CMR in inflammatory vasculitis
© Raman et al.; licensee BioMed Central Ltd. 2012
Received: 15 April 2012
Accepted: 16 November 2012
Published: 30 November 2012
Vasculitis, the inflammation of blood vessels, can produce devastating complications such as blindness, renal failure, aortic rupture and heart failure through a variety of end-organ effects. Noninvasive imaging with cardiovascular magnetic resonance (CMR) has contributed to improved and earlier diagnosis. CMR may also be used in serial evaluation of such patients as a marker of treatment response and as an indicator of subsequent complications. Unique strengths of CMR favoring its use in such conditions are its abilities to noninvasively visualize both lumen and vessel wall with high resolution. This case-based review focuses on the large- and medium-vessel vasculitides where MR angiography has the greatest utility. Because of increasing recognition of cardiac involvement in small-vessel vasculitides, this review also presents evidence supporting greater consideration of CMR to detect and quantify myocardial microvascular disease. CMR’s complementary role amidst traditional clinical, serological and other diagnostic techniques in personalized care for patients with vasculitis is emphasized. Specifically, the CMR laboratory can address questions related to extent and severity of vascular involvement. As ongoing basic and translational studies better elucidate poorly-defined underlying molecular mechanisms, this review concludes with a discussion of potential directions for the development of more targeted imaging approaches.
Vasculitis, the inflammation of blood vessels, is rare [1, 2], yet those affected may suffer high rates of morbidity and mortality. A significant contributor to poor outcomes is delay in diagnosis. While advances in serologic testing have afforded somewhat earlier diagnosis, there remains a need for better techniques to detect vasculitis and improve outcomes. Advances in non-invasive imaging are poised to fill this gap, particularly in vasculitis involving large- and medium-sized arteries where these studies can play a significant role in i) establishing the correct diagnosis, ii) determining disease extent and activity and iii) measuring treatment response .
Recognition that not only vascular but also cardiac sequelae occur in certain vasculitides makes cardiovascular magnetic resonance (CMR) appealing amidst the various imaging options available . Some clinicians may not consider CMR due to concerns surrounding the use of gadolinium-based contrast in vasculitis patients who frequently present with significant renal dysfunction. The availability of excellent non-contrast MR angiography techniques can allay such concerns, allowing CMR in high-risk patients who may have the most to benefit from timely use of the technology.
The paucity of well-defined pathogenic mechanisms for many of these disorders renders in some respect inadequate each of the many vasculitis classification schemes. In this review, we use the common approach that focuses on the sizes of the involved blood vessel that can guide CMR protocols and afford differential diagnosis of imaging findings. This approach, however, requires an appreciation that while specific types of vasculitis classically affect certain-sized blood vessels, there remains a spectrum of involvement across the various levels of the vasculature. What follows is a brief summary of the techniques most relevant to the CMR vasculitis examination followed by case-based illustrations of the major primary inflammatory vasculitides.
While this review focuses on the primary vasculitides, secondary vasculitis and mimics of vasculitis warrant consideration when evaluating a patient with suspected vasculitis . Secondary vasculitis may occur in the setting of infection, malignancy, connective tissue disease , drugs and environmental exposure. Another consideration with vasculitis of medium and small vessels is primary central nervous system (CNS) angiitis or involvement of the CNS with a systemic vasculitis. This, too, is beyond the scope of this review but can be pursued in greater depth in several recent publications of MR’s role in the diagnosis and serial assessment of cerebral vasculitis [7, 8].
CMR techniques in the vasculitis examination
Components of the CMR Examination of Vasculitis
Dark blood stacks typically in axial, coronal and sagittal planes e.g. HASTE
Provides vessel wall imaging as well as complementary information to CE-MRA regarding lumen
Noncontrast bright blood stack(s) e.g. SSFP
3D contrast-enhanced magnetic resonance angiography e.g. spoiled gradient echo
Appropriate vasculature should be covered depending on clinical questions and known or suspected diagnosis (see Table 2)
T1-weighted vessel wall imaging e.g. VIBE or FAME
Additional vessel wall imaging, particularly useful to delineate thickening and thrombus
Multiplane cine imaging e.g. SSFP Aortic valve velocity-encoded cine Myocardial imaging: T2 precontrast, T1W early post contrast, late post-gadolinium imaging
May be appropriate when aortic root disease involves the aortic valve or when myocardial inflammation is suspected, particularly in small-vessel vasculitides
Techniques for angiography include both contrast-enhanced MR angiography (CE-MRA) as well as non-contrast approaches, both recently summarized in this journal by Hartung et al. MRA’s sensitivity is typically at or near 100% while specificity tends to be lower, underscoring the potential to overestimate degree of stenosis particularly in branch vessels of the aorta. The workhorse technique for demonstration of luminal stenosis remains CE-MRA, with improved spatial resolution, better vessel-to-background contrast and reduced volume requirement for exogenous contrast material with higher field strength. These advantages offset limitations imposed by radiofrequency field inhomogeneity that increases with field strength. Technical developments in coil hardware and parallel acquisition techniques make higher field scanners appealing platforms for CE-MRA.
Typical arterial segments involved in the major primary vasculitides
Giant cell arteritis
MRI in inflammatory vasculitidies
Author (Reference #)
Role of CMR
Giant Cell Arteritis
MRA in patients vs. retrospective normal controls
MRA detected GCA in 67% with good inter-observer agreement
MRA vs. Biopsy
16/17 GCA + by biopsy were MRA +, all 3 GCA – were MRA -
MRA in diagnosed GCA patients
MRA demonstrated vascular involvement in all previously diagnosed 9 patients
PET in GCA
30 patients and 31 controls
PET had a sensitivity of 73.3% and specificity of 83.9%
PET vs. MRA
15 FUO patients
MRA and PET had comparable sensitivity and specificity for detecting inflammation. Identical vascular territories were identified in the majority but disparate territories in a large minority
PET vs. MRI
Both Dynamic Contrast Enhanced MRI and PET had identical sensitivity and specificity (86 and 90% respectively) in assessing carotid and vertebral inflammation
PET vs. MRI
MRI and PET found unreliable for assessing large-vessel inflammation in GCA patients on pre-existing immunosuppressive therapy
Whole body MRI
Wall thickness and post-contrast intensity by MRI higher in active group than remissive group (6.12 vs. 4.31 mm and 1.56 vs. 1.17)
Retrospective case series
MRA-inversion recovery prepared gradient-echo MR pulse sequence
All patients had increased wall thickness and 5 had enhancement with contrast (4 had clinically active disease)
26 patients and 16 controls
MR imaging was concordant with clinical findings in 23 patients (88.5%), with laboratory findings in most patients (ESR in 92.3% [24/26] and CRP in 84.6% [22/26])
26 patients-16 classified as active and 10 as inactive
Active group had more stenosis in left SCA than the inactive group (14/16, 87.5% vs. 2/10, 20%; p<0.01) greater vessel wall thickness in left CCA (11/16, 68.75% vs. 1/10, 10%; p<0.01) and left SCA (9/16, 56.25% vs. 0/10, 0%; p<0.01)
MRA revealed vessel wall edema in 94% (17 of 18), 81% (13 of 16), and 56% (24 of 43) of studies during periods of unequivocally active disease, uncertain disease activity, and apparent clinical remission, respectively. ESR and CRP did not correlate with clinical assessment or MR evidence of vascular edema
MRA vs. CA
Takayasu arteritis was diagnosed in 20 patients - MRA accurately revealed 323 (98%) of 330 arteries, but 7 (2%) stenotic lesions were overestimated as occluded. The sensitivity and specificity of MRA for diagnosis of Takayasu arteritis were 100%. PA lesions were demonstrated in 10 (50%) of the 20 patients.
MRA vs. DSA
Diagnosis confirmed by MRA in all patients. MRA with sensitivity, specificity, PPV, NPV and DA for detection of a >50% lesion was 98.33%, 97.25%, 92.18%, 99.43% and 97.52% respectively.
MRA vs. CA
Complete agreement between MRA and CA in detection of coronary aneurysms (n=15).Excellent agreement for aneurysm diameter, length, and distance from the ostium.
MRA vs. Echocardiography
MRA detected coronary aneurysms in 15 patients, whereas echo detected aneurysms in 11.
MRA vs. CA
Excellent agreement for assessment of coronary aneurysm maximal diameter and length
MRA vs. CA
6 patients had coronary aneurysms and 7 had ectasia. MRA and CA agreed completely for the diagnosis of aneurysms
MRA vs. CA
MRA agreed well with CA for detecting aneurysms and stenoses
MRA vs. Multidetector CT vs. CA
100% agreement between MDCT and CA in the detection of aneurysms and stenoses. MRI and CA had 93% agreement for the detection of aneurysms. MRI missed one stenosis.
MRA in Kawasaki disease patients in convalescence
MRA revealed high prevalence of coronary ectasia and myocarditis in 46% (n=13) of convalescing Kawasaki disease patients
Large vessel vasculitis
Giant cell arteritis (GCA)
GCA is a granulomatous, large-vessel vasculitis with a predilection for individuals aged ≥70 years. Up to 60% of patients with GCA have findings consistent with polymyalgia rheumatica such as proximal muscle morning stiffness and aching . The overall incidence is highest in individuals of Scandinavian descent, where it occurs in 18 to 20 per 100,000 individuals . GCA can be diagnosed as present if 3 of the following 5 classical findings are observed: i) age ≥50 years; ii) new-onset or new type of localized pain in the head; iii) temporal artery tenderness; iv) erythrocyte sedimentation rate ≥50 mm/h; and v) arterial biopsy specimen showing vasculitis . However, appreciating that non-classic symptoms may be the initial manifestation of GCA, high clinical suspicion and rapid institution of, for instance, steroid therapy is needed to avoid dreaded complications such as vision loss. Examination of the retina with fluorescein angiography holds particular value in diagnosis .
Classically, GCA affects the extracranial branches of the carotid artery, notably the temporal artery. Risk of developing thoracic and abdominal aortic aneurysms is 17 and 2 times higher, respectively, in patients with GCA compared to age-matched individuals without GCA . Aortic involvement in GCA carries a very high risk of rupture and death, with an average survival of 1 year in GCA patients with thoracic aortic dissection . This considerable increase in mortality due to aortic involvement mandates a low threshold for aortic imaging in this disease [19, 20]. Subclavian artery and axillary artery involvement are not uncommon in GCA, and MR performs well in delineating such . GCA affected lower extremities alone in 17% of patients in a recent series . Recognition of long stenotic segments and vessel wall thickening with MR can prompt specific treatment (e.g., prednisone) in such GCA patients who may present solely with claudication. Follow-up MR may identify reduced vessel wall thickening indicating a favorable response to therapy .
The sensitivity and specificity of Doppler ultrasonography (US) compared to the clinical diagnosis of temporal arteritis in a meta-analysis of 23 studies was 69 and 82% respectively . Additionally, since US assessment was confined to detection of the “halo” sign in the temporal artery, it cannot reliably assess the thoracic aorta, whose involvement can lead to the serious and fatal complications as discussed above. Nonetheless, European League Against Rheumatism (EULAR) guidelines assign US a class Ia recommendation for the diagnosis of GCA vs. IIa for MRA . Alternatively, 3T MRI of the cranial arteries has a high sensitivity and specificity in detecting vessel wall inflammation when compared with temporal artery biopsy (89-94%, and 92-100% respectively), albeit in small studies [25, 26]. Positron emission tomography (PET) may have a higher sensitivity than MRI in detecting GCA according to some retrospective studies [27, 28]. However, PET is limited in its ability to demonstrate temporal artery inflammation because of inadequate spatial resolution and inability to distinguish luminal changes in close proximity to glucose-avid brain tissue. In addition, it involves considerable exposure to ionizing radiation. Recently, high resolution dynamic contrast-enhanced (DCE) MRI performed well in detecting vessel inflammation in patients with suspected arteritis . The abnormal extraction fraction computed from first-pass MR imaging, implying increased endothelial leakiness, correlated well with FDG-uptake in arterial walls by PET-CT.
Current data suggest no clear role for either CMR or PET in GCA patient follow up. PET does detect decline in activity with treatment, but in most cases the uptake does not disappear. This is thought to arise from chronic changes associated with vessel wall remodeling. In one GCA study including patients with a complicated course, PET findings correlated poorly with clinical and laboratory criteria of disease activity and MRI findings. In the same study, PET could not predict disease relapse . Of note, MRI with dark blood imaging may demonstrate wall thickening and edema that persists despite clinical and laboratory improvements .
Takayasu arteritis (TA)
TA shares many of the vascular findings of GCA but occurs in considerably younger patients, classically women more often than men under the age of 50 years. Diagnosis requires angiographic abnormalities  plus one of the following four findings: i) decreased peripheral artery pulse(s) and/or claudication of extremities; ii) blood pressure difference >10 mm Hg between extremities; iii) bruits over aorta and/or its major branches; or iv) hypertension. The mandate for angiographic evidence of disease makes MR an important component of the TA evaluation, especially in children where invasive angiography and CT hold considerably less appeal.
Medium vessel vasculitis
Kawasaki disease (KD)
This leading cause of acquired heart disease in children begins with fever persisting for at least four days. Additionally, diagnosis requires 4 of the following 5 features: i) desquamative rash of the extremities or perineal area; ii) polymorphous exanthema; iii) bilateral conjunctival injection; iv) injection of oral and pharyngeal mucosa; and v) cervical lymphadenopathy [32, 49]. Involvement of the coronary arteries produces much of KD’s mortality and morbidity via myocardial infarction and heart failure. Coronary artery aneurysms develop in up to 25% of untreated children ; intravenous immunoglobulin therapy reduces this incidence to 3 or 4% .
Arnold et al. compared conventional angiography, multi-detector CT (MDCT) and MRI in 16 patients and showed 100% concordance between conventional angiography and MDCT, and 93% concordance between MRI and coronary angiography for aneurysm detection . MRI missed one stenotic lesion, while providing additional information regarding myocardial inflammation and injury. Kan et al. recently summarized the safety and accuracy of contemporary CT with ultra-low radiation exposure for pediatric patients , including 5 with suspected coronary involvement in KD with nondiagnostic CMR examination. More recently, using free-breathing, T2-prepared, 3D-SSFP, whole heart approach with navigator gating and tracking, Greil et al. demonstrated complete and excellent agreement between MRA and coronary angiography .
Mavrogeni et al. reported comprehensive CMR findings using both coronary and myocardial evaluation in 13 KD patients thought to be in convalescence (stage II and III, 20–25 days after disease onset) . Of the six patients with demonstrable myocardial inflammation by T2W STIR (which had resolved in all 6 by repeat CMR 3 months later), only three had evident abnormality by LGE yet all had lower LV ejection fraction by cine imaging. Additional 3D ECG-gated steady state free precession navigator-gated non-contrast coronary MRA identified coronary aneurysms and intracoronary thrombus, some of which were missed by echocardiography. In joint guidelines issued by the American Academy of Pediatrics and the American Heart Association in 2004, echocardiography, MRI, and conventional coronary angiography were all accorded level of evidence C for detection of coronary abnormalities due to lack of prospective data .
Polyarteritis nodosa (PAN)
Whereas KD is considered an acute medium vessel vasculitis, PAN is typically a subacute disorder affecting adults more than children. While all the vasculitides are relatively rare, higher incidences of PAN have been reported in Alaskan and Kuwaiti natives . PAN classically affects visceral arteries such as renal, hepatic and mesenteric arteries. Presenting findings often include hypertension, fever, musculoskeletal symptoms, abdominal angina and neuropathy, occasionally with hepatitis B antigen or DNA in the serum .
Behçet disease (BD)
Pulmonary artery aneurysms contribute to excess mortality via rupture; aggressive treatment with steroids, immunosuppression and occasionally surgery has reduced mortality . Recognizing such, vascular imaging of the patient with BD should at some point include the pulmonary arteries. A recent study identified cardiac complications in 6% of patients with this disease including pericarditis, right ventricular thrombus, myocardial infarction and endomyocardial fibrosis  – all of which can be readily demonstrated with a suitably-prescribed CMR examination.
Small vessel vasculitis: Churg-Strauss syndrome (CSS)
Review and Conclusions
Su and colleagues, in one of the few studies of molecular imaging specifically targeting non-atherosclerotic vascular inflammation, showed feasibility of targeting the enzyme myeloperoxidase that is a marker of certain vasculitides . Ongoing advances in understanding the molecular bases for these varied conditions may translate into novel diagnostic imaging approaches. Remarkably, diagnosis still heavily relies on direct tissue examination; development of MR agents that target IgG4 or ANCA could hopefully improve the diagnostic specificity of noninvasive imaging and reduce the need for histopathology.
In conclusion, diagnosis and serial assessment of patients with inflammatory vasculitis require clinical, laboratory and imaging assessments. The CMR laboratory in particular offers a spectrum of techniques for noninvasive angiography and vessel wall imaging, both with and without need for exogenous contrast administration. The utility of these techniques in patients with inflammatory vasculitis is realized only through 1) their timely use at initial presentation for accurate delineation of both presence and extent of disease and 2) an ongoing dialog among CMR specialists and the clinicians charged with initial diagnosis and long-term management. Such efforts coupled with continued advances in molecular understanding and treatment warrant further investigation given the considerable morbidity and mortality for patients with primary vasculitis.
The authors thank Tam Tran for his assistance in literature compilation.
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