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Cardiac and pericardial calcifications on chest radiographs
Clinical Radiology 65 (2010) 685e694
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Clinical Radiology journal homepage: www.elsevierhealth.com/journals/crad
Review
Cardiac and pericardial calcifications on chest radiographs E.C. Ferguson*, E.A. Berkowitz a The University of Texas Medical School at Houston, Department of Diagnostic and Interventional Imaging, Section of Thoracic Imaging, Houston, TX 77030, USA
art icl e i nformat ion Article history: Received 19 May 2009 Received in revised form 30 November 2009 Accepted 4 December 2009
Many types of cardiac and pericardial calcifications identified on chest radiographs can be recognized and distinguished based on characteristic locations and appearances. The purpose of this review is to emphasize the importance of detecting cardiac and pericardial calcifications on chest radiographs, and to illustrate and describe the various types of calcifications that may be encountered and how they may be differentiated from one another. Each type of cardiac and pericardial calcification is discussed, its location and appearance described, and its significance explained. Recognizing and understanding these calcifications is important as they are often encountered in daily practice and play an important role in patient care. Ó 2010 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.
Introduction
Coronary artery calcification
Various cardiac and pericardial calcifications may be identified on chest radiographs. Calcifications may involve the coronary arteries, aorta, cardiac valves, annuli, cardiac aneurysms, myocardium, pericardium, left atrium, and tumours and thrombi within the cardiac chambers. These calcifications may be distinguished based on characteristic locations, appearances, and shapes. This distinction is essential as cardiac and pericardial calcifications often overlap one another on chest radiographs or occur in similar positions. Often these calcifications are pathognomonic for a particular disease, and the radiologist may be the first to offer a diagnosis. Recognizing and distinguishing cardiac and pericardial calcifications will guide patient care as each has a different aetiology, treatment, and outcome.
The presence of coronary artery calcifications is a recognized marker for atherosclerotic coronary artery disease and may indicate significant stenosis. The radiographic identification of coronary artery calcifications serves as an important indicator of potential ischemic heart disease.1,2 Only relatively severe degrees of calcifications in the coronary arteries are typically visible on a chest radiograph.1 Many calcifications are too small and faint to be detected radiographically, particularly as these calcifications may be obscured by overlying soft tissues or superimposed disease in the chest. The frequency of calcifications is higher in the left coronary artery than in the right, and calcifications are usually greatest in the proximal portions of the coronary arteries. Calcification of the distal part of a coronary artery without involvement of the proximal part is rare.1,3 Coronary artery calcifications may appear as a plaque or double line on a chest radiograph. It must be both dense and extensive to be identified on a chest radiograph. It is most frequently identified on the frontal view in a region just medial to the left atrial appendage, called the coronary arterial calcification triangle.4 On the frontal view, calcification of the left coronary artery is located in the upper left heart border
* Guarantor and correspondent: E.C. Ferguson, The University of Texas Medical School at Houston, Department of Diagnostic and Interventional Imaging, Section of Thoracic Imaging, 6431 Fannin Street, Suite 2.026, Houston, TX 77030, USA. Tel.: þ1 713 628 9218; fax: þ1 713 500 7647. E-mail address: [email protected] (E.C. Ferguson). a Present address: Emory University School of Medicine, 1648 Pierce Drive, Atlanta, GA 30322, USA.
0009-9260/$ e see front matter Ó 2010 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.crad.2009.12.016
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where it branches into the left anterior descending and circumflex branches. The left anterior descending branch courses laterally along the upper left heart border, while the left circumflex runs more medially well inside the cardiac border (Fig.1). Calcification is rarely seen in the right coronary artery because not only is its incidence lower than in the left, but also because it overlies the spine where it is easily obscured. The optimal view for identification of both the right and left coronary arteries is the left anterior oblique view as it shows both arteries in opposite profile. In this view, the left coronary artery is located in the upper left heart border where it branches laterally as the circumflex and anteriorly as the anterior descending branch, while the right coronary artery parallels the right heart border.3,5 Coronary atherosclerosis affects almost every adult, usually beginning as early as childhood with anatomic evidence of involvement by the second or third decade of life. Certain diseases, such as familial hypercholesterolemia, pseudoxanthoma elasticum, and progeria, may lead to premature coronary artery calcification. Any calcium in a vessel wall is usually evidence of at least some degree of atherosclerosis as it is deposited within haemorrhagic areas of atheromatous plaques. Therefore, the calcium is an indicator of the amount of soft plaque burden and the extent of atherosclerotic disease. Heavy calcification is associated with significant coronary artery disease. There is also evidence that the presence of any calcification in a coronary artery signifies a more severe prognosis, independent of the extent of atherosclerotic disease.5e7
Aortic calcification There are two types of aortic calcification: dystrophic and degenerative. Dystrophic calcification is the result of
Figure 1 Coronary artery calcifications in a patient with chest pain and ischaemic heart disease. Frontal radiograph shows these calcifications as a plaque or double line over the left upper portion of the heart involving the left main (short white arrow), left anterior descending (white arrowhead), and left circumflex (black arrowhead) coronary arteries.
a scarred intima or media from aortitis and appears radiographically as a fine and sharp outline around the aortic wall. Degenerative atherosclerotic calcification results from secondary atherosclerosis and appears dense and irregular.8 Atheromatous plaques 4 mm have the highest risk for ulceration and calcification.9 Aortic calcification is most frequently observed in the aortic arch, occurring in more than 25% of patients in their sixth decade. The calcium is initially deposited at two depressions, one at the site of the ligamentum arteriosum and the other near the origin of the left subclavian artery. Calcification then spreads around the aortic wall from these sites. Atherosclerosis is usually the cause for the calcified plaques in the arch and descending thoracic aorta, and may extend into the ascending aorta when the disease is widespread. Otherwise, the ascending aorta is usually spared.5 In general, atherosclerosis is the most common cause for calcification in any part of the aorta. However, some portions of the aorta may preferentially calcify depending on the inciting factor. Syphilis is the classic condition historically associated with a calcified ascending aorta. The calcification in syphilis is typically heavy, linear, and continuous and is located on both the medial and lateral walls of the ascending aorta, whereas ascending aortic calcification due to atherosclerosis is usually deposited as discontinuous plaques at the root of the aorta and along the posteromedial wall of the ascending aorta.5,10 A jet lesion in aortic stenosis may lead to localized calcification in the ascending aorta.5 Younger patients with hyperlipidaemia have accelerated atherosclerosis, especially in the ascending aorta and coronary arteries. Nearly half of patients with hyperlipidaemia have type II hyperlipoproteinaemia, which is characterized by severe calcific atherosclerosis of the aortic root that is often visible on chest films. In these patients, calcification of the ascending aorta frequently extends into the coronary ostia.11 Other causes of a calcified ascending aorta are idiopathic dilatation, localized aneurysm, rheumatoid arthritis, Takayasu’s aortitis, Marfan’s syndrome, and radiation therapy. Aortic arch calcification may occur in aneurysm, aortic coarctation, syphilitic aortitis, atherosclerosis, and rheumatoid arthritis.5,8,12 Calcification of the aortic arch in young individuals, especially females, may suggest a patent ductus arteriosus, particularly when combined with pulmonary artery calcification.13 Dissections, true and false aneurysms may calcify and can occur anywhere in the aorta.14e16 The calcification of a dissection can appear similar to the calcification of atheromatous plaque, although some radiographic features that may suggest the presence of dissection include medial displacement of a calcified plaque by 10 mm or more, widening of the superior mediastinum, an indistinct aortic arch or double aortic contour, or a change in the aortic configuration between successive studies.14,15
Valvular calcification Calcification of cardiac valves identifiable on chest radiographs indicates the presence of significant valvular
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stenosis.10 The extent of calcification of a valve is proportional to the severity of stenosis.17 Aortic valve calcification is detected most frequently. The aortic valve lies in the centre of the heart and overlaps the spine on the frontal view. On the lateral view, most of the valve lies midway between the anterior and posterior cardiac borders above a line drawn from the tracheal bifurcation to the anterior sternodiaphragmatic angle. Three patterns of calcification may be seen in the aortic valve: commissure calcification, which appears linear in configuration; complete or partial ring calcification, which is quite common; and plaque-like calcification.5 The significance of aortic valve calcification seen on chest radiographs is well known and is a marker for clinically significant aortic stenosis. In patients younger than 65 years old, most aortic valve calcification is attributable to a bicuspid valve that produces the commissure and ring patterns of calcification (Fig. 2), followed by rheumatic fever as the next most common cause, which usually forms plaque-like calcification. In the majority of patients older than 65 years of age, aortic valve calcification is due to an idiopathic degenerative process, with a prevalence of 2e7%.5,18,19 A calcified tricuspid aortic valve may be distinguished from a bicuspid aortic valve as it has three distinct cusps forming downward curves, whereas the recognition
of a bicuspid valve is based on the identification of a raphe or a shallow sinus of Valsalva or both.20 If calcification of both the aortic valve and mitral valve is present, rheumatic fever is almost always responsible, unless the calcification has spread from the bicuspid aortic valve into the anterior cusps of the mitral valve or is due to senile calcification involving both valves. A unicuspid valve is a much less common cause of aortic stenosis and calcification. Healed bacterial endocarditis can result in calcification, although this is rare. Less frequent causes for aortic calcification include ankylosing spondylitis, end-stage renal disease, Paget’s disease of the bone, and rarely ochronosis.5,21 The detection of mitral valve calcifications on chest radiographs is uncommon and, when found, has surgical implications. Calcifications may appear nodular or amorphous. On the anterior view, calcification of the mitral valve is visible to the left of the spine and lies lower than aortic valve calcification (Fig. 3). Calcification lies predominately below a line drawn from the tracheal bifurcation to the anterior sternodiaphragmatic angle on the lateral view. Calcification of the mitral valve is nearly always caused by rheumatic heart disease. It is more common in men, and its incidence increases with age. Calcification in the pulmonic valve is a rare finding that may occur in patients of middle age with pulmonary valve stenosis, with tetralogy of Fallot, in pulmonary hypertension,
Figure 2 Aortic valve and aortic calcification. Lateral view of the chest illustrates a combination of ring (white arrowheads) and commissure (long white arrow) patterns of calcification of the aortic valve in this 55-year-old male smoker with a bicuspid aortic valve. Atherosclerotic calcification is also seen throughout the entire thoracic aorta, which typically affects the aortic arch and descending thoracic aorta but may also involve the ascending aorta (short white arrow) when the disease is widespread. The additional pressure placed on the ascending aorta by the jet lesion arising from the stenotic bicuspid aortic valve has contributed to the increased calcification of the ascending aorta observed in this patient.
Figure 3 Mitral valve calcification in a patient with rheumatic heart disease, admitted to the hospital for mitral valve replacement. Frontal chest radiograph shows nodular amorphous calcification in the region of the mitral valve (black arrow), which is visible to the left of the spine and is more caudal in location than aortic valve calcification.
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and after bacterial endocarditis. On the anterior view, it lies below and medial to the pulmonary trunk border between the spine and the left atrial appendage. On the lateral view, it is located within the upper anterior part of the heart, behind the sternum. The pulmonic valve is the most cephalad of the heart valves. Tricuspid valve calcification is rare. It is most frequently caused by rheumatic heart disease. It has also been reported in atrial septal defect, presumably as a result of trauma from high flow. Congenital tricuspid valve defects and infective endocarditis have also been associated with tricuspid valve calcification.5
Annular calcification The annuli or valve rings form the fibrous cardiac skeleton to which the valve leaflets are attached. The annuli are composed of parallel collagen bundles during infancy, but these collagen bundles gradually lose their parallel arrangement during childhood and early adulthood. By the third decade, lipid deposits are evident within the annuli. At an average age of 45 years, calcium deposits are demonstrable. Thus, annular calcification is considered to be a degenerative change related to the aging process. Annular calcification is also influenced by high pressure states. The mitral annulus calcifies most frequently, followed by the tricuspid annulus. As the composition and function of the mitral and tricuspid annuli are similar, the more frequent calcification of the mitral annulus is related to the higher pressure in the left ventricle. Similarly, long-standing elevation of right ventricular pressures leads to accelerated aging of the tricuspid annulus. Massive annular calcification suggests an exaggeration of this aging process.22 Calcification of the mitral annulus occurs in approximately 6% of the population at autopsy, and it is more common in females. It is often asymptomatic. However, it may be associated with atrial arrhythmias or intraventricular conduction defects, or, if massively calcified, may cause mitral regurgitation or congestive heart failure. It is common in patients with end-stage renal disease, indicating that derangements in calcium and phosphorus metabolism may contribute to calcification of the mitral annulus.23 Mitral annular calcification may also be a marker for atherosclerotic disease burden.24 Patients with mitral annular calcifications have a higher incidence of new coronary events than those who do not; right bundle branch block is the only defect that is significantly more common in patients with mitral annular calcification than in controls of similar age; and it is frequently associated with aortic stenosis.23,25 Calcific densities are identifiable on chest radiographs in fewer than 10% of patients with mitral annular calcifications. As the central portion of the mitral annulus adjacent to the aortic root formed by the fibrous trigones usually does not calcify, this often produces a “reverse C” configuration in the left anterior oblique or left lateral projection (Fig. 4). Alternatively, J-, U-, or oval-shaped calcific densities may be seen. Calcific deposits can measure up to 3 cm in calibre and project as far as 3 cm into the myocardium.22,23
Figure 4 Dense calcification of the mitral annulus in a 61-year-old man with atherosclerotic disease and diabetes. Frontal chest radiograph shows reverse “C”-shaped calcification of the mitral annulus (white arrow), with lack of calcification in the central portion of the annulus formed by the fibrous trigones, which usually do not calcify.
Calcification of the tricuspid annulus is rarely seen. Only isolated cases of tricuspid calcification have been reported in association with ventricular septal defect, rheumatic heart disease, congenital malformation of the tricuspid valve, and possibly subacute bacterial endocarditis. It may develop with prolonged elevated right ventricular pressures caused by pulmonary valve stenosis or atrial septal defect with pulmonary artery hypertension. The tricuspid annulus essentially produces a radiographic mirror image of the mitral annulus, as the central portion of this ring formed by the right fibrous trigone is not calcified. This produces a “C” configuration in the left lateral or left anterior oblique projection.22 Aortic annular calcification is usually seen in older patients with a calcified aortic valve. The calcification is often dystrophic and may extend into the ascending aorta or the interventricular septum. Extension of calcification into the conducting system may lead to heart block.26 Otherwise, it is often clinically insignificant.
Calcification of true aneurysms of the left ventricle A true aneurysm of the left ventricle is a localized dilatation of the ventricular wall, which consists of a thinned myocardium interspersed with fibrous tissue and reinforced by an adhesive pericardium. The true aneurysm sac contains endocardium, epicardium, and a thinned fibrous remnant of the left ventricular muscle.27 As the true aneurysm is bounded by epicardium, it will not extend beyond the coronary arteries.28 Cardiac aneurysms most often involve the left ventricle, less often the right ventricle, and rarely the atria. Causes of cardiac aneurysm are ischaemic,
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congenital, surgical, and infectious. Myocardial infarction is the most common cause, and true aneurysms develop in 5 to 10% of patients with acute myocardial infarction.29,30 True aneurysms predominately involve the apical and anterolateral segments of the left ventricle and are usually the result of occlusion of the left anterior descending artery or one of its major branches. These aneurysms produce a localized bulge along the left border of the heart on the frontal chest radiograph, usually at the apex or lower lateral margin of the ventricular contour (Fig. 5a).5,28 On the lateral chest film, a left ventricular aneurysm produces a softtissue opacity retrosternally or superiorly (Fig. 5b).31 The neck of the true aneurysm is wide and its diameter is similar to that of the maximal diameter of the aneurysm.27 Myocardial calcification can be detected on chest radiographs in 3 to 7% of left ventricle aneurysms. The calcification appears thin and curvilinear and may completely surround the aneurysm. The aneurysmal segment of the left ventricle is dyskinetic and does not empty during systole, allowing for stagnation of blood.32 These aneurysms may lead to congestive heart failure or embolic events, and may also give rise to ventricular arrhythmias because of the effects of ventricular scaring on conduction. However, true left ventricular aneurysms may be asymptomatic, especially if small. They can often be managed medically and are compatible with a prolonged survival. They have a lower potential for rupture, which is uncommon, and they are likely to rupture only in the peri-infarct period and rarely in the chronic stage.27,28,30 This is probably due to the intrinsic nature of the wall of the aneurysm, which is composed of scarred myocardium reinforced by an adhesive pericardium. Surgical resection is reserved for refractory angina pectoris, congestive heart failure, systemic embolization, or refractory arrhythmias.
Calcification of false aneurysms of the left ventricle A false aneurysm forms when the myocardium ruptures into the pericardial space and is contained by an overlying, avascular wall of pericardial adhesions and fibrous tissue. This most commonly results from myocardial infarction with rupture of the left ventricle. Rupture of the left ventricle inflames the pericardium and causes a fibrotic reaction that leads to the formation of a pseudochamber to contain the haemorrhage in a localized region. The development of this pseudochamber is necessary to prevent death from haemopericardium and cardiac tamponade.33 The neck of a left ventricular pseudoaneurysm is narrow, unlike the wide neck of a left ventricular aneurysm.28 Pseudoaneurysms form in approximately 4% of patients with infarcts involving the right or left circumflex coronary artery.16,28 Some risk factors that predispose to the development of cardiac rupture and subsequent left ventricular pseudoaneurysm after myocardial infarction include age greater than 60 years, female gender, hypertension, first transmural myocardial infarction, lack of coronary artery
Figure 5 Calcified true aneurysm of the left ventricle. (a, b) Frontal and lateral radiographs reveal thin curvilinear calcification surrounding a true aneurysm of the left ventricle (white arrows), in this patient with a remote history of myocardial infarction. True aneurysms most frequently occur at the apex or anterolateral region of the left ventricle. The neck of the true aneurysm is wide and is a continuum of the left ventricular cavity.
collateral vessels in the area of infarction, among others.34 Additional causes of false aneurysms include cardiac surgery, chest trauma, myocarditis, endocarditis, and infections such as tuberculosis and syphilis.35 A pseudoaneurysm is suggested radiographically by an abnormal lateral or posterior bulge along the left ventricular contour. A retrocardiac double density may be seen on the frontal radiograph. An abnormal cardiac contour may be seen as early as 1 week following myocardial infarction.35 Pseudoaneurysms may calcify, appearing as a thin, curvilinear density outlining the aneurysm sac (Fig. 6a and b). They lie outside the epicardium, unlike true aneurysms, which are bounded by the epicardium. Pseudoaneurysms
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are rarely seen anteriorly, likely because anterior rupture of the left ventricle is usually not contained, and these patients die before diagnostic assessment. Conversely, as only 2e3% of true aneurysms occur posteriorly, a posterior bulge along the left ventricular margin is a strong indicator of a false aneurysm. False aneurysms often enlarge on sequential radiographs. If the cardiac size rapidly increases in a patient with an abnormal cardiac contour, then leakage of the false aneurysm into the pericardium is suspected.28,35 Pseudoaneurysms require surgical repair, as they can rupture at any time after infarction, from the peri-infarct period to years later. Approximately 45% of all pseudoaneurysms rupture.35 Rupture of the free wall is much more common than septal rupture and is usually immediately fatal.36 Other complications associated with false aneurysms include congestive heart failure as the cavity is noncontractile, systemic embolization due to the stagnant flow of blood leading to thrombosis, and ventricular arrhythmias. Even asymptomatic pseudoaneurysms should be resected,33,37 as they are unstable and have a high incidence of frequently fatal rupture. Optimum medical therapy is the only alternative in patients unwilling or unable to undergo surgical repair.38
Myocardial calcification Myocardial calcification most commonly occurs after coronary artery occlusion and myocardial infarction. It is more common in males, and is usually found in patients who have had a large myocardial infarction and have survived at least 6 years after infarction. It is identified in approximately 8% of patients following a large myocardial infarction. Massive myocardial calcification usually forms in patients with coronary artery distributions favouring survival, such as a dominant right coronary artery, which aids in survival after occlusion of the left anterior coronary artery occlusion. Left ventricular aneurysm is often present.5,39 Calcification of the myocardium usually develops toward the apex of the left ventricle. It may be thin or thick and is curvilinear. Rare spherical or cyst-like calcification has also been described.40 Myocardial calcification may mimic the radiographic appearance of pericardial calcification, though distinguishing these two entities is important and is based on characteristic sites of location and appearances. Unlike myocardial calcification, pericardial calcification does not predominate at the cardiac apex. Occasionally, the myocardium may calcify posteriorly; however, this calcification is deposited below the level of the pulmonary valve, whereas pericardial calcification extends over the pulmonary outflow tract. Calcification of the myocardium typically shows a soft-tissue rim of 2 mm or more extending peripherally beyond the calcified myocardium in all projections (Fig. 7), whereas calcification of the pericardium involves the extreme periphery of the cardiac silhouette in at least one projection.39,41 As myocardial calcification also occurs in a similar position as a calcified true aneurysm of the left ventricle, these two entities should also be distinguished. Some features suggestive of the presence of an
aneurysm include a discrete, rounded protrusion of the cardiac contour, bulging, and irregularity of the left heart border, and often an enlarged heart.31 Other causes of myocardial calcification include trauma, cardioversion, infection, and endocardial fibrosis. These calcifications are typically coarse, irregular, and amorphous. Rheumatic fever and other causes of myocarditis may result in calcification. Valvular calcification of the aortic and mitral rings may spread into the adjacent muscle and septum and can cause heart block. Widespread metastatic calcification may rarely involve the myocardium. In some patients, myocardial calcification may have no obvious cause.5,42,43
Pericardial calcification Pericardial calcifications are usually deposited in regions of pericardial inflammation and fibrosis. Causes include tuberculous, fungal, viral or pyogenic infections, trauma and haemopericardium, cardiac surgery, collagen vascular diseases such as lupus, rheumatic heart disease, uremic pericarditis, and radiation. Sometimes, the cause is unknown, and pericardial calcification may occur in apparently healthy individuals.44 Occasionally, pericardial masses or cysts may calcify. The pericardium most frequently calcifies over the rightsided cardiac chambers, over the anterior and diaphragmatic aspects of the heart, and in the atrioventricular grooves (Fig. 8). Calcification over the left ventricle or cardiac apex is rare, unless there is more extensive calcification in the remainder of the pericardium. Thus, pericardial calcifications tend to form more frequently over the less pulsatile right-sided cardiac chambers, indicating that the increased pulsatility of the left-sided cardiac chambers likely hinders calcium deposition. This distribution of calcium aids in distinguishing pericardial calcifications, which are usually right-sided or diffuse over most of the heart, from myocardial calcifications, which are more leftsided and localized. On chest radiographs the calcification appears as a curvilinear density at the extreme margin of the cardiac silhouette, often better visualized on the lateral view. The extension of calcification over the pulmonary outflow tract is an important finding on the lateral view, as this occurs in pericardial but not myocardial calcification. Pericardial calcification develops less frequently over the left atrium, probably because of less pericardial investment over this region and the presence of the pulmonary veins. This lack of calcific investment allows the left atrium to dilate even when pericardial constriction is present, producing a radiographic appearance that can mimic mitral stenosis.41 Pericardial calcification can be detected on chest radiographs in about half the cases of constrictive pericarditis. However, extensive pericardial calcification can be present without signs or symptoms of constrictive pericarditis. Although there are many causes of pericardial constriction, tuberculosis has historically been the leading cause worldwide. Calcifications caused by tuberculous pericarditis are most dense in the atrioventricular grooves and appear as thick, amorphous oblique circles or arcs of calcifications.
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The calcium may then spread from the grooves over the surfaces of the atria and ventricles. This pattern of calcification is seen less often with other forms of pericarditis.5,41,45,46 When pericardial calcifications are identified, it is important to assess for signs of potential constrictive pericarditis, such as dilatation of the superior vena cava or azygos vein, pulmonary venous hypertension, left atrial enlargement, and flattenening of the cardiac contours.30 As medical management is generally ineffective, the diseased pericardium usually must be surgically resected.
Left atrial calcification
Figure 6 Calcified false aneurysm of the left ventricle. (a, b) Frontal and lateral radiographs obtained during a barium oesophagram show a focal bulge along the posterolateral wall of the left ventricle, representing a false aneurysm that is peripherally calcified (white arrowheads). False aneurysms have a narrow neck.
Calcification of the wall of the left atrium is almost always due to rheumatic heart disease with mitral valve involvement. It develops in 2e3% of individuals with this condition. Calcium deposition in the left atrial wall may be due to overstretching of the wall and local tissue necrosis primarily caused by mitral stenosis, or may be the result of active and repeated bouts of rheumatic inflammation. Calcium forms in the endocardial and subendocardial layers. The detection of left atrial calcification is important because it may indicate a number of different abnormalities, such as mitral stenosis with some regurgitation, atrial fibrillation, and mural thrombi. Other much rarer causes of left atrial calcification include metabolic calcinosis and massive intake of vitamin D.47,48 Calcification of the left atrial wall is usually thin and curvilinear measuring a few millimetres in calibre, and is most marked over the posterosuperior aspect. The lateral and oblique radiographs are most helpful in its identification. If the calcium completely encircles the left atrium, it is visible as a ring on the frontal view and as a C-shaped structure on the lateral view with the mitral valve lying anteriorly in the open part of the “C” (Fig. 9). This appearance has been termed a “coconut atrium” or “porcelain atrium”. The mitral valve may also be calcified. The interatrial septum usually does not calcify. If only a portion of the left atrial wall calcifies, it is usually the posterior wall, a finding suggesting that the regurgitant mitral jet may be the causative factor. This produces a focal calcified patch called a MacCallum’s patch. Sometimes, only the left atrial appendage calcifies, which is visible along the left cardiac border on the frontal radiograph and over the middle of the heart on the lateral view. Calcification can occasionally extend into the pulmonary veins. Thrombus is often present within a calcified left atrium, and it can also calcify. Thrombus calcification is laid down in thick, laminated layers. However even when this appearance is seen, it is more often due to uneven deposition of calcium within the walls of the left atrium as thrombus calcifies much less frequently.5,48e51 Recognizing calcium in the left atrial wall is critical, as it indicates significant disease and accompanying health issues. The amount of calcification in the left atrial wall is a marker for the duration of untreated disease. Most of these patients have atrial fibrillation and congestive heart failure from longstanding mitral valve disease. Systemic
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Figure 7 Myocardial calcification in a 52-year-old male with a history of a large myocardial infarction 16 years earlier, necessitating treatment with coronary artery bypass graft and pacemaker. Frontal radiograph shows focal curvilinear calcification over the left side of the heart (white arrow), a location that is more typical of myocardial rather than pericardial calcification. Note the peripheral shadow of myocardial tissue extending beyond the calcification (white arrowheads), which also aids in distinguishing myocardial from pericardial calcification.
Figure 9 Left atrial calcification in a patient with a history of rheumatic heart disease. Lateral chest radiograph shows the reverse “C”-shaped appearance of the calcification encircling the left atrium (white arrows), with the non-calcified mitral valve located anteriorly in the open part of the “C”.
embolization of mural thrombi is common. It is important to report this finding prior to cardiovascular surgery, as the presence of left atrial calcification alters the surgical approach needed to repair the mitral valve and to avoid complications.47,48
Tumour and thrombus calcification
Figure 8 Pericardial calcification in a patient with remote history of cardiac surgery. Frontal radiograph shows pericardial calcifications over the extreme margin of the right side of the cardiac silhouette and along the diaphragmatic surface (black arrows). This location aids in differentiating pericardial from myocardial calcification, which occurs more often over the left side of the heart and not at the extreme margin of the cardiac silhouette.
Calcifications occurring within the cardiac chambers are usually associated with tumours or thrombi. Thrombus develops in the left ventricle following myocardial infarction in approximately 20e60% of cases, and can lead to embolization.52 Thrombus formation may occur in the left atrium when the mitral valve is diseased, with an incidence of 10e25%.53 It is usually found in the left atrial appendage or along the posterior wall of the left atrium extending towards the appendage. Myxomas account for about 50% of primary cardiac tumours, and 5e10% of these contain calcification dense enough to be seen on a chest radiograph. About three-fourths of myxomas are located in the left atrium. They typically obstruct the valve orifice, but if calcified can interfere with valve closure or destroy the cusp tissue leading to regurgitation. Other primary tumours reported to calcify include teratomas, fibromas, rhabdomyomas, carcinoid tumours, and endotheliomas.5,54 Secondary tumours are much more common, and they
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can involve the intracardiac chamber via metastatic deposits, by direct infiltration or by vascular extension. A calcified mass in a neighbouring structure may invade the adjacent cardiac chamber, or calcified metastases may be deposited in the heart. Reported infectious causes of calcific intracardiac lesions include hydatid cysts, calcified tuberculomas, and infectious vegetations.5
Conclusion Many types of calcifications related to the heart and pericardium may be detected on chest radiographs. The chest radiograph is often the first diagnostic tool ordered to assess the cardiovascular structures. Some radiographically identified calcifications may be clinically insignificant, while others are critical, and the ability to make that distinction is crucial to determine when additional tests or emergent intervention is needed. Therefore, recognizing and detecting cardiac and pericardial calcifications, understanding their importance, and distinguishing among them is necessary to make an appropriate diagnosis and to guide patient care.
References 1. Stanford W, Thompson BH, Weiss RM. Coronary artery calcification: clinical significance and current methods of detection. AJR Am J Roentgenol 1993;161:1139e46. 2. Sakuma J, Takeda K, Hirano T, et al. Plain chest radiograph with computed radiography: improved sensitivity for the detection of coronary artery calcification. AJR Am J Roentgenol 1988;151:27e30. 3. Tampas JP, Soule AB. Coronary artery calcification: its incidence and significance in patients over forty years of age. AJR Am J Roentgenol 1966;97:369e76. 4. Higgins CB. Radiography of acquired heart disease. Essentials of cardiac radiology and imaging. Philadelphia: JB Lippincott; 1992. 5. Jefferson K, Rees S. Calcification. In: Jefferson K, Rees S, editors. Clinical cardiac radiology. 2nd ed. London: Butterworth; 1980. p. 76e87. 6. Baron MG. Significance of coronary artery calcification. Radiology 1994;192:613e4. 7. Wexler L, Brundage B, Crouse J, et al. Coronary artery calcification: pathophysiology, epidemiology, imaging methods, and clinical implications. A statement for health professionals from the American Heart Association. Circulation 1996;94:1175e92. 8. Coblentz C, Martin L, Tuttle R. Calcified ascending aorta after radiation therapy. AJR Am J Roentgenol 1986;147:477e8. 9. Tunick PA, Krinsky GA, Lee VS, et al. Diagnostic imaging of thoracic aortic atherosclerosis. AJR Am J Roentgenol 2000;174:1119e25. 10. Higgins CB, Reinke RT. Nonsyphilitic etiology of linear calcification of the ascending aorta. Radiology 1974;113:609e13. 11. Dinsmore RE, Lees RS. Vascular calcification in types II and IV hyperlipoproteinemia: radiographic appearance and clinical significance. AJR Am J Roentgenol 1985;144:895e9. 12. Elliott LP, Eliot RS. Roentgenologic findings in conditions of the ascending aorta simulating aortic valvular insufficiency. AJR Am J Roentgenol 1966;97:390e410. 13. Pochaczevsky R, Dunst ME. Coexistent pulmonary artery and aortic arch calcification. AJR Am J Roentgenol 1972;116:141e5. 14. Petasnick JP. Radiologic evaluation of aortic dissection. Radiology 1991;180:297e305. 15. Itzchak Y, Rosenthal T, Adar R, et al. Dissecting aneurysm of the thoracic aorta: reappraisal of radiologic diagnosis. AJR Am J Roentgenol 1975;125:559e70. 16. Cole TJ, Henry DA, Jolles H, et al. Normal and abnormal vascular structures that simulate neoplasms on chest radiographs: clues to the diagnosis. Radiographics 1995;15:867e91.
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17. Lee VS, Patz EF, Chen JTT. Atypical and unusual calcifications of the heart and great vessels: imaging findings. AJR Am J Roentgenol 1994;163: 1349e55. 18. Lippert JA, White CS, Mason AC, et al. Calcification of aortic valve detected incidentally on CT scans: prevalence and clinical significance. AJR Am J Roentgenol 1995;164:73e7. 19. Koos R, Mahnken AH, Sinha AM, et al. Aortic valve calcification as a marker for aortic stenosis severity: assessment on 16-MDCT. AJR Am J Roentgenol 2004;183:1813e8. 20. Spindola-Franco H, Fish BG, Dachman A, et al. Recognition of bicuspid aortic valve by plain film calcification. AJR Am J Roentgenol 1982;139: 867e72. 21. Porkodi R, Parthiban M, Rukmangathrajan S, et al. Ochronotic arthropathy: a study from Chennai. J Indian Rheumatol Assoc 2004;12:37e9. 22. Rogers JV, Chandler NW, Franch RH. Calcification of the tricuspid annulus. AJR Am J Roentgenol 1969;106:550e7. 23. Lewandowski BJ, Winsberg F. Incidence of aortic cusp and mitral annulus calcification as determined by echocardiography: significance and interrelationship. AJR Am J Roentgenol 1982;138:829e32. 24. Fox CS, Vagan RS, Parise H, et al. Mitral annular calcification predicts cardiovascular morbidity and mortality. Circulation 2003;107:1492e6. 25. Jeon DS, Atar S, Brasch AV, et al. Association of mitral annulus calcification, aortic valve sclerosis and aortic root calcification with abnormal myocardial perfusion single photon emission tomography in subjects age 65 years old. J Am Coll Cardiol 2001;38:1988e93. 26. Higgins CB. Radiography of acquired heart disease. In: Webb WR, Higgins CB, editors. Thoracic imaging: pulmonary and cardiovascular radiology. Philadelphia: Lippincott Williams & Wilkins; 2005. p. 655e78. 27. Kumbasar B, Wu KC, Kamel IR, et al. Left ventricular true aneurysm: diagnosis of myocardial viability shown on MR imaging. AJR Am J Roentgenol 2002;179:472e4. 28. Brown SL, Gropler RJ, Harris KM. Distinguishing left ventricular aneurysm from pseudoaneurysm. Chest 1997;111:1403e9. 29. Jefferson K, Rees S. Cardiac aneurysm, tumour and cyst. In: Jefferson K, Rees S, editors. Clinical cardiac radiology. 2nd ed. London: Butterworth; 1980. 272e277. 30. Konen E, Merchant N, Gutierrez C, et al. True versus false left ventricular aneurysms: differentiation with MR imagingdinitial experience. Radiology 2005;236:65e70. 31. Kittredge RD, Gamboa B, Kemp HG. Radiographic visualization of left ventricular aneurysms on lateral chest film. AJR Am J Roentgenol 1976;126:1140e6. 32. Kittredge RD, Cameron A. Abnormalities of left ventricular wall motion and aneurysm formation. AJR Am J Roentgenol 1972;116:110e24. 33. Spindola-Franco H, Kronacher N. Pseudoaneurysm of the left ventricle. Radiology 1978;127:29e34. 34. Naik H, Sherev D, Hui PYM. The rapid diagnosis of pseudoaneurysm formation in left ventricular free wall rupture. J Invasive Cardiol 2004;16:390e2. 35. Higgins CB, Lipton MJ, Johnson AD, et al. False aneurysms of the left ventricle. Radiology 1978;127:21e7. 36. Gopal A, Pal R, Karlsberg RP, et al. Left ventricular pseudoaneurysm by cardiac CT angiography. J Invasive Cardiol 2008;20:370e1. 37. Winzelberg GG, Miller SW, Okada RD, et al. Scintigraphic assessment of false left ventricular aneurysms. AJR Am J Roentgenol 1980;135:569e74. 38. Varvarigos N, Koletsis E, Zafiropoulos A, et al. A case of left ventricular pseudoaneurysm with long survival and congestive heart failure as first presentation. Case report and review of the literature. Med Sci Monit 2005;11:69e73. 39. Brean HP, Marks JH, Sosman MC, et al. Massive calcification in infarcted myocardium. Radiology 1950;54:33e42. 40. Murray RH. Perispherical calcification at the site of old myocardial infarction. AJR Am J Roentgenol 1968;102:297e300. 41. MacGregor JH, Chen JTT, Chiles C, et al. The radiographic distinction between pericardial and myocardial calcifications. AJR Am J Roentgenol 1987;148:675e7. 42. Barnard DC, Pape L, Missri J, et al. Massive myocardial calcification and normal coronary arteries. Tex Heart Inst J 1985;12:363e5. 43. Bylsma F, Walmsley JBW. Metastatic myocardial calcification. Can Anaesth Soc J 1981;28:167e9. 44. Mathewson FAL. Calcification of the pericardium in apparently healthy people. Circulation 1955;22:44e51.
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45. Shawdon HH, Dinsmore RE. Pericardial calcification: radiological features and clinical significance in twenty-six patients. Clin Radiol 1967;18:205e12. 46. Ling LH, Oh JK, Breen JF, et al. Calcific constrictive pericarditis: is it still with us? Ann Intern Med 2000;132:444e50. 47. Gedgaudas E, Kieffer SA, Erickson C. Left atrial calcification. AJR Am J Roentgenol 1968;102:293e6. 48. Seltzer RA, Harthorne JW, Austen WG. The appearance and significance of left atrial calcification. AJR Am J Roentgenol 1967;100:307e11. 49. Del Campo C, Weinstein P, Kunnelis C, et al. Coconut atrium: transmural calcification of the entire left atrium. Tex Heart Inst J 2000;27:49e51.
50. Pulikal G, Marshall A. Complete calcification of rheumatic left atrium. N Engl J Med 2006;354:2262. 51. Harthorne JW, Seltzer RA, Austen WG. Left atrial calcification: review of literature and proposed management. Circulation 1966;34:198e210. 52. Godwin JD, Herfkens RJ, Sklöldebrand CG, et al. Detection of intraventricular thrombi by computed tomography. Radiology 1981;138:717e21. 53. Matsuyama S, Watabe T, Kuribayashi S, et al. Plain radiographic diagnosis of thrombosis of left atrial appendage in mitral valve disease. Radiology 1983;146:15e20. 54. Gross BH, Glazer GM, Francis IR. CT of intracardiac and intrapericardial masses. AJR Am J Roentgenol 1983;140:903e7.
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Clinical Radiology journal homepage: www.elsevierhealth.com/journals/crad
Review
Cardiac and pericardial calcifications on chest radiographs E.C. Ferguson*, E.A. Berkowitz a The University of Texas Medical School at Houston, Department of Diagnostic and Interventional Imaging, Section of Thoracic Imaging, Houston, TX 77030, USA
art icl e i nformat ion Article history: Received 19 May 2009 Received in revised form 30 November 2009 Accepted 4 December 2009
Many types of cardiac and pericardial calcifications identified on chest radiographs can be recognized and distinguished based on characteristic locations and appearances. The purpose of this review is to emphasize the importance of detecting cardiac and pericardial calcifications on chest radiographs, and to illustrate and describe the various types of calcifications that may be encountered and how they may be differentiated from one another. Each type of cardiac and pericardial calcification is discussed, its location and appearance described, and its significance explained. Recognizing and understanding these calcifications is important as they are often encountered in daily practice and play an important role in patient care. Ó 2010 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.
Introduction
Coronary artery calcification
Various cardiac and pericardial calcifications may be identified on chest radiographs. Calcifications may involve the coronary arteries, aorta, cardiac valves, annuli, cardiac aneurysms, myocardium, pericardium, left atrium, and tumours and thrombi within the cardiac chambers. These calcifications may be distinguished based on characteristic locations, appearances, and shapes. This distinction is essential as cardiac and pericardial calcifications often overlap one another on chest radiographs or occur in similar positions. Often these calcifications are pathognomonic for a particular disease, and the radiologist may be the first to offer a diagnosis. Recognizing and distinguishing cardiac and pericardial calcifications will guide patient care as each has a different aetiology, treatment, and outcome.
The presence of coronary artery calcifications is a recognized marker for atherosclerotic coronary artery disease and may indicate significant stenosis. The radiographic identification of coronary artery calcifications serves as an important indicator of potential ischemic heart disease.1,2 Only relatively severe degrees of calcifications in the coronary arteries are typically visible on a chest radiograph.1 Many calcifications are too small and faint to be detected radiographically, particularly as these calcifications may be obscured by overlying soft tissues or superimposed disease in the chest. The frequency of calcifications is higher in the left coronary artery than in the right, and calcifications are usually greatest in the proximal portions of the coronary arteries. Calcification of the distal part of a coronary artery without involvement of the proximal part is rare.1,3 Coronary artery calcifications may appear as a plaque or double line on a chest radiograph. It must be both dense and extensive to be identified on a chest radiograph. It is most frequently identified on the frontal view in a region just medial to the left atrial appendage, called the coronary arterial calcification triangle.4 On the frontal view, calcification of the left coronary artery is located in the upper left heart border
* Guarantor and correspondent: E.C. Ferguson, The University of Texas Medical School at Houston, Department of Diagnostic and Interventional Imaging, Section of Thoracic Imaging, 6431 Fannin Street, Suite 2.026, Houston, TX 77030, USA. Tel.: þ1 713 628 9218; fax: þ1 713 500 7647. E-mail address: [email protected] (E.C. Ferguson). a Present address: Emory University School of Medicine, 1648 Pierce Drive, Atlanta, GA 30322, USA.
0009-9260/$ e see front matter Ó 2010 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.crad.2009.12.016
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where it branches into the left anterior descending and circumflex branches. The left anterior descending branch courses laterally along the upper left heart border, while the left circumflex runs more medially well inside the cardiac border (Fig.1). Calcification is rarely seen in the right coronary artery because not only is its incidence lower than in the left, but also because it overlies the spine where it is easily obscured. The optimal view for identification of both the right and left coronary arteries is the left anterior oblique view as it shows both arteries in opposite profile. In this view, the left coronary artery is located in the upper left heart border where it branches laterally as the circumflex and anteriorly as the anterior descending branch, while the right coronary artery parallels the right heart border.3,5 Coronary atherosclerosis affects almost every adult, usually beginning as early as childhood with anatomic evidence of involvement by the second or third decade of life. Certain diseases, such as familial hypercholesterolemia, pseudoxanthoma elasticum, and progeria, may lead to premature coronary artery calcification. Any calcium in a vessel wall is usually evidence of at least some degree of atherosclerosis as it is deposited within haemorrhagic areas of atheromatous plaques. Therefore, the calcium is an indicator of the amount of soft plaque burden and the extent of atherosclerotic disease. Heavy calcification is associated with significant coronary artery disease. There is also evidence that the presence of any calcification in a coronary artery signifies a more severe prognosis, independent of the extent of atherosclerotic disease.5e7
Aortic calcification There are two types of aortic calcification: dystrophic and degenerative. Dystrophic calcification is the result of
Figure 1 Coronary artery calcifications in a patient with chest pain and ischaemic heart disease. Frontal radiograph shows these calcifications as a plaque or double line over the left upper portion of the heart involving the left main (short white arrow), left anterior descending (white arrowhead), and left circumflex (black arrowhead) coronary arteries.
a scarred intima or media from aortitis and appears radiographically as a fine and sharp outline around the aortic wall. Degenerative atherosclerotic calcification results from secondary atherosclerosis and appears dense and irregular.8 Atheromatous plaques 4 mm have the highest risk for ulceration and calcification.9 Aortic calcification is most frequently observed in the aortic arch, occurring in more than 25% of patients in their sixth decade. The calcium is initially deposited at two depressions, one at the site of the ligamentum arteriosum and the other near the origin of the left subclavian artery. Calcification then spreads around the aortic wall from these sites. Atherosclerosis is usually the cause for the calcified plaques in the arch and descending thoracic aorta, and may extend into the ascending aorta when the disease is widespread. Otherwise, the ascending aorta is usually spared.5 In general, atherosclerosis is the most common cause for calcification in any part of the aorta. However, some portions of the aorta may preferentially calcify depending on the inciting factor. Syphilis is the classic condition historically associated with a calcified ascending aorta. The calcification in syphilis is typically heavy, linear, and continuous and is located on both the medial and lateral walls of the ascending aorta, whereas ascending aortic calcification due to atherosclerosis is usually deposited as discontinuous plaques at the root of the aorta and along the posteromedial wall of the ascending aorta.5,10 A jet lesion in aortic stenosis may lead to localized calcification in the ascending aorta.5 Younger patients with hyperlipidaemia have accelerated atherosclerosis, especially in the ascending aorta and coronary arteries. Nearly half of patients with hyperlipidaemia have type II hyperlipoproteinaemia, which is characterized by severe calcific atherosclerosis of the aortic root that is often visible on chest films. In these patients, calcification of the ascending aorta frequently extends into the coronary ostia.11 Other causes of a calcified ascending aorta are idiopathic dilatation, localized aneurysm, rheumatoid arthritis, Takayasu’s aortitis, Marfan’s syndrome, and radiation therapy. Aortic arch calcification may occur in aneurysm, aortic coarctation, syphilitic aortitis, atherosclerosis, and rheumatoid arthritis.5,8,12 Calcification of the aortic arch in young individuals, especially females, may suggest a patent ductus arteriosus, particularly when combined with pulmonary artery calcification.13 Dissections, true and false aneurysms may calcify and can occur anywhere in the aorta.14e16 The calcification of a dissection can appear similar to the calcification of atheromatous plaque, although some radiographic features that may suggest the presence of dissection include medial displacement of a calcified plaque by 10 mm or more, widening of the superior mediastinum, an indistinct aortic arch or double aortic contour, or a change in the aortic configuration between successive studies.14,15
Valvular calcification Calcification of cardiac valves identifiable on chest radiographs indicates the presence of significant valvular
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stenosis.10 The extent of calcification of a valve is proportional to the severity of stenosis.17 Aortic valve calcification is detected most frequently. The aortic valve lies in the centre of the heart and overlaps the spine on the frontal view. On the lateral view, most of the valve lies midway between the anterior and posterior cardiac borders above a line drawn from the tracheal bifurcation to the anterior sternodiaphragmatic angle. Three patterns of calcification may be seen in the aortic valve: commissure calcification, which appears linear in configuration; complete or partial ring calcification, which is quite common; and plaque-like calcification.5 The significance of aortic valve calcification seen on chest radiographs is well known and is a marker for clinically significant aortic stenosis. In patients younger than 65 years old, most aortic valve calcification is attributable to a bicuspid valve that produces the commissure and ring patterns of calcification (Fig. 2), followed by rheumatic fever as the next most common cause, which usually forms plaque-like calcification. In the majority of patients older than 65 years of age, aortic valve calcification is due to an idiopathic degenerative process, with a prevalence of 2e7%.5,18,19 A calcified tricuspid aortic valve may be distinguished from a bicuspid aortic valve as it has three distinct cusps forming downward curves, whereas the recognition
of a bicuspid valve is based on the identification of a raphe or a shallow sinus of Valsalva or both.20 If calcification of both the aortic valve and mitral valve is present, rheumatic fever is almost always responsible, unless the calcification has spread from the bicuspid aortic valve into the anterior cusps of the mitral valve or is due to senile calcification involving both valves. A unicuspid valve is a much less common cause of aortic stenosis and calcification. Healed bacterial endocarditis can result in calcification, although this is rare. Less frequent causes for aortic calcification include ankylosing spondylitis, end-stage renal disease, Paget’s disease of the bone, and rarely ochronosis.5,21 The detection of mitral valve calcifications on chest radiographs is uncommon and, when found, has surgical implications. Calcifications may appear nodular or amorphous. On the anterior view, calcification of the mitral valve is visible to the left of the spine and lies lower than aortic valve calcification (Fig. 3). Calcification lies predominately below a line drawn from the tracheal bifurcation to the anterior sternodiaphragmatic angle on the lateral view. Calcification of the mitral valve is nearly always caused by rheumatic heart disease. It is more common in men, and its incidence increases with age. Calcification in the pulmonic valve is a rare finding that may occur in patients of middle age with pulmonary valve stenosis, with tetralogy of Fallot, in pulmonary hypertension,
Figure 2 Aortic valve and aortic calcification. Lateral view of the chest illustrates a combination of ring (white arrowheads) and commissure (long white arrow) patterns of calcification of the aortic valve in this 55-year-old male smoker with a bicuspid aortic valve. Atherosclerotic calcification is also seen throughout the entire thoracic aorta, which typically affects the aortic arch and descending thoracic aorta but may also involve the ascending aorta (short white arrow) when the disease is widespread. The additional pressure placed on the ascending aorta by the jet lesion arising from the stenotic bicuspid aortic valve has contributed to the increased calcification of the ascending aorta observed in this patient.
Figure 3 Mitral valve calcification in a patient with rheumatic heart disease, admitted to the hospital for mitral valve replacement. Frontal chest radiograph shows nodular amorphous calcification in the region of the mitral valve (black arrow), which is visible to the left of the spine and is more caudal in location than aortic valve calcification.
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and after bacterial endocarditis. On the anterior view, it lies below and medial to the pulmonary trunk border between the spine and the left atrial appendage. On the lateral view, it is located within the upper anterior part of the heart, behind the sternum. The pulmonic valve is the most cephalad of the heart valves. Tricuspid valve calcification is rare. It is most frequently caused by rheumatic heart disease. It has also been reported in atrial septal defect, presumably as a result of trauma from high flow. Congenital tricuspid valve defects and infective endocarditis have also been associated with tricuspid valve calcification.5
Annular calcification The annuli or valve rings form the fibrous cardiac skeleton to which the valve leaflets are attached. The annuli are composed of parallel collagen bundles during infancy, but these collagen bundles gradually lose their parallel arrangement during childhood and early adulthood. By the third decade, lipid deposits are evident within the annuli. At an average age of 45 years, calcium deposits are demonstrable. Thus, annular calcification is considered to be a degenerative change related to the aging process. Annular calcification is also influenced by high pressure states. The mitral annulus calcifies most frequently, followed by the tricuspid annulus. As the composition and function of the mitral and tricuspid annuli are similar, the more frequent calcification of the mitral annulus is related to the higher pressure in the left ventricle. Similarly, long-standing elevation of right ventricular pressures leads to accelerated aging of the tricuspid annulus. Massive annular calcification suggests an exaggeration of this aging process.22 Calcification of the mitral annulus occurs in approximately 6% of the population at autopsy, and it is more common in females. It is often asymptomatic. However, it may be associated with atrial arrhythmias or intraventricular conduction defects, or, if massively calcified, may cause mitral regurgitation or congestive heart failure. It is common in patients with end-stage renal disease, indicating that derangements in calcium and phosphorus metabolism may contribute to calcification of the mitral annulus.23 Mitral annular calcification may also be a marker for atherosclerotic disease burden.24 Patients with mitral annular calcifications have a higher incidence of new coronary events than those who do not; right bundle branch block is the only defect that is significantly more common in patients with mitral annular calcification than in controls of similar age; and it is frequently associated with aortic stenosis.23,25 Calcific densities are identifiable on chest radiographs in fewer than 10% of patients with mitral annular calcifications. As the central portion of the mitral annulus adjacent to the aortic root formed by the fibrous trigones usually does not calcify, this often produces a “reverse C” configuration in the left anterior oblique or left lateral projection (Fig. 4). Alternatively, J-, U-, or oval-shaped calcific densities may be seen. Calcific deposits can measure up to 3 cm in calibre and project as far as 3 cm into the myocardium.22,23
Figure 4 Dense calcification of the mitral annulus in a 61-year-old man with atherosclerotic disease and diabetes. Frontal chest radiograph shows reverse “C”-shaped calcification of the mitral annulus (white arrow), with lack of calcification in the central portion of the annulus formed by the fibrous trigones, which usually do not calcify.
Calcification of the tricuspid annulus is rarely seen. Only isolated cases of tricuspid calcification have been reported in association with ventricular septal defect, rheumatic heart disease, congenital malformation of the tricuspid valve, and possibly subacute bacterial endocarditis. It may develop with prolonged elevated right ventricular pressures caused by pulmonary valve stenosis or atrial septal defect with pulmonary artery hypertension. The tricuspid annulus essentially produces a radiographic mirror image of the mitral annulus, as the central portion of this ring formed by the right fibrous trigone is not calcified. This produces a “C” configuration in the left lateral or left anterior oblique projection.22 Aortic annular calcification is usually seen in older patients with a calcified aortic valve. The calcification is often dystrophic and may extend into the ascending aorta or the interventricular septum. Extension of calcification into the conducting system may lead to heart block.26 Otherwise, it is often clinically insignificant.
Calcification of true aneurysms of the left ventricle A true aneurysm of the left ventricle is a localized dilatation of the ventricular wall, which consists of a thinned myocardium interspersed with fibrous tissue and reinforced by an adhesive pericardium. The true aneurysm sac contains endocardium, epicardium, and a thinned fibrous remnant of the left ventricular muscle.27 As the true aneurysm is bounded by epicardium, it will not extend beyond the coronary arteries.28 Cardiac aneurysms most often involve the left ventricle, less often the right ventricle, and rarely the atria. Causes of cardiac aneurysm are ischaemic,
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congenital, surgical, and infectious. Myocardial infarction is the most common cause, and true aneurysms develop in 5 to 10% of patients with acute myocardial infarction.29,30 True aneurysms predominately involve the apical and anterolateral segments of the left ventricle and are usually the result of occlusion of the left anterior descending artery or one of its major branches. These aneurysms produce a localized bulge along the left border of the heart on the frontal chest radiograph, usually at the apex or lower lateral margin of the ventricular contour (Fig. 5a).5,28 On the lateral chest film, a left ventricular aneurysm produces a softtissue opacity retrosternally or superiorly (Fig. 5b).31 The neck of the true aneurysm is wide and its diameter is similar to that of the maximal diameter of the aneurysm.27 Myocardial calcification can be detected on chest radiographs in 3 to 7% of left ventricle aneurysms. The calcification appears thin and curvilinear and may completely surround the aneurysm. The aneurysmal segment of the left ventricle is dyskinetic and does not empty during systole, allowing for stagnation of blood.32 These aneurysms may lead to congestive heart failure or embolic events, and may also give rise to ventricular arrhythmias because of the effects of ventricular scaring on conduction. However, true left ventricular aneurysms may be asymptomatic, especially if small. They can often be managed medically and are compatible with a prolonged survival. They have a lower potential for rupture, which is uncommon, and they are likely to rupture only in the peri-infarct period and rarely in the chronic stage.27,28,30 This is probably due to the intrinsic nature of the wall of the aneurysm, which is composed of scarred myocardium reinforced by an adhesive pericardium. Surgical resection is reserved for refractory angina pectoris, congestive heart failure, systemic embolization, or refractory arrhythmias.
Calcification of false aneurysms of the left ventricle A false aneurysm forms when the myocardium ruptures into the pericardial space and is contained by an overlying, avascular wall of pericardial adhesions and fibrous tissue. This most commonly results from myocardial infarction with rupture of the left ventricle. Rupture of the left ventricle inflames the pericardium and causes a fibrotic reaction that leads to the formation of a pseudochamber to contain the haemorrhage in a localized region. The development of this pseudochamber is necessary to prevent death from haemopericardium and cardiac tamponade.33 The neck of a left ventricular pseudoaneurysm is narrow, unlike the wide neck of a left ventricular aneurysm.28 Pseudoaneurysms form in approximately 4% of patients with infarcts involving the right or left circumflex coronary artery.16,28 Some risk factors that predispose to the development of cardiac rupture and subsequent left ventricular pseudoaneurysm after myocardial infarction include age greater than 60 years, female gender, hypertension, first transmural myocardial infarction, lack of coronary artery
Figure 5 Calcified true aneurysm of the left ventricle. (a, b) Frontal and lateral radiographs reveal thin curvilinear calcification surrounding a true aneurysm of the left ventricle (white arrows), in this patient with a remote history of myocardial infarction. True aneurysms most frequently occur at the apex or anterolateral region of the left ventricle. The neck of the true aneurysm is wide and is a continuum of the left ventricular cavity.
collateral vessels in the area of infarction, among others.34 Additional causes of false aneurysms include cardiac surgery, chest trauma, myocarditis, endocarditis, and infections such as tuberculosis and syphilis.35 A pseudoaneurysm is suggested radiographically by an abnormal lateral or posterior bulge along the left ventricular contour. A retrocardiac double density may be seen on the frontal radiograph. An abnormal cardiac contour may be seen as early as 1 week following myocardial infarction.35 Pseudoaneurysms may calcify, appearing as a thin, curvilinear density outlining the aneurysm sac (Fig. 6a and b). They lie outside the epicardium, unlike true aneurysms, which are bounded by the epicardium. Pseudoaneurysms
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are rarely seen anteriorly, likely because anterior rupture of the left ventricle is usually not contained, and these patients die before diagnostic assessment. Conversely, as only 2e3% of true aneurysms occur posteriorly, a posterior bulge along the left ventricular margin is a strong indicator of a false aneurysm. False aneurysms often enlarge on sequential radiographs. If the cardiac size rapidly increases in a patient with an abnormal cardiac contour, then leakage of the false aneurysm into the pericardium is suspected.28,35 Pseudoaneurysms require surgical repair, as they can rupture at any time after infarction, from the peri-infarct period to years later. Approximately 45% of all pseudoaneurysms rupture.35 Rupture of the free wall is much more common than septal rupture and is usually immediately fatal.36 Other complications associated with false aneurysms include congestive heart failure as the cavity is noncontractile, systemic embolization due to the stagnant flow of blood leading to thrombosis, and ventricular arrhythmias. Even asymptomatic pseudoaneurysms should be resected,33,37 as they are unstable and have a high incidence of frequently fatal rupture. Optimum medical therapy is the only alternative in patients unwilling or unable to undergo surgical repair.38
Myocardial calcification Myocardial calcification most commonly occurs after coronary artery occlusion and myocardial infarction. It is more common in males, and is usually found in patients who have had a large myocardial infarction and have survived at least 6 years after infarction. It is identified in approximately 8% of patients following a large myocardial infarction. Massive myocardial calcification usually forms in patients with coronary artery distributions favouring survival, such as a dominant right coronary artery, which aids in survival after occlusion of the left anterior coronary artery occlusion. Left ventricular aneurysm is often present.5,39 Calcification of the myocardium usually develops toward the apex of the left ventricle. It may be thin or thick and is curvilinear. Rare spherical or cyst-like calcification has also been described.40 Myocardial calcification may mimic the radiographic appearance of pericardial calcification, though distinguishing these two entities is important and is based on characteristic sites of location and appearances. Unlike myocardial calcification, pericardial calcification does not predominate at the cardiac apex. Occasionally, the myocardium may calcify posteriorly; however, this calcification is deposited below the level of the pulmonary valve, whereas pericardial calcification extends over the pulmonary outflow tract. Calcification of the myocardium typically shows a soft-tissue rim of 2 mm or more extending peripherally beyond the calcified myocardium in all projections (Fig. 7), whereas calcification of the pericardium involves the extreme periphery of the cardiac silhouette in at least one projection.39,41 As myocardial calcification also occurs in a similar position as a calcified true aneurysm of the left ventricle, these two entities should also be distinguished. Some features suggestive of the presence of an
aneurysm include a discrete, rounded protrusion of the cardiac contour, bulging, and irregularity of the left heart border, and often an enlarged heart.31 Other causes of myocardial calcification include trauma, cardioversion, infection, and endocardial fibrosis. These calcifications are typically coarse, irregular, and amorphous. Rheumatic fever and other causes of myocarditis may result in calcification. Valvular calcification of the aortic and mitral rings may spread into the adjacent muscle and septum and can cause heart block. Widespread metastatic calcification may rarely involve the myocardium. In some patients, myocardial calcification may have no obvious cause.5,42,43
Pericardial calcification Pericardial calcifications are usually deposited in regions of pericardial inflammation and fibrosis. Causes include tuberculous, fungal, viral or pyogenic infections, trauma and haemopericardium, cardiac surgery, collagen vascular diseases such as lupus, rheumatic heart disease, uremic pericarditis, and radiation. Sometimes, the cause is unknown, and pericardial calcification may occur in apparently healthy individuals.44 Occasionally, pericardial masses or cysts may calcify. The pericardium most frequently calcifies over the rightsided cardiac chambers, over the anterior and diaphragmatic aspects of the heart, and in the atrioventricular grooves (Fig. 8). Calcification over the left ventricle or cardiac apex is rare, unless there is more extensive calcification in the remainder of the pericardium. Thus, pericardial calcifications tend to form more frequently over the less pulsatile right-sided cardiac chambers, indicating that the increased pulsatility of the left-sided cardiac chambers likely hinders calcium deposition. This distribution of calcium aids in distinguishing pericardial calcifications, which are usually right-sided or diffuse over most of the heart, from myocardial calcifications, which are more leftsided and localized. On chest radiographs the calcification appears as a curvilinear density at the extreme margin of the cardiac silhouette, often better visualized on the lateral view. The extension of calcification over the pulmonary outflow tract is an important finding on the lateral view, as this occurs in pericardial but not myocardial calcification. Pericardial calcification develops less frequently over the left atrium, probably because of less pericardial investment over this region and the presence of the pulmonary veins. This lack of calcific investment allows the left atrium to dilate even when pericardial constriction is present, producing a radiographic appearance that can mimic mitral stenosis.41 Pericardial calcification can be detected on chest radiographs in about half the cases of constrictive pericarditis. However, extensive pericardial calcification can be present without signs or symptoms of constrictive pericarditis. Although there are many causes of pericardial constriction, tuberculosis has historically been the leading cause worldwide. Calcifications caused by tuberculous pericarditis are most dense in the atrioventricular grooves and appear as thick, amorphous oblique circles or arcs of calcifications.
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The calcium may then spread from the grooves over the surfaces of the atria and ventricles. This pattern of calcification is seen less often with other forms of pericarditis.5,41,45,46 When pericardial calcifications are identified, it is important to assess for signs of potential constrictive pericarditis, such as dilatation of the superior vena cava or azygos vein, pulmonary venous hypertension, left atrial enlargement, and flattenening of the cardiac contours.30 As medical management is generally ineffective, the diseased pericardium usually must be surgically resected.
Left atrial calcification
Figure 6 Calcified false aneurysm of the left ventricle. (a, b) Frontal and lateral radiographs obtained during a barium oesophagram show a focal bulge along the posterolateral wall of the left ventricle, representing a false aneurysm that is peripherally calcified (white arrowheads). False aneurysms have a narrow neck.
Calcification of the wall of the left atrium is almost always due to rheumatic heart disease with mitral valve involvement. It develops in 2e3% of individuals with this condition. Calcium deposition in the left atrial wall may be due to overstretching of the wall and local tissue necrosis primarily caused by mitral stenosis, or may be the result of active and repeated bouts of rheumatic inflammation. Calcium forms in the endocardial and subendocardial layers. The detection of left atrial calcification is important because it may indicate a number of different abnormalities, such as mitral stenosis with some regurgitation, atrial fibrillation, and mural thrombi. Other much rarer causes of left atrial calcification include metabolic calcinosis and massive intake of vitamin D.47,48 Calcification of the left atrial wall is usually thin and curvilinear measuring a few millimetres in calibre, and is most marked over the posterosuperior aspect. The lateral and oblique radiographs are most helpful in its identification. If the calcium completely encircles the left atrium, it is visible as a ring on the frontal view and as a C-shaped structure on the lateral view with the mitral valve lying anteriorly in the open part of the “C” (Fig. 9). This appearance has been termed a “coconut atrium” or “porcelain atrium”. The mitral valve may also be calcified. The interatrial septum usually does not calcify. If only a portion of the left atrial wall calcifies, it is usually the posterior wall, a finding suggesting that the regurgitant mitral jet may be the causative factor. This produces a focal calcified patch called a MacCallum’s patch. Sometimes, only the left atrial appendage calcifies, which is visible along the left cardiac border on the frontal radiograph and over the middle of the heart on the lateral view. Calcification can occasionally extend into the pulmonary veins. Thrombus is often present within a calcified left atrium, and it can also calcify. Thrombus calcification is laid down in thick, laminated layers. However even when this appearance is seen, it is more often due to uneven deposition of calcium within the walls of the left atrium as thrombus calcifies much less frequently.5,48e51 Recognizing calcium in the left atrial wall is critical, as it indicates significant disease and accompanying health issues. The amount of calcification in the left atrial wall is a marker for the duration of untreated disease. Most of these patients have atrial fibrillation and congestive heart failure from longstanding mitral valve disease. Systemic
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Figure 7 Myocardial calcification in a 52-year-old male with a history of a large myocardial infarction 16 years earlier, necessitating treatment with coronary artery bypass graft and pacemaker. Frontal radiograph shows focal curvilinear calcification over the left side of the heart (white arrow), a location that is more typical of myocardial rather than pericardial calcification. Note the peripheral shadow of myocardial tissue extending beyond the calcification (white arrowheads), which also aids in distinguishing myocardial from pericardial calcification.
Figure 9 Left atrial calcification in a patient with a history of rheumatic heart disease. Lateral chest radiograph shows the reverse “C”-shaped appearance of the calcification encircling the left atrium (white arrows), with the non-calcified mitral valve located anteriorly in the open part of the “C”.
embolization of mural thrombi is common. It is important to report this finding prior to cardiovascular surgery, as the presence of left atrial calcification alters the surgical approach needed to repair the mitral valve and to avoid complications.47,48
Tumour and thrombus calcification
Figure 8 Pericardial calcification in a patient with remote history of cardiac surgery. Frontal radiograph shows pericardial calcifications over the extreme margin of the right side of the cardiac silhouette and along the diaphragmatic surface (black arrows). This location aids in differentiating pericardial from myocardial calcification, which occurs more often over the left side of the heart and not at the extreme margin of the cardiac silhouette.
Calcifications occurring within the cardiac chambers are usually associated with tumours or thrombi. Thrombus develops in the left ventricle following myocardial infarction in approximately 20e60% of cases, and can lead to embolization.52 Thrombus formation may occur in the left atrium when the mitral valve is diseased, with an incidence of 10e25%.53 It is usually found in the left atrial appendage or along the posterior wall of the left atrium extending towards the appendage. Myxomas account for about 50% of primary cardiac tumours, and 5e10% of these contain calcification dense enough to be seen on a chest radiograph. About three-fourths of myxomas are located in the left atrium. They typically obstruct the valve orifice, but if calcified can interfere with valve closure or destroy the cusp tissue leading to regurgitation. Other primary tumours reported to calcify include teratomas, fibromas, rhabdomyomas, carcinoid tumours, and endotheliomas.5,54 Secondary tumours are much more common, and they
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can involve the intracardiac chamber via metastatic deposits, by direct infiltration or by vascular extension. A calcified mass in a neighbouring structure may invade the adjacent cardiac chamber, or calcified metastases may be deposited in the heart. Reported infectious causes of calcific intracardiac lesions include hydatid cysts, calcified tuberculomas, and infectious vegetations.5
Conclusion Many types of calcifications related to the heart and pericardium may be detected on chest radiographs. The chest radiograph is often the first diagnostic tool ordered to assess the cardiovascular structures. Some radiographically identified calcifications may be clinically insignificant, while others are critical, and the ability to make that distinction is crucial to determine when additional tests or emergent intervention is needed. Therefore, recognizing and detecting cardiac and pericardial calcifications, understanding their importance, and distinguishing among them is necessary to make an appropriate diagnosis and to guide patient care.
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