Atrial fibrillation (AF) is the most frequent atrial arrhythmia. During the last few decades, owing to numerous advancements in the field of electrophysiology, we reached satisfactory outcomes for paroxysmal AF with the help of ablation procedures. But the most challenging type is still persistent AF. The recurrence rate of AF in patients with persistent AF is very high, which shows the inadequacy of pulmonary vein isolation (PVI). Over the last few decades, we have been trying to gain insight into AF mechanisms, and have come to the conclusion that there must be some triggers and substrates other than pulmonary veins. According to many studies, PVI alone is not enough to deal with persistent AF. The purpose of our review is to summarize updates and to clarify the role of coronary sinus (CS) in AF induction and propagation. This review will provide updated knowledge on developmental, histological, and macroscopic anatomical aspects of CS with its role as arrhythmogenic substrate. This review will also inform readers about application of CS in other electrophysiological procedures.

The coronary sinus (CS) is the largest cardiac venomuscular structure draining most of cardiac venous blood into the right atrium. The CS musculature is an extension of atrial myocardial fibers [1] providing not only an anatomical bridge between atria but an electrical connection as well [2]. For a long time, CS has only been considered a venous structure, but recently its role in the pathophysiology of atrial tachyarrhythmias has been recognized [3-10]. Knecht et al. [10] showed that focal tachyarrhythmia originates from CS and ablation within the CS eliminates the tachycardia.

Catheter ablation of CS, at the endocardial and epicardial region, increases atrial fibrillation (AF) cycle length that is an indicator of AF termination [3]. The CS also provides percutaneous epicardial access for ablation, even in patients with previously failed endocardial radiofrequency (RF) ablation, which helps improve the outcome [11]. AF is a rapidly growing problem in routine clinical practice. To cope with this expanding health issue first, we need to know the exact substrate for AF. This review is an outline of the knowledge about relation of pathophysiology, mechanism of initiation, maintenance, and recurrence of AF with CS.

The CS has a key role in myocardial venous drainage. About 60% of drainage is performed by CS, the remaining 40% by anterior and small cardiac veins. The CS receives four major tributaries: the great, middle, small, and posterior cardiac veins; the other two groups include anterior veins of the right ventricle also called anterior cardiac veins and the smallest group of cardiac veins named Thebesian veins that drain directly into the tributaries of the greater and smaller cardiac veins [12-14]. The CS is the continuation of the great cardiac vein that runs posteriorly in the left atrioventricular groove (Fig. 1). The anterior wall of the left ventricle and the interventricular septum are drained by the tributaries of the anterior interventricular vein, which collectively form the great cardiac vein on the annulus [4, 7, 13, 14]. The great cardiac vein joins the main posterior lateral vein to form CS. Remaining parts of the heart are drained by small cardiac veins into the ostium of CS [7]. Anatomically, CS starts from the ostium in the right atrium, positioned below the foramen ovale and above the inferior vena cava, and ends as a great cardiac vein [15](Fig. 1).

Fig. 1.

a Posterior view of the heart showing the coronary sinus (CS) connecting the right (RA) and left (LA) atrium. b Posterior aspect of the heart. Yellow arrow demonstrates the extension of atrial fibers on CS. RAA, right atrial appendage; RV, right ventricle; LV, left ventricle; dCS, distal coronary sinus, pCS, proximal coronary sinus; SCV, superior vena cava [16].

Fig. 1.

a Posterior view of the heart showing the coronary sinus (CS) connecting the right (RA) and left (LA) atrium. b Posterior aspect of the heart. Yellow arrow demonstrates the extension of atrial fibers on CS. RAA, right atrial appendage; RV, right ventricle; LV, left ventricle; dCS, distal coronary sinus, pCS, proximal coronary sinus; SCV, superior vena cava [16].

Close modal

CS lies in the coronary groove that is located on the diaphragmatic part of the heart (Fig. 1). Gray’s anatomy describes “the coronary sinus as a wide venous channel, about 2.25 cm in length, situated in the posterior part of atrioventricular sulcus of the heart, usually covered by muscular fibers from the left atrium” and it has been considered as a part of the venous system for long time. In 2004, Barceló et al. [17] demonstrated that it is not a usual venous structure like other cardiac veins and also hypothesized that CS is a fifth small chamber of the heart with atrial myocardial characteristics [17].

Embryologically, the CS originates from the differentiation of the left sinus horn that is vital for the development of the complete venous system of the heart [18, 19]. Maturity and sexual dimorphism of the CS during antenatal period have an impact on its histological and electrophysiological features [20]. The CS and oblique vein of Marshall are both derivatives of sinus venosus. The muscular tissue around CS can be right atrial (RA) myocardial tissue continuation. Some of these muscular sleeve fibers join left atrial (LA) myocardial tissue that makes second most important connection between atria [21]. The proximal two-thirds of the CS have double muscular covering from the embryonic stage [10]. Muscular sheath is a derivative of the left sinus horn with some involvement from developing adjacent LA [21]. This double muscular covering of the CS plays an important role in interatrial connection [22]. The CS anomalies are classified by Mantini et al. [66], e.g. enlargement of CS, absence of CS, atresia of RA CS ostium, and hypoplasia of the CS [23]. These anomalies also affect the electrophysiological characteristics of CS. Ambrose et al.[24] reported the relationship between CS ostium enlargement and supraventricular tachycardia in children. CS ablation can be done in patients with AF with CS anomalies even without prior PVs isolation [25].

Barceló et al.[17] described three discrete layers including endocardium, myocardium, and epicardium similar to those of four cardiac chambers, which makes it different from other cardiac veins. In contrast to veins, the CS contains myocardial tissue, which is a continuation of left atrium muscles [21, 26], consisting of striated myofibrils like those of myocardium with intercalated discs; Jan Evangelista Purkyně was probably the first to discover this important fact [27]. On the posterior surface of CS, multiple Purkinje like cells with typical features like clear perinuclear halo, are present near the entrance of oblique Marshall veins [17]. In addition, cells similar to those of sinus node (P cells) with increased quantity of merged connective tissue were also found. Rossi [28] demonstrated that P-like cells were embryologically derived from primitive myocardial cells; the authors described multiple ganglionic neurons below the epicardial layer of the CS on the posterior aspect. Recently, Kugler et al.[29] discovered Purkinje-like cells in the myocardial layer of CS, which may be an important part of the mechanisms for AF initiation and maintenance due their conduction properties.

The CS is becoming an important subject of investigation in cardiac electrophysiological techniques; mainly, it provides access to the left heart for the implantation of biventricular pacing, epicardial mapping, and ablation techniques. It provides a route through epicardial surface to access atrial and ventricular accessory pathways [3, 30]. Total occlusion of left circumflex artery during ablation inside the CS can lead to life-threatening arrhythmias [31, 32]. Other complications like sudden cardiac death followed by ventricular fibrillation have been reported [31]. Due to its anatomic and electrophysiological relationship with atria, CS can be used to localize the origin of multifocal atrial tachycardia from either atrium by using electrophysiological mapping, where a high-frequency, higher-amplitude component indicates a near-field potential originating from the myocardial tissue of the CS, and a low-frequency, lower-amplitude component indicates a far-field potential from the activation of the adjacent LA [33, 34].

RF is the most common method currently used to ablate into the CS, usually with a three-dimensional anatomic guide system that allows detecting the areas to ablate. RF applications are delivered with maximum power set at 40–45 W and temperature control limited to 55–60°C using a standard, nonirrigated, 4-mm tip catheter. Recently, the use of catheters with irrigation and contact force has increased to deliver RF energy with higher efficacy and safety, with the irrigation rate ranging from 10 to 20 mL/min, maximum power set at 20–25 W and temperature control limited to 40–50°C.

The CS is a myocardial connection between right and left atria, and participates in simultaneous physiological contractions of both atria [21, 35]. As mentioned earlier, the muscular sleeve around the proximal 25–50 mm of its length [35] also connects two atria. These connections may play a role in arrhythmogenesis by acting as a trigger for AF and by forming a part of reentrant circuit [36]. The amplitude of the CS signal is an indicator of LA scarring, which is thought to be an important mechanism in AF maintenance [37]. The electrophysiological properties inside and outside the coronary ostium are completely different. The way of impulse generation in both areas is also variable. Impulse generation outside the CS does not need any force [38], while CS musculature needs external stimulus, even in response to catecholamines to generate impulse [39]. Action potential in CS is similar to atrial myocytes [39]. Norepinephrine enhances and acetylcholine decreases automaticity of the CS cells during spontaneous diastolic depolarization [39]. Resting potentials in CS atrial cells are >–80 mV and also show a plateau phase during repolarization, when the activity is regular. During decreased activity, the action potential also declines to <–70 mV [39]. Conduction block occurs due to a different nature of tissue, on the outside and inside of CS ostium. Habib et al. [42] showed in their study that CS musculature is capable of spontaneous depolarization and slow conduction, showing intrinsic automaticity [12, 40, 41]. Blood flow through CS becomes maximum during slow ejection and protodiastolic phases of cardiac cycle [21]. CS like other veins has compliance and is not influenced by other regulatory mechanisms of coronary vessels. Habib et al. [42] demonstrated clinical importance of connections between right and left atria which could be a source of arrhythmias, like AF [7, 42].

In 1907, Erlanger and Blackman [43] explained rhythmogenicity of CS. They cut atria into small slices and observed rhythmicity of those small pieces and interpreted results on an anatomical basis. AF may be triggered by the spontaneous firing of the CS cells [29, 42], and the main mechanism of its maintenance is re-entry phenomenon, and CS is involved in this re-entry mechanism as suggested by Morita et al. [45], where CS has an important role in triggering, maintenance, and recurrence of AF [36, 44]. The role of pulmonary veins in AF pathogenesis is well established [46] for paroxysmal AF, but pulmonary vein ablation is not sufficient to treat persistent AF. This failure to address persistent AF using pulmonary vein ablation demonstrates an additional re-entry mechanism, probably involvement of CS. Rotter et al.[47] published a case of a 59-year-old patient, who underwent RF catheter ablation (RFCA) of PVIs even with modified substrate ablation including joining superior PVs and anterior mitral annulus. There was clinical improvement, but AF recurrences were evidenced; further mapping showed an independent localized source of AF originating from CS. After CS isolation, there was no more recurrence of AF. CS is the structure observed with focal origin of atrial tachycardia [48, 49].

CS is a well-developed interatrial connection. Interruption in the electrical activity of CS may improve the results of RFCA for AF because usually unstable re-entrant circuits appear in CS musculature and its atrial junctions [45]. This was demonstrated by Morita et al. [45] in their RFCA 3-step procedure of CS isolation with conduction monitoring during CS pacing. The first step was circular ablation of CS ostium to block electrical conduction between CS ostium and RA. Then in the second step, a 13.8 ± 7.5 mm linear ablation was performed between proximal CS and LA junction. After the first two steps, a connection was still found between distal CS and LA junction in 12 tissues. Finally, the third step with a 8.3 ± 2.5 mm linear lesion was made by RF energy. After the first step of RFCA, RA activation was significantly delayed as before RFCA activation of both atria was direct during CS pacing. After the second step of RFCA, LA and RA activation was significantly delayed leading to a complete block after the third step of RFCA. But after complete isolation of CS, there were still some electrical signals from distal CS to LA junction associated with the vein of Marshall [45]. Recently, Yin et al.[50] reported that the frequency of AF was significantly higher in proximal CS and a lower distal CS/proximal CS ratio (<67%) indicates better long-term outcome. Pambrun et al. [51] confirmed these data, showing that RF ablation of epicardium muscular bundles in CS is an important step to achieve the resolution of AF in a short time follow-up as mentioned in Table 1.

Table 1.

Summary of radiofrequency ablation for coronary sinus to treat atrial fibrillation

Summary of radiofrequency ablation for coronary sinus to treat atrial fibrillation
Summary of radiofrequency ablation for coronary sinus to treat atrial fibrillation

In this review, as well as the study by Mainigi et al.[54], it was suggested that CS might be an arrhythmogenic substrate and play a role in AF recurrence in post PVI patients. Di Biase et al.[55] recommend that for treatment of persistent AF, ablation of nonpulmonary vein triggers of AF including CS in addition to PVI, improves the long-term outcome of RFCA by decreasing the recurrences. Sanders et al. [56] have reported a successful electrical disconnection of CS from RA and LA where focal ablation inside CS was not successful.

CS is recognized as a common area for fractionated electrograms and used as a target for ablation in persistent AF [5, 41, 57, 58]. Multiple factors are involved in the pathogenesis and recognition of AF substrate; the most common indicator is complex fractionated atrial electrograms (CFAEs) with short AF cycle length [58]. In 1997, Konings et al.[59] have for the first time explained fractionated electrograms, showing slow conduction areas in AF patients. Nademanee et al.[40] have for the first time demonstrated that CFAEs could be an ideal target for ablations in patients with AF. The targeted ablation of CFAEs has a great impact on long-term maintenance of the sinus rhythm in spite of LA enlargement [60]. In addition to PV ablation, CFAE ablation significantly improves results in persistent AF [61]. Forleo et al. [62] described the highest prevalence of CFAEs in distal CS, while Teh et al.[58] have demonstrated in their study that prevalence of CFAEs and short AF cycle length was higher in proximal CS, whereas the study by Boles et al.[63] suggested their presence in both the proximal and distal CS depending on whether they originated from RA or LA. Yoshida et al. [30] have suggested that the frequency and complexity of CS CFAEs might indicate the presence of AF sources and that dominant frequencies decrease within the CS might predict procedural success. Boles et al.[63] reported that CS CFAEs can predict the recurrence of AF after the ablation procedure. In conclusion, the high prevalence of CFAEs in CS and the good impact of CFAE target ablation on persistent AF suggest a role of CS in AF recurrence even after PV isolation.

AF is the most common atrial arrhythmia in humans [46], which is increasing exponentially. The incidence increases with the advancing age. The PVs are common, and important structures are involved in the initiation of AF [46]. Since the last decade, one of the burning questions has been, “What is the underlying mechanism of AF or which part of the heart is responsible for initiation and maintenance of AF, especially recurrence after PV ablation.” To achieve successful results in chronic AF, emphasis on nonpulmonary triggers is of utmost importance [55]. This is becoming very challenging these days especially with the arrival of novel ablation therapies in the field of electrophysiology, with high hopes of recovery from AF. Initially, these new ablation techniques showed promising results; however, after a short period physicians realized that even PV ablation was not very successful for persistent AF. This indicates that PVs are not the right ablation target for persistent AF. In order to find the right target for ablation, we have tried to systematically analyze the way of mapping and isolating PVs. New techniques of mapping the accessory pathways have allowed us to find answers to our question of failure to achieve significant outcomes with RF ablation. Several studies have provided sufficient evidence about the role of CS in AF maintenance, due to its connections with RA and LA. There is also embryological evidence that CS is involved in conduction and may be the origin of macro re-entrant circuits to maintain AF, even after PVIs. Interesting data come from CFAEs records, which demonstrate good clinical outcome after ablation of CFAEs to terminate persistent AF [64]. Ablation of drivers in CFAE has been found to be sufficient to terminate persistent AF in the majority of patients [65]. As reported earlier, CFAEs with short cycle lengths are suggestive of AF substrate [58], and several studies have identified them in CS. The presence of CFAEs gives us a clue about arrhythmogenicity of CS and its significance that involves the evaluation of cycle length in persistent AF.

The CS is not only a vascular structure but rather a developmental, anatomical, and electrophysiological part of the cardiac electrical conduction system. The CS plays a major role in maintenance and recurrence of AF. This knowledge may help in the management of therapeutic choices for persistent AF ablation.

The authors declare that they have no conflicts of interest.

1.
Matsuyama
TA
,
Ho
SY
,
McCarthy
KP
,
Ueda
A
,
Makimoto
H
,
Satomi
K
, et al
Anatomic assessment of variations in myocardial approaches to the atrioventricular node
.
J Cardiovasc Electrophysiol
.
2012
Apr
;
23
(
4
):
398
403
.
[PubMed]
1045-3873
2.
Morita
H
,
Zipes
DP
,
Morita
ST
,
Wu
J
.
The role of coronary sinus musculature in the induction of atrial fibrillation
.
Heart Rhythm
.
2012
Apr
;
9
(
4
):
581
9
.
[PubMed]
1547-5271
3.
Haïssaguerre
M
,
Hocini
M
,
Takahashi
Y
,
O’Neill
MD
,
Pernat
A
,
Sanders
P
, et al
Impact of catheter ablation of the coronary sinus on paroxysmal or persistent atrial fibrillation
.
J Cardiovasc Electrophysiol
.
2007
Apr
;
18
(
4
):
378
86
.
[PubMed]
1045-3873
4.
Lin
WS
,
Tai
CT
,
Hsieh
MH
,
Tsai
CF
,
Lin
YK
,
Tsao
HM
, et al
Catheter ablation of paroxysmal atrial fibrillation initiated by non-pulmonary vein ectopy
.
Circulation
.
2003
Jul
;
107
(
25
):
3176
83
.
[PubMed]
0009-7322
5.
Haïssaguerre
M
,
Sanders
P
,
Hocini
M
,
Takahashi
Y
,
Rotter
M
,
Sacher
F
, et al
Catheter ablation of long-lasting persistent atrial fibrillation: critical structures for termination
.
J Cardiovasc Electrophysiol
.
2005
Nov
;
16
(
11
):
1125
37
.
[PubMed]
1045-3873
6.
Pavin
D
,
Boulmier
D
,
Daubert
JC
,
Mabo
P
.
Permanent left atrial tachycardia: radiofrequency catheter ablation through the coronary sinus
.
J Cardiovasc Electrophysiol
.
2002
Apr
;
13
(
4
):
395
8
.
[PubMed]
1045-3873
7.
Volkmer
M
,
Antz
M
Fau - Hebe J, Hebe J Fau - Kuck K-H and Kuck KH. Focal atrial tachycardia originating from the musculature of the coronary sinus.
8.
Katritsis
D
,
Ioannidis
JP
,
Giazitzoglou
E
,
Korovesis
S
,
Anagnostopoulos
CE
,
Camm
AJ
.
Conduction delay within the coronary sinus in humans: implications for atrial arrhythmias
.
J Cardiovasc Electrophysiol
.
2002
Sep
;
13
(
9
):
859
62
.
[PubMed]
1045-3873
9.
Eckardt
L
,
Haverkamp
W
,
Breithardt
G
.
Antiarrhythmic therapy in heart failure
.
Heart Fail Monit
.
2002
;
2
(
4
):
110
9
.
[PubMed]
1470-8590
10.
Knecht
S
,
O’Neill
MD
,
Matsuo
S
,
Lim
KT
,
Arantes
L
,
Derval
N
, et al
Focal arrhythmia confined within the coronary sinus and maintaining atrial fibrillation
.
J Cardiovasc Electrophysiol
.
2007
Nov
;
18
(
11
):
1140
6
.
[PubMed]
1045-3873
11.
Gaita
F
,
Paperini
L
,
Riccardi
R
,
Ferraro
A
.
Cryothermic ablation within the coronary sinus of an epicardial posterolateral pathway
.
J Cardiovasc Electrophysiol
.
2002
Nov
;
13
(
11
):
1160
3
.
[PubMed]
1045-3873
12.
Ho
SY
,
Sánchez-Quintana
D
,
Becker
AE
.
A review of the coronary venous system: a road less travelled
.
Heart Rhythm
.
2004
May
;
1
(
1
):
107
12
.
[PubMed]
1547-5271
13.
Ratajczyk-Pakalska
E
,
Błoch
P
,
Kulig
A
.
Termination of the coronary sinus in the left atrium
.
Folia Morphol (Warsz)
.
1989
;
48
(
1-4
):
151
5
.
[PubMed]
0015-5659
14.
Silver
MA
,
Rowley
NE
.
The functional anatomy of the human coronary sinus
.
Am Heart J
.
1988
May
;
115
(
5
):
1080
4
.
[PubMed]
0002-8703
15.
Katritsis
DG
.
Arrhythmogenicity of the coronary sinus
.
Indian Pacing Electrophysiol J
.
2004
Oct
;
4
(
4
):
176
84
.
[PubMed]
0972-6292
16.
Ahmed
N
,
Rungatscher
A
,
Linardi
D
,
Molon
G
,
Luciani
GB
,
Faggian
G
.
PP-158 Coronary Sinus Can Be Target for Permanent Atrial Fibrillation Ablation Therapy?
Am J Cardiol
.
2016
;
117
:
S98
. 0002-9149
17.
Stertzer ABLMDlFSH
.
ANATOMIC AND HISTOLOGIC REVIEW OF THE CORONARY SINUS
.
Int J Morphol
.
2004
.0717-9367
18.
von Lüdinghausen
M
.
The venous drainage of the human myocardium
.
Adv Anat Embryol Cell Biol
.
2003
;
168
:
I
VIII
.
[PubMed]
0301-5556
19.
Wessels
A
,
Sedmera
D
.
Developmental anatomy of the heart: a tale of mice and man
.
Physiol Genomics
.
2003
Nov
;
15
(
3
):
165
76
.
[PubMed]
1094-8341
20.
Kronzon
I
,
Tunick
PA
,
Jortner
R
,
Drenger
B
,
Katz
ES
,
Bernstein
N
, et al
Echocardiographic evaluation of the coronary sinus
.
J Am Soc Echocardiogr
.
1995
Jul-Aug
;
8
(
4
):
518
26
.
[PubMed]
0894-7317
21.
Chauvin
M
,
Shah
DC
,
Haïssaguerre
M
,
Marcellin
L
,
Brechenmacher
C
.
The anatomic basis of connections between the coronary sinus musculature and the left atrium in humans
.
Circulation
.
2000
Feb
;
101
(
6
):
647
52
.
[PubMed]
0009-7322
22.
v. Lüdinghausen M, Ohmachi N and Boot C. Myocardial coverage of the coronary sinus and related veins. Clinical Anatomy. 1992;5:1-15.
23.
Tassinari
CC
,
Munha
JM
,
Teixeira
W
,
Palacios
T
,
Nutman
AP
.
S CS, Santos AP and Calado BO. The imataca complex, NW amazonian craton, venezuela: crustal evolution and integration of geochronological and petrological cooling histories
.
Episodes
.
2004
;
27
:
3
12
.0705-3797
24.
Ambrose
MB
,
Avari Silva
JN
,
Rudokas
M
,
Bowman
TM
,
Murphy
J
,
Van Hare
GF
.
Coronary sinus morphology in pediatric patients with supraventricular tachycardia
.
J Interv Card Electrophysiol
.
2018
Mar
;
51
(
2
):
163
8
.
[PubMed]
1383-875X
25.
Justaniah
A
,
Mckee
B
,
Silver
J
,
Wald
C
,
Flacke
S
.
Coronary sinus to left atrium communication
.
J Radiol Case Rep
.
2013
Dec
;
7
(
12
):
16
20
.
[PubMed]
1943-0922
26.
Zabina
B
,
Singla
RK
,
Sharma
RK
,
Bala
N
.
Morphological and Morphometric Study of Coronary Sinus in North Indian Population
.
J Clin Diagn Res
.
2017
Sep
;
11
(
9
):
AC15
9
.
[PubMed]
2249-782X
27.
Steiner
I
.
[A hitherto unknown priority of Jan Ev. Purkyne—myocardial sleeves of the pulmonary veins. Contribution to the pathogenesis of atrial fibrillation]
.
Cas Lek Cesk
.
2005
;
144
(
10
):
709
10
.
[PubMed]
0008-7335
28.
Rossi
LM
.
L. Clinico-pathological Approach to Cardiac Arrhythmias. A Color Atlas. Clinico-pathological Approach to Cardiac Arrhythmias A Color Atlas
.
Torino
:
Centro Scientifico Torinense Editore
;
1990
.
29.
Kugler
S
,
Nagy
N
,
Rácz
G
,
Tőkés
AM
,
Dorogi
B
,
Nemeskéri
Á
.
Presence of cardiomyocytes exhibiting Purkinje-type morphology and prominent connexin45 immunoreactivity in the myocardial sleeves of cardiac veins
.
Heart Rhythm
.
2018
Feb
;
15
(
2
):
258
64
.
[PubMed]
1547-5271
30.
Yoshida
K
,
Chugh
A
,
Good
E
,
Crawford
T
,
Myles
J
,
Veerareddy
S
, et al
A critical decrease in dominant frequency and clinical outcome after catheter ablation of persistent atrial fibrillation
.
Heart Rhythm
.
2010
Mar
;
7
(
3
):
295
302
.
[PubMed]
1547-5271
31.
Makimoto
H
,
Zhang
Q
,
Tilz
RR
,
Wissner
E
,
Cuneo
A
,
Kuck
KH
, et al
Aborted sudden cardiac death due to radiofrequency ablation within the coronary sinus and subsequent total occlusion of the circumflex artery
.
J Cardiovasc Electrophysiol
.
2013
Aug
;
24
(
8
):
929
32
.
[PubMed]
1045-3873
32.
Takahashi
Y
,
Jaïs
P
,
Hocini
M
,
Sanders
P
,
Rotter
M
,
Rostock
T
, et al
Acute occlusion of the left circumflex coronary artery during mitral isthmus linear ablation
.
J Cardiovasc Electrophysiol
.
2005
Oct
;
16
(
10
):
1104
7
.
[PubMed]
1045-3873
33.
Traykov
VB
,
Pap
R
,
Shalganov
TN
,
Bencsik
G
,
Makai
A
,
Gallardo
R
, et al
Electrogram analysis at the His bundle region and the proximal coronary sinus as a tool to predict left atrial origin of focal atrial tachycardias
.
Europace
.
2011
Jul
;
13
(
7
):
1022
7
.
[PubMed]
1099-5129
34.
Traykov
VB
.
Mapping strategies in focal atrial tachycardias demonstrating early septal activation: distinguishing left from right
.
Curr Cardiol Rev
.
2015
;
11
(
2
):
111
7
.
[PubMed]
1573-403X
35.
Sánchez-Quintana
D
,
López-Mínguez
JR
,
Pizarro
G
,
Murillo
M
,
Cabrera
JA
.
Triggers and anatomical substrates in the genesis and perpetuation of atrial fibrillation
.
Curr Cardiol Rev
.
2012
Nov
;
8
(
4
):
310
26
.
[PubMed]
1573-403X
36.
January
CT
,
Wann
LS
,
Alpert
JS
,
Calkins
H
,
Cigarroa
JE
,
Cleveland
JC
 Jr
, et al;
American College of Cardiology/American Heart Association Task Force on Practice Guidelines
.
2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society
.
J Am Coll Cardiol
.
2014
Dec
;
64
(
21
):
e1
76
.
[PubMed]
0735-1097
37.
Attanasio
P
,
Qaiyumi
D
,
Rohle
R
,
Wutzler
A
,
Safak
E
,
Muntean
B
,
Boldt
LH
,
Pieske
B
,
Haverkamp
W
and
Huemer
M
. Coronary sinus signal amplitude predicts left atrial scarring. cta ardiol.
2017
.
38.
Wit
AL
,
Cranefield
PF
.
Triggered and automatic activity in the canine coronary sinus
.
Circ Res
.
1977
Oct
;
41
(
4
):
434
45
.
[PubMed]
0009-7330
39.
Wit
AL
. coronary sinus electrophysiology and arrhythmogenesis: historical developments. Thoracic vein arrhythmogenesis: mechanisms and treatment.
2004
:21.
40.
Nademanee
K
,
McKenzie
J
,
Kosar
E
,
Schwab
M
,
Sunsaneewitayakul
B
,
Vasavakul
T
, et al
A new approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate
.
J Am Coll Cardiol
.
2004
Jun
;
43
(
11
):
2044
53
.
[PubMed]
0735-1097
41.
Oral
H
,
Chugh
A
,
Good
E
,
Wimmer
A
,
Dey
S
,
Gadeela
N
, et al
Radiofrequency catheter ablation of chronic atrial fibrillation guided by complex electrograms
.
Circulation
.
2007
May
;
115
(
20
):
2606
12
.
[PubMed]
0009-7322
42.
Habib
A
,
Lachman
N
,
Christensen
KN
and
Asirvatham
SJ
.
The anatomy of the coronary sinus venous system for the cardiac electrophysiologist.
Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology.
2009
;11 Suppl 5:v15-21.
43.
J E and JR B.
A study of relative rhythmicity and conductivity in various regions of the auricles of the mammalian heart
.
Am J Physiol
.
1907
.0002-9513
44.
Romero
J
,
Gianni
C
,
Di Biase
L
,
Natale
A
.
Catheter Ablation for Long-Standing Persistent Atrial Fibrillation
.
Methodist DeBakey Cardiovasc J
.
2015
Apr-Jun
;
11
(
2
):
87
93
.
[PubMed]
1947-6094
45.
Morita
H
,
Zipes
DP
,
Morita
ST
,
Wu
J
.
Isolation of canine coronary sinus musculature from the atria by radiofrequency catheter ablation prevents induction of atrial fibrillation
.
Circ Arrhythm Electrophysiol
.
2014
Dec
;
7
(
6
):
1181
8
.
[PubMed]
1941-3149
46.
Haïssaguerre
M
,
Jaïs
P
,
Shah
DC
,
Takahashi
A
,
Hocini
M
,
Quiniou
G
, et al
Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins
.
N Engl J Med
.
1998
Sep
;
339
(
10
):
659
66
.
[PubMed]
0028-4793
47.
Martin Rotter
M
,
Prashanthan Sanders
M
.
PhD; Yoshihide Takahashi M, Li-Fern Hsu M, Frederic Sacher M, Mélèze Hocini M, Pierre Jaïs M and Michel Haïssaguerre M
.
Coronary Sinus Tachycardia Driving Atrial Fibrillation. Images in Cardiovascular Medicine
;
2004
.
48.
Chugh
A
,
Oral
H
,
Good
E
,
Han
J
,
Tamirisa
K
,
Lemola
K
, et al
Catheter ablation of atypical atrial flutter and atrial tachycardia within the coronary sinus after left atrial ablation for atrial fibrillation
.
J Am Coll Cardiol
.
2005
Jul
;
46
(
1
):
83
91
.
[PubMed]
0735-1097
49.
Yamada
T
,
Murakami
Y
,
Plumb
VJ
,
Kay
GN
.
Focal atrial fibrillation originating from the coronary sinus musculature
.
Heart Rhythm
.
2006
Sep
;
3
(
9
):
1088
91
.
[PubMed]
1547-5271
50.
Yin
X
,
Zhao
Z
,
Gao
L
,
Chang
D
,
Xiao
X
,
Zhang
R
, et al
Frequency Gradient Within Coronary Sinus Predicts the Long-Term Outcome of Persistent Atrial Fibrillation Catheter Ablation
.
J Am Heart Assoc
.
2017
Mar
;
6
(
3
):
e004869
.
[PubMed]
2047-9980
51.
Pambrun
T
,
Denis
A
,
Duchateau
J
,
Sacher
F
,
Hocini
M
,
Jaïs
P
, et al
MARSHALL bundles elimination, Pulmonary veins isolation and Lines completion for ANatomical ablation of persistent atrial fibrillation: MARSHALL-PLAN case series
.
J Cardiovasc Electrophysiol
.
2019
Jan
;
30
(
1
):
7
15
.
[PubMed]
1045-3873
52.
Fassini
G
,
Riva
S
,
Chiodelli
R
,
Trevisi
N
,
Berti
M
,
Carbucicchio
C
, et al
Left mitral isthmus ablation associated with PV Isolation: long-term results of a prospective randomized study
.
J Cardiovasc Electrophysiol
.
2005
Nov
;
16
(
11
):
1150
6
.
[PubMed]
1045-3873
53.
Oral
H
,
Ozaydin
M
,
Chugh
A
,
Scharf
C
,
Tada
H
,
Hall
B
, et al
Role of the coronary sinus in maintenance of atrial fibrillation
.
J Cardiovasc Electrophysiol
.
2003
Dec
;
14
(
12
):
1329
36
.
[PubMed]
1045-3873
54.
Mainigi
SK
,
Sauer
WH
,
Cooper
JM
,
Dixit
S
,
Gerstenfeld
EP
,
Callans
DJ
, et al
S D, Gerstenfeld EP, Callans DJ, Russo AM, Verdino RJ, Lin D, Zado ES and Marchlinski FE. Incidence and predictors of very late recurrence of atrial fibrillation after ablation
.
J Cardiovasc Electrophysiol
.
2007
;
18
(
1
):
6
. 1045-3873
55.
Di Biase
L
,
Santangeli
P
,
Natale
A
.
How to ablate long-standing persistent atrial fibrillation?
Curr Opin Cardiol
.
2013
Jan
;
28
(
1
):
26
35
.
[PubMed]
1531-7080
56.
Sanders
P
,
Jaïs
P
,
Hocini
M
,
Haïssaguerre
M
.
Electrical disconnection of the coronary sinus by radiofrequency catheter ablation to isolate a trigger of atrial fibrillation
.
J Cardiovasc Electrophysiol
.
2004
Mar
;
15
(
3
):
364
8
.
[PubMed]
1045-3873
57.
Haïssaguerre
M
,
Hocini
M
,
Sanders
P
,
Takahashi
Y
,
Rotter
M
,
Sacher
F
, et al
Localized sources maintaining atrial fibrillation organized by prior ablation
.
Circulation
.
2006
Feb
;
113
(
5
):
616
25
.
[PubMed]
0009-7322
58.
Teh
AW
,
Kalman
JM
,
Kistler
PM
,
Lee
G
,
Sutherland
F
,
Morton
JB
, et al
Prevalence of fractionated electrograms in the coronary sinus: comparison between patients with persistent or paroxysmal atrial fibrillation and a control population
.
Heart Rhythm
.
2010
Sep
;
7
(
9
):
1200
4
.
[PubMed]
1547-5271
59.
Konings
KT
,
Smeets
JL
,
Penn
OC
,
Wellens
HJ
,
Allessie
MA
.
Configuration of unipolar atrial electrograms during electrically induced atrial fibrillation in humans
.
Circulation
.
1997
Mar
;
95
(
5
):
1231
41
.
[PubMed]
0009-7322
60.
Nair
M
,
Nayyar
S
,
Rajagopal
S
,
Balachander
J
,
Kumar
M
.
Results of radiofrequency ablation of permanent atrial fibrillation of [{GT}]2 years duration and left atrial size [{GT}]5 cm using 2-mm irrigated tip ablation catheter and targeting areas of complex fractionated atrial electrograms
.
Am J Cardiol
.
2009
Sep
;
104
(
5
):
683
8
.
[PubMed]
0002-9149
61.
Estner
HL
,
Hessling
G
,
Ndrepepa
G
,
Wu
J
,
Reents
T
,
Fichtner
S
, et al
Electrogram-guided substrate ablation with or without pulmonary vein isolation in patients with persistent atrial fibrillation
.
Europace
.
2008
Nov
;
10
(
11
):
1281
7
.
[PubMed]
1099-5129
62.
Forleo
GB
,
Mantica
M
,
De Luca
L
,
Dello Russo
A
,
Casella
M
,
Santini
L
, et al
Impact of pre-existent areas of complex fractionated atrial electrograms on outcome after pulmonary vein isolation
.
J Interv Card Electrophysiol
.
2008
Apr
;
21
(
3
):
227
34
.
[PubMed]
1383-875X
63.
Boles
U
,
Gul
EE
,
Enriquez
A
,
Starr
N
,
Haseeb
S
,
Abdollah
H
, et al
Coronary Sinus Electrograms May Predict New-onset Atrial Fibrillation After Typical Atrial Flutter Radiofrequency Ablation (CSE-AF)
.
J Atr Fibrillation
.
2018
Jun
;
11
(
1
):
1809
1809
.
[PubMed]
1941-6911
64.
Anusionwu
O
,
Calkins
H
.
Catheter Ablation of Long Standing Persistent Atrial Fibrillation: lessons Learned
.
J Atr Fibrillation
.
2013
Feb
;
5
(
5
):
680
.
[PubMed]
1941-6911
65.
Ammar-Busch
S
,
Reents
T
,
Knecht
S
,
Rostock
T
,
Arentz
T
,
Duytschaever
M
, et al
Correlation between atrial fibrillation driver locations and complex fractionated atrial electrograms in patients with persistent atrial fibrillation
.
Pacing Clin Electrophysiol
.
2018
Oct
;
41
(
10
):
1279
85
.
[PubMed]
0147-8389
66.
Mantini E, Grondin CM, Lillehei CW, Edwards JE. (1966). Congenital Anomalies Involving the Coronary Sinus. Circulation. 1966;33(2):317-327.

An abstract of this study has been presented at 12th International Congress of Update in Cardiology and Cardiovascular Surgery, Antalya, March 2016, and published in American Journal of Cardiology (supplemental issue).

Copyright / Drug Dosage / Disclaimer
Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.