERP onset kinetics (assessed in a limited number of animals, n = 4) appeared to differ from RV-ERP onset kinetics (t1/2 onset = 2.5 +/- 2.5 days), whereas LV-ERP and RV-ERP offset kinetics appeared similar (t1/2 offset greater than 21 days). In summary, our findings demonstrate that during oral loading, the temporal sequence of onset of amiodarone-induced electrophysiologic effects is site dependent. Similarly, after cessation of amiodarone, the persistence of drug-induced electrophysiologic effects is both variable and site dependent.

Administration, Oral↗

PubMed1985

Prediction of digoxin treatment failure in infants with supraventricular tachycardia: role of transesophageal pacing.

Transesophageal atrial pacing was used to initiate and terminate tachycardia in 24 infants (seven female and 17 male, aged 1 to 34 days) with ECG documentation of supraventricular tachycardia. Six infants received no chronic treatment, and chronic oral digoxin prophylaxis was administered to 18 infants in an effort to prevent recurrences of tachycardia. In these 18 infants, the effectiveness of digoxin therapy in preventing the initiation of tachycardia by transesophageal pacing was compared with its ability to prevent spontaneous recurrences of supraventricular tachycardia. While receiving chronic oral digoxin therapy, tachycardia could be reinitiated in 15/18 (83%) infants. In these infants, the cycle length of tachycardia and the atrioventricular interval were the same before and during chronic digoxin treatment. Three infants in whom tachycardia could not be initiated during chronic digoxin therapy had no spontaneous recurrences during 6 months of follow-up, whereas 10/15 (67%) infants in whom tachycardia could be reinitiated had clinically significant recurrences in spite of chronic digoxin therapy. Six infants who received no chronic drug treatment had no documented recurrences during 6 months of follow-up. This study demonstrates that digoxin was effective in preventing significant spontaneous recurrences of supraventricular tachycardia in only 8/18 (44%) infants treated with digoxin. The ability to initiate supraventricular tachycardia with transesophageal pacing may be useful in determining which digoxin-treated infants are at risk for recurrence. Finally, not all infants with supraventricular tachycardia require chronic prophylaxis; six of the untreated infants had no documented recurrences.

Atrioventricular Node↗

PubMed1985

Atrial flutter in infancy: diagnosis, clinical features, and treatment.

The clinical features and treatment of atrial flutter in eight infants (four male and four female) less than 2 months of age are presented. Atrial flutter was noted during the first week of life in six of the infants and between 6 and 8 weeks of life in the other two infants. Four of the eight infants had associated structural or functional cardiovascular disease, and in three infants a central venous pressure catheter was present in the atrium at the time atrial flutter was diagnosed. Classic flutter waves were apparent on 12-lead ECGs in only two infants. In six infants, flutter waves were not obvious on standard ECGs, but transesophageal electrogram recordings demonstrated the presence of atrial flutter with second degree atrioventricular block. The atrial cycle length during flutter ranged from 135 to 180 ms (mean 149 ms; mean atrial rate 403 beats per minute); there was a 2:1 ventricular response to atrial flutter. Successful termination of atrial flutter was accomplished using three modes of electrical cardioversion in seven of the eight infants: direct current cardioversion in one, transvenous atrial pacing in one, and transesophageal atrial pacing in five. One asymptomatic infant converted to normal sinus rhythm 24 hours following digoxin administration. One infant had multiple atrial flutter recurrences and required chronic procainamide therapy. In seven of the eight infants, no recurrences have been noted in 6 months to 3 1/2 years of follow-up. These results demonstrate that atrial flutter may be difficult to diagnose in infants with tachycardia unless transesophageal electrogram recording is utilized for evaluation.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Flutter↗

PubMed1984

Antiarrhythmic and electrophysiologic actions of bethanidine sulfate in primary ventricular fibrillation or life-threatening ventricular tachycardia.

Antiarrhythmic and electrophysiologic actions of bethanidine sulfate, a chemical analog of bretylium tosylate, were studied using programmed cardiac electrical stimulation in 14 survivors of out-of-hospital cardiac arrest unassociated with acute myocardial infarction. Before bethanidine sulfate was administered sustained ventricular tachyarrhythmias (VT) were inducible in 11 patients and reproducible nonsustained VT was induced in 3 patients. Bethanidine sulfate shortened sinus cycle length and absolute and relative ventricular refractory periods measured during sinus rhythm, but did not alter ventricular effective refractory period measured during ventricular pacing. Bethanidine sulfate prevented inducible VT in 8 patients (57%), increased the number of extrastimuli needed to induce VT in 2 patients, and was ineffective in 4 patients. In contrast, in only 1 of 26 trials with other conventional and investigational antiarrhythmic drugs in these patients was VT prevented. Orthostatic hypotension was a prominent side effect of bethanidine sulfate therapy, but could be reversed in most patients by concomitant administration of protriptyline. Five patients in whom bethanidine sulfate was effective in the laboratory have been treated chronically (400 to 600 mg 4 times daily), and all are alive at 3 to 40 months. In the remaining 9 patients, 8 were treated empirically because no drug was effective in the laboratory and 1 was treated with quinidine, which appeared to be protective during testing. Four of these 9 patients, including the patient treated with quinidine, died suddenly during follow-up. Thus, although bethanidine sulfate therapy is difficult to initiate because of orthostatic hypotensive side effects, it may be useful in treating patients at high risk of recurrent cardiac arrest.

Adult↗

PubMed1984

Cardiac and skeletal myopathy associated with cardiac dysrhythmias.

Electrophysiologic studies, echocardiograms, cardiac catheterizations and histologic and biochemical analyses of skeletal muscle biopsies were performed in 10 patients (aged 10 to 37 years, mean 21) who had dysrhythmias as the initial manifestation of cardiomyopathy. Presenting symptoms and signs attributable to dysrhythmias included sudden cardiac arrest in 2 patients, syncope in 3, presyncope in 3 and palpitations in 2. There was no clinical evidence of skeletal muscle weakness in any patient. Multicatheter electrophysiologic evaluation established diagnoses of ventricular tachycardia in 6 patients, primary atrial tachycardia in 2 and third degree infra-Hisian heart block in 1 patient. One patient presenting with palpitations had no inducible arrhythmia or conduction disturbance. Echocardiographic, angiographic and hemodynamic studies demonstrated previously unsuspected dilated cardiomyopathy in 7 patients and restrictive cardiomyopathy in 3. Skeletal muscle histologic characteristics were abnormal in all 10 patients; increases in lipid droplets and endomysial fibrosis were the characteristic findings. Serum free carnitine and short- and long-chain acylcarnitine were normal in 9 patients. However, skeletal muscle long-chain acylcarnitine was reduced in 9 patients. These findings support the concept that in certain patients presenting with dysrhythmias, the dysrhythmia may be a manifestation of cardiac and skeletal (that is, generalized) myopathy.

Adolescent↗

PubMed1984

Transesophageal atrial pacing threshold: role of interelectrode spacing, pulse width and catheter insertion depth.

This study evaluated the role of interelectrode spacing, pulse widths greater than 10 ms, and depth of esophageal insertion on minimizing transesophageal atrial pacing threshold in 30 patients aged 1 day to 77 years. Interelectrode spacings of 15, 22 and 28 mm were evaluated by establishing strength-duration curves in 2 or more serial studies in 12 patients; electrode spacing had no effect on pacing threshold. In 23 patients studied with 22-mm electrode spacing, pulse widths of 15 and 20 ms had no significant effect on current threshold requirements compared with 10-ms pulse widths. In 20 patients, pacing threshold and esophageal electrograms were obtained at 1.0- to 2.5-cm intervals with a 22-mm lead using a pulse width of 10 ms. Average minimal pacing threshold was 10.2 mA (range 4.5 to 20). The site of minimal pacing threshold was highly correlated with patient height (r = 0.987), and occurred within 1.1 cm (0 to 2.5 cm) of the site of the maximal bipolar atrial electrogram amplitude and 0.95 cm (0 to 3 cm) of the site of the maximal unipolar atrial electrogram. Bipolar electrode spacing of 15, 22 or 28 mm has little effect on transesophageal pacing threshold. In most patients, pulse widths greater than 10 ms do not significantly decrease pacing threshold. Correct catheter insertion depth is critical to minimize pacing threshold and may be predicted by either the site of the maximal atrial electrogram amplitude or patient height.

Adolescent↗

PubMed1984

Atrial flutter, atrial fibrillation, and other primary atrial tachycardias.

Traditional classifications of atrial tachycardias include not only rhythm disturbances arising primarily within the atria, but also dysrhythmias in which it is now recognized that participation of both atrial and non-atrial tissue is required. We prefer to consider those arrhythmias in which the atria are the principal site of electrophysiologic disturbance as "primary" atrial tachyarrhythmias. The mechanisms, diagnosis, and treatment of these "primary" atrial tachycardias are the subject of this article.

Anti-Arrhythmia Agents↗

PubMed1984

Bromocriptine treatment of digitalis-induced ventricular tachyarrhythmias: studies in a canine model.

Ventricular tachyarrhythmias associated with digitalis toxicity are believed to be due, in part, to cardiac glycoside-mediated increased central sympathetic neural activity. Because dopaminergic receptor agonists reduce sympathetic outflow, this study assessed effectiveness of the available dopaminergic agonist, bromocriptine, in slowing or terminating ouabain-induced ventricular tachycardia in anesthetized dogs. In all experiments, ouabain was administered intravenously (20 micrograms/kg body weight bolus injection, followed by 2.5 micrograms/kg per min infusion) until the onset of stable ventricular tachycardia. Of seven untreated dogs (Group 1), ouabain-induced ventricular tachyarrhythmias resulted in ventricular fibrillation in three, while in four dogs tachycardia persisted without significant change in rate until the study was terminated. Fourteen dogs (Group 2) received bromocriptine, either 30 micrograms/kg (Group 2A) or 50 micrograms/kg (Group 2B), after the onset of ventricular tachycardia. Tachycardia slowed in all 14 dogs and terminated with resumption of sinus rhythm in 8 of the 14. In all six dogs pretreated with the peripheral dopaminergic antagonist domperidone (Group 3), bromocriptine, 50 micrograms/kg, slowed ventricular tachycardia and in three of the six, tachycardia terminated. In contrast, of five dogs pretreated with haloperidol, a central and peripheral dopaminergic receptor antagonist (Group 4), bromocriptine, 50 micrograms/kg, failed to slow ventricular tachycardia in three, and two of the three developed ventricular fibrillation. In summary, the dopaminergic receptor agonist, bromocriptine, presumably acting at central dopaminergic receptor sites, consistently slowed and in most cases reversed ouabain-induced ventricular tachycardia in a canine model.

Animals↗

PubMed1984

Inducible ventricular arrhythmias in a naturally occurring model of cardiomyopathy.

This study examined inducibility of ventricular tachyarrhythmias in turkeys with and without naturally occurring dilated cardiomyopathy. Using a transvenously positioned electrode catheter, 32 cardiomyopathy and 12 control unsedated turkeys aged 2 to 4 months were studied by right ventricular endocardial extrastimulus testing at basic pacing cycle lengths of 200 and 170 ms with both 1 and 2 extrastimuli and burst pacing at progressively shorter cycle lengths (200 to 100 ms). Following study, a dilatation index (determined as the ratio of left ventricular endocardial and epicardial diameter at level of the apex-base midpoint) was utilized to assess the functional severity of cardiomyopathy. All control turkeys had a dilatation index less than 0.3. In cardiomyopathic turkeys, dilatation index was normal (less than 0.3) in 3/32, showed mild to moderate dilatation in 25/32 (0.3 to 0.6), and severe dilatation in 4/32 (greater than 0.6). Results showed no difference in right ventricular effective or functional refractory periods between control and cardiomyopathic turkeys. Control turkeys had no inducible ventricular tachyarrhythmias, but 16/32 cardiomyopathic turkeys (p less than 0.005) had inducible ventricular tachyarrhythmias, consisting most frequently of two beats of rapid ventricular tachycardia supervened by ventricular fibrillation. In the cardiomyopathic turkeys, inducible tachyarrhythmias occurred in 1/3 with normal dilatation index, in 11/25 with mild to moderate dilatation, and in 4/4 with severe dilatation. Thus, inducibility of ventricular tachyarrhythmias in cardiomyopathic turkeys is closely associated with increasing ventricular dilatation, but does not correlate with altered right ventricular refractoriness. This model may be suitable for studying the relationship between ventricular tachyarrhythmias and cardiomyopathy.

Animals↗

PubMed1984

Comparative functional effects of chronic ventricular demand and atrial synchronous ventricular inhibited pacing.

We compared the effects of chronic ventricular inhibited (VVI) and atrial synchronous ventricular inhibited (VDD) pacing on functional capacity in 8 patients with complete atrioventricular heart block. Permanent VDD (Medtronic #2409, ASVIP) pacemakers were implanted in four men and four women (age range 27-76 years, mean 58.9 +/- 18.4 years), and randomly assigned to a three-month period of VDD or VVI pacing in this single blinded, crossover study. Functional capacity was assessed by questionnaire, graded treadmill exercise testing and radionuclide angiocardiography prior to pacemaker implant and following each pacing period. Following 3 months of pacing in each of VVI and VDD pacing modes, maximum heart rate (83.4 +/- 14 vs 134.9 +/- 16.4 beats/min, p less than 0.001) and double product (147.5 +/- 58.3 vs 218.9 +/- 52.7, p less than .001) were greater with VDD pacing. Although exercise duration on treadmill exercise testing (5.3 +/- 2.9 vs 6.9 +/- 3.1 minutes, p less than 0.1) was greater in the VDD mode, the difference was not significant. Similarly, there was no significant difference in functional capacity as measured by questionnaire scores (50.1 +/- 8.4 vs 46.9 +/- 8.9, p less than 0.1) or in left ventricular ejection fraction for the two pacing modes (.54 vs .55, p less than .5). Only one patient reported a subjective improvement with physiologic (VDD) pacing, whereas the remaining patients stated no preference. We conclude that VDD pacing offers improved maximal cardiac work during exercise compared to VVI pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1984

Life threatening ventricular tachycardias in late survivors of surgically corrected tetralogy of Fallot.

Electrophysiological tests were performed in three patients with surgically corrected tetralogy of Fallot (mean age at evaluation 25 years, mean age at surgical correction 4 years) who had had either a cardiac arrest or transient neurological disturbances (presyncope, syncope) associated with ventricular arrhythmias. All three patients had an excellent haemodynamic result from surgery as judged by echocardiography and cardiac catheterisation. Ambulatory electrocardiographic monitoring and stress exercise testing were normal in two patients and showed complex ventricular ectopy in one. During invasive electrophysiological evaluation all three patients had inducible ventricular tachycardia (monomorphic QRS in two patients, cycle lengths 230 and 240 ms; polymorphic QRS in one patient, mean cycle length 200 ms) with adverse haemodynamic effects in all three patients. These findings suggest that rapid ventricular tachycardia with detrimental haemodynamic consequences, similar to that induced during laboratory study, was the basis for the presenting symptoms in each patient. This possibility was confirmed in one patient who had identical QRS morphology during both spontaneous ventricular tachycardia and that induced during the laboratory study. Thus sudden death or symptoms of syncope postoperatively in patients with surgically corrected tetralogy of Fallot appear to be due to rapid ventricular tachycardia, which may occur despite an apparently excellent surgical result.

Adult↗

PubMed1984

Enhanced atrioventricular nodal conduction in man: electrophysiologic effects of pharmacologic autonomic blockade.

Enhanced atrioventricular nodal conduction (EAVC) comprises a portion of the spectrum of atrioventricular node electrophysiology in which physiologic slowing of atrioventricular conduction is diminished. To evaluate the basis of EAVC in humans, we compared the effect of pharmacologic autonomic blockade on electrophysiologic characteristics of atrioventricular nodal conduction and refractoriness in 10 patients with EAVC and 12 patients without EAVC (non-EAVC). The effects of autonomic blockade (0.2 mg/kg iv propranolol and 0.04 mg/kg iv atropine) on sinus cycle length and atrial refractory period were similar in both EAVC and non-EAVC patients. After autonomic blockade, minimum atrial paced cycle length with 1:1 atrioventricular conduction lengthened in EAVC patients (control, 268 +/- 25 msec; blockade, 307 +/- 34 msec; p less than .01), but remained unchanged in non-EAVC patients (control, 392 +/- 69 msec; blockade, 382 +/- 49 msec; p = NS). Similarly, atrioventricular nodal functional refractory periods tended to lengthen in EAVC patients, while remaining unchanged or shortening in non-EAVC patients. Furthermore, although autonomic blockade reduced differences between EAVC and non-EAVC patients, both minimum cycle length with 1:1 atrioventricular conduction and atrioventricular functional refractory period remained shorter in EAVC than in non-EAVC patients (p less than .02). Thus, baseline differences in autonomic atrioventricular nodal control differ in EAVC and non-EAVC patients, but do not fully account for differences in atrioventricular nodal electrophysiologic properties in these patients. Consequently, underlying structural functional factors may play an important role in determining the range of atrioventricular nodal electrophysiologic characteristics in man.

Adolescent↗

PubMed1983

Electrophysiologic effects of theophylline in young patients with recurrent symptomatic bradyarrhythmias.

In this study, both acute electrophysiologic actions of intravenously administered theophylline and clinical effects of chronic oral theophylline therapy were assessed in 10 young patients (aged 9 to 41 years) without clinically significant cardiac disease, in whom recurrent symptoms of syncope and dizziness were attributed to transient bradyarrhythmias (sinus pauses, marked sinus bradycardia or paroxysmal atrioventricular [AV] block). Intravenous theophylline infusion (serum concentration range 9.5 to 12.0 mg/liter) shortened means sinus cycle length (control 973 +/- 285 ms versus theophylline 880 +/- 226 ms, p less than 0.005) and decreased both the estimated sinoatrial conduction time (control 169 +/- 56.0 ms versus theophylline 143 +/- 55.3 ms, p less than 0.05) and the maximum corrected sinus node recovery time (control 442 +/- 251.0 ms versus theophylline 255 +/- 146.2 ms, p less than 0.05). In addition, theophylline infusion shortened the minimum atrial paced cycle length with sustained 1:1 AV conduction (control 414 +/- 86 ms versus theophylline 379 +/- 97 ms, p less than 0.05) and consistently reduced AV node functional refractory periods. Subsequent chronic oral theophylline therapy (serum levels 9 to 12 mg/liter) was tolerated in 8 patients (80%). During a follow-up of 5 to 24 months, suppression of symptoms was achieved in 6 of the 8 patients. Thus, theophylline exhibits positive chronotropic and dromotropic effects in man at serum concentrations in the usual therapeutic range (10 to 15 mg/liter). Furthermore, suppression of symptoms during follow-up suggests that theophylline treatment may be a useful therapeutic consideration in some patients with recurrent symptomatic bradyarrhythmias.

Adolescent↗

PubMed1983

Transesophageal study of infant supraventricular tachycardia: electrophysiologic characteristics.

Programmed electrical stimulation of the heart to initiate and terminate tachycardia and analysis of the temporal relation between ventricular and atrial activation during tachycardia have been useful in the evaluation of supraventricular tachycardia (SVT). Such techniques have rarely been applied to evaluate infants with SVT. We used a silicone rubber-coated bipolar electrode catheter (15 or 22 mm interelectrode spacing), positioned in the esophagus, for electrical stimulation of the heart and recording of electrograms for the evaluation of 14 infants aged 1 to 84 days with SVT. Three infants had electrocardiographic features of Wolff-Parkinson-White syndrome, and no infant had other manifestations of congenital heart disease. Tachycardia cycle lengths ranged from 180 to 295 ms and ventriculoatrial intervals recorded from the esophagus were 80 to 220 ms. In 12 infants, transesophageal atrial stimulation was used to terminate and initiate SVT using stimuli of 9.9 ms and 10 to 20 mA. Initiation and termination of SVT by electrical stimulation suggest that SVT in infants is due to reentry, and the presence of ventriculoatrial intervals greater than 70 ms further suggests that accessory atrioventricular connections (usually concealed) constitute a portion of the reentry circuit.

Atrioventricular Node↗

PubMed1983

Cardiac arrest in young, ostensibly healthy patients: clinical, hemodynamic, and electrophysiologic findings.

This study examines the clinical, hemodynamic, and electrophysiologic findings in a unique group of 11 young (aged 15 months to 29 years) survivors of a cardiac arrest. All patients were previously in good health, and cardiac arrest was the initial manifestation of cardiac disease in all. Overt clinical and hemodynamic abnormalities were not as common as previously reported, and in some instances apparent cardiac abnormalities failed to provide a link to cardiac arrest. No patient had congenital heart disease or hypertrophic cardiomyopathy. However, during multicatheter electrophysiologic study, sustained tachyarrhythmia was reproducibly initiated in 8 of 11 patients (73%). Young, ostensibly healthy patients who survive cardiac arrest form a diverse group. Diligent programmed intracardiac electrical stimulation may demonstrate life-threatening tachycardias in these patients. Treatment to prevent recurrence of cardiac arrest is difficult in this group of patients. However, the ability to initiate tachycardia in the electrophysiologic laboratory may be useful in the management of these patients.

Adolescent↗

PubMed1983

Atrial pacing from the esophagus in the diagnosis and management of tachycardia and palpitations.

Recent reports have emphasized the usefulness of programmed electrical stimulation of the heart for predicting the effectiveness of pharmacologic therapy of recurrent tachycardias and for determining the basis of recurrent palpitations. We used programmed electrical stimulation of the atrium from the esophagus to study 12 children (ages 1 to 13 years) with either electrocardiographically documented tachycardia (seven patients) or recurrent palpitations (five patients). Atrial stimulation from the esophagus initiated and terminated tachycardia in all seven patients who had a previously documented tachycardia. In five of these patients tachycardia could not be initiated after therapy with quinidine sulfate, and no recurrences have been noted in 12 to 18 months of follow-up. In two patients tachycardia could be reinitiated despite therapeutic quinidine levels, and tachycardia has recurred despite quinidine therapy. Atrial stimulation from the esophagus initiated tachycardia in four of five patients with a history of palpitations. Electrocardiographic documentation of tachycardia was beneficial, because it provided a basis for determining whether therapy for tachycardia was indicated, and in some instances provided an opportunity for patient education to permit-self termination without medication.

Adolescent↗

PubMed1983

Prevention of recurrent sudden cardiac arrest: role of provocative electropharmacologic testing.

This study evaluates the usefulness of serial provocative electropharmacologic testing for predicting the efficacy of prophylactic antiarrhythmic treatment regimens in patients resuscitated from sudden cardiac arrest in the absence of acute myocardial infarction. Testing was carried out in 34 consecutive patients (28 men and 6 women) who required cardiopulmonary resuscitation and direct current countershock for treatment of primary ventricular fibrillation (28 patients), ventricular tachycardia (5 patients) or excessively rapid heart rate during atrial fibrillation with preexcitation (1 patient). In 8 (24%) of the 34 patients, drug testing either was not feasible because of absence of inducible arrhythmia or was incomplete because of patient withdrawal from study; and 3 of these 8 patients had recurrent sudden cardiac arrest within 10 to 19 months. In an additional five patients, treatment regimens failed to prevent initiation of sustained ventricular tachyarrhythmias in the catheterization laboratory, and two of these five patients had cardiac arrest recurrences within 2 weeks to 25 months of follow-up. In the remaining 21 (62%) of the 34 patients, including 3 patients with preexcitation syndrome, a drug regimen or surgical treatment, or both, was found that prevented inducible life-threatening tachyarrhythmias in the laboratory. Subsequently, only 1 (5%) of these 21 patients died suddenly within a 7 to 38 month (mean +/- standard deviation, 18 +/- 8.3) follow-up period. Thus, provocative electropharmacologic testing appears to be useful in predicting response to therapy in survivors of sudden cardiac arrest.

Adolescent↗

PubMed1983

Dual accessory nodoventricular pathways: role in paroxysmal wide QRS reciprocating tachycardia.

Clinical electrophysiological study in an otherwise healthy 21-year-old male with paroxysmal wide QRS tachycardia (cycle length 300 ms, heart rate 200/min) suggested the presence of two nodoventricular (NV) bypass connections. The first NV connection pre-excited the base of the interventricular septum (NVs), as evidenced by a short HV interval during sinus rhythm (15-20 ms), with local ventricular activation occurring earlier at the septal base than at either the right ventricular apex or the base of the left ventricle. The second NV connection appeared to connect the AV junction with the right ventricle (NVRV). Intracardiac recordings from a portion of the right-bundle branch of the interventricular conduction system demonstrated right ventricular pre-excitation by NVRV during both atrial pacing and reciprocating tachycardia. The latter finding supported participation of NVRV in the tachycardia. Further, following exclusion of atrial participation in the arrhythmia, premature depolarization of the right ventricle and interventricular septum appeared to advance the tachycardia without altering the timing of His bundle depolarization, implicating NVS in the retrograde limb of a re-entry circuit. Consequently, this study demonstrated the presence of two NV connections and provided further support to the concept that NV accessory bypass connections may comprise portions of a re-entry pathway during reciprocating tachycardia in man.

Adult↗