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Rheumatology 2006 45(Supplement 4):iv26-iv31; doi:10.1093/rheumatology/kel309
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Cardiac imaging in rheumatic diseases

R. Maksimovic, P. M. Seferovic1, A. D. Ristic1, B. Vujisic-Tesic1, D. S. Simeunovic1, G. Radovanovic1, M. Matucci-Cerinic2 and B. Maisch3

Center for Magnetic Resonance Imaging and 1Institute of Cardiovascular Diseases, University Clinical Center of Serbia, Belgrade, Serbia, 2Division of Rheumatology, Department of Internal Medicine, University of Florence, Florence, Italy and 3Department of Internal Medicine-Cardiology, Philipps-University, Marburg, Germany.

Correspondence to: R. Maksimovic, MD, PhD, Associate Professor of Radiology, Center for Magnetic Resonance Imaging, University Clinical Center of Serbia, Koste Todorovica 8, 11 000 Belgrade, Serbia. E-mail: rmaksimovic{at}yahoo.com


   Abstract
Top
 Abstract
Introduction
 Involvement of pericardium
 Involvement of heart valves
 Involvement of myocardium
 Involvement of coronary arteries
 Acknowledgements
 References
 
The majority of the imaging techniques in cardiology could be applied in rheumatic diseases (RDs), such as echocardiography, single-photon emission computed tomography (SPECT), radionuclide ventriculography, angiography, cardiovascular MRI and CT. Inflammatory pericardial involvement is the most common cardiac manifestation in various forms of RD. Echocardiography is the gold standard for diagnosis of pericardial abnormalities, demonstrating location and amount of pericardial effusion. Cardiac MRI and CT can be used to assess the features of pericardial effusions and peracardial structures. In patients with valvular heart disease in RD, transoesophageal echocardiography is a superior method and offers reliable information about valve morphology, the severity of the disease and left ventricular (LV) function. In addition, cardiac MRI is a valuable tool for the evaluation of valvular stenosis and regurgitation severity. Myocardial involvement in RD is demonstrated by abnormalities in LV size and function, indicating myocardial inflammation. In these patients Doppler echocardiography and myocardial tissue imaging can provide essential diagnostic information. Both LV angiography and cardiac MRI can provide reliable information on LV size, function and mass. In patients with coronary disease associated with RD, LV ejection fraction and ventricular wall motion can be assessed by echocardiography, radionuclide ventriculography, gated SPECT and MRI. Three-dimensional (3D) echocardiography is considered superior to 2D echocardiographic techniques. Stress echocardiography is the most used method for detection of myocardial ischaemia. The only accurate visualization of the coronary arteries is by selective coronary arteriography, which remains the gold standard. Although new non-invasive techniques have been developed, including CT and MRI angiography, some limitations apply.


   Introduction
Top
 Abstract
 Introduction
Involvement of pericardium
 Involvement of heart valves
 Involvement of myocardium
 Involvement of coronary arteries
 Acknowledgements
 References
 
In patients with rheumatic diseases (RDs), cardiovascular involvement is common, may have serious consequences, and can contribute to worsening of patients outcome (Table 1) [1]. Incidence and prevalence of cardiovascular diseases (CVD) in RD have recently been largely increased due to both the improved biochemical and cardiac imaging diagnostic techniques. CVD can be diagnosed in more than 50% of the patients with systemic lupus erythematosus (SLE) [2], and is the cause of nearly 40% of deaths in rheumatoid arthritis (RA) patients [3]. Patients with RA are more likely to have myocardial infarction and sudden death, and are prone to serious systemic complications. Systemic sclerosis (SSc) is frequently associated with pulmonary hypertension and/or systemic hypertension, which can lead to subsequent complications.


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  		TABLE 1. Heart diseases in major rheumatic diseases

 
The majority of the imaging techniques in cardiology could be also applied in RD, with variable diagnostic accuracy. These include echocardiography, single-photon emission computed tomography (SPECT), radionuclide ventriculography, angiography, cardiovascular MRI and CT. Imaging techniques are essential in the early detection of CVD in RD, having significant therapeutic implications and improving patients long-term outcome.


   Involvement of pericardium
Top
 Abstract
 Introduction
 Involvement of pericardium
Involvement of heart valves
 Involvement of myocardium
 Involvement of coronary arteries
 Acknowledgements
 References
 
Inflammatory pericardial involvement is the most common cardiac manifestation in various forms of RD [2, 3]. In RA, pericardial effusion is seen in 2–10% of the patients as chronic, asymptomatic pericardial effusion, while tamponade and constrictive pericarditis are rare (0.5%) [2]. In patients with SLE, symptomatic pericardial effusion has been reported in 6–50%, clinically significant pericarditis and pericardial thickening are described in <30%, while post-mortem pericardial lesions range from 60–80%. In SSc, pericardial involvement is seen in 70% of the patients, mostly as small pericardial effusion [4].

Echocardiography is the most widely used imaging technique in the evaluation of suspected pericardial disease. Transthoracic echocardiography represents the gold standard for diagnosis of pericardial abnormalities, demonstrating the location and amount of even minimal pericardial effusion. The echocardiogaphic features of pericardial effusion are the pericardial layer separation with an echo-free space and the decrease in the parietal pericardium motion. If tamponade develops, which is a rare complication of RD, a several echocardiographic signs can be appreciated such as diastolic compression of right heart chambers, lack of inspiratory collapse of the dilated inferior vena cava and the swinging of the entire heart [5] (Fig. 1). Doppler echocardiographic patterns of tamponade include marked respiratory variations of right and left ventricular (LV) inflow and pulmonary and hepatic venous flow velocities. Echocardiography is also very instrumental if combined pericardial and valvular pathology is observed (Fig. 2).


Figure 1
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  		FIG. 1. Echocardiography, parasternal short axis view. Tamponade in SLE demonstrating diastolic right atrial free wall collapse (arrow). Ao, aorta; ra, right atrium; la, left atrium.

 

Figure 2
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  		FIG. 2. Transoesophageal echocardiography, four-chamber view. Pericardial effusion (arrowheads) and two endocardial vegetations (arrows) in SLE. The vegetations are localized on atrial side of the base of the mitral leaflets. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; PE, pericardial effusion.

 
Pericardial thickening resulting from fibrosis or calcification can be presented as a small echo-free space or a single dense band of echoes. Since the pericardium is the most echogenic structure in the image, sensitivity and specificity of transthoracic echocardiography for pericardial thickening is low. Doppler assessment of diastolic flow patterns and the respiratory changes in these patients can provide compelling evidence for pericardial constriction and rule out the diagnosis of restrictive cardiomyopathy and cardiac tamponade [6].

Both cardiac MRI and CT in RD can also be used to assess the size and location of pericardial effusions, although they tend to overestimate the amount of fluid in comparison with echocardiography [7] (Fig. 3). Pericardial effusion is hypodense in comparison with the myocardium, with radiodensity ranging from 10–40 Hounsfield units, depending on the protein content (fibrin) and admixture of blood. If the amount of blood in the pericardium is small, differentiation from fibrosis (chronic constrictive pericarditis), which displays about the same density, may be impossible [8].


Figure 3
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  		FIG. 3. Cardiac MRI, four-chamber view. Cine TrueFISP sequence shows high signal intensity of a pericardial effusion in a patient with SSc (arrows). LV, left ventricle; LA, left atrium; RV, right ventricle; RA, right atrium.

 
MRI is useful in patients with loculated or complex configurations of pericardial effusions, which can be often found in RD. MRI has an advantage over CT in differentiating small pericardial effusions from pericardial thickening. However, MRI cannot distinguish between chronic pericardial thickening and calcifications. CT and MRI diagnosis of constrictive pericarditis is established only if the findings of systemic venous hypertension are confirmed, such as dilated superior and inferior vena cava, ascites, hepatomegaly and pleural effusion. MRI has high diagnostic accuracy for the definitive non-invasive diagnosis of constrictive pericarditis and its separation from restrictive cardiomyopathy. Both the increased pericardial thickness and alterations in the heart structures can contribute to the diagnosis with sensitivity of 88%, specificity 100% and accuracy of 93% [9]. Furthermore, MRI could quantify functional abnormalities, namely LV systolic and diastolic dysfunction, which may be associated with pericardial diseases [10].


   Involvement of heart valves
Top
 Abstract
 Introduction
 Involvement of pericardium
 Involvement of heart valves
Involvement of myocardium
 Involvement of coronary arteries
 Acknowledgements
 References
 
Echocardiography is superior and the most frequently used technique for the evaluation of the patients with valvular heart disease in RD. This method offers the non-invasive and reliable information about valve morphology, the severity of valve stenosis or regurgitation, and the impact of valvular lesion on LV size and function. Transoesophageal echocardiography is considered to be more sensitive than transthoracic echocardiography in revealing valve abnormalities in RD [11]. The haemodynamic data are derived from Doppler echocardiography, and valvular regurgitation can be assessed by colour flow imaging of regurgitant jet.

Valvular disease can be frequently diagnosed in SLE, as valvular thickening, vegetations and valvular insufficiency. As the most typical lesion, the Libman–Sacks endocarditis (atypical verrucous endocarditis) is described, echocardiographically characterized by vegetations usually <10 mm in diameter, which vary in shape, have irregular borders, and have various echodensities (Fig. 4). Lesions are easily echocardiographically detected and are usually attached to the basilar portion of the aortic and mitral valve leaflets. The verrucae are near the edge and in only 3–4% of the patients haemodynamically significant. Echocardiographic anatomical abnormalities were reported in 40–50% of these cases, with much higher sensitivity for transoesophageal echocardiography in 50–60% patients [2].


Figure 4
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  		FIG. 4. Transoesophageal echocardiography in a patient with SLE. Endocardial vegetations (arrow) on the ventricular side of the mitral leaflet (Libman–Sacks endocarditis). lv, left ventricle; la, left atrium.

 
Valvular involvement in RA patients can be also confirmed by echocardiography, which usually reveal aortic valve lesions in 5–14% and mitral valve abnormalities (thickening and prolapse) in 5–35% of the patients, depending on the imaging technique applied [6].

In SSc, nodular thickening of the mitral valve could be seen in 38% of the patients, while in only a few cases mitral and tricuspid vegetations are reported [12]. In patients with antiphospholipid syndrome, heart valve abnormalities are the most common cardiac manifestations and could be presented as vegetations, thickening and valvular dysfunction [13]. Mitral valve thickening is found on echocardiogaphy in 63% of the patients, followed by the aortic (32%) and tricuspid valve thickening in 8% of the patients [14]. Ankylosing spondylitis is associated with aortic root and valve disease [15]. Aortic valve thickening is predominantly echocardiographically manifested as nodularities, usually single, homogeneously echoreflectant, with well-defined borders, located on any portion of the three cusps. Mitral valve thickening could be also common and is predominantly localized to the basal anterior mitral leaflet.

Cardiac MRI is a valuable tool for evaluation of valvular regurgitation severity and quantification of the effects of valvular lesion on LV volumes, function and mass [10]. The accepted MRI method for qualitative assessment of severity of valvular regurgitation is based on the dark signal extending from the diseased valve into the receiving chamber during a variable time period of the cardiac cycle. For the valve stenosis evaluation, signal loss distal to an abnormal valve is appreciated, but could not be used as an accurate parameter because it is dependent on MRI settings. Non-invasive quantitative assessment of blood flow can be performed by velocity-encoded cine MRI, not yet available for clinical use. Furthermore, in the absence of a cardiac shunt, any discrepancy between stroke volumes in a patient with regurgitation will identify the regurgitant LV volume. Disadvantage of this method is that only patients with a single regurgitant valve can be assessed although combination with velocity-encoded cine MRI allows assessment and quantification of multivalvular disease [10].


   Involvement of myocardium
Top
 Abstract
 Introduction
 Involvement of pericardium
 Involvement of heart valves
 Involvement of myocardium
Involvement of coronary arteries
 Acknowledgements
 References
 
The myocardium is frequently affected in RD by means of different immunological mechanisms. In RA, myocardium was involved in 19% of the cases on post-mortem study by Lebowitz [16]. Although myocarditis is not usually associated with RA, secondary amyloidosis could cause cardiomyopathy and atrioventricular conduction abnormalities [17]. Acute or chronic congestive heart failure due to SLE and acute myocarditis are not common, the latter could be initial clinical presentation of the disease. Acute myocarditis has been reported in 8–25% of these patients, but due to introduction of steroid therapy decreased to 5% [18]. In SS, myocardial involvement can manifest as incipient cardiomyopathy that could progress to ventricular dysfunction and heart failure [4].

Echocardiography is considered an accurate tool for the assessment of LV size and function, which are indicative of myocardial inflammation and/or dysfunction. 2D echocardiography could be of limited value, but Doppler echocardiography and myocardial tissue imaging can provide essential diagnostic information. The analysis of impaired myocardial relaxation, decreased compliance and increased filling pressure, are important clues in revealing LV diastolic dysfunction [2].

LV angiography demonstrates LV volumes and function and is routinely used in the assessment of these patients. LV angiography using technetium 99 m-labelled red cells can be used to evaluate LV function, but has largely been replaced by echocardiography and recently MRI [10]. CT is not considered the tool of choice for the assessment of LV function in RD due to radiation and application of contrast media.

Cardiac MRI is superior to other techniques in assessment of LV size, function and mass because it is non-invasive, has high spatial resolution, high reproducibility and low interobserver and intraobserver variability. The results are comparable to SPECT and the method is more accurate than 2D echocardiography and radionuclide ventriculography [10]. Myocardial fibrosis, which is considered as a non-specific finding, is demonstrated as a low signal intensity area on T2-weighted images and as a delayed enhanced region after contrast administration. Inflammatory oedema consistent with myocarditis, could be seen as multiple focal areas of increased myocardial signal intensity on T2-weighted images, and early and late gadolinium enhancement images [19] (Fig. 5). Similar to this, increased gallium-67 citrate uptake may be indicative of a myocardial interstitial inflammation [20].


Figure 5
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  		FIG. 5. Cardiac MRI in myocarditis in patient with SLE. (A) Hypocontractility is demonstrated in the lateral wall of the left ventricle in cine TrueFISP sequence as an evidence of ongoing inflammation (arrows). (B) Late enhancement image shows intramural high signal intensity areas (arrows) due to focal inflammatory necrosis. LV, left ventricle; RV, right ventricle.

 

   Involvement of coronary arteries
Top
 Abstract
 Introduction
 Involvement of pericardium
 Involvement of heart valves
 Involvement of myocardium
 Involvement of coronary arteries
Acknowledgements
 References
 
In SLE, risk of developing coronary artery disease (CAD) is 4–8 times higher than in controls, while in the middle-aged women with long-standing disease and a long period of corticosteroid intake the risk is increased 50-fold than in the matching age group [2]. In patients with RA, risk of CAD is 2–3-fold increased in comparison with the general population. In addition, silent ischaemia and sudden cardiac death are more likely to be experienced by RA patients [1].

For assessment of LV ejection fraction and ventricular wall motion in CAD, radionuclide ventriculography, echocardiography, gated SPECT and MRI could be used. According to American Heart Association/American College of Cardiology (AHA/ACC) Task Force on Practice Guidelines in CAD, radionuclide ventriculography should be used for serial measurements of LV ejection fraction [21]. Gated SPECT myocardial perfusion nuclear imaging is preferred for simultaneous assessment of myocardial perfusion and function [22].

2D echocardiography is suggested for routine assessment of LV ejection fraction in patients with CAD in RD. 3D echocardiography is superior to both quantitative and qualitative 2D echocardiographic techniques and correlates well with measurements made using cardiac MRI. Tissue Doppler imaging study [23] revealed that early diastolic velocities and mitral E/A ratio are lower in patients with CAD in comparison with the controls. Recently, a new global index of left ventricular function (TEI index), was introduced by Turiel et al. [14] aimed to assess systolic and diastolic LV function, and was confirmed to be higher in patients with RA and SS compared with control subjects.

Stress echocardiography is a useful method for detection of myocardial ischaemia and for risk stratification of patients with suspected or known CAD. Stressors include exercise, pharmacological agents and pacing. In patients with LV dysfunction and documented CAD, stress echocardiography can differentiate viable from scarred myocardium. In patients who are unable to exercise, pharmacological stressors can be used: sympathomimetic agents (dobutamine) or vasodilatators (dipyridamole or adenosine). This technique is important to differentiate myocardial stunning from necrosis, and it is considered safe, relatively inexpensive and easy to perform.

Cardiac MRI pharmacological stress test is well-established to identify ischaemia-induced wall motion abnormalities. Dobutamine MRI has greater sensitivity than dobutamine echocardiography (86 vs 74%) and specificity (86 vs 70%) [24]. The diagnostic accuracy of adenosine stress cardiac MRI varies significantly according to the MRI parameter evaluated.

Ischaemic territories can be identified with high sensitivity and specificity by using intravenous gadolinium for a first-pass perfusion, when perfusion abnormalities were confined to the subendocardium. Dark areas of low perfusion could be identified visually or using computer analysis (Fig. 6). Usually, both stress and rest myocardial perfusion scans are used and are comparable with myocardial perfusion reserve using flow wire probe, positron emission tomography (PET) and SPECT [22]. More simple approach is to assess stress myocardial perfusion only during vasodilatation, and using late gadolinium enhancement to define areas of non-viability.


Figure 6
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  		FIG. 6. Cardiac MRI in myocardial ischaemia in a patients with SLE. (A) TrueFISP sequence with saturation—recovery preparation shows perfusion defect in the lateral wall of the left ventricle (arrows). (B) This finding corresponds to angiographically proven high-grade stenosis of left circumflex coronary artery (arrow). LV, left ventricle; RV, right ventricle.

 
Severity of stenotic coronary lesion could be measured by coronary flow reserve and direct visualization of coronary artery tree. Coronary flow reserve could be estimated with the combination of coronary flow assessment by Doppler and vasodilatator stress, which increases accuracy of this technique [14]. Determination of coronary flow by cardiac MRI in humans has been only reported to identify stenosis of the left anterior descending artery [10].

The most accurate visualization of the coronary arteries is by selective coronary arteriography, which remains a gold standard. Although new non-invasive techniques have been developed, including CT and MRI angiography, some limitations apply. Coronary angiography using 64-slice CT scanners, does not identify all coronary segments (88%), and has sensitivity of 88–100%, and specificity of 85–97% per patient. Angiography with MRI has even lower diagnostic accuracy than multislice CT angiography [25]. However, neither of the techniques is an alterantive to selective coronary angiography and neither is recommended for screening asymptomatic patients, including those at high risk [26].

The authors have declared no conflicts of interest.


   Acknowledgements
Top
 Abstract
 Introduction
 Involvement of pericardium
 Involvement of heart valves
 Involvement of myocardium
 Involvement of coronary arteries
 Acknowledgements
References
 
This work is part of the project supported by the Ministry of Science and Environmental Protection, Republic of Serbia, ‘Uncovering etiopathogenesis of heart muscle disease, pericardial disease, and congestive heart failure as a comprehensive background for diagnosis and treatment: application of neuronal network and artificial intelligence’, (No. 145063) and Joint European Project, Tempus (No. 19046-2004), ‘Restructuring of postgraduate studies and training in medicine in Serbia’.


   References
Top
 Abstract
 Introduction
 Involvement of pericardium
 Involvement of heart valves
 Involvement of myocardium
 Involvement of coronary arteries
 Acknowledgements
 References
 

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