(Circulation. 1999;99:3017-3023.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
From Pino Hospital, University of Las Palmas (J.A.C., A.M., F.W., E.G., J.G., E.H.), Canary Island, Spain; Facultad de Medicina, Universidad de Extremadura (D.S.-Q.), Badajoz, Spain; and Paediatrics, Imperial College School of Medicine at National Heart and Lung Institute (S.Y.H., R.H.A.), London, UK.
Correspondence to Dr S.Y. Ho, National Heart and Lung Institute, Imperial College School of Medicine, Dovehouse St, London SW3 6LY, UK. E-mail yen.ho{at}ic.ac.uk
| Abstract |
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Methods and ResultsThe gross morphological features and dimensions of the area between the orifice of the inferior caval vein and the attachment of the septal leaflet of the tricuspid valve were determined from angiograms made in 23 patients with documented atrial flutter and 30 control subjects. For comparison, we studied 20 normal heart specimens. When viewed in right anterior oblique projection, 2 morphologically distinct areas were identified. In the specimens, the inferior isthmus measured a mean length of 30±4 mm, not significantly different from the dimensions obtained from angiograms of control subjects. The mean length of the isthmus, however, was greater in patients with common atrial flutter than those without (37±8 versus 28±6 mm). Patients with atrial flutter and structural heart disease had an even longer isthmus than those with flutter alone (39.6±8 versus 33±7 mm). Compared with those without flutter, the atrial diameter was also larger in patients with flutter (57.6±9 versus 48.5±6 mm). Reevaluation carried out at follow-up 10±2 months after ablation did not show any reduction in atrial size, although contractility improved.
ConclusionsThe inferior isthmus and right atrium in patients with common atrial flutter were significantly larger than those in a control population.
Key Words: atrial flutter atrium angiography catheter ablation
| Introduction |
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| Methods |
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Angiographic Studies
We enrolled 53 patients prospectively in the angiographic
study. There were 23 patients (21 men; mean age, 59±15 years; range,
26 to 75 years) seen consecutively with clinically documented typical
AF who subsequently underwent successful radiofrequency ablation and 30
control subjects (16 men; mean age, 50±14 years; range, 22 to 70
years). Requirements for inclusion as a control were absence of any
history of AF, inability to induce this arrhythmia at
electrophysiological study, and absence of
structural heart disease.
In those with flutter, it had been recurrent for a mean of 8 years (range, 2 to 18 years) despite treatment with several antiarrhythmic agents (mean, 3±1). Structural heart disease was present in 12 patients (coronary arterial disease in 7, dilated cardiomyopathy in 4, and surgically repaired atrial septal defect in 1). Atrial flutter was permanent in 16 patients and paroxysmal in 7 patients.
Before every procedure, detailed information was given to all patients and control subjects, and written consent was obtained for the procedures. Angiographic and electrophysiological studies were performed at a single session.
Of the 23 patients with AF, 19 were reinvestigated with electrophysiological and angiographic studies, again at a single session, 6 to 12 months (mean, 10±2 months) after their therapeutic ablation. During follow-up, all 19 patients were in sinus rhythm without any episodes of AF. Of the remaining 4 patients, 2 had atrial fibrillation, and the other 2 declined to be reevaluated.
Angiographic Techniques and Methodology
Thirty minutes after the
electrophysiological procedure, we
performed right atrial angiography and coronary arteriography
in all patients in sinus rhythm. Contrast was injected into the right
atrium at the moment when the venous phase of coronary
arteriography was visualized (Figure 2
).
This allowed the isthmus and the orifice of the coronary sinus
to be displayed simultaneously.
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Right atrial angiography was performed through an 8F sheath, 40 cm long, inserted into the internal femoral vein. Right atrial angiograms were obtained by means of manual injection of 20 mL of nonionic contrast (Hexabrix) into the inferior caval vein.
Coronary arteriography was performed with conventional 5F catheters. Filming was prolonged to visualize the coronary venous phase. Angiographic studies were filmed in the 45° RAO view and recorded on 35-mm cine film. From film records, 2 observers later performed blind qualitative and quantitative analyses using static atrial end-systolic and end-diastolic frames of the right atrial angiograms and ventricular end-systolic frames of the coronary arteriography.
Reevaluation by use of right atrial angiography (as above) was carried out in 19 patients 6 to 12 months after therapeutic ablation for AF with the same 45° RAO views as before.
Angiographic Analysis and Measurement of the Right
Atrial Isthmus
From the right atrial angiograms, it was possible to
visualize the inferior and superior caval veins, right
lateral wall, eustachian valve, area inferior to the
triangle of Koch, and vestibule of the tricuspid valve (Figure 1
). The inferior isthmus was profiled as the area
between the eustachian valve and the hinge of the septal leaflet of the
tricuspid valve. We were able to distinguish 2 components: a pouchlike
area inferior and posterior to the orifice of the
coronary sinus and a smooth area between the pouch and the
tricuspid annulus. Selecting the frames with the largest linear
dimension of the inferior isthmus, we measured both
components. Depth of the pouchlike area was measured as the distance
from the inferior margin of the mouth of the
coronary sinus to the lowest part of the pouch. We correlated
these dimensions with the diameter of the right atrium, which was
obtained in the RAO view by measurement of the distance between the
lateral atrial wall and the tricuspid valvar annulus. All measurements
were corrected for degrees of magnification of the angiographic image
by relation of the diameter of the catheter in each projection to
its true diameter.
We further compared the dimensions of the right atrium and the inferior isthmus in patients with AF as obtained in sinus rhythm 30 minutes after the ablation procedure with the dimensions at reevaluation (10±2 months after ablation). We also evaluated changes in the contractility of the right atrium on both occasions by estimating the contraction fraction (CF) of the right atrium using the ratio CF=(EDA-ESA)/EDA, where EDA is atrial end diastole and ESA is atrial end systole. For each patient, frames in RAO projection were selected for measurement of end-diastolic and end-systolic areas of the right atrium by digital planimetry. These frames showed the largest and smallest areas at atrial end diastole and end systole, respectively. The same method was used to obtain right atrial areas in the control group.
Statistical Analysis
Measurements were expressed as mean±SD (range) (Tables 1
and 2
). Data concerning postmortem
specimens, control subjects, and patients with AF were compared by use
of unpaired and paired t tests. Correlations between
quantitative variables were performed by standard linear regression
studies. A value of P<0.05 was considered not due to
chance.
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| Results |
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Dimensions of the Isthmus: Angiographic and Anatomic
Comparisons
The overall angiographic features of the isthmus were
similar, with a pouchlike area and a smooth area distinguishable in all
patients. The pouchlike area corresponded to the posterior sector
combined with the middle sector; the smooth area corresponded to the
vestibule of the tricuspid valve as observed in the heart specimens
(Figure 1
). The mean angiographic lengths of the
inferior isthmus and its 2 components in the control group
and patients with AF compared with the corresponding measurements
obtained from the heart specimens are listed in Table 1
.
Compared with heart specimens, no significant differences were found in
the overall lengths obtained from angiograms of patients without
flutter. Furthermore, anatomic dimensions of the inferior
recess and vestibule of the tricuspid valve were comparable (Table 1
). In both groups, control and postmortem hearts, there were no
significant differences between measurements obtained from women and
men. The angiographic dimensions of the right atrium in the RAO view
correlated with the dimensions of the inferior isthmus
(r=0.68, P<0.005). Age and body surface area
were unrelated to these measurements. In the specimens, a weak
correlation existed between length of the inferior isthmus
and heart weight (r=0.56, P<0.05).
Right atrial angiograms showed larger linear dimensions of the right atrium (57.6±9 mm; range, 35 to 63 mm)in patients with AF than in control subjects (48.5±6 mm; range, 40 to 77 mm; P<0.001). The mean CF of the right atrium in patients with AF during sinus rhythm when measured 30 minutes after ablation was 0.23±0.06 compared with 0.51±0.1 in control subjects. We also noted a slower "washout" of contrast in these patients at that time. This indicated decreased blood flow from the right atrium, presumably because of its larger dimensions and lesser compliance. This phenomenon of slower washout was not seen at follow-up.
The mean length of the isthmus and its 2 components was
significantly larger in patients with than in those without common AF
(P<0.001; Table 1
). Representative
angiograms demonstrating the differences between the 2 groups are shown
in Figure 3
. The mean depth of the
pouchlike area showed a wide range in its measurements (0.5 to 8
mm), but no significant differences were found between groups. There
was no correlation between measurements of the inferior
isthmus and time of onset of symptoms. Nonetheless, the
inferior isthmus was larger in the 16 patients with
clinically incessant atrial flutter (38.7±9 mm) than in those
whose episodes of flutter were paroxysmal (32.5±6 mm;
P<0.05). Furthermore, although no significant differences
were found in right atrial dimensions (56.7±8 versus 58±10 mm,
respectively), the mean CF was smaller in patients with incessant
compared with paroxysmal episodes of flutter (0.18±0.04 versus
0.27±0.06). In the 12 patients with structural heart disease, the
dimensions of the inferior isthmus were greater compared
with patients with flutter but no structural heart disease
(P<0.005; Table 2
). These differences in isthmus
measurements were due to a wider vestibule of the tricuspid valve
(P<0.05). When we compared the angiographic features and
dimensions of the inferior isthmus in patients without
structural heart disease with the control group, we found that the
inferior recess was larger in patients with atrial flutter
(P<0.05), resulting in a longer inferior
isthmus (P<0.05).
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There were no significant differences in overall dimensions of the right atrium and inferior isthmus in patients with atrial flutter measured in sinus rhythm after ablation and at reevaluation 10±2 months later. We found that the mean right atrial function estimated by use of the CF of the right atrium, however, improved significantly (P<0.001) at follow-up (0.23±0.06 versus 0.53±0.1). The mean CF at reevaluation of patients with previous AF was found to be similar to that previously obtained in the control subjects (0.51±0.1), suggesting a recovery of atrial function.
| Discussion |
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Usefulness of Right Atrial Angiography in the Study of the
Inferior Isthmus
Interpretation of cardiac anatomy derived from
fluoroscopic examination during an
electrophysiological procedure has
previously been abstract because the electrophysiologist had to imagine
the anatomic landmarks from such weak references as the cardiac shadow
and catheter position. Angiographic techniques, when used in the
electrophysiological environment, have
proved useful in identifying coronary venous anomalies during
ablation of epicardial accessory pathways15 and in
elucidating the anatomy of the triangle of Koch and right AV
junction.16 In our study, we sought to overcome the
limitations of previous investigations that studied the anatomy
of the low right atrium area without the benefit of angiographic
contrast. Simple fluoroscopy does not define the orifices of the
inferior caval vein and tricuspid valve. Angiography, in
contrast, has enabled us to visualize structures such as the eustachian
valve, coronary sinus, caval veins, and tricuspid valve, as
well as other cardiac structures not seen on conventional fluoroscopy
as used in the electrophysiology laboratory. Our study also produced
excellent correlation between isthmic measurements made during life and
at postmortem examination, thus establishing the validity of the
technique.
Interest is now increasingly focused on the anatomic substrates of the different arrhythmias. Several nonfluoroscopic and computer-based techniques have been introduced recently to visualize the cardiac anatomy.3 17 18 No systematic investigations, however, have been made of the dimensions of the inferior isthmus with these procedures. With widely used fluoroscopic projections, our results will, we hope, improve understanding of this critical area of the so-called low right atrium during ablation procedures. They will provide a yardstick for future investigations that use electroanatomic mapping techniques, when it may prove possible to distinguish the different morphological components of the isthmus.
Anatomic Determinants for the Development of Atrial
Flutter
Even though our anatomic findings in the normal heart may
provide a clue to the potential substrate for areas of slow conduction
essential for reentry, questions still remain as to the precise
mechanism for the development of common AF and the reason why flutter
does not develop in every human heart. It has been reported
recently12 13 that conduction velocity in the isthmus
during pacing in sinus rhythm was slower in patients with typical AF
compared with those without any history of AF, further stressing the
necessity to investigate the anatomy and dimensions of this
crucial area. Our study shows that the overall dimensions of the right
atrium and inferior isthmus are larger in patients with AF
compared with the control population. The relationship between right
atrial enlargement and atrial arrhythmias has been previously
shown in animal models and experimental studies.19 20 21
Atrial enlargement, presumably caused by stretching, with resultant
thinning of the musculature may provide the potential anatomical
substrate for the recognized areas of slow conduction.5
The cause of the enlargement has not been investigated. In patients
with structural heart disease, it is reasonable to suggest that the
right atrium may be involved, resulting in atrial disease. We have
shown that even in patients with AF but without structural heart
disease, the inferior isthmus is longer compared with
control subjects. Although the relationship between atrial enlargement
and AF is evident, it is still unclear whether AF results in atrial
tachycardiomyopathy, leading to larger right atrial
dimensions or conversely whether previous atrial enlargement
predisposes to the development of flutter. Restoration of normal sinus
rhythm after ablation in patients with chronic AF and
cardiomyopathy has been shown to result in
substantially improved left ventricular
function.22 But the effect of restoration of sinus rhythm
on right atrial function has not been examined. We found that right
atrial dimensions in patients with a history of AF were similar in
sinus rhythm immediately after ablation and at reevaluation. It remains
to be shown with longer follow-up whether the atrium will reduce in
size or whether AF will recur in the setting of persistent atrial
enlargement. Persistence of an enlarged right atrium but with normal
contractility after ablation suggests that a previously
dilated right atrium might contribute to AF. It may, of course, also
simply be a residual feature. It is the enlargement of the isthmus,
particularly its inferior recess, that we believe may set
the scene for development of common AF.
A further finding in our study is that a recovery time is needed after ablation to achieve contractility that is comparable to the normal heart. A serial study is required to determine the minimum time needed, because "recovery" was found in all our patients by the time of reevaluation.
Study Limitations
When correlating anatomic with angiographic measurements, we used
2 different populations because no data were available for patients
undergoing both postmortem examination and previous angiographic study.
In consideration of prolonged exposure to radiation, our
analysis was limited to the dimensions of the
inferior isthmus by use of a single, and standard, RAO
projection. In estimating the contractility of the
right atrium, we used area measurements to avoid assumptions on atrial
geometry. The CF thus calculated is a useful, albeit crude, indicator
of atrial function.
| Acknowledgments |
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Received October 27, 1998; revision received March 12, 1999; accepted March 26, 1999.
| References |
|---|
|
|
|---|
2.
Disertori M, Inama G, Vergara G, Guarnerio M, Del
Favero A, Furlanello F. Evidence of a reentry circuit in the common
type of atrial flutter in man. Circulation. 1983;67:434440.
3.
Shah DC, Jais P, Haissaguerre M, Chouairi S, Takahashi
A, Hocini M, Garrigue S, Clementy J. Three-dimensional mapping of the
common atrial flutter circuit in the right atrium.
Circulation. 1997;96:39043912.
4. Rosenblueth A, Garcia Ramos J. Studies on flutter and fibrillation, II: the influence of artificial obstacles on experimental auricular flutter. Am Heart J. 1947;33:677684.
5. Boineau JP, Schuessler RB, Mooney CR, Miller CB, Wylds AC, Hudson RD, Borremans JM, Brockus CW. Natural and evoked atrial flutter due to circus movement in dogs: role of abnormal pathways, slow conduction, nonuniform refractory period distribution and premature beats. Am J Cardiol. 1980;45:11671181.[Medline] [Order article via Infotrieve]
6.
Olgin JE, Kalman JM, Fitzpatrick AP, Lesh MD. Role of
right atrial endocardial structure as barriers to conduction during
human type I atrial flutter: activation and entrainment mapping guided
by intracardiac echocardiography.
Circulation. 1996;92:18391848.
7. Olshansky B, Okumura K. Hess PG, Waldo AL. Demonstration of an area of slow conduction in human atrial flutter. J Am Coll Cardiol. 1990;16:16391648.[Abstract]
8. Cosio FG, Arribas F, Barbero JM, Kallmeyer C, Goicolea A. Validation of double spike electrograms as markers of conduction delay or block in atrial flutter. Am J Cardiol. 1988;61:775780.[Medline] [Order article via Infotrieve]
9.
Nakagawa H, Lazzara R, Khastgir T, Beckman KJ,
McClelland JH, Imai S, Pitha JV, Becker A, Arruda M, Gonzalez M, Widman
L, Rome M, Neuhause J, Wang X, Calame JD, Goudeau MD, Jackman WM. Role
of the tricuspid annulus and the eustachian valve/ridge on atrial
flutter: relevance to catheter ablation of the septal isthmus and a new
technique for rapid identification of ablation success.
Circulation. 1996;94:407424.
10. Cabrera JA, Sanchez-Quintana D, Ho SY, Medina A, Anderson RH. The architecture of the atrial musculature between the orifice of the inferior caval vein and the tricuspid valve: the anatomy of the isthmus. J Cardiovasc Electrophysiol. 1998;9:11861195.[Medline] [Order article via Infotrieve]
11. Feld GK, Mollerus M, Birgersdotter-Gree U, Fujimura O, Bahnson TD, Boyce K, Rahme M. Conduction velocity in the tricuspid valve-inferior vena cava isthmus is slower in patients with type I atrial flutter compared to those without a history of atrial flutter. J Cardiovasc Electrophysiol. 1997;8:13381348.[Medline] [Order article via Infotrieve]
12.
Tai CT, Chen SA, Chiang CE, Lee SH, Ueng KC, Wen ZC,
Huang JL, Chen YJ, Yu WC, Feng AN, Chiou CW, Chan MS. Characterization
of low right atrium as the slow conduction zone and pharmacological
target in typical atrial flutter. Circulation. 1997;96:26012611.
13.
Feld GK, Fleck RP, Chen PS, Boyce K, Bahnson TD, Stein
JB, Calisi CM, Ibarra M. Radiofrequency catheter ablation for the
treatment of human type 1 atrial flutter: identification of a critical
zone in the reentrant circuit by endocardial mapping techniques.
Circulation. 1992;86:12331240.
14. Cosio FG, Lopez Gil M, Goicolea A, Arribas F, Barroso JL. Radiofrequency ablation of the inferior vena cava-tricuspid valve isthmus in common atrial flutter. Am J Cardiol. 1993;71:705709.[Medline] [Order article via Infotrieve]
15. Stamato N, Goodwing M, Foy B. Diagnosis of coronary sinus diverticulum in Wolff-Parkinson-White syndrome using coronary angiography. PACE Pacing Clin Electrophysiol. 1989;12: 15891591.
16. Cabrera JA, Medina A, Suarez de Lezo J, Wanguemert F, Hernandez E, Delgado A. Angiographic anatomy of Koch's triangle, atrioventricular nodal artery and proximal coronary sinus in patients with and without atrioventricular nodal reentrant tachycardia. In: Farré J, Moro C, eds. Ten Years of Radiofrequency Catheter Ablation. New York, NY: Futura Publishing; 1998:91102.
17.
Chu E, Fitzpatrick AP, Chin MC, Sudhir K, Yock PG, Lesh
MD. Radiofrequency catheter ablation guided by intracardiac
echocardiography. Circulation. 1994;89:13011305.
18. Schilling R, Peters N, Davies W. Characterization of functional and anatomical components of human atrial flutter using a non-contact mapping system. Circulation. 1997;96(suppl I):I-1587. Abstract.
19.
Boyden PA, Hoffman BF. The effects of atrial
electrophysiology and structure of surgically induced right atrial
enlargement in dogs. Circ Res. 1981;49:13191331.
20. de Madron E, Kadish A, Spear JF, Knight DH. Incessant atrial tachycardia in a dog with tricuspid dysplasia: clinical management and electrophysiology. J Vet Intern Med. 1987;1:163169.[Medline] [Order article via Infotrieve]
21. Schoels W, Kuebler W, Yan H, Gough WB, El-Sherif N. A unified functional/anatomic substrate for circus movement in atrial flutter: activation and refractory patterns in the canine right atrial enlargement models. J Am Coll Cardiol. 1993;21:738741.
22.
Luchsinger JA, Steinberger JS. Resolution of
cardiomyopathy after ablation of atrial flutter.
J Am Coll Cardiol. 1998;32:205210.The
inferior right atrial isthmus as displayed by angiography
was compared in patients with and without atrial flutter and with a
series of normal heart specimens. There was no significant difference
in isthmus length in patients without flutter and in the specimens. In
contrast, significantly larger atrial and isthmic dimensions were found
in patients with atrial flutter.
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