Author: Sohail G Contractor, MD, Staff Physician, Department of Radiology, University of Medicine and Dentistry of New Jersey
Coauthor(s): Pierre D Maldjian, MD, Associate Professor, Department of Radiology, University of Medicine and Dentistry, New Jersey Medical School; Consulting Staff, Department of Diagnostic Radiology, University Hospital; Mysore Seetharaman, MD, Consulting Staff, Department of Internal Medicine, Ida G Israel Community Health Center, Coney Island Hospital; Hani H Abu-Judeh, MD, Consulting Staff, Department of Radiology, University of Medicine and Dentistry of New Jersey Hospital; Farid Thanawala, MD, Assistant Professor, Department of Interventional Radiology, University of Massachusetts; Staff Radiologist, Wachussett Radiology, Heywood Hospital
Radiologic detection of calcifications within the heart is quite common. The amount of coronary artery calcification correlates with the severity of coronary artery disease (CAD). Calcification of the aortic or mitral valve may indicate hemodynamically significant valvular stenosis. Myocardial calcification is a sign of prior infarction, while pericardial calcification is strongly associated with constrictive pericarditis. Therefore, detecting and recognizing calcification related to the heart on chest radiography and other imaging modalities such as fluoroscopy, CT, and echocardiography may have important clinical implications.
In patients with diabetes mellitus, by determining the presence of coronary calcifications, patients at risk for future myocardial infarction and coronary artery disease could be identified, and future events could be excluded if no coronary calcifications were present.1
In an asymptomatic population, determination of the presence of coronary calcifications identified patients at risk for future myocardial infarction and coronary artery disease independent of concomitant risk factors. In patients without coronary calcifications, future cardiovascular events could be excluded.2
Calcification of the pericardium usually is preceded by a prior episode of pericarditis or trauma. Infectious etiologies for pericarditis include viral agents (eg, coxsackievirus, influenza A, influenza B), tuberculosis, and histoplasmosis.
Pericardial disease from systemic lupus erythematosus, rheumatic heart disease, uremic pericarditis, and hemopericardium (posttrauma or cardiac surgery) also may result in pericardial calcification. Occasionally, pericardial tumors, such as intrapericardial teratomas and pericardial cysts, can calcify (Images 1-2).
Of patients with pericardial calcification, 50-70% have constrictive pericarditis. Extensive calcification may be present without signs or symptoms of pericardial constriction.
On chest radiographs, pericardial calcification appears as curvilinear calcification usually affecting the right side of the heart (Images 3-4). This is often visualized better on lateral chest radiographs than on frontal views. Calcifications associated with tuberculous pericarditis present as thick, amorphous calcifications along the atrioventricular groove. This pattern may be observed less commonly with other forms of pericarditis as well.
Pericardial calcification is seen more commonly over the right ventricle; in contrast, myocardial calcification is seen more often over the left ventricle (LV) and rarely involves the right atrium or ventricle.
CT is the best technique to detect pericardial calcification; however, overpenetrated films, conventional tomography, fluoroscopy, and MRI may be helpful.
Myocardial calcification is more common in males than in females and usually occurs in patients who have sustained sizable infarcts and have survived more than 6 years after infarction. Most of these patients have a dominant right coronary artery, since this favors longer survival after infarction in the region of the left anterior descending coronary artery.
Approximately 8% of patients who sustain a large myocardial infarction develop myocardial calcification. In these patients, infarcts usually are large and most frequently involve the anterolateral wall of the LV. LV aneurysm usually is present.
Myocardial calcification is identified as thin and curvilinear shaped and usually appears toward the apex of the LV. The associated contour abnormality from the aneurysm is frequently noted. Rarely, calcification can appear spherical or platelike.
The walls of the LV rarely calcify, and calcification of the mural thrombus in the aneurysm is more common. Rarely, calcification is noted in cardiac tumors, such as rhabdomyomas and endotheliomas (Images 5-6).
Detection of left atrial wall calcification has significant clinical implications. Most of these patients have congestive heart failure and atrial fibrillation from long-standing mitral valve disease. Mural thrombi secondary to atrial fibrillation are a frequent source of systemic and pulmonary emboli. Possible complications during cardiac surgery include dislodgement of thrombi, which results in cerebral embolism and uncontrollable hemorrhage if the left atrium (LA) is entered through the calcified region because of LA wall rigidity. LA calcification usually is secondary to endocarditis resulting from rheumatic heart disease, and the amount of calcification is often related to the duration of untreated disease.3
LA calcification may be in the endocardial or subendocardial layer or within a thrombus. Calcification is usually thin and curvilinear (Images 8-9). Three patterns of calcification have been identified.
Type A: Calcification is confined to the LA appendage, the underlying lesion is often mitral stenosis; this type of calcification almost always is associated with thrombus in the appendage.
Type B: The free wall of the LA and mitral valve are calcified, although the valve calcification is not always appreciated from chest radiographs. This pattern indicates advanced mitral stenosis.
Type C: Small area of calcification is confined to the posterior wall of the LA. This results from a jet lesion because of mitral regurgitation and is termed a McCollum patch.
Valvular calcification identified radiographically suggests the presence of a hemodynamically significant stenosis. Dominant valvular insufficiency is not associated with radiographic depiction of calcification, except in patients with calcified stenotic valves secondarily destroyed by endocarditis. The aortic valve calcification is detected most frequently.
In patients younger than 40 years, a calcified aortic valve usually indicates marked aortic stenosis secondary to a congenital bicuspid aortic valve. In these patients, one cusp of the valve is larger than the other; therefore, the valve cannot function properly, resulting in prolapse, fibrosis, calcification, and stenosis. The average age at which calcification first is detected is 28 years. More than 90% of patients with congenital bicuspid valve have calcification by age 40 years.
In older patients, calcification of the aortic valve may be secondary to aortic sclerosis with degeneration of normal valve leaflets and may be associated with hemodynamically significant aortic stenosis. Aortic valve disease associated with rheumatic heart disease frequently is associated with mitral valve disease. The average age at which aortic valvular calcification first is detected is 47 years in patients with a history of rheumatic fever and carditis. However, aortic valvular calcification is infrequently seen in this entity, and fewer than 10% of patients without congenital bicuspid valve have calcification from age 40-65 years.
* In bicuspid aortic valves, calcification may be nodular, semilunar, or mushroom shaped. A dilated ascending aorta often is seen. A thick, irregular, semilunar ring pattern with a central bar or knob is typical of stenotic bicuspid valves and results from calcification of the valve ring and the dividing ridge of the 2 cusps or the conjoined leaflet (Image 10). Rarely, 3 leaflet valves mimic this pattern because of fusion of 2 of the 3 leaflets. However, none of these features has a high sensitivity or specificity in predicting valvular anatomy
* In patients with aortic sclerosis, calcification usually is nodular. Diffuse aortic dilatation can be observed. Heart size may be normal; however, LV dilation can occur with decompensation. Nodular calcification of the valve also is observed in patients with rheumatic aortic disease. The ascending aorta may be dilated, and signs of rheumatic mitral valve disease may be present.
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