A new algorithm to determine complete isthmus conduction block after radiofrequency catheter ablation for typical atrial flutter

TABLE III Social Class and Overcrowding in Childhood According to Coronary Artery Disease and Serology Normal Coronary Arteries (n 5 97)

Abnormal Coronary Arteries (n 5 391)

H. pylori Negative (n 5 32)

H. pylori Positive (n 5 65)

H. pylori Negative (n 5 105)

H. pylori Positive (n 5 286)

13 (41%) 9 (28%)

39 (60%) 34 (52%)†

54 (51%) 48 (46%)

186 (65%)* 138 (48%)

Social class IV/V .7 In house in childhood

*OR 1.8 (95% CI 1.11–2.87) within group with abnormal coronary arteries; p 5 0.016. † OR 2.8 (95% CI 1.13– 6.97) within group with normal coronary arteries, p 5 0.02. Numbers are percentages within each H. pylori group rounded to the nearest numeral.

1. NIH Consensus Development panel. Helicobacter pylori in peptic ulcer

disease. JAMA 1994;272:65– 69. 2. Muhlestein JB, Hammond EH, Carlquist JF, Radicke E, Thomson MJ, Karagounis CA, Woods ML, Anderson JL. Increased incidence of Chlamydia species within the coronary arteries of patients with symptomatic atherosclerotic versus other forms of cardiovascular disease. J Am Coll Cardiol 1996;27:1555–1561. 3. Mendall MA, Goggin PM, Molineaux N, Levy J, Toosy T, Strachan D, Camm AJ, Northfield TC. Relation of Helicobacter pylori and coronary heart disease. Br Heart J 1994;71:437– 439. 4. Patel P, Mendall MA, Carrington D, Strachan DP, Leatham E, Molineaux N, Levy J, Blakeston C, Seymor CA, Camm AJ, Northfield TC. Association of Helicobacter pylori and Chlamydia pneumoniae infections with coronary heart disease and cardiovascular risk factors. Br Med J 1995;311:711–714. 5. Murray LJ, Bamford KB, O’Reilly DPJ, McCrum E, Evans AE. Helicobacter pylori infection: relation with cardiovascular risk factors, ischemic heart disease and social class. Br Heart J 1995;74:497–501. 6. Whincup PH, Mendall MA, Perry IJ, Strachan DP, Walker M. Prospective relations between Helicobacter pylori infection, coronary heart disease, and stroke in middle aged men. Heart 1996;75:568 –572. 7. Niemela¨ S, Karttunen T, Korhonen T, La¨a¨ra¨ E, Karttunen R, Ika¨heimo M, Kesaniemi YA. Could Helicobacter pylori infection increase the risk of

coronary heart disease by modifying serum lipid concentrations? Heart 1996; 75: 573–575. 8. Nieto FJ, Adam E, Sorlie P, Farzadegan H, Melnick JL, Comstock GW, Szklo M. Cohort study of cytomegalovirus infection as a risk factor for carotid intimalmedial thickening, a measure of subclinical atherosclerosis. Circulation 1996;94: 922–927. 9. Mendall MA, Goggin PM, Molineaux N, Levy J, Toosy T, Strachan D, Northfield TC. Childhood living conditions and Helicobacter pylori seropositivity in adult life. Lancet 1992;339:896 – 897. 10. Pocock SJ, Shaper AG, Cook DG, Phillips AN, Walker M. Social class differences in ischemic heart disease in British men. Lancet 1987;2:197–201. 11. Whitaker CJ, Dubiel AJ, Galpin OP. Social and geographical risk factors in Helicobacter pylori infection. Epidemiol Infect 1993;111:63–70. 12. Rose GA. The diagnosis of ischemic heart pain and intermittent claudication in field surveys. Bull World Health Organ 1962;27:645– 658. 13. Rathbone B, Martin D, Stephens J, Thompson JR, Samani NJ. Helicobacter pylori seropositivity in subjects with acute myocardial infarction. Heart 1996; 76:308 –311. 14. Ponzetto A, La Rovere MT, Sanseverino P, Bazzoli F. Association of Helicobacter pylori infection with coronary heart disease: study confirms previous findings [letter]. Br Med J 1996;312:251.

A New Algorithm to Determine Complete Isthmus Conduction Block After Radiofrequency Catheter Ablation for Typical Atrial Flutter Robert Johna,

MD,

Lars Eckardt, MD, Thomas Fetsch, MD, Gu¨nter Breithardt, Martin Borggrefe, MD

he induction of a complete conduction block at the subeustachian isthmus between the tricuspid annulus T and inferior vena cava has been shown to be an excellent predictor for lack of arrhythmia recurrence after radiofrequency catheter ablation for common (counterclockwise) or reverse common (clockwise) atrial flutter.1–3 A complete isthmus conduction block is generally assumed if the low lateral right atrial activation sequence is reversed during coronary sinus pacing and the interatrial septal activation sequence is reversed during low lateral right atrial pacing. The development of a complete isthmus block is associated with prolongation both of proximal coronary sinus to low lateral right atrium and low From the Department of Cardiology and Angiology, Hospital of the Westfa¨lische Wilhelms-Universita¨t, and Institute of Arteriosclerosis Research, Mu¨nster, Germany. This study was supported in part by the Franz Loogen Foundation, Du¨sseldorf, Germany. Dr. Johna’s address is: Westfa¨lische Wilhelms-Universita¨t, Innere Medizin C, D-48129 Mu¨nster, Germany. E-mail:[email protected]. Manuscript received November 16, 1998; revised manuscript received and accepted February 1, 1999.

1666

©1999 by Excerpta Medica, Inc. All rights reserved.

MD,

and

lateral right atrium to proximal coronary sinus conduction times, but no single cutoff value exists.4 We validated a new algorithm incorporating the individual flutter cycle length (CLAFl) to determine complete isthmus conduction block.5 •••

Fifty consecutive patients (43 men and 7 women, age 59 6 10 years, 34 without structural heart disease, 10 with coronary artery disease, 3 with dilated cardiomyopathy, 2 after closure of an atrial septal defect, and 1 with hypertrophic cardiomyopathy) with sustained or paroxysmal common or reverse common isthmus-dependent atrial flutter undergoing catheter ablation were included in the evaluation. Antiarrhythmic drugs other than amiodarone were discontinued at least 5 half-lives before the procedure. By means of femoral and right internal jugular venous approaches, a 4Fr bipolar catheter was placed in the right ventricular apex, a 6Fr quadripolar catheter was positioned in the coronary sinus with the proximal electrode pair at 0002-9149/99/$–see front matter PII S0002-9149(99)00176-9

FIGURE 1. Measurement of isthmus conduction times before and after isthmus ablation. CT 5 christa terminalis; CT1 5 conduction time across isthmus; CT2 5 conduction time over roof of right atrium; ER 5 eustachian ridge; IVC 5 inferior vena cava; LLRA 5 low lateral right atrium; PCS 5 proximal coronary sinus; SVC 5 superior vena cava.

TABLE I Conduction Times Across Isthmus Before/After Isthmus Ablation Before Ablation Isthmus Block Complete (n 5 32) Partial (n 5 11) None (n 5 4) All (n 5 47)

D (ms)*

CT1 (ms) 88 76 83 84

6 6 6 6

19 11 10 17

(55–150) (60–90) (70–90) (55–150)

After Ablation

258 266 250 259

6 6 6 6

24 22 34 24

(2100–225) (2110–245) (2100–230) (2110–225)

CT2 (ms)

D (ms)

156 6 20 (125–200) 102 6 10 (85–120) 88 6 13 (70–100)

13 6 10 (0–30) 238 6 18 (275–220) 245 6 37 (2100–220)

*CT1 was taken instead of CT2 for the preablation D (2 z CT1 2 CLAFl).

the coronary sinus os, and a 7Fr Halo catheter with 10 electrode pairs along the lateral right atrium. A 7Fr deflectable-tip 4-mm electrode catheter (Osypka GmbH, Rheinfelden, Germany, or Cordis/Webster Inc., Cordis Webster, Baldwin Park, California) was used for mapping and ablation. At the beginning of the study, 24 patients were in sinus rhythm, 21 in common atrial flutter, and 5 in reverse common atrial flutter; no attempt was made to induce atrial flutter or to terminate flutter by pacing maneuvers. Before radiofrequency pulses were delivered, the mapping catheter was positioned immediately lateral to the future ablation line in the low lateral right atrium, and conduction time across the subeustachian isthmus (CT1) was determined as follows: CT1 was the activation time from low lateral right atrium to proximal coronary sinus (patients in common flutter, Figure 1a), or the activation time from proximal coronary sinus to low lateral right atrium (patients in reverse common flutter, not shown in diagram). If the patient was in sinus rhythm (Figure 1b), the conduction time from proximal coronary sinus to low lateral right atrium during coronary sinus pacing at a cycle length of 400 ms was taken. Radiofrequency pulses were then directed to the isthmus along a line extending from the tricuspid annulus to the inferior vena cava in the left anterior oblique plane (angle 60°) until atrial flutter terminated, the low lateral right atrial activation sequence during coronary sinus pacing reversed, and unidirectional block was excluded. The ablation procedure was aborted if a total fluoroscopy time of 90 minutes was reached, patient discomfort did not allow continuation, or if atrial fibrillation occurred. Then the mapping catheter was moved precisely to the previous position immediately lateral to the ablation line and the conduction time

between proximal coronary sinus and the mapping catheter (CT2) was measured again at a cycle length of 400 ms (Figure 1c). The isthmus conduction at the end of the study was classified as “complete block” (reversal of low lateral right atrial activation sequence during coronary sinus pacing, exclusion of unidirectional block), “partial block” (conduction slowing but no reversal: CT2 2 CT1 .20 ms), “no block” (CT2 2 CT1 20 ms), and “indeterminate” (atrial fibrillation at end of study). The isthmus conduction block achieved was complete in 32 patients and partial in 11. Isthmus conduction could not be modified in 4 patients. In 3 there was atrial fibrillation at the end of the study; these patients were excluded from further analysis. No unidirectional block was observed in any patient. CT was 84 6 17 ms (range 55 to 150) before ablation and 156 6 20 ms (range 125 to 200) after complete isthmus ablation with a considerable overlap between the groups (Table I). Then, a parameter D was calculated: D 5 CT1 1 CT2 2 CLAFl. CLAFl was either the flutter cycle length at the beginning of the study (patients in atrial flutter) or of the most recently documented episode of atrial flutter (patients in sinus rhythm). CLAFl was measured in a standard 12lead surface electrocardiogram at a paper speed of 50 mm/s as an average of 10 consecutive flutter cycles (233 6 32 ms, range 185 to 325). The parameter D was 259 6 24 ms (range 2110 to 225) before ablation, 240 6 23 ms (range 2100 to 220) after unsuccessful ablation (no or partial isthmus block), and 13 6 10 ms (range 0 to 30) after successful ablation (complete isthmus block). Thus, D was ,0 ms in all cases of unsuccessful and $0 ms in all cases of successful isthmus ablation (p ,0.001, Fisher’s exact test). BRIEF REPORTS

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•••

This study describes a new parameter—D 5 CT1 1 CT2 2 CLAFl —that allows assessment of the degree of conduction block after isthmus ablation for common and reverse common atrial flutter without the need to evaluate right atrial activation sequences with a multipolar catheter. D could predict the degree of isthmus conduction block (complete vs. partial or none) with a diagnostic accuracy of 100% in our series when tested against the gold standard (reversal of low lateral right atrial activation sequence and exclusion of unidirectional block). The parameter D represents graphically the time by which the sum of the conduction times across the isthmus and the conduction time over the roof of the right atrium (in case of complete conduction block) exceeds the atrial flutter cycle length. Its development was based on certain assumptions whose correctness was not explicitly explored in the present study: (1) the low lateral right atrium and the coronary sinus os are within the reentry circuit of both common and reverse common atrial flutter, (2) the conduction velocity is equal during atrial flutter and during atrial pacing at a cycle length of 400 ms, (3) antiarrhythmic drugs other than amiodarone do not influence atrial flutter cycle length (possible delay between flutter cycle length measurement and ablation), and (4) there is no conduction across the crista terminalis, even at long pacing cycle lengths. Given the complete concordance of assessing the atrial activation sequence and measuring D, the present study provides evidence that the above assumptions are sufficiently well

met to make this method a useful tool. If validated in a prospective study, the use of D $0 ms as a surrogate end point to isthmus ablation could obviate the need of multipolar catheters and possibly lead to faster and cheaper procedures without hampering the accuracy of the primary end point. This study describes a new algorithm to determine complete isthmus conduction block without the need to evaluate the low lateral right atrial activation sequence during coronary sinus pacing. If the sum of the conduction times across the isthmus before and after ablation is equal or exceeds the atrial flutter cycle length, complete conduction block may be assumed. 1. Poty H, Saoudi N, Abdel AA, Nair M, Letac B. Radiofrequency catheter ablation of type 1 atrial flutter. Prediction of late success by electrophysiological criteria. Circulation 1995;92:1389 –1392. 2. Cauchemez B, Haissaguerre M, Fischer B, Thomas O, Clementy J, Coumel P. Electrophysiological effects of catheter ablation of inferior vena cava-tricuspid annulus isthmus in common atrial flutter. Circulation 1996;93:284 –294. 3. Schwartzman D, Callans DJ, Gottlieb CD, Dillon SM, Movsowitz C, Marchlinski FE. Conduction block in the inferior vena caval-tricuspid valve isthmus: association with outcome of radiofrequency ablation of type I atrial flutter. J Am Coll Cardiol 1996;28:1519 –1531. 4. Poty H, Saoudi N, Nair M, Anselme F, Letac B. Radiofrequency catheter ablation of atrial flutter. Further insights into the various types of isthmus block: application to ablation during sinus rhythm. Circulation 1996;94:3204 –3213. 5. Johna R, Fetsch T, Eckardt L, Cron T, Breithardt G, Borggrefe M. Radiofrequency catheter ablation of common and reverse common atrial flutter: a new algorithm to determine complete isthmus conduction block (abstr). Eur Heart J 1998;19(suppl):541.

Usefulness of Low-Dose Dobutamine Stress Echocardiography in Predicting Recovery of Poor Left Ventricular Function in Atrial Fibrillation Dilated Cardiomyopathy Bernard Paelinck,

MD,

Paul Vermeersch, MD, Dirk Stockman, and Marc Vaerenberg, MD

he increasing prevalence of congestive heart failure has focused on the search for potentially reT versible etiologies of cardiomyopathy. Different chronic tachyarrhythmias may cause a form of reversible myocardial dysfunction known as tachycardiomyopathy.1 Many studies have shown a significant improvement in cardiac dysfunction after abolition of the arrhythmia or after slowing of the ventricular rate.2–5 Atrial fibrillation (AF) has been reported to cause a form of dilated cardiomyopathy reversible with conversion to sinus rhythm.2– 4 Distinction of idiopathic dilated cardiomyopathy with a secondary arrhythmia From the Department of Cardiology, General Hospital Middelheim, Antwerp, Belgium. Dr. Paelinck’s address is: Department of Cardiology, General Hospital Middelheim, Lindendreef 1, 2020 Antwerp, Belgium. Manuscript received November 30, 1998; revised manuscript received and accepted January 25, 1999.

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©1999 by Excerpta Medica, Inc. All rights reserved.

MD,

Carl Convens,

MD,

from tachycardia-induced cardiomyopathy is important because restoration of sinus rhythm leads to a significant improvement in left ventricular function in tachycardiomyopathy only. However, tachycardiomyopathy can be diagnosed only when ventricular function recovers after restoration of sinus rhythm.2– 4 AF is by far the most common arrhythmia in dilated cardiomyopathy.6 Low-dose dobutamine stress echocardiography is used for the detection of myocardial contractile reserve in reversible ischemic or stunned myocardium.7,8 We conducted this study in a group of patients with dilated cardiomyopathy and long-lasting AF to determine whether low-dose dobutamine stress echocardiography is able to identify tachycardiomyopathy before cardioversion. •••

The study group consisted of 16 consecutive patients (10 men and 6 women, mean age 67 6 7 years) 0002-9149/99/$–see front matter PII S0002-9149(99)00177-0