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Comprehensive CT Cardiothoracic ImagingComprehensive CT Cardiothoracic Imaging: A New Challenge for Chest Imaging FREE TO VIEW

Riccardo Marano, MD; Federica Pirro, MD; Valentina Silvestri, MD; Biagio Merlino, MD; Giancarlo Savino, MD; Claudia Rutigliano, MD; Agostino Meduri, MD; Luigi Natale, MD; Lorenzo Bonomo, MD
Author and Funding Information

From the Department of Radiological Sciences, Institute of Radiology, Catholic University, Rome, Italy.

CORRESPONDENCE TO: Riccardo Marano, MD, Department of Radiological Sciences, Institute of Radiology, Catholic University, “A. Gemelli” Hospital, L.go Agostino Gemelli, 8, 00168, Rome, Italy; e-mail: riccardo.marano@rm.unicatt.it


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;147(2):538-551. doi:10.1378/chest.14-1403
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In the past, thoracic and cardiac imaging were two distinct specialties of radiology. The technical evolution, however, has changed their boundaries with an important impact on CT imaging practices and has opened the new era of “cardiothoracic” imaging, due to the strong anatomic, mechanical, physiologic, physiopathologic, and therapeutic cardiopulmonary correlations. Modern thoracic radiologists can no longer avoid the assessment of heart and coronary arteries, as they used to do with earlier generations of CT scanner. The advent of ECG gating and state-of-art CT scanner faster rotation speed, high spatial and temporal resolution, high-pitch mode, shorter acquisition time, and dedicated cardiac reconstruction algorithms has opened new possibilities for chest imaging, integrating cardiac morphologic and even functional information within a diagnostic chest CT scan. The aim of this review is to briefly show and summarize the concept of integrated cardiothoracic imaging, which redefines the boundaries of chest CT imaging, opening the door to a new radiologic specialty.

The imaging of intrathoracic structures has always been susceptible to movement artifacts, mainly due to physiologic movements caused by heart beats or, depending on the patient’s clinical conditions and compliance, by uncontrolled coughing, inability to perform and keep adequate breath-hold, esophageal peristalsis, or involuntary Valsalva maneuver. The continuous, impressive technical evolution in the field of CT imaging in the last decade has made it possible to achieve adequate CT image quality in patients with poor respiratory compliance, mainly through the reduction of scan time and higher temporal resolution of the scanner. Similarly, the development of ECG-gated CT imaging and its introduction in the clinical routine, with ever-less radiation exposure, has made it possible to scan the thorax, heart, and great intrathoracic vessels, avoiding the classic step artifacts due to the heart beats, with improved detection, analysis, and quantification of findings by suppressing all paracardiac motion artifacts.

In the past, thoracic and cardiac imaging were two distinct specialties of radiology. The technical evolution, however, has changed their boundaries with important impact on CT imaging practices and opened the new era of “cardiothoracic” imaging, given the strong embryologic, anatomic, mechanical, physiologic, physiopathologic, and therapeutic cardiopulmonary correlations. Modern thoracic radiologists can no longer avoid the assessment of heart and coronary arteries as they used to do with earlier generations of CT scanner. The advent of ECG gating and the faster rotation speed, high spatial and temporal resolution, high-pitch mode, shorter acquisition time, and dedicated cardiac reconstruction algorithms of state-of-the-art CT scanners have opened new possibilities for chest imaging, possibly integrating cardiac morphology, and even function information, within a diagnostic chest CT scan. The aim of this review is to briefly show and summarize the concept of integrated cardiothoracic imaging, which redefines the boundaries of chest CT imaging, leading to a new radiologic specialty.

The advent of four-slice multidetector CT (MDCT) imaging systems in 1999 actually made it possible to think about a real cardiothoracic imaging,19 but 64-slice MDCT scanners, available since 2004, are considered a prerequisite for successfully implementing cardiothoracic CT scanning within routine clinical algorithms (Fig 1). This is because of their ability to cover the whole chest in ECG-gated mode and with submillimeter collimation, for a comprehensive assessment of cardiac morphology and even function within one CT scan, including high-resolution imaging of the coronary arteries,1014 heart, pericardium, aortic root (annulus, valve, and sinus), and thoracic aorta. The scan time for this purpose usually does not exceed 20 s, and sufficient contrast enhancement of the coronary arteries, aorta, and pulmonary vessels can be achieved without excessive amount of contrast material. In cardiac CT imaging, as demonstrated by the majority of coronary CT angiography (CTA) studies, image quality degrades with increasing heart rate (HR) and increasing HR variability1517; therefore, β-blocker administration is proposed1820 to patients with HR > 70 beats/min to lower and stabilize HR and avoid movement image artifacts. Many authors have tested different CT technologies with ECG gating, but without β-blocker medication, to visualize the heart and the coronary arteries during a chest CT scan performed for different, noncoronary, clinical reasons.10,13,14 A fair or good image quality was generally obtained for functional cardiac analysis or to visualize the proximal and mid-coronary artery segments, underlying the role of HR as the main image-quality limiting factor. The development and introduction of CT scanners with > 64 detector rows or with dual-source CT (DSCT) imaging technology have made it possible to improve the image quality of mid-proximal coronary artery segments in patients with high HR who undergo chest CT scan.21

Figure Jump LinkFigure 1 –  Evolution of CT imaging technology over the last 14 y from the SDCT scan (A, F); to the 4-row (B, G), 16-row (C, H), and 64-row (D, I) MDCT scan; to the more recent DSCT scan (E, J), with consequent tremendous improvement in image quality of chest CT scan performed without cardiac synchronization. A-E, 3D volume rendering images from a thoracic aorta CT angiography. F-J, Corresponding coronal multiplanar reconstruction images from the same CT angiography displayed in A-E. DSCT = dual-source CT; MDCT = multidetector CT; SDCT = single-detector CT.Grahic Jump Location

Without going into all the technical details, elsewhere well described,22 the cornerstones of cardiothoracic imaging using state-of-art CT imaging technology are the faster scan speed and the controlled and reduced x-ray radiation dose. Faster scan speeds allow coverage of the cardiothoracic anatomy in a shorter scan time, with benefits in patients with reduced compliance and in ability to obtain a snapshot of the whole heart in one cardiac cycle, as offered by using MDCT imaging systems with area detectors (320 detectors) or DSCT scan systems with or without ECG-triggered, high-pitch spiral scan in patients with low (< 65 beats/min) and stable HR.23 Different tools have been developed to reduce the radiation dose, such as ECG-controlled dose modulation, ECG-triggered sequential CT scan, low kV scanning, iterative reconstructions, and, more recently, high-pitch spiral scanning.2328 State-of-art MDCT imaging technology can acquire high-resolution and motion-free images of the heart and coronary arteries, whose assessment during chest CT scanning could further widen CT scan application, as cigarette smoking is an established risk factor for both lung and cardiovascular (CV) diseases. High temporal resolution and high-pitch scanning (typical for a state-of-art CT scanner, eg, second-generation DSCT scan) simplify the realization of integrated cardiothoracic imaging, potentially introducing non-ECG-gated cardiac imaging and reshaping thoracic imaging boundaries (Figs 2, 3).

Figure Jump LinkFigure 2 –  High-grade sarcoma of the right pleura in a 61-y-old woman with infiltration of the right inferior pulmonary vein and extension in the left atrium. A, B, The frontal and lateral chest radiographs show a homogeneous, intrathoracic, basal and posterior opacity with obliteration of the right costophrenic angles and deletion of the right hemidiaphragm (arrowheads). C, D, The axial and coronal images from a chest CT scan performed with ECG gating show the solid lesion (*), associated with extension of solid tissue through the ostium (arrows) of the right inferior pulmonary vein within the left atrium (arrowheads). E-G, The images reconstructed along the short and horizontal long cardiac axes show the left intraatrial extension of the tissue, with a diastolic protrusion through the mitral valve (in E and G).Grahic Jump Location
Figure Jump LinkFigure 3 –  A-C, High-pitch, spiral dual-source CT scan of chest and upper abdomen without ECG synchronization in a 79-y-old male patient with previous right nephrectomy for renal tumor, with a new solid lesion in the left kidney (arrowhead in A) and a small noncalcified lung nodule in the right middle lobe (arrows in B and C). D-H, The chest CT scan shows the presence of a noncalcified coronary artery plaque at the mid-anterior descending artery (ADA) with significant arterial lumen reduction (thin arrow in D), as well as the atheromasic plaque along the descending aortic wall (arrows in E) as confirmed by the three- and two-dimensional rendering reconstructions. I-L, The invasive coronary angiography confirms the significant stenosis of the mid-ADA (arrow in I), successfully treated by percutaneous angioplasty and stenting (arrowhead in L).Grahic Jump Location

The need for an integrated lung and CV assessment within a single chest CT scan arises from the strong cardiopulmonary relationships, which include embryology, anatomy, physiology, physiopathology, and therapy, and supports CT imaging as an essential tool, not only to detect and characterize the nature and extent of lung (parenchymal, vascular, or airway) diseases but also to noninvasively assess CV changes frequently observed in the course of those diseases, and vice versa.

Left-Sided Cardiac Diseases or Anomalies and Lung Involvement

Radiologists and physicians are usually familiar with the close relationships between cardiac hemodynamics and chest radiographs (CXRs) in patients with left-sided cardiac failure, which have been well documented over the years.29,30Figure 4 shows the well-known relationship between the distribution of pulmonary blood flow related to the vascular and alveolar pressure, with the classic definition on orthostatic, frontal CXR of three different zones, according to the relative magnitudes of the pulmonary arterial, venous, and alveolar pressures.31Figure 5 shows the different degree of lung involvement in case of left-sided heart disease, with different progressive CXR patterns of balanced pulmonary flow, interstitial edema, interstitial/alveolar edema, and alveolar edema. CT imaging is more sensitive than CXR to small changes in lung water content, resulting in easier detection of unrecognized pulmonary edema and the ability to differentiate edema from other diseases in patients with multiple medical problems.32

Figure Jump LinkFigure 4 –  A, B, Frontal chest radiograph and zonal model of lung perfusion. Zone I: alvP exceeds aP so that the collapsible vessels are closed and there is no flow. Zone II: aP exceeds alvP, but alvP exceeds vP: there is a constriction at the downstream end of each collapsible vessel and the pressure inside the vessel at this point is equal to alvP, so that the pressure gradient causing flow is arterial-alveolar. This gradient increases linearly with distance down the lung and, therefore, so does blood flow. Zone III: vP exceeds alvP and the collapsible vessels are open: the pressure gradient causing flow is arterial-venous and this is constant down the zone. However, the transmural pressure difference steadily increases down the zone, and part of the vessel dilates. Blood flow, therefore, also increases down this zone, though measurements show that the change is less rapid than in zone II (modified from West et al31). alvP = alveolar pressure; aP = arterial pressure; vP = venous pressure.Grahic Jump Location
Figure Jump LinkFigure 5 –  Frontal chest radiograph and progressive degree of lung involvement in case of left-sided heart failure. A, Balanced pulmonary flow. B, Interstitial edema. C, Interstitial/alveolar edema. D, Alveolar edema.Grahic Jump Location

Changes in cardiac structure or function, like myocardial infarction, arterial hypertension (AHT), valvular diseases, cardiomyopathies (CMPs), and rhythm disorders, or a combination of these factors, may cause left-sided cardiac failure with consequent increased left atrial pressure and, therefore, increased pulmonary microvascular pressure. CT imaging is extremely useful for detecting all pulmonary findings related to left-sided cardiac failure, including ancillary abnormalities (mediastinal fatty haziness or increased lymph nodes), vascular changes (increased vascular pedicle size, vessel dilatation, or vascular redistribution), pleural effusion, bronchial wall thickening (ie, “bronchial cuffing”), interstitial/alveolar edema, and cardiac congestive heart failure with cardiomegaly, allowing for differentiation between cardiogenic vs noncardiogenic edema.

In left-sided heart overload, we may distinguish two main patterns: pressure and volume overload (Table 1). Pressure overload conditions include all situations with obstruction to left ventricle (LV) ejection: subvalvular or aortic valve stenosis, aortic coarctation, and systemic AHT. Volume overload may be due to ventricular septal defect, patent ductus arteriosus, mitral or aortic valve regurgitation, and left-sided heart failure. Radiologists are usually familiar with CT scan pulmonary findings through the different stages of pulmonary edema, moving from the initial phase with peribronchial thickening, smooth interlobular septal thickening, and pleural effusion, toward the more advanced stages with intra- and interlobular septal thickening and involvement of the pulmonary secondary lobules, with a gravitational anterior-posterior gradient (Fig 6). Unusual lung involvement may be represented by unilateral pulmonary edema, mainly in the right upper lobe, in patients with coronary artery disease (CAD), myocardial infarction, and severe mitral valve regurgitation (Fig 7).33,34 Another CT scan finding indicative of left-sided cardiac failure, with high specificity and positive predictive value, is an increased right-to-left contrast material transit time (> 10.5 s) during CT real-time, contrast-enhanced imaging of cardiac chambers (Fig 8).35

Table Graphic Jump Location
TABLE 1 ]  Patterns of Left-Sided Heart Overload

LV = left ventricle.

Figure Jump LinkFigure 6 –  CT scan pulmonary findings through the progressive stages of pulmonary edema. A, The early phase of pulmonary edema with peribronchial thickening, smooth interlobular septal thickening, and pleural effusion. B, A more advanced stage with intra- and interlobular septal thickening associated to pleural effusion. C, Severe and diffuse pulmonary secondary-lobule involvement in alveolar edema with typical anterior-posterior gravitational gradient.Grahic Jump Location
Figure Jump LinkFigure 7 –  Unusual unilateral pulmonary edema in a patient with coronary artery disease and acute mitral valve insufficiency. A, Frontal chest radiograph shows a diffuse right-lung opacity, mainly at the mid and upper third of the lung, associated with minor fissure thickening due to alveolar edema. B, Chest CT scan confirms the wide pulmonary secondary-lobule involvement. C, The mediastinum window shows the calcification along the proximal tract of the anterior descending artery (arrowheads). D, Schematic representation of mitral regurgitation flow toward the right pulmonary veins. E, These may occur in case of papillary muscle rupture due to myocardial infarction.Grahic Jump Location
Figure Jump LinkFigure 8 –  Female patient with left-sided cardiac failure in surgically corrected congenital heart disease and Kartagener syndrome. A, CT scan frontal scout view shows the enlarged heart, a single-lead electrode for a dual-chamber implantable cardioverter defibrillator system along the left superior vena cava and tip in the right ventricle, residual trans left-subclavian vein pacemaker wire, and atelectasis of the left lower lobe with bronchiectasis. B, Three subsequent axial CT scan slices from the bolus tracking acquisition during IV contrast-medium injection and resulting time-to-density curve obtained by a region of interest placed at the left atrial-ventricle junction, in a clear noncompaction LV myocardium. C, The time-to-density curves of the RV and LV show a significant increased (> 10.5 s) transit time of contrast medium from the right side to the left side of the heart, as typically occurs in left-sided cardiac failure. HU = Hounsfield units; LV = left ventricle; RV = right ventricle.Grahic Jump Location
Right-Sided Cardiac Diseases or Anomalies and Lung Involvement

Like left-sided heart overload, right-sided heart overload includes pressure and volume overloads (Table 2). Right-sided heart pressure overload is due to obstruction of right ventricle (RV) ejection, which can be caused by infundibular stenosis; pulmonary valve stenosis; supravalvular stenosis; idiopathic or secondary to acute/chronic pulmonary embolism7,8 or COPD precapillary pulmonary hypertension (PHT); and postcapillary PHT due to left-sided heart disease or failure or pulmonary venous occlusive disease. Right-sided heart volume overload includes atrial septal defect (ASD), partial anomalous pulmonary venous return (PAPVR), tricuspid and pulmonary valve regurgitation, and right-sided heart failure. The unilateral, left hilum enlargement on frontal CXR is the hallmark radiographic finding of pulmonary valve stenosis,36 because of the typical left main pulmonary artery enlargement in presence of high-pressure, leftward preferential pulmonary blood flow downstream of a stenotic valve (Fig 9).

Table Graphic Jump Location
TABLE 2 ]  Patterns of Right-Sided Heart Overload

RV = right ventricle.

Figure Jump LinkFigure 9 –  A 69-y-old male patient with pulmonary valve stenosis. A, B, The frontal and lateral chest radiographs show unilateral left hilum enlargement (arrowheads). C, An axial CT image confirms the left main pulmonary artery enlargement, typically due to leftward high-pressure flow downstream (arrow) of a stenotic pulmonary valve.Grahic Jump Location

It is more difficult to completely assess all findings on plain CXR in case of significant right-side chambers dilatation associated with pulmonary blood flow change, as shown in Figure 10. In this case, CT imaging allows the detection of the enlargement of the right-sided cardiac chambers; in particular, the right atrium (RA) with the associated presence of a large communication between the atria due to a large ostium secundum ASD, with a consequent RA overload and retrograde contrast-enhancement (reflux) of inferior vena cava (IVC) and suprahepatic veins.

Figure Jump LinkFigure 10 –  A 62-y-old man with chronic cor pulmonale and ostium secundum atrial septal defect (ASD). A, The frontal chest radiograph shows cardiac and bilateral vascular hilar enlargement. B-G, CT images allow the detection of right-side cardiac-chambers dilatation, in particular of the right atrium (RA) in the presence of a wide communication between the atria due to a large ostium secundum ASD (* in B and G), with a consequent RA volume overload and significant retrograde reflux into the inferior vena cava (seen in C and D) and suprahepatic veins (seen in E and F).Grahic Jump Location

The ASD, typically associated with RA volume overload, pulmonary hyperafflux, and IVC reflux, and better appreciable on cine-CT or MRI images, can be classified into four different types—ostium primum, ostium secundum, sinus venous, and unroofed coronary sinus—on the basis of the setting of the defect during the different embryologic phases of interatrial septum development.37

Pulmonary Diseases or Anomalies and Cardiac Involvement

Many lung diseases may have important cardiac consequences. Lung hyperinflation typically causes PHT with a decreased RV preload and increased LV afterload, increased breathing may be responsible for increased cardiac output, the increased intrathoracic pressure determines a decreased pulmonary venous return and LV diastolic dysfunction, while severe and chronic PHT may determine RV dysfunction and enlargement,38 as in case of PHT secondary to diffuse pulmonary fibrosis (Fig 11). The CT scan findings are useful to calculate a PHT severity score by the assessment of ratio of the ventricular diameters (Fig 12).

Figure Jump LinkFigure 11 –  An 80-y-old female patient with pulmonary hypertension secondary to diffuse pulmonary fibrosis. A, The frontal chest radiograph shows the typical and diffuse reticular interstitial lung opacity associated with bilateral hilar and cardiac enlargement. B-D, CT axial images show honeycombing cysts and reticular septal thickening with subpleural and posterior basal predominance associated with ground-glass opacities. E, Enlargement of both main pulmonary arteries is seen. F, G, Significant right-side cardiac-chambers dilatation is seen in the presence of leftward ventricular septal bowing (arrowheads in G).Grahic Jump Location
Figure Jump LinkFigure 12 –  Ventricular diameter ratio and changes secondary to pulmonary hypertension. A, The right (a) and left (b) ventricular diameters (black arrows) are measured as the distance between the corresponding ventricular free wall and the interventricular septum on the axial CT image. B, Scheme of the same measures shown in A. C, Changes of the ventricular diameter ratio in presence of RV dilatation. LA = left atrium; n.v. = normal value; RA = right atrium. See Figure 8 legend for expansion of other abbreviations.Grahic Jump Location

Focusing on chronic lung diseases, COPD has been described as “a preventable and treatable disease,…with significant extra-pulmonary effects…and comorbidities characterized by airflow limitation that is not fully reversible…usually progressive and associated with an abnormal inflammatory response.”39 Clinical evidence suggests that the heart and lungs should be assessed together.40 In fact, on the basis of their epidemiologic data and given their relative frequency,41 the possibility of lung and heart diseases being associated in the same patient is high. Furthermore, patients with acute exacerbation of COPD and left-sided heart dysfunction may have higher troponin T levels, suggesting that myocardial ischemia subsequent to hypoxia may have occurred.42 Indeed, this possibility needs to be investigated, but it is likely that this subgroup of patients may benefit from further studies to rule out CAD. Moreover, 40% to 50% of patients with COPD have comorbid conditions, among which CV diseases are frequent. There is a high frequency of LV dysfunction among patients with acute exacerbation of COPD; there is a 20% of unrecognized heart failure in elderly patients with stable COPD; for every 10% decrease in FEV1, the CV mortality increases by 28%; and, finally, nonfatal coronary events increase by almost 20% in mild to moderate COPD.42

Other examples of the close correlation between the two organs are represented by the patent foramen ovale (PFO), PHT, and ischemic heart disease (IHD) in OSA syndrome. A higher prevalence of PFO has been reported in patients with chronic lung disease in comparison with the normal population (70% vs 20%),43 with consequent increased RA pressure, decreased pulmonary venous return, and increased thoracic distension. The RV dysfunction in presence of PHT, the so-called chronic cor pulmonale, is essentially based on alteration of RV structure and function, and recognizes such different mechanisms as hypoxia secondary to pulmonary vasoconstriction, hypercapnia, or acidosis. A predisposition to myocardial ischemia during sleep has been shown in patients with OSA syndrome, while among patients with CAD, those with OSA syndrome have higher mortality rates.44,45 Furthermore, LV function impairment may be due to a multifactorial pathophysiology: The RV dilatation or RV pressure overload with associated leftward ventricular septum bowing may be responsible for a reduced LV filling; the CAD secondary to cigarette smoking or the systemic inflammation may represent a trigger for ischemic CMPs; the alcoholic CMP is often superimposed to COPD; the LV remodeling may be due to hypoxia, increased BP, arterial stiffness, or systemic AHT; and, finally, a significantly decreased LV ejection fraction follows in cases of severe emphysema by intrathoracic hypovolemia and low LV preload decreasing the LV end-diastolic volume.46

Cardiac manifestations are frequent even in presence of immunologic diseases, with involvement of pericardium (pericarditis, adhesion, effusion), valves (vegetation, insufficiency, endocarditis), and arteries (arteritis).47 Many cases of cardiac anomalies or pathologies may be detected in the course of clinical, routine chest or body CT scans. Typical examples may be the detection of intramyocardial fat tissue (Fig 13),48 intracardiac fat lesions (Fig 14),49 mid-intraventricular septum area of enhancement in the delayed-contrast phases of body CT scan due to myocarditis (Fig 15), or intramyocardial calcification with LV apical enlargement and endoventricular thrombosis in IHD in course of lung cancer CT staging (Fig 16). Coronary anomalies also may be detected during unenhanced chest CT scans. The abnormal origin, pathway, and diameter of coronary arteries should be detected and described in patients with COPD because of the high frequency of coronary comorbidities, the possible compression or congenital stenosis of the ectopic coronary artery, COPD-induced coronary atherosclerosis (ATS) or PHT, and the mediastinal rotation secondary to pulmonary volume change that may modify the length and orientation of the straight contact of the ascending thoracic aorta and pulmonary trunk. Other examples of those close relationships are given by the PAPVR, varying from the well-known and easier to detect “scimitar syndrome” (Fig 17) to more subtle forms associated with ASD (Fig 18).50 CTA of the pulmonary arteries may represent another source of cardiac findings, as in case of chronic PHT and Eisenmenger complex (Fig 19).

Figure Jump LinkFigure 13 –  CT axial images without contrast medium. A, Coronary calcification of the anterior descending artery and circumflex artery (arrowheads). B-D, Lipomatous metaplasia (arrowheads) are seen along the anteroseptal wall of the left ventricle in previous myocardial infarction. E-H, Physiologic myocardial fat (arrows) along the anterior wall of the outflow tract of the right ventricle in an elderly patient.Grahic Jump Location
Figure Jump LinkFigure 14 –  Intracardiac fat lesion. A-C, CT axial images without and with contrast medium show a large hypodensity structure (arrows) along the septomarginal trabecula (Leonardo’s moderator band) of the RV due to lipoma in a patient with tuberous sclerosis. D, E, Axial CT images of lipomatous hypertrophy of the interatrial septum (*) with the typical sparing of the fossa ovalis (arrowheads). F, Cardiac MRI correlation without fat-suppression technique. G, Cardiac MRI correlation with fat-suppression technique. AO = aorta; E = esophagus. See Figure 8 and 12 legends for expansion of other abbreviations.Grahic Jump Location
Figure Jump LinkFigure 15 –  A, Axial CT image in the arterial phase. B-D, Axial CT images in the portal venous phase. A-E, These images show the onset, in the latter phase of a mid-intraventricular septum area of contrast enhancement (arrowheads), also appreciable in the two-dimensional coronal reconstruction (arrow in E), of suspected myocarditis, which was confirmed few days later by cardiac MRI. F, G, T2-weighted short-tau inversion recovery images show a diffuse hyperintensity due to edema in the midseptal and anteroseptal left ventricular wall (arrowheads). H, The single frame from steady-state free precession cine-MRI short-axis view acquired after IV gadolinium injection shows a focal area of hyperintensity in the mid-inferior septum and anteroseptal ventricular wall (arrows). I, The late gadolinium enhancement sequence along the short axis view. L, The late gadolinium enhancement sequence along the four-chamber view. These views confirm the presence of pathologic intramyocardial hyperintensity along the septal, anteroseptal, and apical walls of the left ventricle (arrowheads), typical of myocarditis.Grahic Jump Location
Figure Jump LinkFigure 16 –  A, Chest CT scan of a patient with cancer of the right lung. B-D, The precontrast CT images show calcifications (arrows) along the proximal anterior descending artery and the LV apical wall. E, F, Post-contrast axial CT images. G, Two-dimensional multiplanar reconstruction along the vertical long axis. H, Two-dimensional multiplanar reconstruction along the three-chamber view. E-H, These images show the presence along the calcification of the LV apical region of a thin subendocardial thrombosis (arrowheads) as consequence of myocardial infarction. See Figure 8 legend for expansion of abbreviation.Grahic Jump Location
Figure Jump LinkFigure 17 –  The scimitar syndrome. A, The frontal chest radiograph shows the typical presence of a curvilinear density (arrows) along the right-side heart border due to the anomalous pulmonary venous return in the right lung, with a single, anomalous large vein that descends toward the inferior vena cava (IVC). B, The coronal maximum intensity CT image reconstruction. C-F, Three-dimensional CT image reconstructions. B-F, These images depict the anomalous right lung venous drainage into the enlarged IVC (arrowheads).Grahic Jump Location
Figure Jump LinkFigure 18 –  Pulmonary hypertension in right-sided partial anomalous pulmonary venous return (PAPVR) and ASD. A, The frontal chest radiograph shows the typical pulmonary hypertension signs with enlargement of the main and lobar pulmonary arteries, increased pulmonary arterial visualization in the upper lobes, and increased volume of right-side heart chambers (enlargement of the second right-side heart arch [arrowheads] and rotation of cardiac axis with apex displaced up and to the left [curved arrow]). B-D, CT angiography axial images. E, CT angiography using multiplanar reformation image. B-E, These images show a PAPVR represented by segmental, right upper lobe, pulmonary vein confluence in the superior vena cava (arrows) associated with the presence of sinus venosus ASD (arrowheads). F, G, Significant right-side chambers enlargement is seen. See Figure 10 legend for expansion of other abbreviation.Grahic Jump Location
Figure Jump LinkFigure 19 –  Pulmonary hypertension in Eisenmerger complex. A, Chest radiograph shows a severe cardiac enlargement and dilatation of both pulmonary trunk and main pulmonary arteries. B, Pulmonary CT angiography (CTA) using multiplanar coronal reconstruction documents the right main pulmonary artery and pulmonary trunk dilatation with relative sparing of segmental branches, and associated with right atrium dilatation (arrow) and severe intrahepatic contrast-medium reflux (arrowhead). C-L, Axial- and oblique-view CT images show the optimal timing of the pulmonary CTA with selective contrast enhancement of the right-side cardiac chambers, absence of contrast medium in the left side of the heart (thin arrows in F-H), extensive and bilateral pulmonary artery parietal thrombosis, right-sided heart pressure overload with right-side cardiac-chambers enlargement, and increased right ventricular anterior wall thickening (arrowheads in E-G). A poor contrast enhancement of the aortic root and ascending aorta (*) is also seen in presence of right-to-left intracardiac shunt due to an interventricular membranous septal defect (thick arrow in F and H). I, L, The descending aorta shows higher contrast enhancement (#) in comparison with the ascending aorta, in presence of right-to-left extracardiac shunt due to patent ductus arteriosus (white circle) with parietal calcification. The inverted gradient of the intracardiac and extracardiac shunt (with pulmonary pressure higher than systemic pressure) is typical in the advanced form of Eisenmerger syndrome: the so-called Eisenmerger complex.Grahic Jump Location
Cardiothoracic Image Quality

Preliminary experiences with good results in cardiothoracic CT imaging without the use of β-blocker medication have been reported.10,13,14 Salem et al10 obtained good image quality for cardiac function analysis in 92% of the 133 patients who underwent integrated cardiothoracic imaging with ECG-gated, 64-row MDCT imaging without β-blocker administration. Delhaye et al13 assessed the coronary artery image quality obtained from routine ECG-gated, 64-row MDCT scan examinations of the whole thorax without β-blockers, obtaining a good image quality in 75% of all coronary artery segments in 95% of patients, with better results in cases of HR < 80 beats/min. The same authors assessed the coronary artery image quality in preoperative chest CT scan staging performed without β-blockers, with a good image quality in 65.4% of all coronary artery segments and better results for HR < 80 beats/min in 88% of all proximal and mid-coronary segments, and, finally, in 98% of all proximal coronary artery segments.14 Pansini et al21 compared the first generation of DSCT scanners with single-source CT scan for the screening of CAD in respiratory patients without β-blockers. DSCT imaging showed significantly higher image quality (P < .0001) and adequate visualization and assessment of all proximal and mid-coronary artery segments for different HR thresholds: 35.3% vs 11.3% for HR < 110 beats/min, 35.6% vs 12.2% for HR < 100 beats/min, 40% vs 8.8% for HR < 90 beats/min, and 60% vs 10% for HR < 80 beats/min.21 The development of a second-generation DSCT scanner with high-pitch thoracic scanning performed for noncardiac purposes is reliable for the simultaneous diagnostic evaluation of all coronary artery segments in patients with mean HR < 65 beats/min and with low HR variability (< 13 beats/min) (Fig 3).23 All those reports show that HR is still the main limiting factor for image quality and adequate assessment of coronary arteries in course of chest CT scan.

It is well known that in patients with chronic obstructive airways and lung diseases (eg, asthma, COPD), β-blocker medication is frequently contraindicated because of the risk of bronchoconstriction.51,52 A new, specific HR-lowering agent (ivabradine; Amgen Inc) is recently available; it acts via the If (or funny) pacemaker channels in the sinoatrial node without any β-adrenoreceptor activity and was recently approved for the treatment of stable angina. In particular, this agent allows selective and effective HR reduction in patients with asthma and COPD with no alteration in respiratory function or symptoms, offering an interesting alternative as an HR-lowering agent in patients with chronic respiratory diseases and contraindications to β-blockers.53,54

Much evidence supports the development of comprehensive CT cardiothoracic imaging and the birth of a new radiologic subspecialty. Among that evidence, we underline the high prevalence of heart disease or anomalies and CV death among patients with COPD; the epidemiologic evidence, suggesting that impaired lung function is a risk factor for increased CV death (independently from tobacco use); that COPD, like ATS, is an inflammatory disease and, as such, may hasten the progression of ATS disease; that IHD is a leading but underrecognized cause of death in COPD; that patients with COPD are at greater risk (two to three times) for CV death (about 50% of all COPD deaths); the inverse relationship between FEV1 and the presence of ATS or CV deaths; and, finally, that FEV1 is an independent predictor of CV death. Comprehensive CT cardiothoracic imaging should allow evaluation of the lung parenchyma, airways, and pulmonary and bronchial arteries and adequate assessment of the coronary arteries (origin, course, patency, ATS, and stenosis), vascular mediastinum (anatomy and anomalies, eg, PAPVR), pericardium (agenesis, thickness, effusion, cysts, calcification), cardiac valves (aortic valve morphology, leaflet thickness, calcification or vegetation, stenosis or insufficiency), left cardiac chambers (dimension, thrombi, scar, fat infiltration, calcification, wall thickness, aneurysm or pseudoaneurysm, trabeculation, and pulmonary veins), and right-side cardiac chambers (PFO, ASD, ventricular septal defect, RV thickness, IVC reflux).

State-of-art CT imaging technology (second-generation DSCT scan) enables assessment of the heart and lung in one single and fast scan with prospective ECG gating, spiral scanning, and very low radiation dose.23 Generally speaking, coronary CTA is mainly indicated for triaging patients suspected of having CAD,55,56 but “chest” radiologists and physicians should keep in mind that coronary artery imaging assessment from a chest CT scan examination performed for noncardiac purposes and often without a very low HR, may be less precise than that achievable with a dedicated cardiac CT scan. The general objective in chest CT imaging is to screen for asymptomatic CAD in respiratory patients without compromising the evaluation of the underlying respiratory disease, limiting the anatomic level of interest to that of proximal- and mid-coronary segments, which are usually the most predominant sites of coronary ATS lesions. HR control is now feasible and safe for patients with COPD, using the newest HR-lowering agent (ivabradine). Finally, respiratory patients and their physicians can now benefit from comprehensive CT cardiothoracic imaging, a concept worth considering in the management of patients with COPD in whom coronary arteries represent a well-known target of systemic inflammation, and considering that the breakthrough of new CT imaging technologies may counterbalance the limitations of the common noninvasive cardiac tests (eg, echocardiography, ECG, nuclear medicine) in those patients.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

AHT

arterial hypertension

ASD

atrial septal defect

ATS

atherosclerosis

CAD

coronary artery disease

CMP

cardiomyopathy

CTA

CT angiography

CV

cardiovascular

CXR

chest radiograph

DSCT

dual-source CT

HR

heart rate

IHD

ischemic heart disease

IVC

inferior vena cava

LV

left ventricle

MDCT

multidetector CT

PAPVR

partial anomalous pulmonary venous return

PFO

patent foramen ovale

PHT

pulmonary hypertension

RA

right atrium

RV

right ventricle

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Figures

Figure Jump LinkFigure 1 –  Evolution of CT imaging technology over the last 14 y from the SDCT scan (A, F); to the 4-row (B, G), 16-row (C, H), and 64-row (D, I) MDCT scan; to the more recent DSCT scan (E, J), with consequent tremendous improvement in image quality of chest CT scan performed without cardiac synchronization. A-E, 3D volume rendering images from a thoracic aorta CT angiography. F-J, Corresponding coronal multiplanar reconstruction images from the same CT angiography displayed in A-E. DSCT = dual-source CT; MDCT = multidetector CT; SDCT = single-detector CT.Grahic Jump Location
Figure Jump LinkFigure 2 –  High-grade sarcoma of the right pleura in a 61-y-old woman with infiltration of the right inferior pulmonary vein and extension in the left atrium. A, B, The frontal and lateral chest radiographs show a homogeneous, intrathoracic, basal and posterior opacity with obliteration of the right costophrenic angles and deletion of the right hemidiaphragm (arrowheads). C, D, The axial and coronal images from a chest CT scan performed with ECG gating show the solid lesion (*), associated with extension of solid tissue through the ostium (arrows) of the right inferior pulmonary vein within the left atrium (arrowheads). E-G, The images reconstructed along the short and horizontal long cardiac axes show the left intraatrial extension of the tissue, with a diastolic protrusion through the mitral valve (in E and G).Grahic Jump Location
Figure Jump LinkFigure 3 –  A-C, High-pitch, spiral dual-source CT scan of chest and upper abdomen without ECG synchronization in a 79-y-old male patient with previous right nephrectomy for renal tumor, with a new solid lesion in the left kidney (arrowhead in A) and a small noncalcified lung nodule in the right middle lobe (arrows in B and C). D-H, The chest CT scan shows the presence of a noncalcified coronary artery plaque at the mid-anterior descending artery (ADA) with significant arterial lumen reduction (thin arrow in D), as well as the atheromasic plaque along the descending aortic wall (arrows in E) as confirmed by the three- and two-dimensional rendering reconstructions. I-L, The invasive coronary angiography confirms the significant stenosis of the mid-ADA (arrow in I), successfully treated by percutaneous angioplasty and stenting (arrowhead in L).Grahic Jump Location
Figure Jump LinkFigure 4 –  A, B, Frontal chest radiograph and zonal model of lung perfusion. Zone I: alvP exceeds aP so that the collapsible vessels are closed and there is no flow. Zone II: aP exceeds alvP, but alvP exceeds vP: there is a constriction at the downstream end of each collapsible vessel and the pressure inside the vessel at this point is equal to alvP, so that the pressure gradient causing flow is arterial-alveolar. This gradient increases linearly with distance down the lung and, therefore, so does blood flow. Zone III: vP exceeds alvP and the collapsible vessels are open: the pressure gradient causing flow is arterial-venous and this is constant down the zone. However, the transmural pressure difference steadily increases down the zone, and part of the vessel dilates. Blood flow, therefore, also increases down this zone, though measurements show that the change is less rapid than in zone II (modified from West et al31). alvP = alveolar pressure; aP = arterial pressure; vP = venous pressure.Grahic Jump Location
Figure Jump LinkFigure 5 –  Frontal chest radiograph and progressive degree of lung involvement in case of left-sided heart failure. A, Balanced pulmonary flow. B, Interstitial edema. C, Interstitial/alveolar edema. D, Alveolar edema.Grahic Jump Location
Figure Jump LinkFigure 6 –  CT scan pulmonary findings through the progressive stages of pulmonary edema. A, The early phase of pulmonary edema with peribronchial thickening, smooth interlobular septal thickening, and pleural effusion. B, A more advanced stage with intra- and interlobular septal thickening associated to pleural effusion. C, Severe and diffuse pulmonary secondary-lobule involvement in alveolar edema with typical anterior-posterior gravitational gradient.Grahic Jump Location
Figure Jump LinkFigure 7 –  Unusual unilateral pulmonary edema in a patient with coronary artery disease and acute mitral valve insufficiency. A, Frontal chest radiograph shows a diffuse right-lung opacity, mainly at the mid and upper third of the lung, associated with minor fissure thickening due to alveolar edema. B, Chest CT scan confirms the wide pulmonary secondary-lobule involvement. C, The mediastinum window shows the calcification along the proximal tract of the anterior descending artery (arrowheads). D, Schematic representation of mitral regurgitation flow toward the right pulmonary veins. E, These may occur in case of papillary muscle rupture due to myocardial infarction.Grahic Jump Location
Figure Jump LinkFigure 8 –  Female patient with left-sided cardiac failure in surgically corrected congenital heart disease and Kartagener syndrome. A, CT scan frontal scout view shows the enlarged heart, a single-lead electrode for a dual-chamber implantable cardioverter defibrillator system along the left superior vena cava and tip in the right ventricle, residual trans left-subclavian vein pacemaker wire, and atelectasis of the left lower lobe with bronchiectasis. B, Three subsequent axial CT scan slices from the bolus tracking acquisition during IV contrast-medium injection and resulting time-to-density curve obtained by a region of interest placed at the left atrial-ventricle junction, in a clear noncompaction LV myocardium. C, The time-to-density curves of the RV and LV show a significant increased (> 10.5 s) transit time of contrast medium from the right side to the left side of the heart, as typically occurs in left-sided cardiac failure. HU = Hounsfield units; LV = left ventricle; RV = right ventricle.Grahic Jump Location
Figure Jump LinkFigure 9 –  A 69-y-old male patient with pulmonary valve stenosis. A, B, The frontal and lateral chest radiographs show unilateral left hilum enlargement (arrowheads). C, An axial CT image confirms the left main pulmonary artery enlargement, typically due to leftward high-pressure flow downstream (arrow) of a stenotic pulmonary valve.Grahic Jump Location
Figure Jump LinkFigure 10 –  A 62-y-old man with chronic cor pulmonale and ostium secundum atrial septal defect (ASD). A, The frontal chest radiograph shows cardiac and bilateral vascular hilar enlargement. B-G, CT images allow the detection of right-side cardiac-chambers dilatation, in particular of the right atrium (RA) in the presence of a wide communication between the atria due to a large ostium secundum ASD (* in B and G), with a consequent RA volume overload and significant retrograde reflux into the inferior vena cava (seen in C and D) and suprahepatic veins (seen in E and F).Grahic Jump Location
Figure Jump LinkFigure 11 –  An 80-y-old female patient with pulmonary hypertension secondary to diffuse pulmonary fibrosis. A, The frontal chest radiograph shows the typical and diffuse reticular interstitial lung opacity associated with bilateral hilar and cardiac enlargement. B-D, CT axial images show honeycombing cysts and reticular septal thickening with subpleural and posterior basal predominance associated with ground-glass opacities. E, Enlargement of both main pulmonary arteries is seen. F, G, Significant right-side cardiac-chambers dilatation is seen in the presence of leftward ventricular septal bowing (arrowheads in G).Grahic Jump Location
Figure Jump LinkFigure 12 –  Ventricular diameter ratio and changes secondary to pulmonary hypertension. A, The right (a) and left (b) ventricular diameters (black arrows) are measured as the distance between the corresponding ventricular free wall and the interventricular septum on the axial CT image. B, Scheme of the same measures shown in A. C, Changes of the ventricular diameter ratio in presence of RV dilatation. LA = left atrium; n.v. = normal value; RA = right atrium. See Figure 8 legend for expansion of other abbreviations.Grahic Jump Location
Figure Jump LinkFigure 13 –  CT axial images without contrast medium. A, Coronary calcification of the anterior descending artery and circumflex artery (arrowheads). B-D, Lipomatous metaplasia (arrowheads) are seen along the anteroseptal wall of the left ventricle in previous myocardial infarction. E-H, Physiologic myocardial fat (arrows) along the anterior wall of the outflow tract of the right ventricle in an elderly patient.Grahic Jump Location
Figure Jump LinkFigure 14 –  Intracardiac fat lesion. A-C, CT axial images without and with contrast medium show a large hypodensity structure (arrows) along the septomarginal trabecula (Leonardo’s moderator band) of the RV due to lipoma in a patient with tuberous sclerosis. D, E, Axial CT images of lipomatous hypertrophy of the interatrial septum (*) with the typical sparing of the fossa ovalis (arrowheads). F, Cardiac MRI correlation without fat-suppression technique. G, Cardiac MRI correlation with fat-suppression technique. AO = aorta; E = esophagus. See Figure 8 and 12 legends for expansion of other abbreviations.Grahic Jump Location
Figure Jump LinkFigure 15 –  A, Axial CT image in the arterial phase. B-D, Axial CT images in the portal venous phase. A-E, These images show the onset, in the latter phase of a mid-intraventricular septum area of contrast enhancement (arrowheads), also appreciable in the two-dimensional coronal reconstruction (arrow in E), of suspected myocarditis, which was confirmed few days later by cardiac MRI. F, G, T2-weighted short-tau inversion recovery images show a diffuse hyperintensity due to edema in the midseptal and anteroseptal left ventricular wall (arrowheads). H, The single frame from steady-state free precession cine-MRI short-axis view acquired after IV gadolinium injection shows a focal area of hyperintensity in the mid-inferior septum and anteroseptal ventricular wall (arrows). I, The late gadolinium enhancement sequence along the short axis view. L, The late gadolinium enhancement sequence along the four-chamber view. These views confirm the presence of pathologic intramyocardial hyperintensity along the septal, anteroseptal, and apical walls of the left ventricle (arrowheads), typical of myocarditis.Grahic Jump Location
Figure Jump LinkFigure 16 –  A, Chest CT scan of a patient with cancer of the right lung. B-D, The precontrast CT images show calcifications (arrows) along the proximal anterior descending artery and the LV apical wall. E, F, Post-contrast axial CT images. G, Two-dimensional multiplanar reconstruction along the vertical long axis. H, Two-dimensional multiplanar reconstruction along the three-chamber view. E-H, These images show the presence along the calcification of the LV apical region of a thin subendocardial thrombosis (arrowheads) as consequence of myocardial infarction. See Figure 8 legend for expansion of abbreviation.Grahic Jump Location
Figure Jump LinkFigure 17 –  The scimitar syndrome. A, The frontal chest radiograph shows the typical presence of a curvilinear density (arrows) along the right-side heart border due to the anomalous pulmonary venous return in the right lung, with a single, anomalous large vein that descends toward the inferior vena cava (IVC). B, The coronal maximum intensity CT image reconstruction. C-F, Three-dimensional CT image reconstructions. B-F, These images depict the anomalous right lung venous drainage into the enlarged IVC (arrowheads).Grahic Jump Location
Figure Jump LinkFigure 18 –  Pulmonary hypertension in right-sided partial anomalous pulmonary venous return (PAPVR) and ASD. A, The frontal chest radiograph shows the typical pulmonary hypertension signs with enlargement of the main and lobar pulmonary arteries, increased pulmonary arterial visualization in the upper lobes, and increased volume of right-side heart chambers (enlargement of the second right-side heart arch [arrowheads] and rotation of cardiac axis with apex displaced up and to the left [curved arrow]). B-D, CT angiography axial images. E, CT angiography using multiplanar reformation image. B-E, These images show a PAPVR represented by segmental, right upper lobe, pulmonary vein confluence in the superior vena cava (arrows) associated with the presence of sinus venosus ASD (arrowheads). F, G, Significant right-side chambers enlargement is seen. See Figure 10 legend for expansion of other abbreviation.Grahic Jump Location
Figure Jump LinkFigure 19 –  Pulmonary hypertension in Eisenmerger complex. A, Chest radiograph shows a severe cardiac enlargement and dilatation of both pulmonary trunk and main pulmonary arteries. B, Pulmonary CT angiography (CTA) using multiplanar coronal reconstruction documents the right main pulmonary artery and pulmonary trunk dilatation with relative sparing of segmental branches, and associated with right atrium dilatation (arrow) and severe intrahepatic contrast-medium reflux (arrowhead). C-L, Axial- and oblique-view CT images show the optimal timing of the pulmonary CTA with selective contrast enhancement of the right-side cardiac chambers, absence of contrast medium in the left side of the heart (thin arrows in F-H), extensive and bilateral pulmonary artery parietal thrombosis, right-sided heart pressure overload with right-side cardiac-chambers enlargement, and increased right ventricular anterior wall thickening (arrowheads in E-G). A poor contrast enhancement of the aortic root and ascending aorta (*) is also seen in presence of right-to-left intracardiac shunt due to an interventricular membranous septal defect (thick arrow in F and H). I, L, The descending aorta shows higher contrast enhancement (#) in comparison with the ascending aorta, in presence of right-to-left extracardiac shunt due to patent ductus arteriosus (white circle) with parietal calcification. The inverted gradient of the intracardiac and extracardiac shunt (with pulmonary pressure higher than systemic pressure) is typical in the advanced form of Eisenmerger syndrome: the so-called Eisenmerger complex.Grahic Jump Location

Tables

Table Graphic Jump Location
TABLE 1 ]  Patterns of Left-Sided Heart Overload

LV = left ventricle.

Table Graphic Jump Location
TABLE 2 ]  Patterns of Right-Sided Heart Overload

RV = right ventricle.

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