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Biomedical subjects

M Talajic

Publications and source records attributed to M Talajic.

At least 73 records · Page 4Linked to original sources
PubMed1991

Low energy direct current ablation in patients with the Wolff-Parkinson-White syndrome: clinical outcome according to accessory pathway location.

Forty-five patients with the Wolff-Parkinson-White syndrome underwent direct current (DC) ablation using a low energy power source (Cardiac Recorders). Anodal shocks of 10-40 joules were given to either a 6 French quadripolar catheter (Bard), a 7 French bipolar contoured catheter (Bard), or a 7 French deflectable catheter with a 4-mm distal electrode (Mansfield). The indifferent electrode consisted of a large patch that was positioned under the left scapula. There were 26 males and 19 females, with a mean age of 34 years (range 9-67). Accessory pathways were located in the left free wall in 30 patients (67%) and were posteroseptal in 15 patients (33%). The shortest ventriculoatrial interval during mapping (89 +/- 21 msec), the mean cumulative amount of energy per patient (322 +/- 283 joules), and the mean CK-MB rise (45 +/- 30 units, normal 0-30 units) were not significantly different between both groups. Ablation was successful in 29/30 patients (97%) with a left free-wall accessory pathway, and in 13/15 patients (87%) with a posteroseptal accessory pathway. All three patients with failure of ablation had multiple accessory pathways, and two of these patients had Ebstein's anomaly. Patients with left free-wall and posteroseptal accessory pathways, respectively, differed significantly in terms of: total session time (4.1 +/- 1 hours vs 5.3 +/- 1.3, p = 0.0001), total procedure time for ablation (2.6 +/- 0.8 hours vs 3.2 +/- 1.2, P = 0.02), and fluoroscopy time (46 +/- 24 min vs 64 +/- 29, P = 0.006). In 13 patients (29%) with a concealed accessory pathway, these variables were not significantly different from patients with overt preexcitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Quantitation of dynamic AV nodal properties and application to predict rate-dependent AV conduction.

A number of functional properties of the atrioventricular (AV) node have been described in response to changes in the atrial input rate. The purpose of this study was 1) to develop quantitative descriptors of these properties, and 2) to determine whether they can account for rate-dependent changes in AV nodal conduction. The delay in AV nodal conduction of single premature beats (recovery) was found to be an exponential function of coupling interval with a time constant of 66 +/- 2 (+/- SE) ms. A single abbreviated (facilitation) cycle did not alter the time constant of recovery or basal conduction for a subsequent beat but shifted its recovery curve to the left to an extent exponentially related to the facilitation cycle length. The induction of a tachycardia with HA interval fixed so as to control the recovery and facilitation variables resulted in a first-order onset of AV conduction slowing (fatigue). The fatigue process had a time constant in the range of 70 beats and a magnitude that was a decaying exponential function of HA interval. An equation incorporating quantitative descriptors of recovery, facilitation, and fatigue accurately predicted rate-dependent changes in AH interval. We conclude that 1) the AV nodal properties of recovery, facilitation, and fatigue are amenable to quantitative characterization, and 2) rate-dependent changes in AV nodal conduction time can be well described in terms of these underlying properties.

Animals↗
PubMed1991

In vitro and in vivo effects within the coronary sinus of nonarcing and arcing shocks using a new system of low-energy DC ablation.

DC shocks within the coronary sinus have been abandoned because of the risk of cardiac rupture and tamponade. Catheter ablation using DC energy to electrodes straddling the ostium of the coronary sinus, when used clinically, has been reported to result in cardiac tamponade in as many as 16% of patients. A new system of energy delivery maximizes voltage while decreasing the undesirable effects caused by barotrauma. This system includes 1) a low-energy ablation power supply with a brief time-constant capacitive discharge that delivers up to 40 J and 3,000 V and 2) a low-energy ablation catheter with a contoured distal electrode. We performed in vitro and in vivo studies of this new system and compared arcing shocks with nonarcing shocks. Ablations were performed using unipolar distal shocks (D) and unipolar shocks to both electrodes made electrically common (P-D). In vitro studies were done in a large tank filled with physiological saline while recording voltage, current, and pressure. High-speed cinematography (32,000 frames/sec) of shocks of 10-40 J permitted detailed analysis of the vapor globe. Anodal shocks of less than 20 J showed no arcing or only minimal vapor globe formation. For D and P-D anodal shocks of 40 J, the diameters of the vapor globe were 31 and 22 mm, respectively, corresponding to pressure recordings of 11 and 4.9 atm. The pressure rise lasted less than 50 mu sec. In vivo studies involved 18 dogs that received nonarcing shocks (one to six shocks of 15 J) and 18 dogs that received arcing shocks (one to three shocks of 40 J). Each group was divided between D and P-D shocks; catheter ablation was performed at a mean +/- SEM distance of 2.94 +/- 0.92 cm within the coronary sinus. All dogs tolerated the procedure without cardiac rupture or tamponade. When killed 2-4 days later, the dogs had edema and hyperemia or hemorrhage in the area of the coronary sinus. We compared the effects of multiple (three to six) nonarcing shocks with the effects of one to three arcing shocks. Disruption or rupture of the coronary sinus within the epicardial fat space occurred in two of 12 dogs (17%) with multiple nonarcing shocks but in 13 of 18 dogs (72%) with arcing shocks (p less than 0.003). Occlusion of the coronary sinus occurred in two of 12 dogs (17%) with multiple nonarcing shocks and in nine of 18 dogs (50%) with arcing shocks (p less than 0.06).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Kinetics of use-dependent ventricular conduction slowing by antiarrhythmic drugs in humans.

BACKGROUND: Rate-dependent conduction slowing by class I antiarrhythmic agents has clinically important consequences. Class I drugs are known to produce use-dependent sodium channel blockade. If rate-dependent conduction slowing by class I agents is due to sodium channel blocking actions, the kinetics of conduction slowing should be similar to those of depression of sodium current indexes in vitro. The purpose of the present investigation was to study the onset time course of ventricular conduction slowing caused by a variety of class I agents in humans. METHODS AND RESULTS: Twenty-seven patients undergoing electrophysiological evaluation for antiarrhythmic therapy were studied. Changes in QRS duration at initiation of ventricular pacing at cycle lengths of 400 and 500 msec were used to evaluate the kinetics of drug action. Mean time constants for each drug were similar to values for Vmax depression reported in vitro studies: flecainide, 24.9 +/- 11.6 beats in eight patients (versus 34.5 beats reported for Vmax block); propafenone, 17.8 +/- 6.9 beats in five patients (versus 8.4-20.8 beats); quinidine, 7.0 +/- 2.4 beats in six patients (versus 5.6-6.2 beats); and amiodarone, 3.6 +/- 2.0 beats for eight patients (versus 3.0 beats). Time constants were significantly different among the various drugs tested (p = 0.0002 at a cycle length of 400 msec; p = 0.002 at 500 msec), and there was a strong correlation (r = 0.89, p less than 0.0001) between values obtained at a cycle length of 400 msec and those at a cycle length of 500 msec. No rate-dependent changes in QRS duration were seen at onset of ventricular pacing among eight age- and disease-matched control patients not taking class I antiarrhythmic drugs, including three patients subsequently showing such changes during type I antiarrhythmic drug therapy. CONCLUSIONS: We conclude that class I agents produce use-dependent QRS prolongation in humans with characteristic kinetics for each agent that are similar to the kinetics of Vmax depression in vitro. These results suggest that rate-dependent ventricular conduction slowing by antiarrhythmic drugs in humans is due to use-dependent sodium channel blockade.

Anti-Arrhythmia Agents↗
PubMed1991

A unified model of atrioventricular nodal conduction predicts dynamic changes in Wenckebach periodicity.

The atrioventricular (AV) node responds in a complex fashion to changes in activation rate. A variety of approaches have been used to explain these dynamic AV nodal responses, but none has been able to account fully for AV nodal behavior. Three specific rate-dependent properties of the AV node have been described: 1) time-dependent recovery after excitation, 2) an effect of short cycles to advance recovery ("facilitation"), and 3) a gradual slowing of conduction in response to sustained, high-frequency activation ("fatigue"). We hypothesized that a model incorporating quantitative descriptors of all three processes might be able to account for a wide variety of AV nodal behaviors. Quantitative descriptors of AV nodal recovery, facilitation, and fatigue were developed based on AV nodal conduction changes during selective pacing protocols in seven autonomically blocked dogs. These descriptors were incorporated into a set of mathematical equations that define AV nodal conduction of any beat based on activation history. The equations were then applied to predict pacing-induced Wenckebach periodicity in each dog. Experimental data were obtained after nine to 19 step decreases in atrial cycle length into the Wenckebach zone in each animal. Observed behaviors included complex patterns of block, a progressive increase in the level of block over 5 minutes of rapid pacing, and periods of alternating patterns of block. The model accurately predicted the onset of AV block at each cycle length, the relation between conduction ratio and cycle length as a function of time, and the changing patterns of Wenckebach periodicity during sustained atrial pacing. All three terms of the model equation (describing recovery, facilitation, and fatigue) were essential to account fully for the observed behaviors. Elimination of AV nodal fatigue from the model resulted in failure to account for time-dependent changes in Wenckebach patterns, whereas exclusion of facilitation led to consistent overestimation of the degree of AV block at each cycle length. We conclude that a mathematical model incorporating terms to describe recovery, facilitation, and fatigue accurately predicts a wide range of Wenckebach-type behavior and that complex conduction patterns of the AV node can be fully accounted for by simple functional AV nodal properties.

Animals↗
PubMed1991

The effects of stress, emotion, and behavior on the heart.

The relationships between emotional status, neurohormonal control and the cardiovascular function are reviewed. In the first part of this paper, we reviewed (1) the pathways between brain and heart, physiology of the defense reaction and the role of the autonomic nervous system in the mediation of the effects of stress; (2) the cardiac manifestations of emotional stress, and (3) the role of stress and the influence of circadian variations in the occurrence and development of myocardial ischemia, myocardial infarction and sudden death. In the second part, we discussed the relationship between behavior, coronary heart disease and particularly the role of the so-called type A behavior and hostility. Finally, we emphasize the importance of life-style changes to improve the prognosis of coronary disease and to limit the progression and ultimately to cause a regression of atherosclerosis. Thus, it appears that a transdisciplinary approach associating cardiologists, neuroscientists and behavior scientists will help to devise more effective strategies for the prevention and early therapy of cardiovascular disease.

Animals↗
PubMed1990

Determinants and significance of diltiazem plasma concentrations after acute myocardial infarction. The Multicenter Diltiazem Postinfarction Trial Research Group.

A total of 1,975 plasma diltiazem concentrations were obtained from 1,067 patients enrolled in a multicenter secondary intervention study of diltiazem after acute myocardial infarction. To evaluate the determinants and significance of diltiazem concentrations in this patient population, we related drug concentrations to a variety of clinical variables recorded on the case history forms. Multiple linear regression analysis showed that (1) time from the last drug dose, (2) drug dose taken, (3) patient height (an index of lean body weight), and (4) patient age were important determinants of plasma concentration. For an equivalent dose, plasma diltiazem concentrations in a 75-year-old patient were about double those of a 25-year-old patient. Total weight and drug dose prescribed did not significantly affect plasma concentrations. Whereas drug concentrations were higher (p = 0.01) among patients with left-sided heart failure, they were not altered by renal dysfunction, hepatic disease or beta blockers. Diltiazem concentrations were a significant determinant of diastolic arterial pressure (p less than 10(-9), but neither systolic pressure nor heart rate were significantly related to diltiazem concentration. The overall incidence of adverse experiences was not related to drug concentrations, but the occurrence of second- and third-degree atrioventricular block in the coronary care unit and the need for a temporary pacemaker were substantially higher among patients with a drug concentration greater than 150 ng/ml (7.4 and 1.9%, respectively) than among patients with lower concentrations (2.6% for atrioventricular block, 0.3% for pacemaker; p = 0.02 for each). The risk of atrioventricular block was particularly increased by high diltiazem concentrations in the face of acute inferior infarction. These results suggest that diltiazem's pharmacologic and clinical effects in a large population are concentration-related, and that the consideration of patient size, age, and left ventricular function in selecting a diltiazem dose may allow for effective drug therapy with a reduced likelihood of adverse effects.

Adult↗
PubMed1990

Cycle length alternation during supraventricular tachycardia: occurrence and mechanism in a canine model of AV reentrant tachycardia.

Cycle length alternation (CLA) is commonly observed during supraventricular tachycardia (SVT) onset and termination. The present study was designed to gain insights into the mechanism and potential clinical relevance of CLA by comparing computer simulations of tachycardia to directly observed behavior in a canine model of AV reentrant tachycardia (AVRT). The computer model was based on the hypothesis that CLA is secondary to feedback between AV nodal output during SVT and subsequent AV nodal input, and used the measured anterograde AV nodal recovery curve (AV vs A1A2) to predict sequential AV and RR intervals during SVT. Orthodromic AVRT was created experimentally in 11 open-chested, autonomically-blocked (atropine plus nadolol) dogs using a sensing and pacing circuit that mimicked a retrograde-conducting accessory pathway. Steady-state cycle length and AV interval during experimental AVRT closely paralleled predictions made by the computer model. CLA appeared consistently at the onset of experimental AVRT at programmed VA intervals less than or equal to 100 msec (corresponding to VA less than or equal to 150 msec as measured clinically) in all dogs. The amplitude and duration of CLA increased as the VA interval decreased, and closely paralleled predictions based on the computer model. Abrupt accelerations in atrial pacing to the same rate as AVRT did not result in alternation of cycle length. In conclusion, alternation of cycle length results from feedback between AV nodal output and subsequent AV nodal input at the onset of reentrant supraventricular tachycardia, and does not require changes in autonomic tone or dual AV nodal pathways. CLA occurrence, amplitude, and duration are predictable based on AV node recovery properties, and depend on retrograde conduction properties of the reentrant circuit. The presence of CLA suggests that the AV node is an integral component of the SVT reentry circuit, and may be useful clinically to identify the mechanism of supraventricular tachycardias.

Animals↗
PubMed1990

Electrophysiological effects of alpha-adrenergic stimulation.

Autonomic blockade for in vivo electrophysiological studies generally involves atropine and beta blockers, ignoring the potential role of alpha-adrenergic activity. To evaluate the importance, if any, of alpha-adrenergic tone, the electrophysiological effects of incremental doses of phenylephrine were examined in eight chloralose-anesthetized dogs. In order to study direct effects, all dogs were both beta blocked (with nadolol) and vagally blocked (with the combination of vagotomy and atropine). Results were also obtained after normalization of blood pressure with nitroprusside or the alpha-blocker, prazosin. Phenylephrine caused dose-dependent increases in systolic and diastolic blood pressure. This was accompanied by consistent but modest decreases in sinus cycle length (control RR interval 492 +/- 34 msec vs 459 +/- 29 msec after dose 1 of phenylephrine, P less than 0.05, 516 +/- 41 vs 484 +/- 34 msec control versus dose 2, P less than 0.05). These increases in automaticity were not prevented after normalization of arterial pressure by nitroprusside, but were reversed when concomitant alpha-receptor blockade was achieved with prazosin, suggesting that sinus node acceleration resulted directly from alpha-receptor stimulation. No effects on atrial, AV nodal or His-Purkinje conduction were noted. In addition, phenylephrine did not affect atrial, AV nodal, or ventricular refractoriness. In conclusion, conduction and refractoriness of normal cardiac tissue (other than the sinus node) are unaffected by direct alpha-receptor stimulation. This justifies the use of combined beta and muscarinic blockers to achieve autonomic blockade under most circumstances.

Adrenergic alpha-Agonists↗
PubMed1990

Antiarrhythmic actions of diltiazem during experimental atrioventricular reentrant tachycardias. Importance of use-dependent calcium channel-blocking properties.

The purpose of this study was to determine if the known frequency-dependent effects of diltiazem on inward calcium current result in selective actions during supraventricular tachycardia. These effects were evaluated by use of an experimental model of orthodromic atrioventricular reentrant tachycardia (AVRT). AVRT was induced in 15 dogs over a wide range of retrograde conduction times before and after two doses of diltiazem. Diltiazem produced a tachycardia-related suppression of atrioventricular nodal conduction resulting in greater efficacy for faster than for slower AVRTs. The degree of slowing for tachycardias that remained inducible after diltiazem administration was greater for AVRTs with a rapid initial rate (dose 1, 29%; dose 2, 40%) than for slower AVRTs (dose 1, 11%, p less than 0.01; dose 2, 18%, p less than 0.001). Rate-dependent AVRT slowing occurred because of a time-dependent phase of AH interval prolongation after the onset of tachycardia, which was observed only after diltiazem administration. to further clarify the mechanism of diltiazem's selective actions against faster tachycardias, its effects on the minimum pathway for reentry, or wavelength, were examined in four dogs. The ratio of refractory period to revolution time (RP/RT), an index of wavelength, was measured for each AVRT before and after diltiazem administration. Diltiazem increased the positive slope of the relation between RP/RT and the AVRT rate threefold compared with control (p less than 0.05). This rate-dependent effect prevented AVRT when RP/RT became greater than unity. In conclusion, rate-dependent atrioventricular node depression by diltiazem results in greater tachycardia slowing and higher rates of termination during atrioventricular reentrant tachycardias with faster initial rates and shorter retrograde conduction intervals.

Animals↗
PubMed1990

Effects of flecainide and quinidine on human atrial action potentials. Role of rate-dependence and comparison with guinea pig, rabbit, and dog tissues.

Flecainide and other class IC antiarrhythmic drugs are effective in the prevention and termination of atrial fibrillation, but the mechanism of this action is unknown. To gain insights into potential cellular mechanisms, we evaluated the response of human atrial action potentials to equimolar therapeutic concentrations of flecainide and quinidine and compared this response to that of guinea pig, rabbit, and dog atria. Both compounds reduced Vmax more as activation rate increased, but flecainide was more potent than quinidine and had slower kinetics. The rate-dependence of Vmax reduction was similar for all species, but human tissue was more sensitive to the drugs tested. In contrast to changes in Vmax, drug-induced alterations in action potential duration showed opposite rate-dependence for the two drugs. Quinidine increased action potential duration to 95% repolarization (APD95) in human atria by 33 +/- 7% (mean +/- SD) at a cycle length of 1,000 msec, but this effect was reduced as cycle length decreased, to 12 +/- 4% (p less than 0.001) at a cycle length of 300 msec. Flecainide increased APD95 (by 6 +/- 3%) much less than quinidine at a cycle length of 1,000 msec, but its effect was increased by faster pacing, to 27 +/- 12% at a cycle length of 300 msec and 35 +/- 8% (p less than 0.001) at the shortest 1:1 cycle length. The rate-dependent response of APD to drugs was qualitatively similar but quantitatively different among species. Human tissue showed the greatest frequency-dependent drug effects on repolarization, followed by tissue from dogs and rabbits. Guinea pig atria showed the least (and statistically nonsignificant) rate-dependence of drug effect on APD. Drug-induced changes in refractoriness paralleled those in APD. We conclude that: 1) flecainide and quinidine both increase APD in human atrial tissue but with opposite rate-dependence, 2) the effects of flecainide to increase atrial APD and refractoriness are enhanced by the rapid rates typical of atrial fibrillation, and 3) animal tissues may differ importantly from human in both their sensitivity and rate-dependent response to antiarrhythmic drugs. The salutary response of atrial fibrillation to flecainide may be due to enhancement of drug action by the rapid atrial activation rates characteristic of this arrhythmia.

Action Potentials↗
PubMed1990

Vagal modulation of the rate-dependent properties of the atrioventricular node.

Vagal effects on atrioventricular (AV) nodal conduction are accentuated by increases in heart rate. To establish the mechanism of these rate-dependent negative dromotropic actions, we studied the properties governing AV nodal adaptation to changes in heart rate in chloralose-anesthetized dogs in the absence and presence of bilateral cervical vagal nerve stimulation (20 Hz, 0.2 msec). Stimulation protocols were applied to evaluate the contributions of changes in AV nodal recovery, facilitation, and fatigue independently of each other. Vagal stimulation slowed AV nodal recovery in a voltage-dependent way, increasing the time constant of recovery (tau r) from 80 +/- 7 to 194 +/- 16 msec (mean +/- SEM, p less than 0.01) at the highest voltage studied. The facilitating effect of a premature (A2) beat was manifested by a leftward shift of the recovery curve (A3H3 versus H2A3) of a subsequent A3 beat. The magnitude of shift depended on the A1A2 coupling interval and was reduced by vagal stimulation at all A1A2 intervals (maximum shift: control, 63 +/- 12 msec; vagus, 24 +/- 11 msec; p less than 0.01). When recovery and facilitation were kept constant, abrupt increases in AV nodal activation rate caused a slow (tau = 75 beats) increase in AH interval (fatigue). Vagal stimulation increased the magnitude of this process (maximum: control, 11 +/- 2 msec; vagus, 27 +/- 3 msec; p less than 0.001), without altering its time course. At activation rates comparable to sinus rhythm in humans, vagal stimulation at an intermediate voltage increased the AH interval by 25 msec. As heart rate increased, vagally induced changes in dynamic processes amplified AH prolongation up to fivefold at maximum rate. The role of vagal changes in individual functional properties depended on heart rate, but slowing of recovery was the single most important factor, constituting over 50% of overall vagal action at rapid rates. We conclude that vagal stimulation alters the ways in which the AV node responds to changes in activation rate and that at rapid rates most of the negative dromotropic action of the vagus is due to changes in the AV nodal response to tachycardia. Alterations in rate-dependent AV nodal properties are a novel and potentially important mechanism through which interventions may affect AV nodal conduction.

Animals↗
PubMed1990

Autonomic modulation of the frequency-dependent actions of diltiazem on the atrioventricular node in anesthetized dogs.

Calcium antagonists have rate-dependent effects on atrioventricular node refractoriness in autonomically blocked dogs. Autonomic reflexes can attenuate diltiazem's actions and could alter their frequency-dependence. We evaluated the effects of four steady-state drug concentrations in each of seven dogs with intact autonomic tone, six with muscarinic blockade (atropine) and eight with combined muscarinic and beta adrenergic blockade. Diltiazem depressed atrioventricular nodal function less in autonomically intact dogs than in the other two groups. The concentration-response relationship for increases in Wenckebach cycle length (compared to intact dogs) was twice as steep among dogs with muscarinic blockade (P less than .001) and three times as steep with combined blockade (P less than .001). For an equal dose of diltiazem, the slope of drug-induced refractory period prolongation vs. pacing cycle length was similar (-0.20 +/- 0.11%/msec, mean +/- S.D.) in intact dogs compared to atropinized dogs (-0.21 +/- 0.10%/msec) and dogs with combined blockade (-0.24 +/- 0.14%/msec). Amplification of diltiazem's actions by the rapid atrial rate during atrial fibrillation was associated with increases in mean RR interval which were 8.3 times as large as changes in refractory period produced by the drug at slow heart rates. We conclude: 1) autonomic reflexes reduce diltiazem's effect for any given plasma concentration; 2) changes in vagal tone can play an important role in the autonomic response to diltiazem; and 3) despite altering the magnitude of diltiazem's effects, autonomic mechanisms do not prevent frequency-dependent drug action.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1989

Concentration dependence of class III and beta-adrenergic blocking effects of sotalol in anesthetized dogs.

Sotalol is unique among beta-adrenergic blocking drugs in possessing significant class III antiarrhythmic actions. The present study was designed to assess the relative concentration dependence of beta-blocking and class III actions of sotalol and to relate the findings to concentrations achieved during oral sotalol therapy in humans. Measurements were made in anesthetized dogs under control conditions, and then in the presence of a series of stable sotalol plasma concentrations produced by sequential loading and maintenance infusions. Beta-blocking effects of sotalol, determined by attenuation of the chronotropic actions of isoproterenol, were seen at the lowest dose used. Increases in atrial and ventricular refractory periods (observed in dogs with autonomic blockade to exclude beta-receptor-mediated or reflex autonomic effects) required much larger doses of sotalol. Half-maximal beta-blocking effects occurred at an average sotalol concentration of 0.8 +/- 0.3 mg/liter, an order of magnitude lower than the concentrations required for half-maximal effects on atrial (6.9 +/- 1.2 mg/liter, p less than 0.01) and ventricular (6.8 +/- 2.8 mg/liter, p less than 0.05) refractoriness. These results show that substantially higher concentrations are needed for the class III effects of sotalol than for its beta-blocking action. These pharmacodynamic differences need to be considered in evaluating the antiarrhythmic efficacy and mechanisms of this unusual drug.

Adrenergic beta-Antagonists↗
PubMed1989

Cost-benefit analysis of medical vs surgical treatment of symptomatic patients with accessory atrioventricular pathways.

Surgical treatment of patients with an accessory atrioventricular pathway leading to symptomatic arrhythmias provides effective control. However, surgical treatment is usually considered only when medical treatment fails. To assess the cost-benefit ratio of medical vs surgical treatment 77 patients treated with antiarrhythmic drugs were compared with 50 patients treated surgically. Cost was calculated by considering current costs for drugs, surgery and pacemakers, electrophysiological investigations, outpatient clinic controls, and costs of readmissions because of tachycardia. Mean cost per treated patient and mean cost per successfully treated patient (total cost divided by the number of patient not requiring readmission during follow-up) was respectively 4242 and 6949 US dollars after 56 months for the medically treated group and 10800 and 11250 US dollars for the surgically treated group. A projection of costs demonstrated that costs of medical treatment was the same as costs of surgical treatment after 12.5 years of treatment but a higher number of medically treated patients remain symptomatic. We conclude that surgical treatment of symptomatic patients with accessory pathways has a better cost-benefit ratio than medical treatment and should be considered earlier without waiting for failure for medical treatment.

Adolescent↗