AJR Women's Imaging Online
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow CME
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bruzzi, J. F.
Right arrow Articles by Rémy, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bruzzi, J. F.
Right arrow Articles by Rémy, J.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
Hotlight (NEW!)
Right arrow
What's Hotlight?
DOI:10.2214/AJR.05.0718
AJR 2006; 186:333-341
© American Roentgen Ray Society

Perspective

When, Why, and How to Examine the Heart During Thoracic CT: Part 2, Clinical Applications

John F. Bruzzi1,2, Martine Rémy-Jardin1, Damien Delhaye1, Antoine Teisseire1, Chadi Khalil1 and Jacques Rémy1

1 Department of Radiology, Hospital Calmette, Boulevard Pr. J. Leclerq, Lille 59037, France.
2 Present address: Department of Thoracic Imaging, The University of Texas M. D. Anderson Cancer Center, Box 57, 1515 Holcombe Blvd., Houston, TX 77030-4095.

Received April 27, 2005; accepted after revision July 16, 2005.

Address correspondence to J. F. Bruzzi.

CME

This article is available for 1 CME credit. See supplemental data for this article at www.ajronline.org or visit www.arrs.org for more information.

Abstract

OBJECTIVE. CT examination of the thorax is often requested for the investigation of disorders that may have an important underlying cardiac cause or association that is not clinically obvious. Conditions such as idiopathic and acquired cardiomyopathy, ischemic heart disease, and valvular dysfunction may underlie symptoms such as dyspnea, chest pain, and hemoptysis that prompt the request for CT of the thorax. Other conditions such as pulmonary thromboembolic disease, chronic obstructive airways disease, pectus excavatum, sleep apnea, and many intrathoracic malignancies may have an important effect on cardiac structure and function. Patients undergoing thoracic surgery may have unsuspected coronary artery disease that can be detected in the course of preoperative evaluation by CT; similarly, postoperative complications often have a cardiogenic basis.

CONCLUSION. Examination of the heart in the course of CT of the chest often can provide important and clinically relevant information that is not otherwise easily available.

Keywords: cardiac gating • cardiopulmonary imaging • chest • heart • MDCT • motion artifact • thoracic CT

In the preceding article [1], we discussed the rationale for including an examination of the heart in the course of chest CT, provided an overview of the basic technical principles involved in performing a cardiac study, and described some of the normal and abnormal appearances of the heart commonly seen on CT. In this article, we discuss some specific clinical situations in which evaluation of the cardiac structures may be particularly useful.

Unsuspected Cardiomyopathy with Respiratory Symptoms

Cardiogenic Edema
Cardiomyopathies can present clinically in a variety of fashions. They may present as dyspnea on exertion and be wrongly diagnosed as obstructive airways disease; they may be discovered in the course of respiratory complications in patients with a history of alcohol abuse or smoking, or even in otherwise healthy patients; or they may complicate rare conditions such as viral infections and hypereosinophilia (viral cardiomyopathy and eosinophilic restrictive cardiomyopathy). In many situations, clinical symptoms may be misinterpreted, and a chest CT examination may be requested to exclude other disorders.

The most typical presentation of cardiogenic edema on thoracic CT is that of interstitial edema involving infiltration of the interlobular septa, the peribronchial and peribronchiolar interstitium, and the bronchial and bronchiolar walls, resulting in thickening of the airway walls and consequent reduction of their endoluminal diameter, which results in dyspnea simulating asthma (cardiac pseudoasthma) (Figs. 1A and 1B). Compared with healthy patients, patients with smoking-related chronic obstructive airways disease, and patients with asthma, patients with cardiac insufficiency have the thickest airway walls and present with symptoms that are more often temporally heterogeneous.


Figure 1
View larger version (94K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Fig. 1A —Contrast-enhanced CT scans of thorax (360° rotation, no cardiac gating) in 45-year-old man evaluated for chronic obstructive airways disease. High-resolution 1-mm-thick axial slices through right upper lobe at level of tracheal bifurcation obtained at lung parenchymal window settings (window center: -600 H; window width: 1,600 H). Thickening of septal lines (arrows) and of peribronchial walls (arrowheads) is characteristic of interstitial pulmonary edema. In certain situations, irregular thickening of lymphatic vessels in interstitium can mimic other diseases such as lymphangitic carcinomatosis or sarcoidosis.

 

Figure 2
View larger version (85K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Fig. 1B —Contrast-enhanced CT scans of thorax (360° rotation, no cardiac gating) in 45-year-old man evaluated for chronic obstructive airways disease. Six months after treatment of cardiogenic pulmonary edema, CT abnormalities are no longer seen.

 
Mediastinal adenopathy, which is often observed in such patients, reflects absorption of interstitial edema by the lymphatics and stasis of lymphatic flow in mediastinal and bronchopulmonary nodes. This appearance can simulate that of lymphangitis carcinomatosis, especially in the presence of bulky lymphadenopathy [2]. With the appearance on CT of a pure interstitial pattern of septal thickening in the lungs and mediastinal or bronchopulmonary lymphadenopathy, the heart must be examined carefully. A cardiac cause might be suggested by cardiomegaly, pericardial thickening or effusions, or abnormal myocardial thickening.

When cardiogenic edema is suspected, a control scan after treatment can be useful to confirm the reduction in volume of the lymphadenopathy. The association between ischemic cardiomyopathy and smoking, in which adenopathy can also be observed in both the mediastinum and in the peribronchial lymphatic chains, may be the cause of a lack of change in such lymphadenopathy after diuretic treatment.

The detection of interstitial edema can lead to the discovery of previously unsuspected primary or secondary cardiomyopathies affecting the left ventricle. Primary, or idiopathic, cardiomyopathies include hypertrophic, dilated, and restrictive cardiomyopathies that have overlapping functional and morphologic features but are characterized by impairment of diastolic relaxation that is frequently accompanied by abnormalities in the relative heart wall thickness (ratio of the thickness of the heart wall to endoluminal chamber diameter), global systolic dysfunction, and valvular incompetence [3]. Acquired cardiomyopathies have similar features and are caused by a wide range of disorders such as ischemic heart disease, smoking- and drinking-related illnesses, amyloidosis, connective tissue disorders, sarcoidosis, hemochromatosis, endomyocardial fibrosis, and metabolite storage diseases [4].

One form of secondary cardiomyopathy that is particularly common and that may simulate ischemic cardiomyopathy is alcohol-related cardiomyopathy [5], characterized by dilatation of the left ventricle and associated with a myocardial thickness that is either normal or reduced, but rarely thickened. This is the most frequent cause of nonischemic dilated cardiomyopathy (Fig. 2). Alcohol-related cardiomyopathy affects men more often than women and can coexist with ischemic cardiomyopathy, systemic arterial hypertension, and chronic obstructive airways disease. Patients usually have a history of alcohol dependency of longer than 15 years and often have an associated history of cigarette smoking.


Figure 3
View larger version (129K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Fig. 2 —Contrast-enhanced CT scan of thorax in 49-year-old man with recurrent congestive heart failure. Axial 5-mm-thick image at level of both ventricles shows dilated left ventricle with relative preservation of myocardial thickness (arrow), evoking possibility of dilated and hypertrophic cardiomyopathy of left ventricle. Such an appearance would be compatible with mixed ischemic and alcoholic cardiomyopathy.

 
On CT, cardiomyopathy may be suspected by the detection of abnormalities in cardiac volumes and myocardial thicknesses, which can be depicted on routine thoracic CT without recourse to cardiac gating or supplementary contrast administration. On axial images, cardiomyopathy should be suspected by the finding of abnormally thickened heart muscle in the absence of any discernable cause, or by discrepancies between ventricular and atrial volumes and ventricular wall thickness (Fig. 2).

Acquiring images of the heart with ECG gating can permit quantification of myocardial mass and ejection fraction, facilitate detection of endoluminal thrombi, and help differentiate ischemic cardiomyopathy (which is characterized by regional wall abnormalities of systolic function and subendocardial perfusion defects) from nonischemic cardiomyopathy (in which global systolic and diastolic impairment is more common). However, MRI is more suited to the analysis of intracardiac blood flow, diastolic filling pressures, and valvular function, and it is the imaging technique of choice for a comprehensive assessment of suspected cardiomyopathy [3].

Hemoptysis
Hemoptysis of cardiogenic origin can often occur as a complication of a known cardiomyopathy, but it may also be the presenting symptom, in particular in the context of mitral insufficiency. Such a cause may be suspected in the presence of idiopathic hemoptysis originating from the right lung, and especially from the right upper lobe [6]. In patients in whom a cardiogenic origin of hemoptysis is suspected, contrast-enhanced CT of the thorax performed with cardiac gating can be useful to enable an examination of the mitral orifice. ECG gating may also be useful in cases of massive hemoptysis requiring bronchial artery embolization, by permitting detailed analysis of the coronary arteries: it is not rare for anastomoses to exist between the coronary arteries and hypertrophied bronchial arteries, and this information can help avoid inadvertent embolization of the coronary arteries in the course of therapeutic embolotherapy [7].


Figure 4
View larger version (145K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Fig. 3 —Axial contrast-enhanced CT image obtained without cardiac gating in 52-year-old man with atypical chest pain and hypertension shows focal area of poor enhancement in subendocardial region of anterior wall of left ventricle (arrow), which is consistent with ischemic or infarcted myocardium in territory of left anterior descending coronary artery.

 
Atypical Chest Pain
Thoracic CT examinations are often requested by clinicians in the investigation of atypical chest pain for which an immediate cardiac cause is not suspected. Atypical chest pain can often be a symptom of cardiac ischemia, and knowledge of the patient's history and cardiac risk factors can direct the CT examination appropriately. Signs of atherosclerotic coronary artery disease on CT include heavy calcification of the coronary arteries, early-phase perfusion defects in the endomyocardium, endocardial or myocardial calcification, and ventricular aneurysms. In the acute assessment of atypical chest pain, myocardial enhancement patterns should be studied because myocardial ischemia and infarction can be detected on CT [8] (Fig. 3). In the early arterial phase of enhancement at CT examination, the attenuation of normal myocardium should exceed 100 H, whereas infarcted myocardium has an attenuation of less than 60 H [9]. Acquisition of a second phase 5 min later enables the detection of late perfusion defects and regions of surrounding late enhancement, which have been shown to correlate with fixed infarcts detected at later technetium-99m sestamibi SPECT [10].

In the nonemergent CT assessment of atypical chest pain, the possibility of a prior unrecognized myocardial infarct should be borne in mind, and signs of such an event should be sought. Ventricular aneurysm formation can complicate previous myocardial infarction in up to 8-10% of cases, occurring between 2 weeks and 2 years after ischemic myocardial necrosis and being located most often on the anterior wall of the left ventricle or at the cardiac apex. On CT images, a true ventricular aneurysm is seen as a broad bulge of the ventricular wall. Suspicion of an aneurysm may be supported in the presence of thinning of the involved myocardium, a hypodensity in the abnormal ventricular wall that approaches that of fat, myocardial calcification, or local endoluminal thrombus formation. The apical ventricular aneurysm can be particularly difficult to detect: it may be represented by a spherical shape of the left ventricular apex rather than the usual pointed triangular shape (Figs. 4A and 4B). On cine CT images of the heart in different phases of the cardiac cycle, ventricular movement is often abnormal at the site of a new aneurysm, which is hypokinetic compared with the adjacent normal myocardium.


Figure 5
View larger version (80K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Fig. 4A —Contrast-enhanced thoracic CT scans in 63-year-old man evaluated for extension of right upper lobe carcinoma (360° rotation, no cardiac gating). Axial 1-mm-thick image at level of cardiac apex (window center: 50 H; window width: 350 H) shows aneurysm of left ventricular apex that was discovered incidentally on CT performed for investigation of exertional dyspnea. Aneurysm is characterized by spherical aspect of left ventricular apex. Involved myocardium (arrow) is thinned.

 

Figure 6
View larger version (120K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Fig. 4B —Contrast-enhanced thoracic CT scans in 63-year-old man evaluated for extension of right upper lobe carcinoma (360° rotation, no cardiac gating). At slightly more caudal level, 5-mm-thick axial image shows local thrombus in aneurysm (arrow) that was formed as result of local dyskinesis.

 
True ventricular aneurysms arising from previous myocardial infarction with associated scar formation and thinning of the myocardium should be differentiated from ventricular pseudoaneurysms, which are characterized by actual rupture of the myocardium and containment of the aneurysm by only the thin pericardium, and which are therefore at high risk of fatal rupture [11, 12]. Ventricular pseudoaneurysms are typically inferior in location and have a more discrete, narrower neck than true aneurysms. Both true and pseudoaneurysms can be complicated by the formation of mural thrombus.

The discovery of a ventricular aneurysm in the CT evaluation of atypical chest pain should stimulate a more focused search for other signs of coronary artery disease.

Cardiogenic chest pain can also be caused by myocardial ischemia in the absence of atherosclerotic coronary artery disease. For example, the coronary steal syndrome is characterized by recurrent cardiac angina caused by shunting of blood from the coronary arteries to the pulmonary artery system by way of systemic-to-bronchial-to-pulmonary anastomoses, which can develop in conditions of diminished pulmonary artery blood flow [7, 13-19]. Such anastomoses can be depicted on ECG-gated cardiac CT examination (Fig. 5). They most commonly occur in the retrocardiac bare areas of the heart and can arise from branches of both coronary arteries supplying the atria [20, 21].


Figure 7
View larger version (79K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Fig. 5 —ECG-gated cardiac CT examination of heart, performed on 16-MDCT scanner, in 34-year-old man with recurrent hemoptysis resulting from severe cystic bronchiectasis. Axial oblique maximum-intensity-projection 5-mm-thick image at mediastinal soft-tissue window setting shows abnormally dilated bronchial artery coursing toward left anterior descending coronary artery in retrocardiac region (arrow). Images at slightly more caudal level confirmed coronary artery-to-bronchial artery anastomosis.

 
Another rare cause of nonatherosclerotic cardiac angina is an aberrant right or left coronary artery originating from the contralateral sinus of Valsalva. If the aberrant artery follows a subsequent course between the aorta and the main pulmonary trunk, an increased risk exists of angina pectoris, myocardial infarction, and sudden death [22, 23] for reasons that have not been fully elucidated but that may be due to spasm in the coronary artery [24]. In such cases, CT can suggest the diagnosis by identifying the anomalous origin of the aberrant coronary artery, and CT is superior to coronary angiography in depiction of the subsequent course of the artery between the aorta and the right ventricular outflow tract [25].

Disorders of the Chest Wall, Lung Parenchyma, Airways, and Pulmonary Vasculature Affecting the Heart or Having a Cardiac Cause

Pulmonary Hypertension
A strong correlation exists between pressure in the pulmonary artery system and dilatation of the pulmonary trunk and central branches. However, estimation of the pulmonary artery pressure on echocardiography in patients with disorders of the lung parenchyma, airways, or pulmonary arteries is possible in only 40% of cases, has a margin of error of 10 mm Hg, and is prone to overestimating the incidence of pulmonary artery hypertension [26]. CT may be more useful than echocardiography because it can depict the cardiac structures in all patients, including those with extensive parenchymal lung abnormalities, and can estimate both right ventricular function and pulmonary artery pressure. Arcasoy et al. [26] have shown than in the absence of abnormalities of the right ventricle (dilatation, hypertrophy, and systolic dysfunction [Fig. 6]), the diagnosis of pulmonary artery hypertension can be reliably excluded.


Figure 8
View larger version (94K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Fig. 6 —CT scan obtained for evaluation of chronic thromboembolic disease in 38-year-old woman with primary pulmonary hypertension (360° rotation, no cardiac gating). Axial 5-mm-thick image at level of ventricles (window center: 50 H; window width: 350 H) shows marked dilatation of right ventricular lumen; partial posterior convexity of interventricular septum (arrow); dilatation of right atrium, coronary sinus (star), and inferior vena cava; and minor pericardial effusion (arrowhead).

 
A search for signs of right ventricular strain is particularly important in patients with severe chronic obstructive airways disease, in whom emphysema may be responsible for a pulmonary tamponade effect that causes left ventricular dysfunction, primarily affecting diastolic volume, and which may be cured by lung reduction surgery [27]. Lung reduction surgery, however, is contraindicated in the presence of pulmonary hypertension. An estimation of the pulmonary artery pressure on echocardiography is nearly impossible in these patients because of hyperinflation of the lungs, distention of the thoracic cage, or modification of the position of the heart.

Similarly, chest CT is often requested to exclude pulmonary parenchymal disease in obese patients suffering from dyspnea and fatigue related to chronic airway outflow obstruction. In such patients, sleep apnea syndrome (pickwickian syndrome) can cause right ventricular strain that is poorly seen on echocardiography but may be readily detected on CT [28].

Pulmonary Embolic Disease
Two of the most important disorders reflecting the close relationship between the heart and the pulmonary arteries are acute pulmonary embolism and chronic thromboembolic disease. In acute pulmonary embolism, the detection of right ventricular strain is an important prognostic factor [29-31]. In chronic thromboembolic disease or in nonembolic pulmonary hypertension, changes in right ventricular function can reflect the efficacy of medical treatment and influence surgical decisions among thromboendarterectomy, lung transplantation, and heart-and-lung transplantation (Fig. 7). In addition to the well-recognized signs of right heart strain—including dilatation of the inferior vena cava, the hepatic veins, the coronary sinus, and the azygous vein; tricuspid incompetence; and right ventricular dilatation—the phenomenon of ventricular interdependence should also be appreciated. Specifically, one should note the presence of a "paradoxical septum," which is a posterior convexity of the interventricular septum that can impede filling of the left ventricle during diastole.


Figure 9
View larger version (106K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Fig. 7 —CT scan obtained for evaluation of chronic thromboembolic disease in 45-year-old woman (360° rotation, no cardiac gating). Axial 1-mm-thick image at level of ventricles (window center: 50 H; window width: 350 H) shows pericardial effusion, ventricular dilatation, and moderate hypertrophy of right ventricular myocardium (arrows) resulting from chronic pulmonary artery hypertension and consequent right ventricular decompensation. Pulmonary arteries in basal segments of right lower lobe (arrowheads) are smaller than their counterparts in left lower lobe, consistent with sequelae of chronic pulmonary thromboembolic disease.

 
An association also exists between arterial distensibility and pulmonary vascular resistance. Immobility of the proximal pulmonary artery walls represents a loss of distensibility in the context of raised pulmonary vascular resistance. In healthy patients, displacement of the right and left main pulmonary arteries during the cardiac cycle can be as great as 4 mm, an effect that can be measured on ECG-gated cardiac studies.

The discovery of pulmonary emboli on CT angiography does not always indicate thrombotic pulmonary emboli. The heart should always be examined to exclude the possibility of emboli arising from an intracardiac myxoma in the right ventricle (Fig. 8), from intracardiac hydatid disease, or from infective endocarditis of the tricuspid valves arising in IV drug abusers.


Figure 10
View larger version (99K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Fig. 8 —Contrast-enhanced CT scan of thorax (360° rotation, no cardiac gating) in 55-year-old man hospitalized for pyrexia and shortness of breath. Axial 5-mm-thick image (window center: 50 H; window width: 350 H) at level of left atrium depicts prominent intraluminal soft-tissue mass (arrow) that was proven at subsequent surgery to be intraatrial myxoma. Note extensive consolidation and pleural effusion in left lung resulting from superimposed pneumonia.

 
Pectus Excavatum
The preoperative workup of a patient with pectus excavatum often includes CT of the chest. Its purpose is to identify the costal cartilages responsible for the thoracic cage malformation (which may be symmetric or asymmetric), to quantify the degree of sternal depression, to exclude associated malformations, and to assess the degree of compression of the left lower lobe. In this malformation, the right ventricular outflow tract may be compressed by sternal depression. No precise correlation has been established between the severity of sternal depression and the importance of right ventricular compression [32]. The principal reason for this is the difficulty of visualizing on echocardiography the volume of the right ventricular chamber and, more particularly, of the pulmonary infundibulum [33]. These functional consequences of a pectus excavatum that may arise because of cardiac compression and pulmonary restrictive disease can be evaluated on CT, and they deserve further research.

Thoracic Disorders and Complications Resulting from Extension of Disease into the Heart or Pericardium

Certain pulmonary diseases can involve the heart, pericardial structures, mediastinum, and lung parenchyma simultaneously. In such situations, the heart should be attentively examined, and supplementary gating studies used when movement artifacts interfere with confident image interpretation.

The most common example of thoracic abnormality involving the heart and pericardium through direct extension is non-small cell lung carcinoma. Invasion of the pericardium, pulmonary veins, or left atrium must be precisely described with a view to influencing the surgical decision between extra- and intrapericardial resection [34]. Other mediastinal malignancies such as esophageal carcinoma can also cause complications from direct invasion of adjacent cardiac structures, which may only be detected by careful attention to the heart.

Mediastinal masses may present with pericardial complications, such as pericardial effusions resulting from direct invasion by mediastinal tumors or abscesses. In other cases, it may be difficult to confidently determine the intra- or extrapericardial location of certain mediastinal tumors such as thymomas, teratomas, bronchogenic cysts, and hydatid cysts (Fig. 9). Thoracic mesothelioma, for example, can invade the pericardial sac or the myocardium, but it may also be primarily pericardial in origin. In nearly all cases, careful attention to the normal CT appearances of the heart and pericardium can help interpretation.


Figure 11
View larger version (103K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Fig. 9 —Contrast-enhanced CT scan of thorax (360° rotation, no cardiac gating) for evaluation of abnormality of cardiomediastinal silhouette on standard chest radiograph in 45-year-old man. Cystic tracheobronchial mass (star) is seen compressing superior vena cava (arrow) and, on adjacent slices (not shown), displacing right main pulmonary artery inferiorly and indenting roof of left atrium. Whether cystic lesion is intra- or extrapericardial is uncertain. Arguments in favor of intrapericardial nature include origin from region of subaortic pericardial reflections, whereas two signs arguing against infra- or retrocarinal position are compression of superior vena cava and inferior displacement of right pulmonary artery. Mass was subsequently confirmed to be intrapericardial hydatid cyst.

 
Diagnosis and Treatment of Pulmonary Disorders That Complicate Latent Coronary Artery Disease or Lead to Postoperative Cardiac Complications

Cardiac complications after thoracic surgery, particularly pneumonectomy, are relatively frequent and may prompt a chest CT examination. The most frequent cardiac complications include cardiac arrhythmia, myocardial ischemia, cardiac failure, pulmonary edema, right-to-left shunts, and pulmonary embolism [35]. Occult coronary artery disease in patients at risk may become obvious only in the postoperative period [36]. In patients for whom major thoracic surgery is considered and who are at risk of coronary artery disease, the preoperative anesthetic evaluation often includes a stress test and, if this has positive results, coronary angiography [37]. However, it is technically possible to combine preoperative CT of the thorax for the evaluation of thoracic malignancy with a cardiac CT study for the evaluation of ejection fractions and assessment of the coronary arteries, thereby combining an assessment of both tumor resectability and cardiovascular risk in a single, noninvasive, "one-stop shopping" examination.

Furthermore, in patients for whom adjuvant radiation therapy is anticipated, the increased radiation exposure incurred by preoperative CT angiography may be of secondary importance. The benefits of such an approach over conventional preoperative cardiovascular evaluation have not previously been evaluated in a clinical setting but deserve further attention.

Deformity of the Cardiomediastinal Silhouette

The origin of a pericardial defect can be congenital, posttraumatic, or postoperative. Congenital defects may be complete or partial, involving the entire pericardium or predominantly affecting the left and apical portions of the pericardium. When partial, the defect may be localized to the level of the left atrium [38] or may extend over the whole left ventricle [39]. It is often an isolated abnormality and is usually asymptomatic, but it may be responsible for chest pain or sensations of thoracic discomfort that are not typically anginalike [40]. When asymptomatic, a congenital defect may be revealed incidentally in the course of the evaluation of respiratory symptoms: for example, a pneumothorax may be associated with a pneumopericardium, and subsequent pleuroscopy may discover the pericardial defect. Pericardial defects may also be associated with congenital bronchial atresia and resultant obstructive hyperinflation.


Figure 12
View larger version (80K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Fig. 10 —Unenhanced CT examination of thorax for evaluation of spontaneous left-sided pneumothorax in 35-year-old woman depicts incidental discovery of congenital pericardial defect over left side of heart (arrow). Note minor intrapericardial pulmonary herniation between ascending aorta and pulmonary trunk, which is displaced anterolaterally.

 
On CT, the defect may be suspected because of an anomaly in the position of the heart: levocardia with levorotation; intrapericardial herniation of a lung (Fig. 10); extrapericardial herniation of the left atrium or the left ventricle; abnormal mobility of the heart between changes in position (Figs. 11A and 11B). The detection of a pericardial defect on CT justifies a study of the cardiac chambers because the right ventricle may be dilated and the interventricular septum may have a paradoxical configuration. Such a finding also justifies a study of the coronary arteries, whose smaller branches may exhibit stenoses at the edges of the defect [41].


Figure 13
View larger version (97K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Fig. 11A —Congenital left-sided pericardial defect suspected on posteroanterior chest radiograph of 38-year-old man. Excessive mobility of heart is shown on two unenhanced CT images obtained with cardiac gating (temporal resolution, 250 msec) at level of inferior pulmonary veins with patient in supine (A) and left lateral decubitus (B) positions. Note cardiac levorotation and increased contact between left ventricle and anterolateral thoracic wall in left lateral decubitus position (B).

 

Figure 14
View larger version (97K):
[in this window]
[in a new window]
[as a PowerPoint slide]
  		Fig. 11B —Congenital left-sided pericardial defect suspected on posteroanterior chest radiograph of 38-year-old man. Excessive mobility of heart is shown on two unenhanced CT images obtained with cardiac gating (temporal resolution, 250 msec) at level of inferior pulmonary veins with patient in supine (A) and left lateral decubitus (B) positions. Note cardiac levorotation and increased contact between left ventricle and anterolateral thoracic wall in left lateral decubitus position (B).

 

A rare complication of pulmonary resection is extrapericardial herniation of the heart, which usually complicates intrapericardial pneumonectomy without closure of the pericardial defect and which may occur with or without cardiac volvulus. To establish the diagnosis, herniation must be strongly suspected clinically and radiologically [42] and can be confirmed on CT.

Conclusion

This limited review attempts to convince the reader of the importance of "throwing an eye" on the heart in the course of the planning, acquiring, and interpreting a thoracic CT study.

References

  1. Bruzzi JF, Rémy-Jardin M, Delhaye D, Teisseire A, Khalil C, Rémy J. When, why, and how to examine the heart during thoracic CT. Part 1. Basic principles. AJR 2006;186 : 324-332[Abstract/Free Full Text]
  2. Chabbert V, Canevet G, Baixas C, et al. Mediastinal lymphadenopathy in congestive heart failure: a sequential CT evaluation with clinical and echocardiographic correlations. Eur Radiol2004; 14:881 -889[CrossRef][Medline]
  3. Soler R, Rodriguez E, Remuinan C, Bello MJ, Diaz A. Magnetic resonance imaging of primary cardiomyopathies. J Comput Assist Tomogr 1996; 27:724 -734
  4. Richardson P, McKenna W, Bristow M, et al. Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of Cardiomyopathies. Circulation 1996;93 : 841-842[Free Full Text]
  5. Piano MR. Alcoholic cardiomyopathy: incidence, clinical characteristics, and pathophysiology. Chest2002; 121:1638 -1650[Abstract/Free Full Text]
  6. Gurney JW, Goodman LR. Pulmonary edema localized in the right upper lobe accompanying mitral regurgitation. Radiology1989; 171:397 -399[Abstract/Free Full Text]
  7. Matsunaga N, Hayashi K, Sakamoto I, et al. Coronary-to-pulmonary artery shunts via the bronchial artery: analysis of cineangiographic studies. Radiology 1993;186 : 877-882[Abstract/Free Full Text]
  8. Koyama Y, Mochizuki T, Higaki J. Computed tomography assessment of myocardial perfusion, viability, and function. J Magn Reson Imaging 2004; 19:800 -815[CrossRef][Medline]
  9. Gosalia A, Haramati LB, Sheth MP, Spindola-Franco H. CT detection of acute myocardial infarction. AJR 2004;182 : 1563-1566[Abstract/Free Full Text]
  10. Paul JF, Wartski M, Caussin C, et al. Late defects on delayed contrast-enhanced multi-detector row CT scans in the prediction of SPECT infarct size after reperfused acute myocardial infarction: initial experience. Radiology 2005;236 : 485-489. Epub 2005 Jun 21[Abstract/Free Full Text]
  11. Agramunt Lerma M, Blanc Garcia E, Marti-Bonmati L. Helical CT in left ventricular pseudoaneurysm rupture [in Spanish]. Rev Esp Cardiol 2002; 55:1201[Medline]
  12. White RD. MR and CT assessment for ischemic cardiac disease. J Magn Reson Imaging 2004;19 : 659-675[CrossRef][Medline]
  13. Kochiadakis G, Chrysostomakis S, Igoumenidis N, Skalidis E, Vardas P. Anomalous collateral from the coronary artery to the affected lung in a case of congenital absence of the left pulmonary artery: effect on coronary circulation. Chest 2002;121 : 2063-2066[Abstract/Free Full Text]
  14. Bjork L. Angiographic demonstration of extracardiac anastomoses to the coronary arteries. Radiology 1966;87 : 274-277[Medline]
  15. Spindola-Franco H, Weisel A, Delman AJ. Pulmonary steal syndrome: an unusual case of coronary-bronchial pulmonary artery communication. Radiology 1978;126 : 25-27[Abstract]
  16. St. John Sutton MG, Miller GA, Kerr IH, Traill TA. Coronary artery steal via large coronary artery to bronchial artery anastomosis successfully treated by operation. Br Heart J 1980;44 : 460-463[Abstract/Free Full Text]
  17. Green CE, Kelley MJ, Higgins CB, Bookstein JJ. Acquired coronary-to-bronchial artery communication: a possible cause of coronary steal. Cathet Cardiovasc Diagn 1981;7 : 191-196[Medline]
  18. Stefas L, Assayag P, Aubry P, et al. Coronary to bronchial artery anastomosis with bronchial steal syndrome demonstrated by thallium-201 myocardial tomoscintigraphy. Eur Heart J1990; 11:275 -279[Abstract/Free Full Text]
  19. Jarry G, Bruaire JP, Commeau P, et al. Coronary-to-bronchial artery communication: report of two patients successfully treated by embolization. Cardiovasc Intervent Radiol 1999;22 : 251-254[CrossRef][Medline]
  20. Arvidsson H, Moberg A. Extracardiac anastomoses to the myocardium: preliminary report of angiographic and anatomic studies. Acta Radiol Diagn (Stockh) 1966;4 : 385-394[Medline]
  21. Petelenz T. Extracoronary shunts with coronary arteries in man. Cardiology 1965;47 : 323-336
  22. Roberts W. Major anomalies of coronary arterial origin seen in adulthood. Am Heart J 1986;111 : 941-963[CrossRef][Medline]
  23. Khouzam R, Marshall T, Lowell D, Siler JR. Left coronary artery originating from right sinus of Valsalva with diagnosis confirmed by CT: a case report. Angiology 2003;54 : 499-502[Medline]
  24. Rossi PA, Rapeport K, Fisher EA, Depasquale N. Coronary artery spasm as a cause of chest pain in a patient with anomalous origin of the right coronary artery from the left sinus of Valsalva. Tex Heart Inst J 1988; 15:124 -127[Medline]
  25. Mousseau E, Harnigou A, Sapoval M, et al. Coronary arteries arising from the contralateral aortic sinus: electron beam computed tomographic demonstration of the initial course of the artery with respect to the aorta and the right ventricular outflow tract. J Thorac Cardiovasc Surg 1996; 112:836 -840[Free Full Text]
  26. Arcasoy SM, Christie JD, Ferrari VA, et al. Echocardiographic assessment of pulmonary hypertension in patients with advanced lung disease. Am J Respir Crit Care Med 2003;167 : 735-740[Abstract/Free Full Text]
  27. Jorgensen K, Houltz E, Westfelt U, Nilsson F, Schersten H, Ricksten SE. Effects of lung volume reduction surgery on left ventricular diastolic filling and dimensions in patients with severe emphysema. Chest 2003; 124:1863 -1870[Abstract/Free Full Text]
  28. Guidry UC, Mendes LA, Evans JC, et al. Echocardiographic features of the right heart in sleep-disordered breathing: the Framingham Heart Study. Am J Respir Crit Care Med 2001;164 : 933-938[Abstract/Free Full Text]
  29. Reid JH, Murchison JT. Acute right ventricular dilatation: a new helical CT sign of massive pulmonary embolism. Clin Radiol 1998; 53:694 -698[CrossRef][Medline]
  30. Collomb D, Paramelle PJ, Calaque O, et al. Severity assessment of acute pulmonary embolism: evaluation using helical CT. Eur Radiol 2003; 13:1508 -1514[CrossRef][Medline]
  31. Contractor S, Maldjian PD, Sharma VK, Gor DM. Role of helical CT in detecting right ventricular dysfunction secondary to acute pulmonary embolism. J Comput Assist Tomogr 2002;26 : 587-591[CrossRef][Medline]
  32. Mansour KA, Thourani VH, Odessey EA, Durham MM, Miller JI Jr, Miller DL. Thirty-year experience with repair of pectus deformities in adults. Ann Thorac Surg 2003;76 : 391-395[Abstract/Free Full Text]
  33. Kowalewski J, Brocki M, Dryjanski T, Zolynski K, Koktysz R. Pectus excavatum: increase of right ventricular systolic, diastolic, and stroke volumes after surgical repair. J Thorac Cardiovasc Surg 1999; 118:87 -92, discussion 92-93[Abstract/Free Full Text]
  34. Chiles C, Woodard PK, Gutierrez FR, Link KM. Metastatic involvement of the heart and pericardium: CT and MR imaging. RadioGraphics 2001;21 : 439-449[Abstract/Free Full Text]
  35. De Decker K, Jorens PG, Van Schil P. Cardiac complications after noncardiac thoracic surgery: an evidence-based current review. Ann Thorac Surg 2003; 75:1340 -1348[Abstract/Free Full Text]
  36. Licker M, Spiliopoulos A, Frey JG, et al. Risk factors for early mortality and major complications following pneumonectomy for non-small cell carcinoma of the lung. Chest 2002;121 : 1890-1897[Abstract/Free Full Text]
  37. Burke JR, Duarte IG, Thourani VH, Miller JI Jr. Preoperative risk assessment for marginal patients requiring pulmonary resection. Ann Thorac Surg 2003; 76:1767 -1773[Abstract/Free Full Text]
  38. Bennett KR. Congenital foramen of the left pericardium. Ann Thorac Surg 2000;70 : 993-998[Abstract/Free Full Text]
  39. Gatzoulis MA, Munk MD, Merchant N, Van Arsdell GS, McCrindle BW, Webb GD. Isolated congenital absence of the pericardium: clinical presentation, diagnosis, and management. Ann Thorac Surg 2000; 69:1209 -1215[Abstract/Free Full Text]
  40. Rusk RA, Kenny A. Congenital pericardial defect presenting as chest pain. Heart 1999;81 : 327-328[Free Full Text]
  41. Nguyen DQ, Wilson RF, Bolman RM 3rd, Park SJ. Congenital pericardial defect and concomitant coronary artery disease. Ann Thorac Surg 2001; 72:1371 -1373[Abstract/Free Full Text]
  42. Kim EA, Lee KS, Shim YM, et al. Radiographic and CT findings in complications following pulmonary resection. RadioGraphics 2002;22 : 67-86[Abstract/Free Full Text]

Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 Am. J. Roentgenol.Home page
H. Scheffel, S. Baumueller, P. Stolzmann, S. Leschka, A. Plass, H. Alkadhi, and T. Schertler
Atrial Myxomas and Thrombi: Comparison of Imaging Features on CT
Am. J. Roentgenol., March 1, 2009; 192(3): 639 - 645.
[Abstract] [Full Text] [PDF]

Home page
 Proc Am Thorac SocHome page
M. Remy-Jardin and J. Remy
Vascular Disease in Chronic Obstructive Pulmonary Disease
Proceedings of the ATS, December 15, 2008; 5(9): 891 - 899.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow CME
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bruzzi, J. F.
Right arrow Articles by Rémy, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bruzzi, J. F.
Right arrow Articles by Rémy, J.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
Hotlight (NEW!)
Right arrow
What's Hotlight?

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS