- Email: [email protected]
Effects of adenosine on paroxysmal atrial tachycardia
patients are systemically treated with the anticoagulant drug heparin during the procedure and subsequently treated with oral acetylsalicylic acid or warfarin for variable lengths of time.1-5Thus, the magnitude of the potential risk of systemic embolism and the possible salutary effect of any preventive strategies is unknown. Endocardial application of radiofrequency energy with cathetersresults in a spherical zone of necrosis surrounded by a hemorrhagic area.6,7Pathologic examination of lesion sites in animal models have shown thrombus formation on the endocardium.6,7Jackman et al1 performed transesophagealechocardiography within 72 hours of the ablation procedure in 128 patients and did not find any evidence of thrombus formation at the ablation site in any of the patients. However, they observed thrombi in 3 patients: in the high right atrium, the left atria1 appendage, and on the atrial side of the anterior tricuspid leaflet at a site in contact with a permanent pacemakerlead. Only the thrombus in the high right atrium was believed to be procedure related. All 3 patients were treated with a course of warfarin for an unspecified period of time and were free of subsequentthromboembolic complications. We observed 3 embolic complications in 153patients after ablation on the left side of the heart. These patients were young and otherwise healthy and did not have any other identifiable explanation for thromboembolism. The embolism event rate was 2%, with 95% confidenceintervals of 0 to 4.2%.8 These observations are of concern for several reasons. First, embolic events occurred despite the fact that patients received adequateanticoagulant therapy during the procedure and were treated with 325 mg of acetylsalicylic acid daily for 3 months. Second,embolic events occurred up to 3.5 months after ablation. Third, patients with embolic eventshad had fewer radiofrequency applications with shorter total duration than did other patients. These observations suggest that the risk of systemic embolic complications may be greater than originally thought. It is possible that a larger number of subclinical emboli occurred but were undetected. Furthermore, the risk of embolic complications may not be directly
related to the extent of endocardial damage,but that any endocardial damage or left heart catheter manipulation may predisposeto thromboembolic complications. These observations also suggestthat intraoperative heparin and postoperative acetylsalicylic acid therapy for 3 months may not eliminate the risk of embolic complications. Also, embolic complications occurred up to 3.5 months after ablation, thus raising the question of how long postoperative therapy should continue in order to eliminate the risk of thromboembolism. Although radiofrequency catheter ablation of accessory pathways is very efftcacious and the procedure is well tolerated with a relatively low risk of serious complications, some concern is warranted for ablations in the left heart. The risk of systemic embolism may be quite significant despite heparinization during the procedure and therapy with 325 mg acetylsalicylic acid orally for 3 months. The issue of anticoagulation during ablation and the method and duration of therapy after ablation requires further scrutiny.
1. Jackman WM, Wang X, Friday KJ, Roman CA, Moulton KP, Beckman KJ, McClelland JH, Twidale N, Hazlitt HA, Prior MI, Margolis PD, Calmane JD, Overholt ED, Lazzara R. Catheter ablation of accessory ahioventticular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current. N Engl J Med 1991;324:160-1611. 2. C&ins H, Sousa J, El-Atassi R, Rosenheck S, DeBuitleir M, Kou WH, Kadish AH, Langberg JJ, Morady F. Diagnosis and cure of the Wolff-Parkinson-White syndrome or paroxysmal supravemicular tachycardia during a single electrophysiologic test. N Engl J Med 1991;324:1612-1618. 3. Lesch MD, Van Hare GF, Schamp DJ, Chien W, Lee MA, Griffin JC, Langberg JJ, Cohen TJ, Lurie KG, Scheinman MM. Curative percutaneous catheter ablation using radiofrequency energy for accessory pathways in all locations: results in 100 consecutive patients. JAm Coil Cardiol 1992;19:130313G9. 4. Swartz JF, Tracy CM, Fletcher RD. Radiofrequency endocmlial catheter ablation of accessory atrioventricular pathway atrial insertion sites. Circulation 199287: 481-499. 5. Kuck KH, Schluter M, Geiger M, Siebels J, Duckeck W. Radiofrequency current catheter ablation of accessoty ahioventricular pathways. Lancer 1991;337: 1557-1.561. 6. Hoyt RH, Hung SK, Marcus FI, Ode11 RC. Factors influencing tram-catheter radiofrequency ablation of the myocardium. JAppl Cardiol 1986;1:469-487. 7. Huang SK, Graham AR, Hoyt RH, Ode11RC. Tramcatheter de&cation of the canine left ventricle using radiofrequency energy-a pilot study. Am Heart J 1987;114:42-48. 8. Colton T. Statistics in Medicine. Boston: Little, Brown, 1974: 160.
Effects of Adenosine on Paroxysmal
Atrial Tachycardia
I-Chang Hsieh, MD, San-Jou Yeh, MD, Ming-Shien Wen, MD, Chun-Chieh Wang, MD, Fun-Chung Lin, MD, and Delon Wu, MD aroxysmal tachycardia originating from the atrium is P an uncommon but well-recognized entity.’ The focus may arise from the sinus node, the perinodal area,or oth-
ever, the definitive mechanisms responsible for paroxysmal atial tachycardia remain unsettled. Adenosine has been shown to be a useful therapeutic agent and a valuer parts of the right or left atrium. Reentry,triggered auto- able diagnostic tool in certain forms of supraventricular maticity, or abnormal automaticity have been implied as and ventricular tachycardias.3,4Adenosine has been being operative in paroxysmal atrial tachycardia.2How- shown to be capableof terminating paroxysmal or incessant atrial tachycardia in 3 previously reported cases.5-7 In this study, we report the effect of adenosine triphosFrom the 2nd Section of Cardiology, Department of Medicine, Chang Gung Memorial Host&al, Chang Gung Medical College. Taioei. Taiphate on paroxysmal atrial tachycardia that was wan-This report w&supported% parfby Grants NSC%-04lkl!%182inducible and terminable by programmed stimulation. 022 and NSC82-0115-B 182-08 1 from the National Science Council, and Grant DOH83-HR.205 from the National Health Institute of the Republic of China, Taipei, Taiwan. Manuscript received December 7, 1993; revised manuscript received January 14, 1994, and accepted January 15.
The study group consisted of 15 patients (6 men and 9 women, aged 19 to 79 years [mean f SD, 51 f 91). All had clinical documentation of paroxysmal supravenBRIEFREPORTS 279
ATF’ 10 mg ,,,,,,,,,,,,,,,,,,,,,,,,rllllllrlllrllllrrlllllllllllllllIlilllllllllllllllilllllllllllllllllllllllll L A I-
AVF h
A
A
A
A
360 “. 390 I A
A
A
h,
360 1. $30 _.
PlGURE 1. Termination of paroxysmal atrial tachycardia after intravenous bolus of 10 mg adenosine triphosphate (ATP) in 1 patient. Note atrioventricular nodal Wenckebach block with minor irregularity of the tachycardia cycle length occurring before termination. A q low septal right atrial response during sinus rhythm; Ae q low septal right atrial response during tachycardia; HBE q His bundle electrogram; HRA and BB q atrial electrogram recorded from high right atrium and coronary sinus.
tricular tachycardia. Three patients presented with syncope or near syncope, 8 with dizziness, and others with palpitation during attacks of tachycardia. Threepatients had known structural heart disease: I with pulmonic stenosisand severetricuspid regurgitation, 1 with anomalous drainage of the inferior vena cava to the high right atrium at the junction of superior vena cava and the right atrium, and another with dextrocardia. Four of the 5 patients subject to treadmill exercisetesting hadprovocable atria1 tachycardia. Verapamil 5 to 10 mg given intravenously terminated the spontaneoustachycardia in 5 of the 8 patients when this agent was administered in the emergencyroom. All 15 patients underwent a complete electrophysiologic study after giving informed written consent and after discontinuance of cardioactive drugs for 23 half lives. The stimulation protocol included incremental atria1 pacing, and single or double extrastimulus testing during sinus rhythm, and at an atrial driven cycle lengthfiom the high right atrium. Diagnosis of an atria1 origin of an induced tachcyardia was based on previously described criteria that exclude atrioventricular node reentry tachycardia or atrioventricular reentry tachycardia incorporating an accessorypathway.‘a2If sustained tachycardia could not be induced, isoproterenol I to 4 pglmin was infused intravenously to achievea 20% increase in sinus rate, andprogrammed stimulation was repeated during isoproterenol infusion. After induction of sustained tachycardia, mapping within both right and left atria was performed to locate the earliest activation site. Entrainment study was conducted using incremental atria1 pacing starting at a cycle length slightly shorter than that of tachycardia. Termination of tachycardia was then attempted by delivery of single or double atria1 extrastimulus, or a short burst of rapid atrialpacing. On successfultermination, sustained atria1 tachycardia was induced once again. This time, intravenous adenosine triphosphate was administered through an intravenous catheter positioned at the superior vena cava in incremental doses,from 2.5 to 30 mg maximum (if tolerated by patient) or until a positive 280
THE AMERICANJOURNALOF CARDIOLOGY@ VOLUME74
responsewas noted. A positive responsewas defined as slowing with a >20% increment of cycle length or termination of tachycardia occurring within 30 secondsof the bolus administration. When a positive responsewas observed, sustained atria1 tachycardia was induced at least one more time and adenosine administration repeated to ensure result reproducibility. Tenpatients had induction of sustained atria1 tachycardia during baseline study, 3 had induction of sustained tachycardia during isoproterenol, and 2 had incessant tachycardia. None had a P-wave cor@guration, atria1 electrogram morphology, or atria1 activation sequenceduring tachycardia that were identical to those during sinus rhythm. The tachycardia was terminable with programmed stimulation in all 15 patients; however, it resumedspontaneously in the 2 patients with incessant tachycardia. In the 13 patients with inducible atrial tachycardia, there was no correlation betweenthe$rst coupling interval of tachycardia and the coupling interval of the atria1 extrastimulus that initiated the tachycardia. There also was no correlation betweenthe tachycardia cycle length and the cycle length of the rapid atria1 pacing that induced tachycardia. Thesejmdings argue against triggered automaticity as being operative in thesepatients. The earliest atria1 activation site was noted to occur at the high right atrium in 4 patients, midposterior right atrium in 2, midlateral right atrium in I, low posterior septal right atrium in 5, and left atrium in 3. The cycle length of tachycardia ranged from 330 to 480 ms (mean f SD, 393 I!I 56) in these 15 patients. Entrainment of tachycardia could not be demonstrated in any of the 15 patients with overdrive incremental atria1 pacing during tachycardia, and none exhibited an area of slow conduction with fragmentation of the atria1 electrogram. TheseJindings do not favor a mechanismof intraatrial reentry to be operating in these patients. A positive responsewith termination of tachycardia to the bolus administration of adenosine triphosphate was noted in 13 patients (Figures 1 and 2). In these 13 patients, the tachycardia terminated in 9.6 f AUGUST 1, 1994
ATP 5 rW ~1111111111111111111lliifllllllllllllllllliltlllllllllllllllllllflilllllllllllllilllllllllllllllllllllll~llllllllllllllillll~lllllllllllllllllllfllillllll1llillllllflll
AVF fl Vl HRA’--’
*-
w
Ig
.rwrYrWvr
” ;
540
RGURE 2. Termination of paroxysmal atrial tachycardia (ATP) in another patient. LSRA = low septal right atrial
after intravenous response.
5.2 seconds (range 4 f 22) after drug administration. Three of the 13 patients exhibited slowing of tachycardia and 5 demonstrated second-degreeatrioventricular block before termination of tachycardia. The mean dose required was 6 + 2 mg (range 2.5 + 10). In the other 2 patients, 1 displayed a transient lengthening of tachycardia cycle length from 360 to 480 ms and the other exhibited no response to adenosine. Both patients displayed transient second-degreeatrioventricular block. Adenosine has a negative chronotropic effect on the sinus node and a negative dromotropic effect on the atrioventricular node. It causeshyperpolarization of the resting membranepotential toward the potassium equilibrium potential and shortening of action potential duration by increasing the potassium conductance in atrial myocytes.* It has no known direct effect on adult ventricular tissues or Purkinje fibers. However, it reduces intracelhtlar cyclic adenosine monophosphate and thus suppressesP-adrenergic-mediated triggered activities in ventricular myocytes or Purkinje tissues. With these unique properties, adenosinehas been thought to be useful in differentiating tachycardias of various mechanisms.3,4A previous study has demonstrated ineffectiveness of adenosineon intraatrial reentry tachycardia.3 In contrast, our study shows slowing and termination of paroxysmal atrial tachycardia in response to adenosine administration. The difference in outcome between these 2 studies may well reflect the heterogenousnature of the so-called “intraatrial reentry tachycardia,” implying several different operative mechanisms.In our patients, the tachycardias were electrically inducible and terminable and were frequently exercise-provocable and verapamilresponsive. However, on the basis of our data and current knowledge, we are still unable to deduce whether
w
A
A
A.
*
”
V
=
bolus
of 5 mg adenosine
triphosphate
the paroxysmal atrial tachycardia in our patients resulted from intraatrial reentry or from triggered automaticity. Both intraatrial reentry tachycardia incorporating partially depolarized atrial tissue with a depressedfast action potential and atrial tachycardia due to P-adrenergic-mediated triggered activities can be expected to respond to adenosine. In conclusion, adenosine is effective in terminating paroxysmal atria1 tachycardia that is electrically inducible and terminable. Because both reentry and triggered automaticity could be operative in this arrhythmia, “adenosine-sensitive paroxysmal atria1 tachycardia” would be a better descriptive term for this form of arrhythmia.
1. Wu D, Am&-y-Leon F, Denes P, Dhmgm R, Pietras R.J, Rosen KM. Demonstration of sustained sinus and auial m-entry as a mechanism of paroxysmal supraventricular tachycardia. Circulation 1975;51:234-243. 2. Wu D, Denes P, Amat-y-Leon F, Dhingra R, Wyndham CRC, Bauemfeind R, Latif P, Rosen KM. Clinical electrocardiographic and electrophysiologic observation in patients with paroxysmal supravenhicular tachycardia. Am .I Cardiol 1978; 41:1045-1051. 3. DiMarco JP, Sellers TD, Lerman BB, Greenberg ML, Beme RM, Belardinelli L. Diagnostic and therapeutic use of adenosine in patients with supraventricular tachyarrhytbmias. .I Am Coil Cardiol 1985;6:417425. 4. Lerman BB. Response of nonreentrant catecholamine-mediated ventricular tachycardia to endogenous adenosine and acetylcholine: evidence for myocardial receptar-mediated effects. Circulation 1993;87:382-390. 1. Tajima T, Muramatsu T, Kanak S, Yanagisbita Y, Dohi Y. Intravenous adenosine hiphosphate discdimn: its efficacy and electmphysiologic effects on patients with paroxysmal supraventicular tachycanlias. PACE 1986;9:401410. 6. Perelman MS, Kri!der DM. Termination of focal atrial tachycardia by adenosine hiphosphate. Br Heart J 1987;58:528-530. 7. Sharma A, Klein G, Yee R. Intravenous adenosine triphosphate during wide QRS complex tachycardia: safety, therapeutic efficacy, and diagnostic utility. An J Med 1990;88:337-343. 8. Belardinelli L, Isenberg G. Isolated atrial myocytes: adenosine and acetylcholine increase potassium conductance. Am J Physiol 1983;224:H734-H737,
BRIEFREPORTS 281
related to the extent of endocardial damage,but that any endocardial damage or left heart catheter manipulation may predisposeto thromboembolic complications. These observations also suggestthat intraoperative heparin and postoperative acetylsalicylic acid therapy for 3 months may not eliminate the risk of embolic complications. Also, embolic complications occurred up to 3.5 months after ablation, thus raising the question of how long postoperative therapy should continue in order to eliminate the risk of thromboembolism. Although radiofrequency catheter ablation of accessory pathways is very efftcacious and the procedure is well tolerated with a relatively low risk of serious complications, some concern is warranted for ablations in the left heart. The risk of systemic embolism may be quite significant despite heparinization during the procedure and therapy with 325 mg acetylsalicylic acid orally for 3 months. The issue of anticoagulation during ablation and the method and duration of therapy after ablation requires further scrutiny.
1. Jackman WM, Wang X, Friday KJ, Roman CA, Moulton KP, Beckman KJ, McClelland JH, Twidale N, Hazlitt HA, Prior MI, Margolis PD, Calmane JD, Overholt ED, Lazzara R. Catheter ablation of accessory ahioventticular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current. N Engl J Med 1991;324:160-1611. 2. C&ins H, Sousa J, El-Atassi R, Rosenheck S, DeBuitleir M, Kou WH, Kadish AH, Langberg JJ, Morady F. Diagnosis and cure of the Wolff-Parkinson-White syndrome or paroxysmal supravemicular tachycardia during a single electrophysiologic test. N Engl J Med 1991;324:1612-1618. 3. Lesch MD, Van Hare GF, Schamp DJ, Chien W, Lee MA, Griffin JC, Langberg JJ, Cohen TJ, Lurie KG, Scheinman MM. Curative percutaneous catheter ablation using radiofrequency energy for accessory pathways in all locations: results in 100 consecutive patients. JAm Coil Cardiol 1992;19:130313G9. 4. Swartz JF, Tracy CM, Fletcher RD. Radiofrequency endocmlial catheter ablation of accessory atrioventricular pathway atrial insertion sites. Circulation 199287: 481-499. 5. Kuck KH, Schluter M, Geiger M, Siebels J, Duckeck W. Radiofrequency current catheter ablation of accessoty ahioventricular pathways. Lancer 1991;337: 1557-1.561. 6. Hoyt RH, Hung SK, Marcus FI, Ode11 RC. Factors influencing tram-catheter radiofrequency ablation of the myocardium. JAppl Cardiol 1986;1:469-487. 7. Huang SK, Graham AR, Hoyt RH, Ode11RC. Tramcatheter de&cation of the canine left ventricle using radiofrequency energy-a pilot study. Am Heart J 1987;114:42-48. 8. Colton T. Statistics in Medicine. Boston: Little, Brown, 1974: 160.
Effects of Adenosine on Paroxysmal
Atrial Tachycardia
I-Chang Hsieh, MD, San-Jou Yeh, MD, Ming-Shien Wen, MD, Chun-Chieh Wang, MD, Fun-Chung Lin, MD, and Delon Wu, MD aroxysmal tachycardia originating from the atrium is P an uncommon but well-recognized entity.’ The focus may arise from the sinus node, the perinodal area,or oth-
ever, the definitive mechanisms responsible for paroxysmal atial tachycardia remain unsettled. Adenosine has been shown to be a useful therapeutic agent and a valuer parts of the right or left atrium. Reentry,triggered auto- able diagnostic tool in certain forms of supraventricular maticity, or abnormal automaticity have been implied as and ventricular tachycardias.3,4Adenosine has been being operative in paroxysmal atrial tachycardia.2How- shown to be capableof terminating paroxysmal or incessant atrial tachycardia in 3 previously reported cases.5-7 In this study, we report the effect of adenosine triphosFrom the 2nd Section of Cardiology, Department of Medicine, Chang Gung Memorial Host&al, Chang Gung Medical College. Taioei. Taiphate on paroxysmal atrial tachycardia that was wan-This report w&supported% parfby Grants NSC%-04lkl!%182inducible and terminable by programmed stimulation. 022 and NSC82-0115-B 182-08 1 from the National Science Council, and Grant DOH83-HR.205 from the National Health Institute of the Republic of China, Taipei, Taiwan. Manuscript received December 7, 1993; revised manuscript received January 14, 1994, and accepted January 15.
The study group consisted of 15 patients (6 men and 9 women, aged 19 to 79 years [mean f SD, 51 f 91). All had clinical documentation of paroxysmal supravenBRIEFREPORTS 279
ATF’ 10 mg ,,,,,,,,,,,,,,,,,,,,,,,,rllllllrlllrllllrrlllllllllllllllIlilllllllllllllllilllllllllllllllllllllllll L A I-
AVF h
A
A
A
A
360 “. 390 I A
A
A
h,
360 1. $30 _.
PlGURE 1. Termination of paroxysmal atrial tachycardia after intravenous bolus of 10 mg adenosine triphosphate (ATP) in 1 patient. Note atrioventricular nodal Wenckebach block with minor irregularity of the tachycardia cycle length occurring before termination. A q low septal right atrial response during sinus rhythm; Ae q low septal right atrial response during tachycardia; HBE q His bundle electrogram; HRA and BB q atrial electrogram recorded from high right atrium and coronary sinus.
tricular tachycardia. Three patients presented with syncope or near syncope, 8 with dizziness, and others with palpitation during attacks of tachycardia. Threepatients had known structural heart disease: I with pulmonic stenosisand severetricuspid regurgitation, 1 with anomalous drainage of the inferior vena cava to the high right atrium at the junction of superior vena cava and the right atrium, and another with dextrocardia. Four of the 5 patients subject to treadmill exercisetesting hadprovocable atria1 tachycardia. Verapamil 5 to 10 mg given intravenously terminated the spontaneoustachycardia in 5 of the 8 patients when this agent was administered in the emergencyroom. All 15 patients underwent a complete electrophysiologic study after giving informed written consent and after discontinuance of cardioactive drugs for 23 half lives. The stimulation protocol included incremental atria1 pacing, and single or double extrastimulus testing during sinus rhythm, and at an atrial driven cycle lengthfiom the high right atrium. Diagnosis of an atria1 origin of an induced tachcyardia was based on previously described criteria that exclude atrioventricular node reentry tachycardia or atrioventricular reentry tachycardia incorporating an accessorypathway.‘a2If sustained tachycardia could not be induced, isoproterenol I to 4 pglmin was infused intravenously to achievea 20% increase in sinus rate, andprogrammed stimulation was repeated during isoproterenol infusion. After induction of sustained tachycardia, mapping within both right and left atria was performed to locate the earliest activation site. Entrainment study was conducted using incremental atria1 pacing starting at a cycle length slightly shorter than that of tachycardia. Termination of tachycardia was then attempted by delivery of single or double atria1 extrastimulus, or a short burst of rapid atrialpacing. On successfultermination, sustained atria1 tachycardia was induced once again. This time, intravenous adenosine triphosphate was administered through an intravenous catheter positioned at the superior vena cava in incremental doses,from 2.5 to 30 mg maximum (if tolerated by patient) or until a positive 280
THE AMERICANJOURNALOF CARDIOLOGY@ VOLUME74
responsewas noted. A positive responsewas defined as slowing with a >20% increment of cycle length or termination of tachycardia occurring within 30 secondsof the bolus administration. When a positive responsewas observed, sustained atria1 tachycardia was induced at least one more time and adenosine administration repeated to ensure result reproducibility. Tenpatients had induction of sustained atria1 tachycardia during baseline study, 3 had induction of sustained tachycardia during isoproterenol, and 2 had incessant tachycardia. None had a P-wave cor@guration, atria1 electrogram morphology, or atria1 activation sequenceduring tachycardia that were identical to those during sinus rhythm. The tachycardia was terminable with programmed stimulation in all 15 patients; however, it resumedspontaneously in the 2 patients with incessant tachycardia. In the 13 patients with inducible atrial tachycardia, there was no correlation betweenthe$rst coupling interval of tachycardia and the coupling interval of the atria1 extrastimulus that initiated the tachycardia. There also was no correlation betweenthe tachycardia cycle length and the cycle length of the rapid atria1 pacing that induced tachycardia. Thesejmdings argue against triggered automaticity as being operative in thesepatients. The earliest atria1 activation site was noted to occur at the high right atrium in 4 patients, midposterior right atrium in 2, midlateral right atrium in I, low posterior septal right atrium in 5, and left atrium in 3. The cycle length of tachycardia ranged from 330 to 480 ms (mean f SD, 393 I!I 56) in these 15 patients. Entrainment of tachycardia could not be demonstrated in any of the 15 patients with overdrive incremental atria1 pacing during tachycardia, and none exhibited an area of slow conduction with fragmentation of the atria1 electrogram. TheseJindings do not favor a mechanismof intraatrial reentry to be operating in these patients. A positive responsewith termination of tachycardia to the bolus administration of adenosine triphosphate was noted in 13 patients (Figures 1 and 2). In these 13 patients, the tachycardia terminated in 9.6 f AUGUST 1, 1994
ATP 5 rW ~1111111111111111111lliifllllllllllllllllliltlllllllllllllllllllflilllllllllllllilllllllllllllllllllllll~llllllllllllllillll~lllllllllllllllllllfllillllll1llillllllflll
AVF fl Vl HRA’--’
*-
w
Ig
.rwrYrWvr
” ;
540
RGURE 2. Termination of paroxysmal atrial tachycardia (ATP) in another patient. LSRA = low septal right atrial
after intravenous response.
5.2 seconds (range 4 f 22) after drug administration. Three of the 13 patients exhibited slowing of tachycardia and 5 demonstrated second-degreeatrioventricular block before termination of tachycardia. The mean dose required was 6 + 2 mg (range 2.5 + 10). In the other 2 patients, 1 displayed a transient lengthening of tachycardia cycle length from 360 to 480 ms and the other exhibited no response to adenosine. Both patients displayed transient second-degreeatrioventricular block. Adenosine has a negative chronotropic effect on the sinus node and a negative dromotropic effect on the atrioventricular node. It causeshyperpolarization of the resting membranepotential toward the potassium equilibrium potential and shortening of action potential duration by increasing the potassium conductance in atrial myocytes.* It has no known direct effect on adult ventricular tissues or Purkinje fibers. However, it reduces intracelhtlar cyclic adenosine monophosphate and thus suppressesP-adrenergic-mediated triggered activities in ventricular myocytes or Purkinje tissues. With these unique properties, adenosinehas been thought to be useful in differentiating tachycardias of various mechanisms.3,4A previous study has demonstrated ineffectiveness of adenosineon intraatrial reentry tachycardia.3 In contrast, our study shows slowing and termination of paroxysmal atrial tachycardia in response to adenosine administration. The difference in outcome between these 2 studies may well reflect the heterogenousnature of the so-called “intraatrial reentry tachycardia,” implying several different operative mechanisms.In our patients, the tachycardias were electrically inducible and terminable and were frequently exercise-provocable and verapamilresponsive. However, on the basis of our data and current knowledge, we are still unable to deduce whether
w
A
A
A.
*
”
V
=
bolus
of 5 mg adenosine
triphosphate
the paroxysmal atrial tachycardia in our patients resulted from intraatrial reentry or from triggered automaticity. Both intraatrial reentry tachycardia incorporating partially depolarized atrial tissue with a depressedfast action potential and atrial tachycardia due to P-adrenergic-mediated triggered activities can be expected to respond to adenosine. In conclusion, adenosine is effective in terminating paroxysmal atria1 tachycardia that is electrically inducible and terminable. Because both reentry and triggered automaticity could be operative in this arrhythmia, “adenosine-sensitive paroxysmal atria1 tachycardia” would be a better descriptive term for this form of arrhythmia.
1. Wu D, Am&-y-Leon F, Denes P, Dhmgm R, Pietras R.J, Rosen KM. Demonstration of sustained sinus and auial m-entry as a mechanism of paroxysmal supraventricular tachycardia. Circulation 1975;51:234-243. 2. Wu D, Denes P, Amat-y-Leon F, Dhingra R, Wyndham CRC, Bauemfeind R, Latif P, Rosen KM. Clinical electrocardiographic and electrophysiologic observation in patients with paroxysmal supravenhicular tachycardia. Am .I Cardiol 1978; 41:1045-1051. 3. DiMarco JP, Sellers TD, Lerman BB, Greenberg ML, Beme RM, Belardinelli L. Diagnostic and therapeutic use of adenosine in patients with supraventricular tachyarrhytbmias. .I Am Coil Cardiol 1985;6:417425. 4. Lerman BB. Response of nonreentrant catecholamine-mediated ventricular tachycardia to endogenous adenosine and acetylcholine: evidence for myocardial receptar-mediated effects. Circulation 1993;87:382-390. 1. Tajima T, Muramatsu T, Kanak S, Yanagisbita Y, Dohi Y. Intravenous adenosine hiphosphate discdimn: its efficacy and electmphysiologic effects on patients with paroxysmal supraventicular tachycanlias. PACE 1986;9:401410. 6. Perelman MS, Kri!der DM. Termination of focal atrial tachycardia by adenosine hiphosphate. Br Heart J 1987;58:528-530. 7. Sharma A, Klein G, Yee R. Intravenous adenosine triphosphate during wide QRS complex tachycardia: safety, therapeutic efficacy, and diagnostic utility. An J Med 1990;88:337-343. 8. Belardinelli L, Isenberg G. Isolated atrial myocytes: adenosine and acetylcholine increase potassium conductance. Am J Physiol 1983;224:H734-H737,
BRIEFREPORTS 281