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Europace 2004 6(4):307-315; doi:10.1016/j.eupc.2004.03.011
© 2004 by European Society of Cardiology
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Anatomical diversity and age-related histological changes in the human right atrial posterolateral wall

Taka-aki Matsuyamaa,*, Shin Inoueb, Youichi Kobayashic, Tetsuo Sakaic, Tsukasa Saitoc, Takashi Katagiric and Hidekazu Otaa

aSecond Department of Pathology, Showa University School of Medicine 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan; bDepartment of Internal Medicine Showa University Toyosu Hospital, Tokyo, Japan; cThird Department of Internal Medicine, Showa University School of Medicine Tokyo, Japan

Manuscript submitted 24 September 2003. Accepted after revision 28 March 2004.

*Corresponding author. Tel.: +81-3-3784-8122; fax: +81-3-3784-2959. E-mail address: zan42100{at}nifty.com


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Conclusion
 Acknowledgements
 References
 
AIMS: Recent clinical observations suggest that the right atrial posterolateral wall structures originate ectopic beats and function as anatomical obstacles. Because atrial arrhythmias increase in incidence after middle age, we investigated histological diversity and age-related changes in right atrial posterolateral wall.

METHODS AND RESULTS: Twenty-six autopsied hearts (mean 65.2 years, 16 men and 10 women) were studied. The entire posterolateral right atrium was cut serially. We determined the distribution of the sinoatrial node and localized it in relation to the crista terminalis and sinus venosus. We also compared histopathological changes in these tissues between three groups consisting of 31- to 50-year-old, 51- to 70-year-old and 71- to 90-year-old hearts. Total mean length of the crista terminalis, the sinoatrial node, and the sinus venosus was 46 mm, 21 mm and 29 mm, respectively, and showed no age-related changes, but the distribution of the sinoatrial node was varied. Mean muscular volume of the sinus venosus was significantly reduced in the two older groups, though that of the crista terminalis showed no age related-changes.

CONCLUSION: Histological diversity of the sinoatrial node and age-related changes in the sinus venosus beneath the sinoatrial node may enhance histological heterogeneity and hence arrhythmogenicity.

Key Words: atrial arrhythmia, crista terminalis, histopathology, sinoatrial node, sinus venosus


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Conclusion
 Acknowledgements
 References
 
Recent electrophysiological observations have suggested that the right atrial posterolateral wall, which contains the crista terminalis and sinus venosus, may be an arrhythmogenic substrate such as micro or macro-reentrant right atrial arrhythmia. For example, the crista terminalis and its vicinity are considered to be the focus of atrial ectopic beats or sinoatrial reentry, and the posterior boundary of flutter [1–Go5]Go. Although this phenomenon has been attributed to anisotropy, the anatomy of this area of the atrium has not been described in detail. The sinoatrial node, a structure adjacent to the orifice of the superior vena cava (SVC), has been found to vary in position and length along the crista terminalis, and in some cases the tail extends inferiorly close to the orifice of the inferior vena cava (IVC) [6,Go7]Go. Recent papers have emphasized the importance of this lower extension of the sinoatrial node, postulating that distribution of the sinoatrial node or its junction toward the sinus venosus may affect conduction across the area [8,Go9]Go. The purpose of the present study was to explore the arrangement of these tissues in the posterolateral region of the right atrium by examination of serial sections of autopsied human hearts. We also concentrated on age-related changes in the musculature of this area, especially in the vicinity of the orifice of the IVC. Because of the high incidence of atrial flutter prevalent in 50- to 70-year-olds [10]Go, detailed understanding of the anatomy and the age-related changes in this area may improve our understanding of the basic background of atrial flutter and other variations of macro-reentrant atrial tachycardia.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Conclusion
 Acknowledgements
 References
 
Subjects
We studied 26 autopsied adult human hearts without obvious structural anomaly from 16 men and 10 women ranging in age from 31 to 89 years (mean 65.2 ± 16.8 years). None of the individuals had been recorded as having a supraventricular tachyarrhythmia on his or her surface electrocardiogram. Seventeen individuals died of malignant disease, and the remaining 9 died of pneumonia, liver disease, cerebral infarction, or traumatic injury. None died of cardiac-related causes. We divided the hearts into three age groups according to the age of the individuals at death: 31–50 years (4 men, 1 woman), 51–70 years (6 men, 4 women), and 71–90 years (6 men, 5 women).

Tissue preparation
All hearts were examined for macroscopic abnormality after fixation with 10% formalin. We removed the right atrial myocardium including the SVC and IVC orifices, the right lateral free wall, and the sinus venosus, as indicated in Fig. 1A. The complete crista terminalis and adjacent musculature consisting of the sinus venosus and pectinate muscles were included, as shown in Fig. 1B.



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  		Figure 1 A. Panoramic view of the posterolateral wall of the right atrium based on the right oblique view of the fluoroscope (Heart 2). Arrowheads indicate the sulcus terminalis, the probable junction between the sinoatrial node and the sinus venosus. The frame containing the SVC, IVC, and the posterolateral free wall indicates the subject area of this study and is the area of the right atrium removed for tissue preparation. B. Endocardial aspect of the excised tissue based on the left oblique view of the fluoroscope. The crista terminalis is unfolded from its originally curved shape. The entire crista terminalis (arrowheads) lies between the pectinate muscles and the sinus venosus. The crista terminalis and its adjacent musculature were cut into sections 10-mm thick and perpendicular to the longitudinal axis, as shown. Because the inferior border of the crista terminalis was unclear in some cases, we defined it as the first bifurcation from the main trunk (dotted line). ANT = anterior, CT = crista terminalis, FO = foramen ovale, IVC = inferior vena cava, LAT = lateral, PM = pectinate muscle, POST = posterior, RA = right atrium, RAA = right atrial appendage, RSPV = right superior pulmonary vein, SVC = superior vena cava, SV = sinus venosus. Bar = 10 mm.

 
Each specimen was cut into pieces 10-mm wide. All tissue sections were carefully embedded in paraffin and cut serially into sections of 10-µm thickness. Every 100th section was stained with Azan-Mallory and observed histological age-related changes. In addition, we determined the distribution of the sinoatrial node and localized it in relation to the endocardial aspect of the posterolateral right atrium.

Dimension of the crista terminalis
The crista terminalis was identified as a thick muscular ridge that began near the junction of the atrial septum and right atrial appendage and ended in the vicinity of the IVC orifice. The length of the crista terminalis was determined macroscopically, as shown in Fig. 1B. Because the inferior border of the crista terminalis near the IVC orifice was unclear in some cases, we defined it at the first bifurcation from the main trunk (Fig. 1B, dotted line).

Dimension of the sinoatrial node
The sinoatrial node was identified as a structure adjacent to the sinoatrial nodal artery running along the epicardial border of the crista terminalis. We identified it from microscopic observation of the specific nodal cells located in a reconsiderable amount of elastic and collagen fibres [11–Go14]Go. The length of the node was calculated from the number of sections it occupied. The transitional cell zone was not included in this measurement since short tongues of traditional cells sometimes extend into the myocardium [15]Go.

Dimension of the sinus venosus
The sinus venosus was mainly located in the posterolateral wall of the right atrium between the SVC and the IVC orifices. The craniocaudal length of the sinus venosus was also calculated from the number of sections between the SVC and IVC myocardial sleeves. The upper and lower borders were determined as the junction of the SVC and IVC myocardial sleeves consisted of thin musculature and the sinus venosus thick myocardial bundle.

Quantitative analysis of the crista terminalis and sinus venosus musculature
We determined the approximate muscular volume of the crista terminalis and the sinus venosus of each heart by reconstructing the digital images, obtained at 5-mm intervals (Fig. 2A). The sinus venosus was divided into two segments, an upper segment located abreast of the sinoatrial node (Fig. 2B) and a lower segment located beneath the inferior margin of the sinoatrial node (Fig. 2C). Colour images were obtained with a digital microscope camera (Polaroid PDMC Ie) and were stored as 24-bit 800 × 600-pixel colour images. Quantitative histological assessments were derived from a computer digital optical analyzer (Win ROOF, MITANI).



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  		Figure 2 Digital measurement of the musculature on a computer image. A. Muscular volume was estimated by measuring the areas of the digital images obtained at 5-mm intervals, and these images were then reconstructed on the endocardial aspect of the same heart. The images are oppressed 1/3 in thickness. The musculature of the crista terminalis (black), the sinoatrial node (yellow), the sinus venosus (red), and the sleeve of the superior and inferior vena cava (blue) are depicted. These artificial colours were automatically selected by computer image analyzer. Note the relatively low position of the sinoatrial node at the posterolateral free wall and the myocardial connection at the lower crista terminalis and the sinus venosus. The boundary between the superior and inferior vena cava and the posterior margin of the atrial septum is indicated by a dotted line (Heart 7). B. Low-power photomicrograph taken at the superior margin of the sinoatrial node in A. At this level, the sinoatrial node is adjacent to thin muscular sleeve of the superior vena cava. Note the paucity of epicardial adipose tissue in the superior vena cava sleeve. C. Low-power photomicrograph at the mid level of the sinoatrial node in A. At this level, the sinoatrial node infiltrates the musculature of the crista terminalis and the sinus venosus. The sinus venosus musculature consists of some myocardial layers within epicardial adipose tissue. D. Low-power photomicrograph taken beneath the inferior margin of the sinoatrial node in A. The sinus venosus shows little collagenous or adipose tissue alteration. Both the sinus venosus and the crista terminalis are connected without infiltration of the sinoatrial node. ANT = anterior, CT = crista terminalis, IVC = inferior vena cava, LAT = lateral, POST = posterior, SAN = sinoatrial node, SEP = septum, SVC = superior vena cava, SV = sinus venosus. Azan-Mallory stain. Bar = 10 mm.

 
Statistical analysis
We compared heart weight, longitudinal length of the sinoatrial node, craniocaudal lengths of the crista terminalis and sinus venosus, and volumes of the crista terminalis and sinus venosus musculature across three age groups. Values are shown as mean ± SD. Fisher's protected least significant difference test was used for statistical comparisons between the three groups. A P value of <0.05 was considered significant.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Conclusion
 Acknowledgements
 References
 
Macroscopically, concentric left ventricular hypertrophy was observed in 14 hearts: 1 heart in the 31- to 50-year-old group, 6 hearts in the 51- to 70-year-old group, and 7 hearts in the 71- to 90-year-old group. This was presumably caused by an increase of blood pressure in elderly patients. No heart showed massive fibrotic scar formation due to ischaemia, myocardial degeneration due to chemotherapy, specific inflammatory infiltrates, right ventricular hypertrophy, tricuspid valvular deformity, or significant atherosclerotic narrowing of the coronary arteries.

Measurements
Measurement details are summarized in Table 1. Heart weight varied from 230 to 480 g. Mean heart weight did not significantly differ in three groups (Fig. 3A). Mean length of the crista terminalis was 51 ± 9 mm in the 31- to 50-year-old group, 47 ± 11 mm in the 51- to 70-year-old group, and 42 ± 7 mm in the 71- to 90-year-old group. Mean length of the sinoatrial node was 20 ± 3 mm (range 18–25 mm), 22 ± 7 mm (range 13–38 mm), and 21 ± 9 mm (range 11–40 mm), respectively. Mean craniocaudal length of the sinus venosus was 33 ± 8 mm, 28 ± 5 mm, and 27 ± 5 mm, respectively. These differences were not significant. The ratio of the sinoatrial node length overlapping on the sinus venosus to the sinus venosus length also did not differ significantly between the groups, but the ratio exceeded 0.50 in 17 of the 26 hearts. Namely, the sinoatrial node extended inferiorly beyond the midline between the SVC and IVC orifices in these 17 hearts. The extent of the sinoatrial node varied greatly, and its length was not related to that of the crista terminalis or the sinus venosus.



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  		Figure 3 Graphs show quantitative data comparisons between 31- to 50-year-old, 51- to 70-year-old, and 71- to 90-year-old hearts. A. Heart weight. B. Muscular volume of the crista terminalis (CT). C. Muscular volume of the sinus venosus (SV) at the level of the sinoatrial node (SAN). D. Muscular volume of the SV at the level beneath the SAN. (All values are mean ± SD), y = years.

 


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  		Table 1 Study hearts and related pathological features per age group

 
Muscular volume and histological findings of the crista terminalis and the sinus venosus
Mean muscular volume of the crista terminalis was slightly but not significantly decreased in the two older groups (Fig. 3B). Mean muscular volume of the sinus venosus in the upper segment abreast of the sinoatrial node was 75.4 mm3, 80.5 mm3 and 65.3 mm3, respectively. That of the sinus venosus in the lower segment beneath the sinoatrial node was 104.7 mm3, 61.7 mm3 and 42.5 mm3, respectively (Fig. 3C, D). The sinus venosus musculature of the 31- to 50-year-old group was relatively preserved in the upper and lower segments (Fig. 4). The sinoatrial node, especially in the lower segment is sandwiched by the sinus venosus musculature epicardially and the crista terminalis endocardially. At the lower segment beneath the sinoatrial node, the massive myocardial bundle of the crista terminalis and the thin musculature of the sinus venosus meet each other beyond the nodal artery. The sinus venosus musculature of the two older groups showed fibro-fatty change (Fig. 5), a phenomenon that was particularly conspicuous in the lower segment beneath the sinoatrial node (P<0.05). This fibro-fatty infiltration from the epicardium eventually interrupted the myocardial continuity between the crista terminalis and the sinus venosus.



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  		Figure 4 Thirty-four-year-old man (Heart 2). A. Endocardial aspect based on the left anterior oblique view. The sinoatrial node is 25 mm in length and the crista terminalis is 53 mm in length. Bar = 10 mm. B. Low-power photomicrograph shows the sinoatrial node located beneath epicardium infiltrating the sinus venosus and the crista terminalis. The musculature of the sinus venosus (arrowheads) shows slight interstitial fibrosis and continues to the junction with the sinoatrial node. Bar = 1 mm. C. Low-power photomicrograph at level C of A shows attenuation of the sinoatrial nodal tissue and predominance of the musculature of the sinus venosus (arrowheads). Bar = 1 mm. ANT = anterior, CT = crista terminalis, IVC = inferior vena cava, LAT = lateral, POST = posterior, SAN = sinoatrial node, SEP = septum, SV = sinus venosus, SVC = superior vena cava. Azan-Mallory stain.

 



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  		Figure 5 Eighty-two-year-old man (Heart 21). A. Endocardial aspect based on the left anterior oblique view. The sinoatrial node is 25 mm in length and that of the crista terminalis is 47 mm in length. Bar = 10 mm. B. Low-power photomicrograph at the level of the main sinoatrial node. Sinus venosus musculature is decreased and replaced by fibro-fatty tissue (arrowheads). Bar = 1 mm. C. Low-power photomicrograph of the crista terminalis and sinus venosus beneath the sinoatrial node. The musculature of the sinus venosus and the junction of the crista terminalis show severe fibrosis. Bar = 1 mm. ANT = anterior, CT = crista terminalis, IVC = inferior vena cava, LAT = lateral, POST = posterior, SAN = sinoatrial node, SV = sinus venosus, SVC = superior vena cava. Azan-Mallory stain.

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Conclusion
 Acknowledgements
 References
 
Keith and Flack [6]Go in 1907 first described the location of the human sinoatrial node near the superior margin of the right atrial appendage. The only variation reported by Koch [7]Go was inferior extension of the laterally located node toward the orifice of the IVC. Subsequently, many investigators described the sinoatrial node as located within a relatively narrow area straddling the crest of the right atrial appendage, presumably because they were technologically limited in their ability to observe the vicinity of the junction of the right atrium and the SVC [11–Go13]Go. Anderson et al. [8,Go16]Go investigated the nodal arteries in relation to the position of the sinoatrial node and pointed out the variability of the vascular supply and the possibility of nodal elongation along the crista terminalis. The morphological diversity of the sinoatrial node was suggested to be a reflection of the node's embryological development [17]Go. The longitudinal length of the sinoatrial node did not differ between the three groups, however the sinoatrial node was elongated more than 30 mm in three cases, and extended inferiorly beyond the midline between the SVC and IVC orifices in more than half cases. The elongated nodal tissue seems to correspond to the widely distributed pacemaker complex and the phenomenon of the wandering pacemaker [18]Go. Elongated nodal tissue with heterogeneous atrionodal connection or specific nodal conductivity may evoke sinoatrial reentry or other atrial tachycardias observed near the crista terminalis [4,Go5]Go. In regard to age-related changes of the sinoatrial node and its vicinity, reduction of sinoatrial nodal cells and increase of collagen fibre after middle age have previously been shown [14]Go. Furthermore, James [19]Go pointed out the susceptibility of the sinoatrial node to disease due to its proximity to the epicardium. This means that any disease causing pericarditis can potentially involve at least the epicardial margin of the junction between the crista terminalis and the sinus venosus.

In describing the anatomy of the posterolateral right atrial wall, Papez [20]Go detailed the orientation of several bundles of the atrial musculature. He referred to the musculature running through the sinus venosus as "the intercaval bundle." This intercaval bundle was recently referred to by Ho et al. as the interatrial muscular bridge [21]Go. A recently published histological study suggests that the age-related fibrosis occurring at the border between the crista terminalis and the pectinate muscle is relevant to atrial reentrant arrhythmias [22]Go, and another clinical study suggested that the thickness of the crista terminalis may lead to the development of typical atrial flutter [23]Go. In our study, however, muscular volume of the crista terminalis did not change with age. Furthermore, fibrous change with myocardial cell reduction was more conspicuous in the lower than the upper segment of the sinus venosus. Regarding muscular continuity in the posterolateral right atrium, age-related changes in the sinus venosus musculature seems to explain the results of some recent mapping studies indicating that the posterior line of block is not in the crista terminalis but rather in the region of the sinus venosus [3]Go. Connection, interruption, or nodal interference between the crista terminalis and the sinus venosus may also be related to the variant form of atrial flutter, termed "lower loop reentry," that is more rapid and at times more irregular than typical atrial flutter. In this unique arrhythmia, conduction across the lower part of the crista terminalis has been suggested by pacing from the coronary sinus [24]Go.

Study limitations
Our study did not include hearts from individuals less than 30 years of age. Nor did it include hearts with a history of atrial flutter because of this arrhythmia's short duration and good prognosis. Sinoatrial nodal tissue identified histologically does not always correspond to that identified electrophysiologically. Our work was done by means of conventional histological staining. We do not know whether immunostaining for the gap junction proteins, i.e., connexin 40, 43, and 45, might have yielded alternative findings to explain functional block in the posterior wall. With respect to an internodal or preferential pathway, both the sinoatrial and atrioventricular nodes varied considerably in dimension [14,Go25]Go; however, the myocardial connection between these two nodes appeared to be broadly distributed within the right atrium.


   Conclusion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
Acknowledgements
 References
 
In our autopsied hearts, distribution of the sinoatrial node varied, and the node was sometimes unexpectedly long. In the ≥51 year-old hearts, the musculature of the sinus venosus showed significant fibro-fatty replacement, especially in its lower segment. Diversity of sinoatrial node anatomy and age-related changes in the sinus venosus may enhance histological heterogeneity and hence arrhythmogenicity.


   Acknowledgements
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
 Acknowledgements
References
 
The authors express appreciation to Ms. Yoshiko Sasaki for her technical assistance.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
 Acknowledgements
 References
 
[1] Olgin JE, Kalman JM, Fitzpatrick AP, Lesh MD. Role of right atrial endocardial structures as barriers to conduction during human type I atrial flutter. Activation and entrainment mapping guided by intracardiac echocardiography. Circulation 1995; 92: 1839–1848.[Abstract/Free Full Text]

[2] Arenal A, Almendral J, Alday JM, Villacastin J, Ormaetxe JM, Sande JLM, et al. Rate-dependent conduction block of the crista terminalis in patients with typical atrial flutter: influence on evaluation of cavotricuspid isthmus conduction block. Circulation 1999; 99: 2771–2778.[Abstract/Free Full Text]

[3] Friedman PA, Luria D, Fenton AM, Munger TM, Jahangir A, Shen WK, et al. Global right atrial mapping of human atrial flutter: the presence of posteromedial (sinus venosa region) functional block and double potentials: a study in biplane fluoroscopy and intracardiac echocardiography. Circulation 2000; 101: 1568–1577.[Abstract/Free Full Text]

[4] Kalman JM, Olgin JE, Karch MR, Hamdan M, Lee RJ, Lesh MD. "Cristal tachycardias": origin of right atrial tachycardias from the crista terminalis identified by intracardiac echocardiography. J Am Coll Cardiol 1998; 31: 451–459.[Abstract/Free Full Text]

[5] Sanders WE Jr., Sorrentino RA, Greenfield RA, Shenasa H, Hamer ME, Wharton JM. Catheter ablation of sinoatrial node reentrant tachycardia. J Am Coll Cardiol 1994; 23: 926–934.[Abstract]

[6] Keith A and Flack M. The form and nature of the muscular connections between the primary divisions of the vertebrate heart. J Anat Physiol 1907; 41: 172–189.[Medline]

[7] Koch W. Weiter Mitteilungen uber den Sinusknoten der Herzens. Verh Dtsch Pathol Anat 1909; 13: 85–92.

[8] Anderson RH and Ho SY. The architecture of the sinus node, the atrioventricular conduction axis, and the internodal atrial myocardium. J Cardiovasc Electrophysiol 1998; 9: 1233–1248.[Web of Science][Medline]

[9] Taylor JR and Taylor AJ. The relationship between the sinus node and the right atrial appendage. Can J Cardiol 1997; 13: 85–92.[Medline]

[10] Hejtmancik MR, Herrmann GR, Bradfield JY. Atrial flutter. Am Heart J 1950; 40: 884–890.[Medline]

[11] Lev M and Watne AL. Laboratory methods and technical notes. Method for routine histopathologic study of human sinoatrial node. A M A Arch Pathol 1954; 57: 168–177.

[12] Hudson REB. The human conducting-system and its examination. J Clin Path 1963; 16: 492–498.[Free Full Text]

[13] Truex RC, Smythe MQ, Taylor MJ. Reconstruction of the human sinoatrial node. Anat Rec 1967; 159: 371–378.[CrossRef][Medline]

[14] Inoue S, Shinohara F, Niitani H, Gotoh K. A new method for the histological study of aging changes in the sinoatrial node. Jpn Heart J 1986; 27: 653–660.[Medline]

[15] Davies MJ, Anderson RH, Becker AE. Anatomy of the conduction tissues. The conduction system of the heart. 1983; London Butterworth 9–70.

[16] Anderson KR, Ho SY, Anderson RH. Location and vascular supply of sinus node in human heart. Br Heart J 1979; 41: pp. 28–32.[Abstract/Free Full Text]

[17] Anderson RH, Ho SY, Becker AE, Gosling JA. The development of the sinoatrial node. In Bonke FIM (Ed.). The sinus node 1978; Den Haa g Martinus Nijoff pp. 166–182.

[18] Boineau JP, Canavan TE, Schuessler RB, Cain ME, Corr PB, Cox JL. Demonstration of a widely distributed atrial pacemaker complex in the human heart. Circulation 1988; 77: 1221–1237.[Abstract/Free Full Text]

[19] James TN. The sinus node. Am J Cardiol 1977; 40: 965–986.[CrossRef][Web of Science][Medline]

[20] Papez JW. Heart musculature of the atria. Am J Anat 1920; 27: 255–285.[CrossRef][Web of Science]

[21] Ho SY, Anderson RH, Sanchez-Quintana D. Atrial structure and fibres: morphologic bases of atrial conduction. Cardiovasc Res 2002; 54: 325–336.[Abstract/Free Full Text]

[22] Sanchez-Quintana D, Anderson RH, Cabrera JA, Climent V, Martin R, Farre J, et al. The terminal crest: morphological features relevant to electrophysiology. Heart 2002; 88: 406–411.[Abstract/Free Full Text]

[23] Mizumaki K, Fujiki A, Nagasawa H, Nishida K, Sakabe M, Sakurai K, et al. Relation between transverse conduction capability and the anatomy of the crista terminalis in patients with atrial flutter and atrial fibrillation: analysis by intracardiac echocardiography. Circ J 2002; 66: 1113–1118.[CrossRef][Medline]

[24] Cheng J, Cabeen WR, Scheinman MM. Right atrial flutter due to lower loop reentry: mechanism and anatomic substrates. Circulation 1999; 99: 1700–1705.[Abstract/Free Full Text]

[25] Inoue S and Becker AE. Posterior extension of the human compact atrioventricular node: a neglected anatomic feature of potential clinical significance. Circulation 1998; 97: 188–193.[Abstract/Free Full Text]


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