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Ethan J. Halpern and Alyson N. Owen

Quantitative analysis of cardiac chamber geometry and ventricular function is an essential component of a complete cardiac evaluation. Many cardiac imaging studies—including echocardiography, nuclear scintigraphy, and cardiac magnetic resonance (MR) imaging—evaluate cardiac morphology and function. As part of a comprehensive cardiac imaging study, gated cardiac CT can provide an anatomically precise evaluation of chamber morphology and function, along with a detailed assessment of coronary anatomy and valves. With respect to chamber size, assessment of chamber enlargement is optimally performed with measurements indexed to body size.1 As cardiac CT is a relatively young technology, however, there are few published studies that quantify CT measurements for the assessment of cardiac morphology and function. Most of the criteria provided in this chapter are based on accepted echocardiographic standards.²

Is it appropriate to use echocardiographic standards when interpreting cardiac CT? Linear measurements of cardiac wall thickness and chamber size, as well as global measures of left ventricular (LV) function by electrocardiographically (ECG)-gated CT demonstrate a high correlation with echocardiography.³ However, several studies suggest that left atrial volume may be substantially underestimated by echocardiography compared with both CT^4,5 and MR.⁶ Our own analysis suggests that volume measurements of the left atrium obtained during ECG-gated CT are approximately twice as large as the corresponding volumes calculated from transthoracic echocardiography with apical four-chamber and two-chamber measurements.⁷ Although the discrepancy can be explained in part by geometric assumptions used for echocardiographic calculations, much of the discrepancy persists when the same echocardio-graphic formulas are applied to CT data. Our findings therefore suggest that underestimation of left atrial volume by transthoracic echocardiography is related primarily to foreshortening of the left atrium and suboptimal definition of the back wall of the atrium when visualized from the cardiac apex.

Based on our experience with cardiac CT and echocardiography, we believe that linear measurements of chamber size and wall thickness on CT correspond very well to conventional echocardiographic measurements obtained in the parasternal three-chamber view. There is no substantial foreshortening of anterior–posterior echocardiographic measurements in the parasternal view. CT measurements of ejection fraction also seem to correlate well with echocardiography.⁸ Although we provide additional echocardio-graphic standards for chamber area and volume in Table 9.1 that are generally calculated from apical views, the reader is cautioned that normative values for chamber area and volume on CT will be much larger than those defined by echocardiography. Further studies are needed to establish normative data for cardiac chamber volumes with ECG-gated CT and MR studies.

Standard Imaging Views

To assess cardiac chamber morphology, size, and function, standard views that should be obtained include the four-chamber view, three-chamber view, two-chamber view, and short-axis projection. The three-chamber and five-chamber views are useful to assess the LV outflow tract (LVOT) and aortic valve. All of these views are typically created with a maximum intensity projection (MIP) technique with 2- to 5-mm slab MIPs. Normal values are available for chamber measurements obtained from these views (see Table 9.1). LV function should be reviewed in long axis (four-chamber view, three-chamber view, and two-chamber view) as well as short axis. Accurate calculation of LV volume and ejection fraction should be performed in two orthogonal long-axis planes or with short-axis views through the entire LV.

Four-Chamber View

The four-chamber view provides an overview of all four cardiac chambers and allows a side-by-side comparison of the right-sided and left-sided chambers (Fig. 9.1). To obtain a four-chamber MIP, the heart is rotated along its short axis so that both the mitral and tricuspid valves are visible. Once both valves are optimally imaged, the image is rotated into the long axis of the heart to extend the cardiac chambers and visualize the cardiac apex. The plane of this image is different from the standard axial image obtained on CT. A four-chamber view of the normal heart demonstrates that the cardiac apex is formed by the LV and that the right-sided chamber diameters are smaller than the corresponding left-sided chamber diameters. In the four-chamber projection, the lateral wall of the LV is observed as the free wall, whereas the interventricular septum separates the two ventricles. The interatrial septum and interventricular septum may be evaluated in this view by scrolling superiorly and inferiorly. Diastolic and systolic frames in the four-chamber projection demonstrate normal motion of the atrioventricular valves, as well as normal thickening and contraction of the ventricular walls.

The three-chamber view demonstrates the LV, left atrium, and aortic root in one image (Fig. 9.2). As discussed in Chapter 10, the three-chamber view is required to assess for mitral valve prolapse. It is also the standard view (from the parasternal window) for echocardiographic M-mode assessment of the size of the LV, left atrium, and aortic root. This view is most easily obtained by identifying the shared portion of the annulus between the aortic and mitral valves—the mitral–aortic intervalvular fibrosa—on an axial image. The intervalvular fibrosa is selected as a fixed center of rotation. The heart is rotated around this point such that both the aortic and mitral valves are visualized, and the LV is elongated to image the apex of the heart. The aorta and left atrium are demonstrated above the LV. The anteroseptal wall is ipsilateral to the aortic valve; the inferolateral wall (formerly known as the posterior wall) is ipsilateral to the left atrium.

The LV diameter is measured on the three-chamber view at the level of the chordal attachments just below the tips of the mitral leaflets (Fig. 9.2). The aortic root is typically measured at the level of the sinuses of Valsalva, just above the aortic valve, although measurement of the diameter at the sinotubular junction may also be useful. The left atrium is measured along its minor axis (antero-posterior dimension), in a plane that is roughly parallel to the aortic root. This convention derives from M-mode data, although now measurements will frequently be performed on the two-dimensional image. The maximum diameters of the LV and the aortic root are measured at end diastole; the maximum diameter of the left atrium is measured at end systole. Normal values for the left atrium and ventricle are presented in Table 9.1. The expected aortic root diameter is slightly smaller than the left atrium diameter. Published equations are available that relate the precise limits of normal aortic root diameter to age and body surface area.⁹

The LVOT diameter is traditionally measured at midsystole in the (parasternal) three-chamber view, just below the plane of the aortic valve, at the level of the insertion points of the aortic valve leaflets (Fig. 9.2D). This measurement is used for echocardiographic calculation of aortic valve area with the continuity equation. Measurement errors in the echocardio-graphic assessment of LVOT diameter are a common cause of errors in calculation of aortic valve area, particularly because any measurement error is compounded by its squaring to obtain area. A more accurate estimate of the true LVOT area may be obtained with a two-dimensional CT cross-section of the LVOT. To visualize the LVOT in cross-section, an MIP is created in the short axis of the aortic valve and stepped caudally to demonstrate the short axis of the LVOT (Fig. 9.2E).

Two-Chamber View

The two-chamber projection demonstrates only the left atrium and LV, with the mitral valve separating these two chambers (Fig. 9.3). The right-sided chambers and the aorta are not visible in this projection. Starting with a four-chamber or a three-chamber view, the two-chamber view is obtained by setting the center of rotation at the center of the mitral valve and rotating the image so that the right–sided chambers and aorta are no longer visible. As with the four-chamber and three-chamber views, the imaging plane is adjusted to maximize the length of the LV and to demonstrate the LV apex. The two-chamber projection demonstrates the inferior wall of the LV along the diaphragm. The anterior wall is opposite the inferior wall.

Five-Chamber View

The four-chamber, three-chamber, and two-chamber views are obtained by rotating the imaging plane in the true long axis of the LV. Each of these views is rotated about 60 degrees from the adjacent view to provide a complete picture of the LV walls for assessment of function. The five-chamber projection is tilted away from the true long axis of the four-chamber view to provide an additional assessment of the LVOT and aortic valve (Fig. 9.4). The five-chamber view is obtained from the four-chamber view by setting the center of rotation on the cardiac apex and tilting the base of the heart in a cranial direction to demonstrate the aortic root. As with the four-chamber view, this view demonstrates the septum and the lateral walls of the LV, although the portion of the septum that is demonstrated is more anterior than that seen in the four-chamber view.

Atrial Anatomy

The two atria serve as antechambers for blood entering into their respective ventricles. The left atrium is the most superior and the most posterior of all four cardiac chambers. Inflow from the left atrium to the LV is directed in an anterior–inferior–leftward direction through the mitral valve into the LV. The right atrium is anterior, to the right, and inferior relative to the left atrium. A thin septum separates the right and left atria. The tricuspid valve is located on the anterior or left aspect of the right atrium. The right ventricular inflow (tricuspid valve) and right ventricular outflow (infundibulum to pulmonic valve) form an arc anterior to the aortic valve, perpendicular to the long axis of aortic outflow; both the tricuspid and pulmonic valves are visible along this arc on a short-axis image through the aortic valve.

Atrial diastole, the time during which the two atria fill with blood, corresponds to ventricular systole. In normal sinus rhythm, the atria distend to their maximum volume during ventricular systole. Rapid ventricular filling in early diastole results from active relaxation of the ventricles, as well as elastic recoil from the force of systolic contraction. Additional ventricular filling in late diastole is related to active contraction of the atria (atrial systole). To obtain a consistent and accurate measurement of atrial size, atrial measurements should be obtained at end systole (Fig. 9.2).

The right and left atria demonstrate narrow anterior extensions, the atrial appendages, which are visible on the surface of the heart (Figs. 9.5 and 9.6). The right atrial appendage is a relatively flat triangular structure that extends anteriorly over the right anterior surface of the heart. The anterior margin of this appendage often covers the proximal right coronary artery in the right atrioventricular (AV) groove. The left atrial appendage is a crescent-shaped structure that extends anteriorly from the left atrium, covering the left AV groove, and terminating over the junction of the left AV groove with the anterior inter-ventricular groove. The left atrial appendage often covers the left main coronary artery, as well as the origin of the circumflex and left anterior descending artery. The left atrial appendage may have a more complex configuration with accessory lobes. Both atrial appendages contain trabecular fibers known as pectinate muscles.

Anatomic variations of normal right atrial anatomy can mimic the presence of a mass. A ridge of muscle along the right side of the right atrium, the crista terminalis, extends from the IVC orifice up to the SVC orifice. The crista terminalis separates the smooth sinus venosus portion of the right atrium from the more anterior trabeculated right atrial appendage (Fig. 9.7). The crista terminalis has a variable thickness and can appear masslike within the right atrium.¹⁰ The sulcus terminalis is a subtle groove on the epicardial surface of the heart corresponding to the crista terminalis. The sinoatrial node is located in the sulcus terminalis.

The Chiari network consists of long fibers that extend from the crista terminalis to the eustachian valve. These fibers may interfere with device placement during a percutaneous interventional procedure and are a potential, although infrequent, site of right atrial thrombus or attachment of an embolus in transit. Pectinate muscles along the right atrial appendage and along the free wall of the right atrium can appear prominent and can mimic the presence of thrombus. Lipomatous hypertrophy of the interatrial septum (see below) bulges preferentially into the right atrium and may be associated with thickening of the crista terminalis. The typical location, shape, and density of these anatomic structures distinguish them from intracardiac tumor or thrombus (Fig. 9.8).¹¹

As the antechamber for the LV, the left atrium receives inflow from the pulmonary veins. Anatomic variation in the drainage of the pulmonary veins into the left atrium is discussed in detail in Chapter 11. Left atrial size has been traditionally reported by a single diameter measurement on the three-chamber view. More recent echocardiographic studies suggest that atrial volumes, calculated from four-chamber and two-chamber views, provide a more clinically relevant estimate of chamber size compared with one-dimensional measurements of atrial diameter or two-dimensional measurements of atrial area.^12,13 Area measurements of the left atrium can be quantified on the four-chamber view (Fig. 9.9) and on the two-chamber view. These areas can be converted to a volume measurement via the area-length equation: 8/3π [(A1)(A2)/L], where A1 and A2 are the areas from the four- and two-chamber views, respectively, and L is the shortest inferior–superior length from the annular plane to the back wall of the atrium. However, as noted in the introduction to this chapter, normative values for atrial volumes computed from apical four-chamber and two-chamber views by echocardiography underestimate the volumes measured by cardiac CT. Thus, although we believe it is important to assess chamber morphology on CT in standard echocardiographic projections, one must be careful not to overcall chamber enlargement based on published echocardiographic standards for chamber volume. Enlargement of the left atrium may be suggested when the atrium appears larger than the adjacent aortic root in the three-chamber view (Fig. 9.10A) or when the left atrium appears large relative to the LV on the four-chamber view (Fig. 9.10B).

Left atrial dilatation is associated with many disease processes, including LV failure, hypertension, and mitral valve disease. A dilated left atrium may be present in association with atrial fibrillation, both as a contributing cause and as a consequence of atrial fibrillation. Clot may form in a dilated left atrium, most commonly within the left atrial appendage (Fig. 9.11). Left atrial thrombus may result in embolic complications, including stroke.

The interatrial septum is a thin-walled structure between the right and left atria. The interatrial septum develops from two separate structures, the septum primum and the septum secundum. The septum primum develops first and extends toward the AV junction. The gap that is present during development between the septum primum and the AV junction is called the ostium primum. As the septum primum closes this gap, a series of fenestrations within the septum primum coalesce into the ostium secundum. The septum secundum then grows to the right of the septum primum to cover this ostium secundum. During fetal life, a connection between the atria remains as an oblique pathway that courses between the septum primum and septum secundum and through the ostium secundum, taking oxygenated blood from the placenta to the systemic circulation, bypassing the pulmonary circuit. This pathway, the foramen ovale, generally closes after birth. However, the resultant fossa ovalis may be visible as an area of thinning within the interatrial septum (Fig. 9.12A). In patients with incomplete fusion of the septum primum to the septum secundum, the residual space between the septum primum and septum secundum may be visible on imaging (Fig.9.12B). A redundancy of the interatrial septum is often present at the level of the fossa ovalis (Fig. 9.12C). When this redundancy is large, the finding is called an interatrial septal aneurysm (Fig. 9.12D,E). Atrial septal aneurysms are diagnosed when the septum protrudes 11 mm off the mid-line or demonstrates a total excursion of 15 mm during the cardiac cycle.¹⁴ Atrial septal aneurysms are associated with an increased incidence of thromboembolic events, with the presence of a patent foramen ovale (PFO) (Fig. 9.13), and with small perforations in the atrial septum associated with interatrial shunting (see Fig. 14.3).

Lipomatous hypertrophy of the interatrial septum is increasingly recognized with CT of the heart (Fig. 9.14) and can present as an area of increased 2-fluoro-2-deoxyglucose (FDG) uptake during positron emission tomography (Fig.9.15).¹⁵ Lipomatous hypertrophy consists of unencapsulated mature adipose cells that proliferate within the interatrial septum. This entity was first described in 1964.¹⁶ In a prospective study using CT, lipomatous hypertrophy was identified in 2.2% of the patients.¹⁷ Lipomatous hypertrophy is associated with obesity and is seen more frequently in older patients. The diagnosis of lipomatous hypertrophy of the interatrial septum is based on a characteristic fat density with thickening of the interatrial septum in a dumb-bell shape that spares the fossa ovalis. Lipomatous hypertrophy is generally a benign entity, although it may be associated with supraventricular arrhythmia and, in singular cases, with sudden death.¹⁸ Rarely, lipomatous hypertrophy may present with SVC obstruction or intractable arrhythmia (Fig. 9.14D).¹⁹

The patent foramen ovale is a hemodynamically insignificant communication between the right and left atria at the level of the fossa ovalis. The foramen ovale normally closes spontaneously after birth. However, a probe PFO may be present in upward of 25% of the adult population.20 A probe PFO is not generally associated with an intracardiac shunt,²¹ but it may be detected echocardiographically with a Valsalva maneuver during injection of agitated saline. A PFO is prone to serve as a conduit for paradoxical right-to-left embolization. Paradoxical embolism is often cited as one possible cause of ischemic stroke.²² Clinical studies suggest an increased prevalence of migraine headaches with aura in patients with a PFO.23 Trials are currently under way to evaluate the efficacy of PFO closure for prevention of migraine headaches and for secondary prevention of embolic stroke. The site of a PFO may be visible on cardiac CT (Fig. 9.16), but interatrial shunting is uncommonly demonstrated. PFO can be differentiated from an atrial septal defect (ASD) based on its tunneled intraseptal course (Fig. 9.12B) or the presence of a flap valve on the left atrial side of the foramen, representing the free margin of the septum primum that overlaps the septum secundum (Figs. 9.13 and 9.16).^24,25 The shunt from a PFO is generally directed toward the orifice of the IVC (Fig. 9.16C and see Fig. 16.1E).

Intracardiac shunts found in the adult include ASDs, ventricular septal defects (VSDs), partial anomalous pulmonary venous return (PAPVR), and patent ductus arteriosus (PDA). Intracardiac shunts generally result in flow from the high (systemic) pressure left-sided circulation into the lower (pulmonary) pressure right-sided circulation. Increased flow related to intracardiac shunts results in volume overload and dilatation of the right side of the heart (Figs. 9.18, 9.19, 9.20, 9.21, 9.22, 9.23, 9.24, 9.25, 9.26, 9.27, 9.28, 9.29, 9.30, and 9.31). PDA is associated with increased blood flow through both sides of the heart and results in dilatation of the LV along with right-sided chamber dilatation. Elevation of pulmonary pressure is initially related to increased volume without a change in pulmonary resistence; but when a shunt of sufficient volume persists for an extended period, increased pulmonary resistance may result as well. Once right-sided pressures are elevated beyond the left-sided pressures, Eisenmenger physiology develops with reversal of shunt flow from the right-sided circulation into the left-sided circulation and an associated decrease in left-sided oxygen saturation.

Fig. 9.16 Patient foramen ovale (PFO). (A) Four-chamber view in diastole demonstrates a patent tunnel within the interatrial septum between the septum primum and septum secundum (arrow). (B) Oblique sagittal view of the left atrium (LA) and right atrium (RA) demonstrates the flap of the septum primum on the LA side of the PFO (arrow). Patient foramen ovale (PFO). (C) Oblique sagittal view in a second patient demonstrates that the left-to-right shunt through the PFO is directed inferiorly (arrowhead) toward the orifice of the inferior vena cavaI (IVC). (D) Oblique sagittal view in a third patient with elevation of right-sided pressures (Eisenmenger physiology) demonstrates the flap of the septum primum on the LA side of the PFO (arrow) as well as a dilated RA. (E) Similar view during reinjection of contrast into the RA demonstrates right-to-left shunting of contrast through the foramen ovale and along the superior aspect of the LA (arrowheads).

ASDs are present in about 10% of newborns with congenital heart disease and are also encountered in adults. Most small ASDs (<8 mm in diameter) diagnosed in the first 3 months of life will close spontaneously before 18 months of age.26 Larger ASDs do not generally close spontaneously and may persist into adult life.

ASDs are classified based on location. The ostium secundum defect, located in the midportion of the interatrial septum, accounts for 50 to 75% of ASDs (Figs. 9.17, 9.18, 9.19, and 9.20). An ostium primum defect, located adjacent to the AV valve plane, accounts for about 15 to 30% of defects. This type of defect is often associated with endocardial cushion defects and may be associated with abnormalities of the AV valves, including cleft anterior mitral leaflet and mitral regurgitation. Ostium primum ASD is a cardiac anomaly associated with Down syndrome. The next most common subtype of ASD is the sinus venosus ASD. Most sinus venosus ASDs are located in the upper septum adjacent to the entrance of the SVC (Figs. 9.21, 9.22, and 9.23). These superior sinus venosus defects are often associated with a superior SVC that overrides both atria and anomalous drainage of the superior right pulmonary vein into the SVC. Rarely, a sinus venosus ASD may be located in the inferior portion of the interatrial septum, adjacent to the IVC (Fig. 9.24). An inferior sinus venosus ASD is not generally associated with anomalous pulmonary venous drainage. Finally, a rare form of ASD is the unroofed coronary sinus that communicates with the left atrium. Unroofed coronary sinus is frequently associated with other forms of congenital heart disease and is also frequently associated with a persistent left SVC. When treatment of an ASD is required, both surgical and percutaneous treatment options are available for closure.²⁷

Fig. 9.17 Small ostium secundum atrial septal defects (ASDs). (A) Four-chamber view demonstrates thinning of the atrial septum at the level of the foramen ovale (black arrow). Subtle left-to-right shunting of contrast is visible through this portion of the septum (white arrow). (B) Four-chamber view in a second patient demonstrates normal-sized cardiac chambers with two defects in the atrial septum (arrowheads). The recognition of multiple defects or a fenestrated ASD can be important if the patient is to have successful percutaneous repair of the ASD (Chapter 12).

Fig. 9.20 Ostium secundum atrial septal defect (ASD) with right-sided heart enlargement and hypertrophy. (A) Four-chamber view of the heart demonstrates a large atrial septal defect with contrast shunting (*) from the left atrium (LA) to the right atrium (RA). In addition to enlargement of the right side of the heart (RA and right ventricle [RV]), there are prominent trabeculations in the RV (arrowheads) suggesting hypertrophy. (B) Short-axis view again demonstrates dense contrast shunting from the left atrium (LA) to the right atrium (RA). (C) Coronal view through the atria demonstrates a wide communication between the RA and LA (*). The superior vena cava (SVC) and inferior vena cava (IVC) are seen to empty into the RA.

Fig. 9.23 Sinus venosus atrial septal defect (ASD) with pressure or volume overload of the right side of the heart. (A) Four-chamber view at a superior level demonstrates a complex communication between the left atrium (LA) and right atrium (RA) via an overriding vessel (arrow). (B) Four-chamber view at a more caudal level demonstrates bowing of the atrial septum (arrowhead) toward the LA and straightening of the interventricular septum (arrow). (C) Sagittal view demonstrates multiple pulmonary veins (arrows) entering the superior vena cava (SVC). A dilated inferior vena cava (IVC) is also noted. (D) Oblique sagittal view demonstrates that the SVC overrides both the RA and LA at the level of the sinus venosus ASD. (E) Oblique sagittal view during the early venous phase of the study demonstrates contrast from the SVC entering both the RA and the LA. The right-sided heart enlargement, bowing of the atrial septum, flattening of the interventricular septum, and dilated IVC are all indicators of severe right-sided pressure or volume overload.

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