Superior Right Atrium Landmarks

The most important landmark of the roof of the RA is the superior cavoatrial junction and the structures around it (Fig. 12‑14). In this region, the crista terminalis originates anterior to the orifice of the SVC (Fig. 12‑19 , Fig. 12‑20). Laterally, the crista terminalis continues its normal anatomical course in the lateral RA wall. Medially, the crista terminalis blends with the interatrial muscular bundle commonly known as Bachmann’s bundle (Fig. 12‑19).

In some CT images of the heart a large pectinate muscle trabeculation band is seen arising from the precaval portion of the crista terminalis. This parasagittal band is a remnant of the septum spurium and should not be mistaken with intra-atrial thrombus (Fig. 12‑20).

Another important landmark in the superior portion of the RA is the SA node. The SA node is a banana-shaped structure in the subepicardial side of superior cavoatrial junction within the crista terminalis ⁴ (Fig. 12‑21). The mean length of the SA node is reported 20 ± 3 mm ⁴ and its cross-sectional diameter is usually less than 5 mm. ⁵ It is the source of the cardiac impulse and composed of specialized cells slightly smaller than normal working cells. With age, the amount of connective and fatty tissue increases with respect to the area occupied by the nodal cells and the node becomes atrophic. ^{5 ,​ 6} The SA node can be localized in axial CT images by locating the SA node artery passing along the crista terminalis (Fig. 12‑22). The SA node gradually penetrates musculature of the crest to rest in the subendocardium. Because of the vicinity of the SA node to the epicardial surface, it may be damaged in selected cardiac surgeries or extensive pericardial diseases. ⁷ Modification of the sinus node activity using radiofrequency ablation (RFA) has been established as a treatment for inappropriate sinus tachycardia. ⁸

The SA node artery is usually, a single branch, arising from the proximal RCA (60%) or left circumflex (LCx) artery (40%) ^{7 ,​ 9} (Fig. 12‑23). In an anatomical study of the conduction system arteries by CT scan, single SA node artery from the RCA was seen in 66% and from the LCx artery in 28% of studies. ¹⁰ A dual blood supply to SA node was seen in 6%: one from the RCA and the other from the LCx artery. Regardless of its artery of origin, the SA node artery usually courses along the superior interatrial groove toward the superior cavoatrial junction (Fig. 12‑23). At the cavoatrial junction, SA node artery course becomes variable and may circle either anteriorly (precaval) or posteriorly (retrocaval) to enter the node ¹⁰ (Fig. 12‑24).

Anterolateral Right Atrium Landmarks

The body of the crista terminalis is an important structure in the lateral RA wall that could be the source of several forms of atrial tachyarrhythmias. ¹¹ The crista terminalis varies in size and extent in different individuals and should not be mistaken with intra-atrial pathology (Fig. 12‑25). Excess epicardial fat can infiltrate around the RA causing marked thickening of the crista terminalis which may mimic a mass (Fig. 12‑25, lower row). It may be associated with lipomatous hypertrophy of the interatrial septum. ¹² Both conditions are due to excessive accumulation of fat in the epicardial space. ¹³

Medially and superiorly, the crista terminalis connects to the interatrial Bachmann bundle (Fig. 12‑19). On the right, this broad band of circumferential interatrial myofibers can be traced to the junction of the RA and SVC (Fig. 12‑27). On the left, the bundle blends on the epicardial musculature of the LA toward the neck of the left atrial appendage (LAA) (Fig. 12‑27). ^{14 ,​ 15} This interatrial band ensures rapid interatrial conduction, leading to physiological biatrial contraction. Changes in the musculature of Bachmann’s bundle could block or prolong interatrial conduction resulting in abnormal atrial excitability, atrial dysfunction, atrial fibrillation (AF), and other arrhythmias. ¹⁶ The principal vascular supply of Bachmann’s bundle is believed to stem from the SA node artery and its branches ¹⁷ (Fig. 12‑26). Anatomical variants of this region are common (Fig. 12‑27). An anatomical study of Bachmann’s bundle and its vascular supply by CT in normal and abnormal patients showed that Bachmann’s bundle was less visible in the patients with severe coronary artery disease as it was replaced with fat ¹⁷ (Fig. 12‑27).

Inferior Right Atrium Landmarks

The inferior part of the RA is an interesting area with several important anatomical landmarks. The IVC and the coronary sinus connect to this portion of the RA. The Eustachian valve is seen at the anterior margin of the IVC (Fig. 12‑28). It is a remnant of the embryonic right valve of the sinus venosus. Embryologically, the Eustachian valve directs oxygenated blood from the IVC across the patent foramen ovale (PFO) into the systemic circulation. ¹⁸ It is usually membranous and variably developed. It may look fenestrated or contain muscles. Usually, it inserts medially to the Eustachian ridge at the medial atrial wall. In some cases, the Eustachian valve is large, causing difficulty to pass a catheter (Fig. 12‑29). Patients with large Eustachian valve have a higher incidence of PFO. ¹⁶

The inferior wall of the RA between the IVC and the tricuspid valve is a quadrilateral region known as “cavotricuspid isthmus.” ¹⁹ This part of the right atrial vestibule is the target of catheter ablation techniques for isthmus-dependent atrial flutter. ²⁰ There are variable sizes and morphology that changes with cardiac cycle with the largest diameters during midventricular systole. ²¹ Obstacles such as large Eustachian ridge/valve, aneurysmal pouches, or even a concave deformation of the entire isthmus may lead to more difficult ablation sessions. Therefore, knowledge of anatomical variants of this region is very important ²¹ (Fig. 12‑30 , Fig. 12‑31 , Fig. 12‑32).

It is common to observe outpouchings in the medial and lateral margins of the inferior wall of the RA. The medial outpouching inferior to the orifice of the coronary sinus is known as the sub-Eustachian sinus of Keith. It is an extension of a pouch-like isthmus under the orifice of the coronary sinus. Since it is sub-Thebesian rather than sub-Eustachian, some prefer to call it sub-Thebesian sinus/recess ² (Fig. 12‑32 , Fig. 12‑33). This anatomical variant is recognized as one of the major procedural difficulties in catheter interventions of the RA and could also be the substrate for reentrant circuit during atrial flutter.

The coronary sinus also connects the inferomedial aspect of the RA. The coronary sinus drains most epicardial coronary venous flow into the RA. Its orifice is guarded by the Thebesian valve. The valve is usually a thin semilunar fold in anteroinferior rim of the ostium and can be seen in most CT angiography studies of the heart ²² (Fig. 12‑34). The Thebesian valve is continuous with the Eustachian valve.

The Chiari network represents coarse or fine fibers in the RA, arising from the Eustachian or Thebesian valve, and strands within the RA connecting these valves with the crista terminalis, right atrial wall, or interatrial septum (Fig. 12‑35). It is a remnant of the embryonic right valve of the sinus venosus, ^{23 ,​ 24} and should be differentiated from a large Eustachian valve. The Chiari network fibers may be seen in high-quality CT or MR studies (Fig. 12‑35). It could be a risk factor for clot formation. ¹⁸

Medial Right Atrium Landmarks

The inferior part of the medial RA wall above the orifice of the coronary sinus is called the triangle of Koch. It is of significant importance to electrophysiologists because the AV node resides in this triangle and it is the site for catheter ablation procedures which are guided largely by anatomical landmarks (Fig. 12‑36 , Fig. 12‑37). The AV node consists of a compact portion near the apex and an area of transitional cells near the base of the triangle (Fig. 12‑37). The central fibrous body resides in the apex of the triangle and the ostium of the coronary sinus holds its base. When viewed from the RA, the triangle is delimited by the hinge line of the septal tricuspid leaflet on the ventricular side and the Eustachian ridge (tendon of Todaro) on the atrial side. ²⁵ The triangle of Koch is the target of ablation for AV node reentrant tachycardia (AVNRT), septal and paraseptal accessory pathways, and atypical forms of atrial flutter. ^{26 ,​ 27} The size of the triangle varies in different individuals with a mean height of 26 ± 8 mm. ^{28 ,​ 29} Patients with large triangles require additional ablations of the septal region which may increase the rate of complication. ²⁸

The vestibular atrial wall between the coronary sinus ostial rim and the hinge line of the septal leaflet of the tricuspid valve is known to electrophysiologists as the septal isthmus (Fig. 12‑36). It is one of the targets of ablation of the ”slow pathway” AVNRT. The AV node artery can run very close to the septal isthmus (3.5 ± 1.5 mm) being at risk of coagulation during ablation ^{28 ,​ 30} (Fig. 12‑14 b). In general, ablations for slow pathway are performed near the base of triangle where the transitional part of the AV node is located to avoid injury of the compact AV node (fast pathway) or the AV node artery. ²⁹

The tendon of Todaro runs deep in the atrial musculature (the sinus septum) between the coronary sinus and the fossa ovalis. It extends from the commissure between the Eustachian and Thebesian valves to the central fibrous body ³¹ (Fig. 12‑36). The tendon of Todaro is not visible in the internal view of the RA. Visible representative of it on the internal atrial surface is the Eustachian ridge which can be prominent enough to be visible in CT angiographies in 25% of individual ²¹ (Fig. 12‑31 , Fig. 12‑36). The significance of demonstration of a large Eustachian ridge is more related to the need for its catheter ablation to achieve a complete paraseptal isthmus block in patients with atrial flutter. ³² The AVN artery originates from the distal RCA and penetrates into the base of the posterior interatrial septum (inferior pyramidal space) at the level of crux of the heart in 80 to 90% of patients (Fig. 12‑38). In the remaining, it originates from the distal LCx artery. ^{10 ,​ 33 ,​ 34 ,​ 35}

Components of the Left Atrium

As with the RA, the LA consists of a venous component, an appendage and a supravalvular vestibule (Fig. 12‑41). Most part of the LA except the appendage is smooth-walled. The superior and posterior walls of the LA form the pulmonary venous component, with the venous orifices at each corner ³⁶ (Fig. 12‑39). In early embryonic stage, the pulmonary venous component is a small single vein that opens into the posterior LA adjacent to the developing left AV junction. Subsequent to atrial septation the venous component expands and gradually shifts superiorly to form the roof of the LA with four venous orifices on the sides.

The vestibular component surrounds the mitral orifice (Fig. 12‑16 , Fig. 12‑41). As with the developing RA, part of the initial AV canal also forms the vestibule of the mitral valve. ⁴⁰ Large branches of the LCx artery extend to the posterior aspect of the LA vestibule usually 10 mm above the ostium of the LV. In a dominant LCx artery distal branches can reach to the external crux of the heart. However, exceptions occur and large RCA branches may run in contact with the vestibule. An anatomical area of the vestibule located between the orifice of the left inferior pulmonary vein and the mitral annulus is known as left atrial or mitral isthmus ⁴¹ (Fig. 12‑42). There is marked variability in the dimensions and wall thickness of the mitral isthmus. This area may be the source of recurrence after circumferential pulmonary vein catheter ablation for AF. ⁴²

Pulmonary Vein Ostia

Normal pulmonary vein anatomy consists of two right-sided and two left-sided pulmonary veins with separate ostia (Fig. 12‑39). This arrangement is commonly variable. The pulmonary vein ostia are ellipsoid with a longer superior–inferior dimension. The right superior pulmonary vein is located close to the SVC, and the right inferior pulmonary vein projects horizontally (Fig. 12‑14). The left superior pulmonary vein is close to the LAA and the left inferior pulmonary vein courses near the descending aorta. The veins are larger in men. In patients with enlarged LA or persistent AF veins can be larger. The superior pulmonary vein ostia are larger (19–20 mm) than the inferior ostia (16–17 mm). ⁴³ The ostium of the pulmonary veins is a common location for radiofrequency catheter ablation to treat AF. The ostial diameters influence the selection of the ablation catheter size used. The pulmonary vein trunk is defined as the distance from the ostium to the first-order branch.

Common anomalies include a conjoined (common) left or right pulmonary vein in 25% of individuals. ⁴³ A conjoined pulmonary vein is seen more frequently on the left than the right side. ⁴⁴ Supernumerary veins are also frequent. The most common is a separate right middle PV, which drains the middle lobe of the lung ⁴⁵ (Fig. 12‑43). One or two middle lobe vein ostia can be seen in 26% of patients. ⁴⁴ The ostial diameter of the right middle PV is smaller than that of the other veins (mean, 9.9 ± 1.9 mm). The ectopic focus originating from the right middle PV could initiate AF, which is cured by catheter ablation of the right middle PV. In some patients, there is a supernumerary PV that shows an aberrant insertion, with a perpendicular position in relation to the LA posterior wall. The supernumerary branch usually drains the superior or posterior segment of the right upper lobe and characteristically passes behind the bronchus intermedius. In the absence of one pulmonary vein, careful examination of the intrathoracic venous system is required to exclude presence of a partial anomalous pulmonary venous return (Fig. 12‑44).

The presence of atrial myocardial tissue extending over the first centimeter of ostial wall of the pulmonary veins has been confirmed both histological examinations. ⁴⁶ The myocardial sleeve is thickest at the venoatrial junction especially in the left superior pulmonary vein. Although, different mechanisms of AF exist, these myocardial sleeves are believed to be the major source for the development of reentry that triggers AF. ⁴⁷ In the past, the most common ablation strategy was electrical isolation of the pulmonary veins by creating circumferential ablation lines around the individual or bilateral pulmonary vein ostia. The lines are either guided by fluoroscopy, 3D electroanatomical mapping, or intracardiac echocardiography. ^{48 ,​ 49} The focus of radiofrequency or cryoablation strategies shifted from the pulmonary vein to the atrial tissue located in the antrum due to the fact that many nonpulmonary vein trigger points for AF are located in the antrum rather than the pulmonary veins and that radiofrequency delivery may cause pulmonary vein stenosis. ⁵⁰ In antrum ablation, the most common sites are the LA “roof” connecting the superior aspects of the left and right upper pulmonary vein isolation lesions and the region of tissue between the mitral valve and the left inferior pulmonary vein (the mitral isthmus). ⁵¹

Incidental discovery of small membranes within the LA near the orifices of the pulmonary veins and adjacent to the superior part of the atrial septum is not rare (Fig. 12‑45). Large membranes should raise the possibility of cor triatriatum sinister. This congenital anomaly is rare but surgically correctable. ⁵²

Left Atrial Appendage

The LAA is derived from the primitive atrium and has a rough trabeculated surface. The LAA interior surface is lined by complicated network of fine pectinate muscles. The LAA is a potential site for deposition of thrombus owing to its narrow neck with the LA. ⁵³ It also appears to be responsible for triggering AF in some patients presenting for repeat procedures of catheter ablation. ⁵⁴

There is a wide variation in the configuration of the LAA (Fig. 12‑46). The LAA is characteristically a small finger-like extension of the LA with a multilobulated appearance in 80% of hearts ⁵³ (Fig. 12‑46). The tip of the LAA can be in a variety of positions, lying over the left anterior descending (LAD) coronary artery, pointing posteriorly, or even directed medially toward the back of the aorta. Using imaging, the LAA morphologies are classified into cactus (30%), chicken wing (48%), windsock (19%), and cauliflower (3%). ⁵⁴ The rate of thrombus formation is less in nondilated LAA with simple morphology compared with dilated LAAs with complicated shapes. The orifice of the LAA is at the junction of the anterior and the lateral wall, anterior to the left superior pulmonary vein. The axis is directed posteriorly, inferiorly, or anteriorly. It may rotate internally into the transverse sinus (Fig. 12‑46 c). Rarely, the tip of the LAA may reopen into the anterior wall of the LA (double orifice). The proximal portion of the LCx artery runs in contact with the inferior wall of the LAA. A variable relationship of the coronary arteries to the LAA exists.

The left lateral “ridge” between the LAA and the left pulmonary veins was first described by Keith in 1907 as the “left tenia terminalis.” The thickness of the ridge is less than 5 mm in 75% of the hearts (Fig. 12‑47, Fig. 12‑48). Thickened ridge can be mistaken for a thrombus or atrial mass. Within the fold runs the remnant of the vein of Marshall, multiple autonomic nerve bundles, and a small atrial artery which, in some cases, is the left SA node artery (S-shaped SA node artery) ^{55 ,​ 56} (Fig. 12‑47). Persistent left SVC also passes in this region. The S-shaped SA node artery is an anatomical variant of the SA node artery in 14% of coronary CT angiographies. It originates from the posterolateral part of the LCx artery ⁵⁷ (Fig. 12‑47). Surgical or catheter ablation interventions of the LA may pose this artery at risk of injury.

Accessory LAA or LA diverticula are common anatomical variants in 30% of the hearts ^{58 ,​ 59} These outpouchings are seen in two anatomical locations: the anterior wall of the LA (projects into the transverse sinus) and the left atrial isthmus (Fig. 12‑49). Description of this anatomical variant in radiology reports is required as they may interfere with ablation procedures or be a potential cause of thrombus formation.

Important Periatrial Structures

Important periatrial structures include the esophagus, vagus nerves, phrenic nerves, and descending thoracic aorta. Posterior to the posterior left atrial wall is a layer of fibrous pericardium and fibrofatty tissue of irregular thickness that contains esophageal arteries and the vagus nerve plexus (Fig. 12‑50). These anatomical structures may be affected by RFA. The esophagus follows a variable course along the posterior aspect of the LA and it is a movable structure. ⁶⁰ In 40% of cases, it passes along the middle portion of the posterior LA wall ^{37 ,​ 60} (Fig. 12‑51). Damage to the esophageal wall may rarely result in the formation of an atrial esophageal fistula.

The vagus nerves pass behind the root of the lungs and form right and left posterior pulmonary plexuses (Fig. 12‑50). Branches of the pulmonary plexuses form the posterior and anterior esophageal plexuses which enter the abdomen through the esophageal diaphragmatic opening to become the posterior and anterior vagal trunks that innervate the stomach and pyloric canal and the digestive tract as far as the proximal part of the colon. ⁶¹ Thermal injury may involve the periesophageal vagal nerves resulting in a syndrome of acute delayed gastric emptying. ⁶²

The phrenic nerves lie along the lateral mediastinum and run from the thoracic inlet to the diaphragm (Fig. 12‑52). Phrenic nerve injury results from direct thermal injury, usually to the right phrenic nerve, which is located lateral to the SVC and anterior to the right superior pulmonary vein. ^{63 ,​ 64} Less frequently, ablation within the LAA can result in the left phrenic nerve damage which may pass close to the apex of the LAA in 30% of the hearts. ⁶³ On the other hand, the left phrenic nerve passes close to the LV. CT coronary angiography can demonstrate the left phrenic neurovascular bundle as it passes over the LV pericardium in two-thirds of the studies ⁶⁵ (Fig. 12‑52).

Patent Foramen Ovale

Closure of the septum primum is complete when the valve becomes adherent to the rim to form the fossa ovalis. The size of fossa ovalis and its margins may vary greatly. In 25 to 35% in autopsy studies, ^{66 ,​ 70} the seal is incomplete leaving a crevice at the anterosuperior quadrant of the rim that allows a probe to be passed obliquely from the RA into the LA (PFO) (Fig. 12‑57). This nonfusion creates the tunnel-like PFO orientated in a craniocaudal, PA, and right-to-left axis. ⁷¹ The incidence and size of PFO do not differ with gender but varies significantly with age; 34% of PFOs occurs in the first three decades, 25% in the 4th to 8th decades, and 20% in the 9th and 10th decades. ⁶⁶ The size of PFO increases progressively from a mean of 3.4 mm in the first decade to 5.8 mm in the tenth decade (possibly because smaller defects seal with age).

Normally, the PFO is closed by the higher left atrial-to-right atrial pressure gradient. If the left atrial pressures rise (i.e., pulmonary hypertension), a small clot may pass directly from the RA into the left side and resides in different organs such as brain to cause a stroke. This condition is called paradoxical embolism. The presence of shunting through the PFO not only depends on the transatrial pressure gradient, but also likely relates to anatomical features of the PFO. These include the size of opening into the RA, length of the PFO tunnel, and the extent of excursion of the flap membrane. Moreover, the risk of stroke appears to increase in the presence of structures that direct flow toward a PFO (i.e., prominent Eustachian valve) or hemodynamic changes that increase right-sided pressure (i.e., large pulmonary embolism) (Fig. 12‑28 , Fig. 12‑29). PFO tunnel length is another important factor in increasing the chance of right-to-left shunting. In a recent MDCT study of asymptomatic individuals, 92% of the shunts occurred with a PFO tunnel length of 6 mm or less. ⁷⁰ This information may be important in patients being evaluated for possible candidates of percutaneous closure. When the flap length is very short, a bidirectional shunt is more probable. In a recent postmortem study by Ho et al, ⁷² two types of PFO were described: valve-competent and valve-incompetent. PFOs with a short, overlapping flap with an atrial septal aneurysm were classified as incompetent with high likelihood of bidirectional flow. Similar incompetent morphology has also been described using CT scanning in patients with a short PFO tunnel length or those with an atrial septal aneurysm ⁷⁰ (Fig. 12‑58).