Biomedical subjects

A D Sharma

Publications and source records attributed to A D Sharma.

At least 37 records · Page 2Linked to original sources

PubMed1991

Characteristics of accessory pathways exhibiting decremental conduction.

The prevalence, electrophysiologic characteristics and functional significance of decremental conduction over an accessory pathway were examined in this retrospective study of 653 patients who had an accessory pathway demonstrated at electrophysiologic study. Decremental conduction was identified in 50 patients (7.6%). In 15 patients with anterograde decremental conduction, the accessory pathway was right parietal or septal in 14 patients and left parietal in 1 patient. In the 40 patients with retrograde decrement, the accessory pathway was left parietal in 19, posteroseptal in 13, right parietal in 2 and right anteroseptal in 6 patients. Anterograde conduction over the accessory pathway was absent in 11 of the 40 patients with retrograde decrement. Retrograde conduction over the accessory pathway was absent in 9 patients with anterograde decrement. There was no significant difference in the accessory pathway effective refractory period, or shortest cycle length with 1:1 conduction over the accessory pathway in anterograde and retrograde directions. The shortest RR interval in atrial fibrillation between 2 preexcited QRS complexes was longer in patients with anterograde decremental conduction than in a control group of patients with anterograde-conducting accessory pathways without decremental properties. These data demonstrate that decremental conduction over accessory pathways is uncommon. Anterograde decremental conduction usually occurs in right-sided or septal pathways that often do not conduct in the retrograde direction.

Adolescent↗

PubMed1991

Effects of lidocaine and verapamil on defibrillation in humans.

Patients with automatic defibrillators frequently require chronic antiarrhythmic drug therapy or receive acute therapy with the onset of symptoms. The effects on energy requirements for defibrillation of lidocaine hydrochloride and verapamil hydrochloride, two commonly used antiarrhythmic agents, were examined in 20 successive patients undergoing corrective arrhythmia surgery. The minimum energy requirement for ventricular defibrillation before and 5 minutes after the administration of 150 mg of lidocaine intravenously (n = 8), or 10 minutes after 10 mg of verapamil intravenously (n = 12), were determined. Each patient was assigned to receive either verapamil or lidocaine. Three mesh coil defibrillating electrodes (Medtronic 6891, 6892) were sutured to the epicardium of the right and left ventricles. Ventricular fibrillation was induced using alternating current. After a minimum of 10 seconds of fibrillation, the minimum energy for defibrillation was established using sequential pulse defibrillation. The preselected drug was then infused and the ventricular defibrillation energy was again determined after 5 or 10 minutes circulation time. Lidocaine did not alter the minimum energy for defibrillation (3.0 +/- 1.4 J vs. 3.0 +/- 1.8 J, mean +/- SD), despite plasma levels of lidocaine that averaged 13.2 +/- 1.9 mumol/l. In contrast, verapamil significantly increased (3.9 +/- 2.2 J vs. 6.5 +/- 2.9 J) the minimum energy necessary for defibrillation. The difference in defibrillation energy was significantly correlated to the fall in systolic blood pressure induced by verapamil administration (r = 0.72). These data reinforce the necessity for determining efficacy of defibrillation when medication changes are instituted. Verapamil should be used with caution in patients with automatic defibrillators and marginal defibrillation threshold.

Adult↗

PubMed1991

Near miss sudden death in an infant with Wolff-Parkinson-White syndrome.

A 6 month old infant with known Wolff-Parkinson-White syndrome presented with an out of hospital cardiac arrest. An electrocardiogram in the emergency department demonstrated atrial fibrillation with rapid ventricular response. The child subsequently was resuscitated and underwent successful interruption of an accessory connection after failing medical therapy. This case underlines the need to reassess the indications for invasive electrophysiologic testing in young children.

Heart Arrest↗

PubMed1990

Adenosine for paroxysmal supraventricular tachycardia: dose ranging and comparison with verapamil. Assessment in placebo-controlled, multicenter trials. The Adenosine for PSVT Study Group.

OBJECTIVE: To assess the safety and efficacy of intravenous adenosine in terminating acute episodes of paroxysmal supraventricular tachycardia. DESIGN: Two prospective, double-blind, randomized, placebo-controlled trials to evaluate dose response in patients receiving adenosine and to compare the effects of adenosine with those of verapamil. PATIENTS: A total of 359 patients with a tachycardia electrocardiographically consistent with paroxysmal supraventricular tachycardia were entered into the two protocols. Patients subsequently found to have arrhythmias other than paroxysmal supraventricular tachycardia were excluded from the efficacy analysis. INTERVENTIONS: The first protocol compared sequential intravenous bolus doses of 3, 6, 9, and 12 mg of adenosine to equal volumes of saline. In the second protocol, patients received either 6 mg and, if necessary, 12 mg of adenosine or 5 mg and, if necessary, 7.5 mg of verapamil. MEASUREMENTS AND MAIN RESULTS: When data are expressed in terms of cumulative response in eligible patients, intravenous adenosine terminated acute episodes of paroxysmal supraventricular tachycardia in 35.2%, 62.3%, 80.2%, and 91.4% of patients who received maximum doses of 3, 6, 9, and 12 mg, respectively, in a four-dose sequence, whereas 8.9%, 10.7%, 14.3%, and 16.1% of patients responded to four sequential placebo doses (P less than 0.0001). In the second trial, cumulative response rates after 6 mg followed, if necessary, by 12 mg of adenosine were 57.4% and 93.4%, and after 5 mg followed, if necessary, by 7.5 mg of verapamil were 81.3% and 91.4%. The average time after injection to termination of tachycardia by adenosine was 30 seconds. Adenosine caused adverse effects in 36% of patients, but they lasted less than 1 minute and were usually mild. CONCLUSIONS: Adenosine in graded doses up to 12 mg rapidly and effectively terminates acute episodes of paroxysmal supraventricular tachycardia in which the atrioventricular node is an integral part of the re-entrant circuit. The overall efficacy of adenosine is similar to that of verapamil, but its onset of action is more rapid. Adverse reactions to adenosine are common but are minor and brief.

Acute Disease↗

PubMed1990

Relation of amiodarone hepatic and pulmonary toxicity to serum drug concentrations and superoxide dismutase activity.

Hepatic enzymes, pulmonary function, serum amiodarone and desethylamiodarone (DEA) concentrations and erythrocyte superoxide dismutase (SOD) activity were monitored at regular intervals for 1 year in 30 patients receiving amiodarone. Subclinical hepatotoxicity developed in 5 patients. These patients had higher baseline alanine transaminase values (42.6 +/- 6.8 vs 22.9 +/- 1.8 U/liter) and had an increase in serum aspartate transaminase from 27 +/- 4.1 at baseline to 147 +/- 77.3 U/liter at 12 months. The other patients had little variation in aspartate transaminase. Six patients with normal baseline carbon monoxide diffusing capacity had subclinical pulmonary toxicity develop with a mean decrease in diffusing capacity to 0.7 +/- 0.05 of the baseline value, which correlated with decreasing erythrocyte SOD activity. Mean carbon monoxide diffusing capacity and SOD activity remained unchanged in the other patients. The mechanisms of hepatic and pulmonary injury remain unknown, but appear to be associated with exposure to higher total serum concentrations of amiodarone plus DEA. Patients who had hepatic and/or pulmonary abnormalities develop received higher doses of amiodarone (440 +/- 27 vs 340 +/- 18 mg/day), but also had a higher amiodarone:DEA ratio suggesting that dose-dependent kinetics contributed to the higher concentrations. Elevated baseline alanine transaminase may indicate increased risk for hepatotoxicity while a progressive decrease in erythrocyte SOD may be an early indication of pulmonary toxicity. The latter finding indicates a need to investigate the role of free radicals in the pathogenesis of amiodarone pulmonary toxicity.

Alanine Transaminase↗

PubMed1990

Right ventricular pressure during ventricular arrhythmias in humans: potential implications for implantable antitachycardia devices.

Implantable defibrillators use algorithms based on ventricular electrographic data to detect the onset and termination of arrhythmias, but these algorithms do not always differentiate hemodynamically stable from unstable arrhythmias. Although, ideally, left ventricular function should be used to assess the hemodynamic state, right ventricular pulse pressure can be assessed in humans on a long-term basis with a transvenous lead. The potential utility of right ventricular pulse pressure to assess hemodynamic stability was studied in 22 patients with induced ventricular arrhythmias. Right ventricular pressure was measured with use of a transvenous right ventricular endocardial pacing lead with a piezoelectric bender pressure sensor 3 cm from its tip. Single ventricular premature paced beats administered in up to a bigeminal frequency did not alter the mean right ventricular pulse pressure (control 33.7 +/- 26, bigeminy 35.7 +/- 26 mm Hg). Twenty-one episodes of induced ventricular tachycardia were studied in the electrophysiology laboratory. Five seconds after tachycardia induction, hemodynamically stable ventricular tachycardia had a longer cycle length (294 +/- 41 ms) and the right ventricular pulse pressure ratio was higher (0.55 +/- 0.26) than that in unstable ventricular tachycardia (cycle length 256 +/- 55 ms, p = 0.06; pulse pressure ratio 0.26 +/- 0.09, p less than 0.05). Twenty episodes of ventricular fibrillation were induced in eight patients. One second after induction, right ventricular pulse pressure decreased from 25 +/- 5 to 6 +/- 3 mm Hg (p less than 0.05). On the first beat after defibrillation, right ventricular pulse pressure increased to 24 +/- 14 mm Hg, a level not significantly different from that before the induction of ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Value of a revised procainamide test in the Wolff-Parkinson-White syndrome.

A shortest preexcited RR interval less than 250 ms during atrial fibrillation identifies the patient with Wolff-Parkinson-White syndrome potentially at risk for ventricular fibrillation. Loss of preexcitation after infusion of up to 10 mg/kg of procainamide during sinus rhythm has been reported to correlate with a slow ventricular response during atrial fibrillation and has been proposed as a noninvasive test to establish risk of sudden death in these patients. Others have failed to establish this relation and have questioned the usefulness of the procainamide test. Such conflicting results were hypothesized to be a result of differing dosages and methodology. Consequently, this study tested the effect of incremental doses of procainamide (to a cumulative dose of 1 g) on the anterograde effective refractory period of the accessory pathway and related the reliability of the procainamide test to the dose at which preexcitation was lost. The effect of procainamide on the anterograde effective refractory period of the accessory pathway was dose dependent; patients who lost preexcitation had a steeper dose-response curve. Loss of preexcitation by a cumulative dose of 550 mg provided the best balance for sensitivity (60%) and specificity (89%) in identifying patients with preexcited shortest RR greater than 250 ms. Specificity fell steeply after this dosage and higher doses were not useful. The diagnostic accuracy of the procainamide test is critically related to dosage and method of infusion.

Adolescent↗

PubMed1990

Intravenous adenosine triphosphate during wide QRS complex tachycardia: safety, therapeutic efficacy, and diagnostic utility.

PURPOSE: Inappropriate administration of intravenous verapamil to patients with wide QRS complex tachycardia due to ventricular tachycardia or atrial fibrillation with Wolff-Parkinson-White syndrome occurs frequently because of misdiagnosis, and may precipitate a cardiac arrest. We evaluated the safety and the diagnostic and therapeutic utility of adenosine triphosphate administered to a consecutive series of 34 patients during wide QRS complex tachycardia due to a variety of mechanisms. PATIENTS AND METHODS: Patients who had a hemodynamically and electrically stable, monomorphic, wide (greater than 120 msec) QRS complex tachycardia induced during an invasive cardiac electrophysiologic test were studied. Hemodynamic stability was defined by a systolic blood pressure greater than 80 mm Hg and no clinical evidence of cerebral or myocardial ischemia. Adenosine triphosphate, 20 mg, was administered as a rapid intravenous bolus via a peripheral vein during wide QRS complex tachycardia. Five surface electrocardiogram leads, at least three intracardiac electrograms, and blood pressure were monitored. RESULTS: Ventricular tachycardia was present in 14 patients (mean age 50.6 +/- 19 years, cycle length 326 +/- 67 msec) and adenosine triphosphate terminated the arrhythmia in one case. Ventricular tachycardia cycle length did not change. Among 10 patients with supraventricular tachycardia with mechanisms not involving the AV node (average ventricular cycle length 346 +/- 82 msec), one case of ectopic atrial tachycardia was terminated. The ventricular rate was transiently increased in patients with Wolff-Parkinson-White syndrome and atrial fibrillation (average R-R interval 351 +/- 84 msec in control and 317 +/- 82 msec after adenosine triphosphate, p less than 0.001). Reentrant tachycardias involving the AV node (cycle length 302 +/- 52 msec) terminated in seven of 10 patients. The drug was well tolerated, and no patient developed hemodynamic compromise necessitating cardioversion as a result of adenosine triphosphate. CONCLUSION: In the setting of electrophysiology testing, adenosine triphosphate is a safe agent, even when administered inappropriately during arrhythmias for which it is relatively ineffective, such as ventricular tachycardia, and Wolff-Parkinson-White syndrome with atrial fibrillation. It is an effective agent in terminating supraventricular tachycardia involving the AV node. Tachycardia termination following adenosine triphosphate, when used as a diagnostic test to indicate obligatory participation of the AV node, had a sensitivity of 70%, specificity of 92%, and a positive predictive accuracy of 85%. Thus, adenosine triphosphate also has diagnostic utility, but should be used after the appropriate arrhythmia diagnosis has been made based on the clinical history and analysis of the 12-lead electrocardiogram.

Adenosine Triphosphate↗

PubMed1990

Skeletonization of the atrioventricular node for AV node reentrant tachycardia: experience with 32 patients.

We describe our experience with operative therapy for atrioventricular (AV) node tachycardia using an anatomically guided procedure. The operative rationale was to dissect the AV node from most of its atrial inputs (AV node "skeletonization") with the intent of altering the perinodal substrate and preventing reentry. The anteroseptal and posteroseptal regions were initially approached epicardially to facilitate identification of anatomical structures. Under normothermic cardiopulmonary bypass, the right atrial septum was mobilized and the intermediate AV node was exposed anterior to the tendon of Todaro. Atrioventricular node conduction was monitored electrocardiographically throughout the procedure. Ablation of concomitant accessory pathways was done prior to AV node skeletonization. Thirty-two patients aged 9 to 67 years (mean age, 30 years) underwent operation. Five patients had concomitant accessory pathways in addition to AV node reentry. At electrophysiological study before discharge, no patient had AV block although anterograde and retrograde Wenckebach cycle lengths were significantly prolonged. Six patients had retrograde AV block. Twenty-nine patients are free from arrhythmia and require no antiarrhythmic medication after a follow-up of 1 month to 45 months (mean follow-up, 17 months). Three patients had recurrence of tachycardia ten days, 2 months, and 7 months postoperatively. All patients subsequently had a successful reoperation.

Adolescent↗

PubMed1990

Mode of onset of atrial fibrillation in the Wolff-Parkinson-White syndrome: how important is the accessory pathway?

The mode of onset of 103 episodes of atrial fibrillation lasting greater than or equal to 30 s was studied in 79 patients with the Wolff-Parkinson-White syndrome during electrophysiologic study. No patient had organic heart disease, and 31 had clinical atrial fibrillation before study. These 79 patients were then compared with a control group of 53 patients with Wolff-Parkinson-White syndrome in whom atrial fibrillation could not be induced. Ninety-five of the 103 episodes were technically suitable for analysis. Atrial fibrillation invariably began with rapid atrial tachycardia that became progressively disorganized within 10 to 20 cycles. It was initiated during right atrial stimulation (n = 52), right ventricular stimulation (n = 8), reciprocating tachycardia (n = 33) and spontaneously (n = 2). Most episodes started at a high right atrial site regardless of accessory pathway location, with only 19% of episodes starting at the electrode closest to the accessory pathway. During reciprocating tachycardia (n = 33), either atrial (n = 8) or ventricular (n = 5) extrastimuli initiated atrial fibrillation. Atrial fibrillation started at the accessory pathway site in 6 of 20 episodes occurring spontaneously during reciprocating tachycardia. Patients with atrial fibrillation had a longer PA interval (54 +/- 14 versus 42 +/- 12 ms, p less than 0.0001), shorter atrial functional refractory period (226 +/- 38 versus 240 +/- 30 ms, p = 0.049) and shorter anterograde effective refractory period of the accessory pathway (279 +/- 26 versus 304 +/- 75 ms, p = 0.03). Clinical reciprocating tachycardia was documented with equal frequency in both the atrial fibrillation and control groups (59.5% versus 52.9%, p = 0.58).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Termination of acute atrial fibrillation in the Wolff-Parkinson-White syndrome by procainamide and propafenone: importance of atrial fibrillatory cycle length.

The effects of intravenous procainamide (n = 30) or propafenone (n = 25) were evaluated in 55 patients with acute atrial fibrillation and the Wolff-Parkinson-White syndrome. All patients received either procainamide (12 to 15 mg/kg body weight) or propafenone (1 to 2 mg/kg) during sustained (greater than 10 min) atrial fibrillation or after termination of nonsustained atrial fibrillation. Termination of atrial fibrillation was attributed to a drug if it occurred less than or equal to 15 min after infusion. Measurements included mean cycle length of fibrillatory electrograms (mean AA interval) as measured at the high right atrium and shortest RR interval between pre-excited cycles during atrial fibrillation. Atrial fibrillation terminated more frequently after procainamide administration (65%) than after propafenone (46%), although this difference was not significant. Procainamide prolonged the shortest pre-excited RR interval (228 +/- 41 to 339 +/- 23 ms, p = 0.0001) as did propafenone (215 +/- 40 to 415 +/- 198 ms, p = 0.0001) and the magnitude of increase was greater for propafenone (p = 0.048). Patients with sustained atrial fibrillation had shorter mean AA intervals than did their counterparts with nonsustained atrial fibrillation (123 +/- 25 versus 186 +/- 35 ms, p = 0.0001). Termination of sustained atrial fibrillation by either drug was accompanied by prolongation of the mean AA interval but not necessarily by the shortest pre-excited RR interval. Termination of atrial fibrillation was heralded by a 68% increase in the mean AA interval after procainamide administration compared with a 30% increase when the arrhythmia persisted. For propafenone the increases were 90% and 68%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1990

Hemodynamic effects of intravenous procainamide during ventricular tachycardia.

Radionuclide angiography was used to study the hemodynamic effects of intravenous procainamide during stable monomorphic ventricular tachycardia. In four patients studied without procainamide, the ejection fraction was 25% +/- 2.4% during normal sinus rhythm, dropped to 11.3% +/- 2.2% (p less than 0.05) at the onset of ventricular tachycardia, increased to 16.7% +/- 1.7% after remaining in ventricular tachycardia for 10 minutes, and returned to 25.3% +/- 3.7% in sinus rhythm. In the 10 study patients, ejection fraction dropped from 36% +/- 5.8% in sinus rhythm to 25% +/- 5.1% in ventricular tachycardia (p less than 0.2). Ejection fraction decreased further (23% +/- 5.0%) following low doses of procainamide (140 +/- 52 mg) despite cycle length prolongation (354 +/- 18 msec versus 373 +/- 21 msec, p less than 0.5). In 8 of 10 patients, there was a progressive increase in the ejection fraction (28.8% +/- 4.1%). Ventricular tachycardia onset also resulted in a decrease in cardiac output and end-diastolic and end-systolic volumes. Two patients who tolerated procainamide in sinus rhythm showed hemodynamic collapse secondary to procainamide during ventricular tachycardia. We conclude that in some patients hemodynamic intolerance to an antiarrhythmic drug may only become evident during ventricular tachycardia.

Adult↗

PubMed1990

Incidence and clinical significance of ST segment depression in supraventricular tachycardia.

To evaluate the clinical significance of ST segment depression observed during paroxysmal supraventricular tachycardia, the data of 100 patients who underwent electrophysiologic testing between 1981 and 1986 in the drug free state were reviewed. Twelve lead electrocardiograms were taken within 20 s of tachycardia induction. Patients with antidromic tachycardia, tachycardia using multiple accessory pathways or tachycardia associated with bundle branch aberration or concomitant electrolyte abnormalities were excluded from the study. Significant ST depression was defined as at least 0.1 mV horizontal or downsloping or 0.2 mV upsloping depression, measured 80 ms after the J point. ST segment changes were correlated with historical data and the results of exercise tests and radionuclide or coronary angiograms. There were 52 males and 48 females, aged 11 to 67 years (mean 32.8 +/- 13.2). Tachycardia was due to atrioventricular reentry via an overt or concealed accessory pathway in 85 patients, and atrioventricular nodal reentry in 15 patients. Significant ST depression was seen in 51 patients (aged 11 to 65 years). Thirty-three of 70 patients younger than 40 years old had significant ST depression. There was no relationship between the presence of significant ST depression and age, sex, mechanism or rate of tachycardia. Only three patients had significant coronary artery disease, and all manifested significant ST depression during tachycardia. Thus the specificity of this finding was 51% and the predictive value only 6%. In conclusion, ST segment changes observed during narrow QRS complex tachycardia are common, nonspecific and a poor predictor of underlying coronary artery disease.

Adolescent↗

PubMed1990

Initial clinical experience with the pacemaker-cardioverter-defibrillator.

The implantation of a new multiprogrammable pacemaker-cardioverter-defibrillator is reported in four patients suffering from drug-refractory ventricular tachycardia or fibrillation. The generator (PCD 7215; Medtronic Inc) was interfaced to the epicardium by three countershock patch electrodes and one ventricular myocardial screw-in lead for sensing/pacing. The device employs separate rate detection criteria for ventricular tachycardia and ventricular fibrillation with automatic delivery of up to four therapies per episode. Therapeutic options include: antitachycardia burst or autodecremental pacing, synchronized cardioversion, defibrillation and ventricular demand pacing at 30 to 90 beats/min. Four men and one woman (ages 29 to 75 years) underwent intraoperative implant evaluation, and the device was implanted in the four men. Over a follow-up of 1.5 to 23 months, 161 spontaneous episodes of ventricular tachycardia and nine episodes meeting ventricular fibrillation criteria (cycle length less than 280 to 290 ms) were detected and treated by the device. Ramp pacing was initially employed to terminate 140 ventricular tachycardia episodes and was successful 88.5% of the time while 10 (7.2%) required low energy epicardial cardioversion (4 to 10 J). Six (4.3%) episodes terminated spontaneously prior to therapy delivery. All nine spontaneous episodes of ventricular fibrillation were defibrillated using 10 to 15 J. Two patients continue to do well with the device functioning reliably. The device was removed at the time of heart transplant in one patient, while another patient died suddenly from drug overdose. No other complications, device malfunctions or inappropriate therapy delivery have been observed. These early results demonstrate the potential usefulness of a programmable device which provides graded therapy for ventricular tachycardia with added defibrillation and bradycardia pacing capability.

Adult↗

PubMed1989

The diagnostic sensitivity of electrophysiologic testing in patients with syncope caused by transient bradycardia.

Although electrophysiologic testing accurately delineates abnormalities in patients with fixed cardiac-conduction defects, its sensitivity in identifying transient rhythm disturbances is unknown. We prospectively studied 21 patients who had electrocardiographically documented intermittent atrioventricular block (n = 13) or sinus pauses (n = 8) causing syncope, but whose cardiac rhythm had reverted to normal by the time of referral. There were 14 men and 7 women, with a mean age (+/- SD) of 63 +/- 13 years. Fourteen patients had organic heart disease, and 8 were taking cardioactive medications. Electrophysiologic testing was performed before the implantation of a permanent pacemaker. Only three of the eight patients with documented sinus pauses had abnormalities during their tests that suggested the correct diagnosis (sensitivity, 37.5 percent), including a prolonged sinus-node recovery time in one and carotid-sinus hypersensitivity in two. Three of the eight patients had abnormalities detected that were unrelated to syncope, including atrial flutter, dual atrioventricular nodal pathways, and sustained monomorphic ventricular tachycardia. Of the 13 patients with documented atrioventricular block, only 2 had abnormalities suggesting the correct diagnosis (sensitivity, 15.4 percent). Additional observations unrelated to syncope among these 13 patients included abnormal sinus-node function, atrial flutter, and atrial fibrillation causing hypotension. These preliminary observations suggest that a negative electrophysiologic test in a patient with a normal cardiac rhythm who has experienced syncope does not exclude a transient bradyarrhythmia as a cause of the syncope. Furthermore, electrophysiologic testing may sometimes reveal unrelated rhythm disturbances that may mistakenly be designated as the cause of the syncope.

Aged↗

PubMed1989

Surgical alternatives for supraventricular tachycardias.

Since Sealy's pioneering surgical intervention for Wolff-Parkinson-White syndrome, surgical electrophysiologic interventions have been developed for all supraventricular arrhythmias. The surgical rationales are based on the site of origin of the arrhythmic mechanism and the associated pathology that characterizes the "arrhythmogenic substrate." The Wolff-Parkinson-White syndrome is characterized by an accessory atrioventricular (AV) connection distinct from the AV node-His bundle system. It is associated with AV reentrant tachycardia or atrial fibrillation, or both, with fast ventricular responses through the accessory pathway. The current surgical management involves ablation of the accessory pathway using either an endocardial or an epicardial approach. Surgical ablation is associated with high efficiency and low morbidity. Epicardial dissection of the accessory pathway on the beating heart has helped to localize variant accessory pathways associated with Coumel's tachycardia or the Mahaim fiber. AV nodal reentrant tachycardia can be cured using direct AV nodal dissection (or perinodal cryoablation). Atrial flutter can be interrupted by cryoablation of the arrhythmogenic substrate located in the coronary sinus orifice region. The chronotropic atrial function, abolished by incessant or paroxysmal idiopathic atrial fibrillation, can be restored using the corridor operation (sinus node-AV node insulation). The success of surgical intervention in atrial tachycardias is uncertain, but it may be an option in selected patients with resistant atrial tachycardias.

Adolescent↗

PubMed1989

Operative therapy of atrioventricular node reentry and results of an anatomically guided procedure.

Operative therapy for atrioventricular (AV) node reentrant tachycardia consisting of dissection guided by anatomic landmarks is described. Of the 21 patients studied, 17 had the common type ("slow-fast") and 4 had the uncommon type ("fast-slow") of AV node reentry. Under normothermic cardio-pulmonary bypass, perinodal dissection was performed guided by anatomic landmarks: the atrial membranous septum, posterior superior process of the left ventricle, tendon of Todaro and os of the coronary sinus. There were no deaths or major complications. Seven to 10 days postoperatively, all patients had normal AV conduction except for one who continued to have AV node Wenckebach-type block. Postoperatively, the shortest cycle length capable of 1:1 conduction over the AV node changed from 323 +/- 66 to 421 +/- 90 ms (p less than 0.0001) anterogradely and from 330 +/- 86 to 449 +/- 164 ms (p = 0.004) retrogradely. Anterograde effective refractory period of the AV node prolonged from 264 +/- 49 to 358 +/- 107 ms (p = 0.012). Discontinuous AV conduction curves were no longer seen in 14 of 17 patients and 5 patients lost retrograde conduction. During follow-up (14.8 +/- 8.2 months), 19 patients have been free of arrhythmia without medication. Two patients required a second operation for recurrent tachycardia with success. No patient required a permanent pacemaker. These data show that operative therapy of AV node reentrant tachycardia can be guided by anatomic landmarks. Successful cure of tachycardia with perinodal dissection while preserving AV node conduction supports the view that the reentrant circuit is, at least in part, perinodal.

Adolescent↗

PubMed1989

Correlation of amiodarone dosage, heart rate, QT interval and corneal microdeposits with serum amiodarone and desethylamiodarone concentrations.

Pharmacokinetic-dynamic relations for amiodarone have been difficult to define. Few studies have successfully correlated serum amiodarone concentration with either dose or pharmacodynamic effects. Reduction in heart rate, prolongation of corrected QT interval and accumulation of corneal microdeposits are 3 clinical effects well suited for making kinetic-dynamic comparisons because they occur in virtually all patients receiving amiodarone. Data on heart rate, corrected QT interval, corneal microdeposits, cumulative dose and serum concentrations of amiodarone and desethylamiodarone (DEA) were collected over the course of 1 year after initiation of therapy in 27 patients (mean age 55.4 +/- 2.35 years). Mean elimination half-lives in this study population were 56 days for amiodarone and 129 days for DEA, as estimated from cumulation kinetics without drug withdrawal. The extremely long half-lives of amiodarone and DEA make demonstration of steady-state concentration-response relations difficult. A new approach using analysis of sequential data before steady-state reveals general relations between dose, DEA concentration and 3 clinically observable effects of amiodarone. A linear relation was evident between DEA concentration and log mean cumulative amiodarone dose (mg/kg) for the population. The steep segments of the concentration-response curves for heart rate, microdeposits and corrected QT interval occurred at low, medium and high serum amiodarone and DEA concentrations, respectively. Patients not developing a decrease in heart rate or corneal microdeposits likely have very low serum drug concentrations and may not be adequately treated. The monitoring of heart rate, corrected QT interval and corneal microdeposits as an aid to assessing adequacy of amiodarone therapy requires further study.

Amiodarone↗