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Biomedical subjects

M Talajic

Publications and source records attributed to M Talajic.

At least 55 records · Page 3Linked to original sources

Depression and 18-month prognosis after myocardial infarction.

BACKGROUND: We previously reported that major depression in patients in the hospital after a myocardial infarction (MI) substantially increases the risk of mortality during the first 6 months. We examined the impact of depression over 18 months and present additional evidence concerning potential mechanisms linking depression and mortality. METHODS AND RESULTS: Two-hundred twenty-two patients responded to a modified version of the National Institute of Mental Health Diagnostic Interview Schedule (DIS) for a major depressive episode at approximately 7 days after MI. The Beck Depression Inventory (BDI), which measures depressive symptomatology, was also completed by 218 of the patients. All patients and/or families were contacted at 18 months to determine survival status. Thirty-five patients met the modified DIS criteria for major in-hospital depression after the MI. Sixty-eight had BDI scores > or = 10, indicative of mild to moderate symptoms of depression. There were 21 deaths during the follow-up period, including 19 from cardiac causes. Seven of these deaths occurred among patients who met DIS criteria for depression, and 12 occurred among patients with elevated BDI scores. Multiple logistic regression analyses showed that both the DIS (odds ratio, 3.64; 95% confidence interval [CI], 1.32 to 10.05; P = .012) and elevated BDI scores (odds ratio, 7.82; 95% CI, 2.42 to 25.26; P = .0002) were significantly related to 18-month cardiac mortality. After we controlled for the other significant multivariate predictors of mortality in the data set (previous MI, Killip class, premature ventricular contractions [PVCs] of > or = 10 per hour), the impact of the BDI score remained significant (adjusted odds ratio, 6.64; 95% CI, 1.76 to 25.09; P = .0026). In addition, the interaction of PVCs and BDI score marginally improved the model (P = .094). The interaction showed that deaths were concentrated among depressed patients with PVCs of > or = 10 per hour (odds ratio, 29.1; 95% CI, 6.97 to 122.07; P < .00001). CONCLUSIONS: Depression while in the hospital after an MI is a significant predictor of 18-month post-MI cardiac mortality. Depression also significantly improves a risk-stratification model based on traditional post-MI risks, including previous MI, Killip class, and PVCs. Furthermore, the risk associated with depression is greatest among patients with > or = 10 PVCs per hour. This result is compatible with the literature suggesting an arrhythmic mechanism as the link between psychological factors and sudden cardiac death and underscores the importance of developing screening and treatment programs for post-MI depression.

Aged↗

The impact of negative emotions on prognosis following myocardial infarction: is it more than depression?

This study examine the importance of major depression symptoms, history of major depression, anxiety, anger-in, anger-out, and perceived social support, measured in the hospital after a myocardial infarction (MI), in predicting cardiac events over the subsequent 12 months in a sample of 222 patients. Cardiac events included both recurrences of acute coronary syndromes (unstable angina admissions and survived and nonsurvived MI recurrences) and probable arrhythmic events (survived cardiac arrests and arrhythmic deaths). Major depression, depressive symptoms, anxiety, and history of major depression all significantly predicted cardiac events. Multivariate analyses showed that depressive symptoms, anxiety, and history of major depression each had an impact independent of each other, as well as of measures of cardiac disease severity.

Adult↗

Catheter ablation using radiofrequency or low-energy direct current in pediatric patients with the Wolff-Parkinson-White syndrome.

Percutaneous ablation of accessory pathways was performed in 22 consecutive children and adolescents (9 boys and 13 girls, age range 8 to 18 years). Low-energy direct current (DC) was used exclusively in the first 6 patients, whereas ablation was performed with radiofrequency energy in the following 16. Accessory pathways were located in the left free wall in 15 patients, were posteroseptal in 3, were in the right free wall in 3 and were anteroseptal in 1. A concealed accessory pathway was present in 7 patients (32%). There was no significant difference in clinical or electrophysiologic variables between both groups. Catheter ablation was successful in the initial 6 patients using low-energy DC, as compared with 13 of 16 patients using radiofrequency ablation. Low-energy DC was successful as a backup power source in all 3 patients who had unsuccessful radiofrequency ablation. There was no complication. The median procedural and fluoroscopic times for successful ablation were 2.5 hours and 49 minutes, respectively (p = NS between both power sources). Accessory pathway conduction recurred in 2 patients (33%) who had low-energy DC as compared with 1 (6%) who had radiofrequency ablation (p = NS). These 3 patients had successful reablation of their accessory pathways. In children and adolescents with accessory pathways, both new power sources compare favorably, with an overall success rate of ablation of 100% (22 of 22 patients). Radiofrequency ablation should be used initially because it does not require general anesthesia and is associated with a lower rate of recurrence of accessory pathway conduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

The treatment of atrial fibrillation. An evaluation of drug therapy, electrical modalities and therapeutic considerations.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia in clinical practice, and is responsible for considerable morbidity. Basic studies have shown that AF is usually due to the coexistence of multiple functional atrial re-entry circuits, and that the main determinant of its haemodynamic manifestations is the ventricular response rate. The major adverse clinical consequences of AF include palpitations, impaired cardiac function and thromboembolism. One approach to treating AF is to convert the patient's cardiac rhythm to sinus rhythm by direct current electrical cardioversion, which is initially successful in about 90% of cases. However, the AF recurrence rate over the year subsequent to cardioversion is very high, in the order of 75% in patients receiving no drug therapy. Class I and class III antiarrhythmic drugs reduce the rate of recurrence of AF, but at the expense of a variety of potential adverse effects including ventricular proarrhythmia. The latter is a rare effect (occurring in 1 to 2% of patients receiving most drugs), but can be lethal. A second approach to therapy is to leave the patient in AF, but to control the ventricular response rate and to prevent thromboemboli with oral anticoagulants. Disadvantages of this approach include the possibilities of functional limitations imposed by the arrhythmia, adverse effects of drug therapy, and major bleeding related to anticoagulation. New approaches currently under study include surgery to prevent AF from sustaining itself, implantable cardioverter devices to maintain sinus rhythm, and modification of AV nodal function by the induction of controlled radiofrequency injury.

Animals↗

Depression following myocardial infarction. Impact on 6-month survival.

OBJECTIVE: To determine if the diagnosis of major depression in patients hospitalized following myocardial infarction (MI) would have an independent impact on cardiac mortality over the first 6 months after discharge. DESIGN: Prospective evaluation of the impact of depression assessed using a modified version of the National Institute of Mental Health Diagnostic Interview Schedule for major depressive episode. Cox proportional hazards regression was used to evaluate the independent impact of depression after control for significant clinical predictors in the data set. SETTING: A large, university-affiliated hospital specializing in cardiac care, located in Montreal, Quebec. PATIENTS: All consenting patients (N = 222) who met established criteria for MI between August 1991 and July 1992 and who survived to be discharged from the hospital. Patients were interviewed between 5 and 15 days following the MI and were followed up for 6 months. There were no age limits (range, 24 to 88 years; mean, 60 years). The sample was 78% male. PRIMARY OUTCOME MEASURE: Survival status at 6 months. RESULTS: By 6 months, 12 patients had died. All deaths were due to cardiac causes. Depression was a significant predictor of mortality (hazard ratio, 5.74; 95% confidence interval, 4.61 to 6.87; P = .0006). The impact of depression remained after control for left ventricular dysfunction (Killip class) and previous MI, the multivariate significant predictors of mortality in the data set (adjusted hazard ratio, 4.29; 95% confidence interval, 3.14 to 5.44; P = .013). CONCLUSION: Major depression in patients hospitalized following an MI is an independent risk factor for mortality at 6 months. Its impact is at least equivalent to that of left ventricular dysfunction (Killip class) and history of previous MI. Additional study is needed to determine whether treatment of depression can influence post-MI survival and to assess possible underlying mechanisms.

Adult↗

Results of a comparative study of low energy direct current with radiofrequency ablation in patients with the Wolff-Parkinson-White syndrome.

OBJECTIVE: To compare two new power sources for catheter ablation in patients with the Wolff-Parkinson-White syndrome. DESIGN: 120 consecutive patients with accessory pathways had catheter ablation. Low energy direct current (DC) was used in the first 60 patients and radio-frequency current in the next 60 patients. SETTING: Electrophysiological laboratory of a large heart institute. PATIENTS: 72 men and 48 women (mean (SD) age 35 (14) years (range 9-75)). The accessory pathways were in the left free wall in 73 patients. They were posteroseptal in 35 patients, in the right free wall in five, and anteroseptal in seven. There was no significant difference in the clinical or electrophysiological variables between the two ablation groups. RESULTS: Catheter ablation with low energy direct current was successful in 55/60 patients (92%) and radiofrequency energy was successful in 52/60 patients (87%). Low energy direct current was also successful in four of the eight patients in whom radiofrequency ablation had failed. Radiofrequency ablation was successful in two of the five patients in whom low energy direct current ablation had failed. The mean (SD) procedure and fluoroscopy times for successful ablation were 3.2 (1.5) h and 61 (40) min respectively. These times were similar for both power sources. Accessory pathway conduction recurred in 17 patients (28%) who had low energy direct current and four patients (7%) who received radiofrequency energy (p < 0.004). All patients with recurrence of an accessory pathway had successful re-ablation. CONCLUSIONS: Both new power sources successfully ablated accessory pathways, (overall success rate 94% (113/120 patients)). Radiofrequency ablation, however, did not require general anaesthesia and was associated with a significantly lower rate of recurrence of accessory pathway conduction. Therefore radiofrequency should be used initially for ablation. Low energy direct current may be most useful as a back-up in patients in whom radiofrequency ablation fails.

Adolescent↗

Rate-dependent functional properties of retrograde atrioventricular nodal conduction in experimental animals.

While rate-dependent atrioventricular (AV) nodal functional properties play a major role in determining antegrade AV nodal conduction, their existence and characteristics have not been assessed during retrograde AV nodal impulse propagation. Pacing protocols were used to study selectively AV nodal recovery, facilitation, and fatigue in 6 isolated, superfused rabbit AV nodal preparations and in 11 morphine-chloralose anesthetized dogs. All three properties were identifiable during retrograde AV nodal activation in rabbits. Retrograde recovery and fatigue were clearly demonstrated in dogs, but facilitation could not be evaluated because of echo beats during retrograde premature stimulation. Functional properties were qualitatively similar during retrograde and antegrade propagation; however, important quantitative differences were noted. The time constant for recovery from activation was significantly greater in the retrograde [rabbits, 69 +/- 8 (SE) ms; dogs, 93 +/- 11 ms] compared with the antegrade direction (rabbits, 50 +/- 5 ms; dogs, 58 +/- 4 ms; P < 0.05 vs. retrograde for each species). The magnitude of fatigue resulting from sustained increases in rate was also substantially greater in the retrograde direction in both rabbits (17 +/- 2 vs. 10 +/- 1 ms antegrade, P = 0.01) and dogs (20 +/- 4 vs. 6 +/- 1 ms antegrade, P < 0.01). Conduction time and refractory period were both greater in the retrograde compared with antegrade direction, and directional differences in conduction properties were magnified as activation rate increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Comparative mechanisms of antiarrhythmic drug action in experimental atrial fibrillation. Importance of use-dependent effects on refractoriness.

BACKGROUND: Antiarrhythmic drugs are considered to terminate atrial fibrillation by prolonging refractoriness, but direct experimental evaluation of this concept has been limited. The atria are activated rapidly during atrial fibrillation, and antiarrhythmic drugs are known to have important rate-dependent actions. The potential role of such properties in determining drug effects during atrial fibrillation has not been evaluated. METHODS AND RESULTS: We evaluated the effects of representative class Ia (procainamide), Ic (propafenone), and III (sotalol) antiarrhythmic drugs on sustained cholinergic atrial fibrillation and atrial electrophysiological properties in anesthetized, open-chest dogs. Loading and maintenance doses were used to produce stable plasma concentrations, and computer-based 112-electrode epicardial mapping was used to study atrial conduction and activation during atrial fibrillation. Clinically used doses of procainamide and propafenone terminated atrial fibrillation in 13 of 13 (100%) and 7 of 10 (70%) dogs, respectively, but a dose of sotalol (2 mg/kg IV) in the clinical range terminated atrial fibrillation in only 2 of 8 (25%) dogs (P = .0005 vs procainamide, P = .08 vs propafenone). Procainamide and propafenone prevented atrial fibrillation induction in 13 of 13 (100%) and 7 of 10 (70%) dogs, respectively, compared with none of 8 dogs for 2 mg/kg sotalol (P < .0001 vs procainamide, P = .004 vs propafenone). A larger dose of sotalol (cumulative dose, 8 mg/kg) was uniformly effective in terminating atrial fibrillation and preventing its induction. All drugs significantly increased atrial refractory period, with effects that were use dependent for propafenone but reverse use dependent for sotalol. Effective doses of all drugs significantly increased the wavelength for reentry at rapid atrial rates in the presence of vagal stimulation into the range observed under drug-free conditions in the absence of vagal input. The inefficacy of clinical doses of sotalol was explained by the reverse use dependence of its effects on refractoriness, which resulted in reduced effects on wavelength at rapid rates. The effects of propafenone on refractoriness were significantly increased at rapid rates, contributing to its ability to increase wavelength and terminate atrial fibrillation. Activation mapping showed that drugs terminated atrial fibrillation by reducing the number and increasing the size of reentry circuits, leading to termination by mechanisms related to block in the remaining circuit(s). CONCLUSIONS: We conclude that antiarrhythmic drugs terminate experimental atrial fibrillation by increasing the wavelength for reentry at rapid rates, leading to a reduction in the number of functional reentry circuits and, eventually, failure of reentrant excitation. Use-dependent effects on refractoriness can limit (in the case of the reverse use dependence of sotalol) or contribute (in the case of propafenone) to antiarrhythmic drug efficacy against atrial fibrillation by determining drug-induced changes in wavelength at rapid atrial rates.

Animals↗

Effects of flecainide on the rate dependence of atrial refractoriness, atrial repolarization and atrioventricular node conduction in anesthetized dogs.

UNLABELLED: Flecainide is effective against certain supraventricular arrhythmias (atrial fibrillation and atrioventricular [AV] node reentrant tachycardia), but its mechanisms of action are unknown. Previous in vitro work suggests that flecainide attenuates rate-dependent action potential duration shortening, producing tachycardia-dependent prolongation of the refractory period. This study was designed to assess whether similar changes occur in vivo and whether the effects of flecainide on AV node conduction depend on heart rate and on direction of propagation (anterograde vs. retrograde). The effects of flecainide at three clinically relevant concentrations were assessed in open chest, morphine-chloralose-anesthetized dogs. Flecainide increased atrial refractory period in a concentration- and rate-related fashion (e.g., dose 3 increased the atrial effective refractory period by 9 +/- 4% at a cycle length of 1,000 ms but by 36 +/- 5% and 55 +/- 10% at a basic cycle length of 400 and 300 ms, respectively; p less than 0.001 for each). Flecainide attenuated the action potential duration accommodation (measured by monophasic action potentials) to heart rate, causing tachycardia-dependent action potential duration prolongation and accounting for most of the rate-dependent atrial effective refractory period changes. Flecainide increased Wenckebach cycle length, but the concentration-response curve was much steeper in the retrograde (slope 41 +/- 7 ms/mumol.liter-1) than in the anterograde direction (17 +/- 4 ms/mumol.liter-1; p less than 0.01), indicating more potent effects on retrograde conduction. The depressant action of the drug on the AV node was also rate dependent, with an effect on the AH interval at a basic cycle length of 400 ms that averaged 1.8, 1.5 and 2 times that at a basic cycle length of 1,000 ms for doses 1 (p less than 0.05), 2 (p less than 0.01) and 3 (p less than 0.001), respectively. CONCLUSIONS: 1) Flecainide suppresses atrial action potential duration accommodation to heart rate changes in vivo, leading to rate-dependent atrial effective refractory period prolongation, which may be important in suppressing atrial fibrillation. 2) The drug has frequency- and direction-dependent effects on AV node conduction, which may lead to selective antiarrhythmic actions during AV node reentry.

Action Potentials↗

Success, safety, and late electrophysiological outcome of low-energy direct-current ablation in patients with the Wolff-Parkinson-White syndrome.

BACKGROUND: Percutaneous ablation of accessory pathways with the use of a defibrillator can be accomplished with high-energy direct-current (DC) shocks of 150-400 J, but complications include cardiac tamponade and sudden cardiac death, mostly resulting from significant electrical arcing and barotrauma. A new low-energy DC power source with a brief time-constant capacitive discharge delivers shocks of 2-40 J and eliminates or greatly reduces arcing. This report describes our initial experience with this device in 60 consecutive patients (mean age, 34 years; range, 9-67 years) with Wolff-Parkinson-White syndrome. Accessory pathways were located in the left free wall in 36 patients, in the right free wall in two, were posteroseptal in 18, and anteroseptal in four. Most patients (77%) had their initial diagnostic electrophysiological study and catheter ablation during the same session. METHODS AND RESULTS: Selective ablation of accessory pathways was successful in 55 patients (92%). The mean cumulative energy was 312 +/- 284 J and the mean creatine kinase MB peak (normal, 0-30 units) was 42 +/- 27 units. Patients with left free wall accessory pathways required less procedure time for ablation (2.7 +/- 0.8 versus 3.6 +/- 1.5 hours, p less than 0.0007) and less fluoroscopy time (46 +/- 24 versus 66 +/- 33 minutes, p less than 0.002). Complications were limited to transient pericarditis (three patients), one iliac artery dissection, and cardiac tamponade probably caused by catheter repositioning in the coronary sinus (one patient). An electrophysiological study was repeated in 50 of the 55 successful cases at a mean of 9 +/- 5 months. This study was normal in 48 of 50 (96%) patients. CONCLUSIONS: Low-energy DC ablation is safe and effective treatment for accessory pathways in children and adults. The long-term outcome is excellent as documented by electrophysiological restudy.

Adult↗

A quantitative analysis of use-dependent ventricular conduction slowing by procainamide in anesthetized dogs.

BACKGROUND: Use-dependent effects of antiarrhythmic drugs on phase 0 sodium current result in rate-dependent conduction slowing with important potential clinical consequences. The purpose of the present study was to determine whether state-dependent interactions of procainamide with sodium channels can be analyzed based on conduction changes in vivo. METHODS AND RESULTS: Procainamide infusions were used to produce stable drug concentrations causing greater than or equal to 25% conduction slowing at a basic cycle length (BCL) of 300 msec in morphine/chloralose-anesthetized dogs with formalin-induced atrioventricular block. Computer-based epicardial activation mapping was applied to assess the time course and pattern of conduction over a wide range of BCLs before and after drug administration. Action potential duration was measured from recordings of monophasic action potentials. The onset and steady-state values of fractional sodium channel block estimated from conduction changes were fitted to equations obtained from a stepwise exponential analysis. The rate constant for the onset of block (lambda *) decreased, as predicted, with decreasing cycle length. The slope of the relation between lambda * and recovery time at each BCL averaged 0.29 +/- 0.03 sec-1, resulting in a calculated recovery time constant (3.4 seconds) similar to values previously obtained by direct measurement. Estimates of binding and unbinding rate constants for the sodium channel during the action potential plateau and after repolarization were of the same order as previous results obtained using microelectrode methods in vitro. CONCLUSIONS: Use-dependent conduction changes produced by procainamide in vivo closely follow the predictions of mathematical models of drug-channel interactions, and underlying kinetic interactions with the sodium channel inferred from conduction changes agree with previous, more direct observations. These results support the relevance of basic concepts about antiarrhythmic drug actions on sodium channels for understanding drug effects on conduction in vivo and advance analytical tools that can be used to explore the latter in humans.

Action Potentials↗

Rate-dependent effects of diltiazem on human atrioventricular nodal properties.

BACKGROUND: Tachycardia enhances the channel-blocking effects of antiarrhythmic drugs. In contrast to the extensive data regarding the rate-dependent effects of sodium channel blockers in humans, little is known about the frequency-dependent effects of calcium channel blockers on human atrioventricular (AV) nodal properties. Accordingly, the purpose of this study was to evaluate the importance of heart rate in modulating the electrophysiological effects of diltiazem in humans. METHODS AND RESULTS: Electrophysiological studies were performed in 25 patients. Sinus node, atrial, and AV nodal function were evaluated at multiple atrial rates under control conditions and after administration of one of three intravenous doses of diltiazem designed to produce low, intermediate, and high stable plasma concentrations (designated doses 1, 2, and 3, respectively). Results were analyzed in terms of the longest and shortest cycle lengths obtainable in each patient under control and drug conditions. Plasma concentrations of diltiazem were stable and averaged 43 +/- 4, 73 +/- 6, and 136 +/- 11 ng/ml for doses 1, 2, and 3, respectively. Sinus node recovery time, intra-atrial conduction time, atrial effective refractory period, and HV interval were unaffected by diltiazem infusion. Effects of diltiazem were limited to changes in AV nodal parameters. Stable, dose-dependent increases in Wenckebach cycle length were observed after all three doses of diltiazem (increases of 54 +/- 13, 84 +/- 18, and 174 +/- 33 msec for doses 1, 2, and 3, respectively). Small nonsignificant increases in AH interval and atrioventricular effective refractory period (AVERP) were observed after dose 1 of diltiazem. At long cycle lengths, diltiazem caused modest increases in AH interval (3 +/- 4 and 25 +/- 8 msec for doses 2 and 3, respectively) and AVERP (36 +/- 12 and 70 +/- 25 msec). Drug effects were far greater at short cycle lengths (45 +/- 17 msec, 58 +/- 12 msec for AH interval and 80 +/- 24 msec, 163 +/- 41 msec for AVERP; p less than 0.05 versus values at long cycle lengths). At rapid rates, effects of diltiazem on AVERP substantially exceeded those on AV conduction, a result that could account for the beneficial effects of diltiazem during paroxysmal AV reentrant tachycardia by decreasing the excitable gap. CONCLUSIONS: Depressant effects of diltiazem on human AV nodal function are highly dependent on atrial rate; the rate-dependent actions on AV nodal refractoriness probably contribute to beneficial effects of diltiazem in patients with supraventricular arrhythmias.

Atrioventricular Node↗

Effects of beta-adrenergic receptor stimulation and blockade on rate-dependent atrioventricular nodal properties.

Recent work has shown that alterations in the dynamic atrioventricular (AV) nodal response to changes in heart rate can significantly modify AV nodal function. The present study was designed to evaluate the nature and potential importance of sympathetic regulation of the rate-dependent properties of the AV node. Selective stimulation protocols and mathematical formulations were used to independently quantify AV nodal recovery, facilitation, and fatigue in 12 morphine-chloralose-anesthetized dogs. Vagal effects were prevented by bilateral vagal transection and intravenous atropine, and the sinus node was crushed to allow a broader range of pacing cycle lengths. In seven dogs with sympathetic nerves intact, beta-adrenergic receptor blockade increased the recovery time constant (tau rec) for the conduction of premature test beats from 47 +/- 2 (mean +/- SEM) msec (control) to 62 +/- 1 msec (p less than 0.001), whereas isoproterenol decreased tau rec to 38 +/- 1 msec (p less than 0.001). In addition, beta-blockade increased the maximum amount of rate-dependent AV nodal fatigue from 7 +/- 1 msec (at a cycle length of 198 +/- 9 msec [control]) to 17 +/- 2 msec (p less than 0.001). In five dogs with decentralized stellate ganglia, tau rec was decreased from 71 +/- 3 msec (control) to 57 +/- 4 msec and 48 +/- 2 msec (p less than 0.001 for each) by left stellate ganglion stimulation at 5 and 10 Hz, respectively. Maximum fatigue was similarly reduced from 16 +/- 1 msec (control) to 12 +/- 2 msec (p = NS) and 8 +/- 1 msec (p less than 0.01), respectively. Stellate ganglion stimulation, isoproterenol, and beta-blockade did not alter AV nodal facilitation. A mathematical model incorporating quantitative indexes of AV nodal function accurately accounted for tachycardia-dependent increases in the atrial-His activation interval, which were enhanced by beta-adrenergic receptor blockade and reduced by isoproterenol. Furthermore, this model showed that beta-adrenergic effects were increased by increasing heart rate, with the majority of the rate-dependent action being due to changes in the time course of AV nodal recovery. We conclude that beta-adrenergic receptor stimulation alters functional properties that govern the AV nodal response to changes in heart rate. These changes in functional properties alter the ability of the AV node to conduct impulses during tachycardia and, as such, could play a major role in the ability of sympathetic stimulation to promote and beta-adrenergic receptor blockade to prevent the occurrence of AV nodal reentrant arrhythmias.

Adrenergic beta-Antagonists↗

Atrial fibrillation in patients with an accessory pathway: importance of the conduction properties of the accessory pathway.

To investigate how the electrophysiologic properties of the accessory pathway affect the occurrence of atrial fibrillation in the Wolff-Parkinson-White syndrome, programmed stimulation data of 57 patients with overt pre-excitation and 33 patients with a concealed accessory pathway with documented circus movement tachycardia were reviewed. Atrial fibrillation had occurred spontaneously in 31 (54%) of the 57 patients with the Wolff-Parkinson-White syndrome and in 1 (3%) of the 33 with a concealed accessory pathway (p less than 0.001). Sustained atrial fibrillation was induced in 23 of 31 patients with the Wolff-Parkinson-White syndrome and spontaneous atrial fibrillation (Group A), in 7 of 26 patients with the Wolff-Parkinson-White syndrome without spontaneous atrial fibrillation (Group B) and in 5 of 33 patients with a concealed accessory pathway (Group C). The anterograde effective refractory period of the accessory pathway was shorter in Group A than in Group B (252 versus 297 ms, p less than 0.001). There were no differences among groups in PA interval, right to left atrium conduction time, cycle length of tachycardia and atrial and retrograde accessory pathway effective refractory period. Atrial fibrillation is more frequent in patients with the Wolff-Parkinson-White syndrome than in those with a concealed accessory pathway. Patients with overt pre-excitation and atrial fibrillation have a shorter anterograde accessory pathway refractory period. It seems therefore that the anterograde rather than the retrograde conduction properties of the accessory pathway are the critical determinants of atrial fibrillation in the Wolff-Parkinson-White syndrome.

Adult↗

Electrophysiologic evaluation and outcome of patients with syncope of unknown origin.

Electrophysiologic studies were performed in 134 patients (87 males, mean age 59 years) with unexplained syncope. Seventy-one patients had organic heart disease (ischaemic in 50). Electrophysiologic studies revealed conduction abnormalities and tachyarrhythmias that could account for syncope in 40 patients (30%). Thirty-seven (93%) of these patients received pacing or antiarrhythmic therapy compared with 23 (24%) of the remaining 94 patients who had a negative study and received empiric therapy (P less than 0.0001). Risk of having an abnormal electrophysiologic study was greater in patients with underlying heart disease (P less than 0.05). During a mean follow-up of 22 +/- 17 months, 26 patients (19%) either had recurrent syncope (22 patients) or died (four patients) suddenly. Men had a higher incidence of recurrent syncope than women (26% vs 6%, P less than 0.005). Other clinical characteristics, electrophysiologic findings, final diagnosis and therapy at discharge were not predictive of outcome. We conclude that (1) 19% of patients investigated for syncope will have a recurrent event, (2) female gender may be an independent predictor of favourable outcome.

Adolescent↗

Ventricular fibrillation in the Wolff-Parkinson-White syndrome.

Ventricular fibrillation (VF) is a well-known but rare complication of the Wolff-Parkinson-White syndrome (WPW). Clinical and electrophysiological data of 23 patients with spontaneous VF were compared with data from 100 consecutive patients with WPW without VF but with symptomatic supraventricular tachycardia. The 23 patients were collected in a multicentre retrospective study in seven European centres. VF occurred in only one patient who was receiving antiarrhythmic drugs, and was the first manifestation of the syndrome in six. No significant differences were found between those with VF and without VF in age, complaints of palpitations, syncope, and presence of structural heart disease. The retrograde effective refractory period of the accessory pathway, the atrial refractory period and the fastest atrial pacing rate with 1:1 anterograde conduction over the accessory pathway were similar in both groups. Significant differences were found for sex, permanent pre-excitation on the electrocardiogram, type of documented supraventricular tachyarrhythmias, shortest RR interval less than or equal to 220 ms during spontaneous atrial fibrillation (AF), inducibility of supraventricular tachycardias, ventricular effective refractory period less than or equal to 190 ms, mean shortest RR interval during induced AF less than or equal to 180 ms and presence of multiple accessory pathways.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗