PICTORIAL REVIEW
Year : 2022 | Volume
: 6 | Issue : 2 | Page : 116--128
Diverse Radiologic Presentations of Common Pathology: Role of Cardiac Magnetic Resonance in the Workup of Intracardiac Thrombi and Mimics- A Pictorial Review
Amol Anil Kulkarni1, Rajeshkannan Ramiah1, Priya Darshan Chudgar2, Nitin J Burkule3,
1 Department of Radiology, Amrita Institute of Medical Sciences and Research Centre, Kochi, Kerala, India
2 Department of Radiology, Jupiter Hospital, Thane, Maharashtra, India
3 Department of Cardiology, Jupiter Hospital, Thane, Maharashtra, India
Correspondence Address:
Dr. Amol Anil Kulkarni
Department of Radiology, Amrita Institute of Medical Sciences and Research Centre, Ponekkara, P. O. Kochi - 682 041, Kerala
India
Abstract
Thrombus represents the most common cardiac mass compared to primary or secondary cardiac tumors. It has variable size, shape, location, and imaging features. Differentiating the cardiac mass as a tumor, thrombus, or vegetation is clinically important due to their different therapeutic implications and prognostic outcomes. Thrombi carry an inherent risk of systemic and pulmonary embolism and warrant appropriate anticoagulation. For over two decades, echocardiography (transthoracic as well as transesophageal) has been the gold standard investigation to detect intracardiac thrombi. However, recent advances in cardiac magnetic resonance imaging allow higher sensitivity and specificity in the detection of thrombi and the assessment of the age of the thrombi by characterization of their contents. The objective of this review is to demonstrate different imaging presentations of cardiac thrombi and how imaging can help differentiate it from other mimics.
How to cite this article:
Kulkarni AA, Ramiah R, Chudgar PD, Burkule NJ. Diverse Radiologic Presentations of Common Pathology: Role of Cardiac Magnetic Resonance in the Workup of Intracardiac Thrombi and Mimics- A Pictorial Review.J Indian Acad Echocardiogr Cardiovasc Imaging 2022;6:116-128
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How to cite this URL:
Kulkarni AA, Ramiah R, Chudgar PD, Burkule NJ. Diverse Radiologic Presentations of Common Pathology: Role of Cardiac Magnetic Resonance in the Workup of Intracardiac Thrombi and Mimics- A Pictorial Review. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2022 [cited 2023 Mar 20 ];6:116-128
Available from: https://jiaecho.org/text.asp?2022/6/2/116/354319 |
Full Text
Introduction
The classical Virchow's triad describes factors predisposing to thrombus formation. These are hypercoagulability, blood stasis, and endothelial injury. Although initially described for venous thrombosis, these can very well be applied to the formation of arterial as well as cardiac thrombi[1] [Figure 1].{Figure 1}
Thrombus is the most common intracardiac mass. The prevalence of intracardiac thrombus is approximately 30% in acute or healed myocardial infarction (MI). Left heart thrombus is often a source of stroke and peripheral arterial embolism, while right heart thrombi lead to pulmonary thromboembolism. An accurate diagnosis of thrombus has prognostic implications due to the risk of thromboembolic complications and is a clinical indication for anticoagulation therapy.[2]
Due to its larger field of view, greater spatial resolution, multiplanar ability to assess all chambers, and the unique capability of tissue characterization, cardiac magnetic resonance (CMR) imaging has enhanced the ability to identify thrombi and differentiate them from other cardiac masses.[3],[4]
Imaging Options
Transthoracic echocardiography is the first line of investigation to detect cardiac thrombi due to its easy availability, portability, reasonable accuracy, and low cost. Limitations include technical challenges such as left ventricle (LV) apical cluttering, inadequate assessment of left and right atrial appendages (LAA and RAA, respectively), inadequate spatial resolution and image noise in obese patients, those with lung emphysema, and the patients with poor echo window. The use of ultrasound-enhancing agents can improve the detection of protruding LV apical thrombi.[5],[6],[7]
Transesophageal echocardiography (TEE) is more sensitive to detect thrombi due to its ability to provide high-resolution images of left atrium (LA), right atrium (RA), LAA, RAA, and systemic and pulmonary venous openings. However, it is semi-invasive, associated with patient discomfort and carries the small risk of complications related to esophageal intubation. TEE also has difficulty in visualizing the LV apex and distal ascending aorta where the left bronchus crosses in front of the esophagus. Furthermore, differentiating myocardium from subactute or organized layered clots may be difficult on echocardiography. Finally, echogenicity of the thrombi does not distinguish a subacute from organized thrombus, which is important to predict the risk of embolic complications.[5],[6]
CMR has emerged as a noninvasive technique that can provide additional information complementary to echocardiography. It allows thrombus detection and characterization following its relative avascular composition. It provides a reproducible assessment of cardiac morphology, function, viability, and certain structural risk factors predisposing to thrombus formation.[8]
Cardiac Magnetic Resonance Protocol and Principles
We recommend a tailored protocol for the detection of cardiac thrombus as outlined in [Figure 2].{Figure 2}
Precontrast T1, T2 fast/turbo spin echo with and without inversion recovery pulses
The signal characteristics of the thrombus depend on its age and composition. Fresh thrombi are usually homogeneous and isointense or slightly hyperintense on T1-weighted magnetic resonance imaging (MRI) and isointense or hyperintense on T2-weighted imaging. In the subacute stage, after 1–2 weeks, clots appear hyperintense on T1 and hypointense on T2 due to T1 and T2 shortening by paramagnetic compounds in the organizing thrombus, such as deoxyhemoglobin and methemoglobin. Chronic thrombi appear hypointense on both T1 and T2 because of low water content, fibrosis, and occasional calcifications. Using an inversion recovery pulse highlights the bright thrombus signal by nulling the signals from fat (using a water-selective excitation) and blood (from its long T1). These techniques are however limited by artifacts from slow-flowing blood. This problem is overcome by using gradient-echo sequences.[2],[9]
Cine steady-state free precession imaging
Cine images are used to confirm the location and morphology of the thrombus. Thrombus always appears isointense or hypointense compared to the myocardium with a background of high signal of the blood pool. Cine MRI allows an assessment of the size, shape, and mobility of the thrombus and its relationship with the adjacent structures, akinetic wall segment, and any functional consequences. The thrombus size, mobility, and morphological characteristics such as protruding or convex toward the cavity help in identifying the risk of embolization. However, similar to echocardiography, cine MRI can miss the layered subacute or old clots.[10],[11]
Parametric mapping
Conventional spin-echo sequences show gray scale signal intensities depending on the “weighting” of T1 and T2 parameters without measurement of absolute values. Parametric images measure pixel-wise T1 and T2 values before and/or after contrast injection and are displayed by various vivid color coding. Acute thrombi show shorter T1 values, whereas older thrombi show longer T1 values. T2 values are longer than myocardial T2, regardless of their age. Postcontrast T1 values of thrombi decrease by about 30% compared to precontrast T1. This could be explained either by some degree of gadolinium soaking inside the thrombus and/or by a partial volume effect in small thrombi (owing to the inclusion of some blood in the image slice).[12]
T2* imaging is helpful in cases of intramyocardial hemorrhage which occurs in areas of microvascular obstruction. Occasionally, dissecting intramyocardial hematoma may be present in acutely infarcted segments. Hence, adding this extra multi-echo sequence may be beneficial.[13]
Perfusion imaging
This should be performed in an imaging plane that best demonstrates the thrombus. Intraluminal filling defects suggest an intracavitary mass. Vascular tumors show prompt contrast hyperenhancement, as opposed to the avascular thrombus. In addition, perfusion defects in the myocardium can be detected due to coronary occlusive disease.[10]
Early enhancement
Early gadolinium enhancement imaging is performed within the first 2–3 min of contrast administration, using an inversion recovery segmented fast (or turbo) gradient-echo (IR-FGE) sequence with a long inversion time of 450–600 ms. It is particularly useful to identify thrombus on the scarred myocardial segment or surface thrombus over an irregular tumor. The thrombus appears dark due to lack of contrast uptake, whereas the blood pool or tumor appears bright, and the myocardium has intermediate-signal intensity.[14]
Delayed enhancement
Late gadolinium enhancement (LGE) imaging is used for assessing myocardial scar burden and the extent of mural involvement. It is acquired 7–10 min after contrast administration using an IR-FGE sequence. Infarcted tissue appears bright, and the myocardium is black or has the lowest shades of gray (nulled). Avascular thrombi are nonenhancing, appearing black surrounded by a brighter blood pool or gray myocardium. Conventional LGE uses an inversion time of about 200–300 ms for myocardial nulling. Both thrombus and myocardium may appear relatively hypointense, limiting thrombus identification. To overcome this challenge, a “long inversion time” (i.e., 450–600 ms) is used to selectively null the thrombi against the backdrop of gray myocardium.[8],[14]
Contrast-enhanced magnetic resonance angiography
Acquiring a high-resolution isotropic three-dimensional (3D) dataset and/or using time-resolved imaging are the two common contrast-enhanced MR angiography techniques. These are especially useful for detecting thrombi in central large arteries and veins.[10]
Contrast-enhanced three-dimensional inversion recovery spoiled gradient-echo sequence with a blood-pool contrast agent
This is an electrocardiogram-gated technique with diaphragmatic tracking compensating for both cardiac and respiratory motions. Thrombi of all ages will appear dark in 3D inversion recovery spoiled gradient-echo (3D IR-SGE) sequence. Due to excellent spatial resolution and respiratory and cardiac motion compensation, 3D IR-SGE is a sequence of choice for the detection of thrombi in cardiac chambers, large vessels, Fontan conduits, as well as the epicardial coronary arteries.[10]
Phase-contrast flow velocity mapping
It adds value by identifying hemodynamic effects caused by the thrombus.[15]
Cardiac Magnetic Resonance Findings in Cardiac Thrombi
Based on the above discussion of CMR protocols and principles, we summarize the CMR findings in intracardiac thrombi as follows:[2],[8],[9],[10],[11],[12],[13],[14],[15]
Cine imaging depicts thrombi as dark-signal intensity on a background of a bright blood pool. In addition, it can show morphofunctional abnormalities predisposing to thrombus formationContrast administration improves the detection of thrombus. The avascular thrombus will appear dark on all postcontrast sequences (perfusion, early or delayed enhancement, and angiography). Out of these, LGE (delayed enhancement) is the most useful sequence to identify intracardiac clots. Thrombus shows low-signal intensity on both conventional and long time to inversion imagesThe age of the clot can be determined by its T1 and T2 characteristics depending on its composition. Newer sequences such as parametric mapping also suggest the age of the thrombus depending upon the composition-related changes in T1 and T2 values. Recent thrombi show intermediate to high signal on T1-weighted image (intermediate-to-short T1 mapping values) and high signal on T2/short tau inversion recovery (STIR) (intermediate T2 values). Older thrombi appear dark on T1-weighted image (intermediate-to-long T1 mapping values) and dark on T2/STIR (intermediate T2 values).
Relevant findings regarding thrombi in different cardiac chambers are discussed below.
Left atrium
Thrombi in the LA and LAA are the main sources of cardioembolic stroke. The appendage is a blind-ended pouch with trabeculations. This morphology promotes stasis and thrombus formation. Other predisposing factors [Figure 3] include mitral valve stenosis, prosthetic mitral valve, poor LV function, abnormal LA contractile function, atrial fibrillation (AF), and cactus, or cauliflower shaped LAA. Thrombi are often multiple and of varying sizes. In the presence of stasis, they may be present even along the LA wall or the interatrial septum and may show mobility.[2],[3],[6] The patients with cardiac amyloidosis have a higher incidence of LA thrombi even with normal sinus rhythm.[16]{Figure 3}
Left ventricle
LV thrombi are commonly found in the presence of LV dysfunction after MI or in patients with dilated cardiomyopathy. These usually form within the first 24 h to 2 weeks after MI. The most common location is the LV apex in cases of anterior wall MI with large regional wall motion abnormalities (RWMAs). Risk factors for LV thrombus formation include anterior wall MI, LGE size and extent, and global wall motion abnormality or RWMA. LV thrombi are clinically important because of their ability to embolize. Patients with subacute, protruding, and mobile thrombi are at higher risk of embolic events, compared with those presenting with sessile, laminated, and organized thrombi[2],[3],[6] [[Figure 4], [Figure 5], [Figure 6], [Figure 7][17] and [Video 1] and [Video 2]a, [Video 1]b.{Figure 4}{Figure 5}{Figure 6}{Figure 7}
[SUPPORTING:1]
Video 1: 2C SSFP cine images show dilated LV with globular morphology and apparent thickening of the anterior wall [later confirmed as a layered clot in [Figure 6]]. Severe LV dysfunction was noted with dephasing artifacts, suggestive of slow flow stasis. The anterior wall and LV apex are dyskinetic with severe hypokinesia of the inferior wall. Mitral regurgitation is also seen. Note that the hypointensity within the LA is consistent with the coumadin ridge. 2C: Two-chamber, LA: Left atrium, LV: Left ventricle, SSFP: Steady-state free precession.
[SUPPORTING:2]
Video 2: (a) Precontrast 4C cine SSFP and (b) postcontrast 4C cine SSFP images show a large clot almost obliterating the LV cavity. It is better appreciated in postcontrast cine
[SUPPORTING:3]
(b). LV wall thickness is preserved with severely impaired contractility. Mitral and tricuspid regurgitant jets and pericardial and pleural effusions are also noted. 4C: Four-chamber, LV: Left ventricle, SSFP: Steady-state free precession.
Right heart
Right heart thrombi often originate from embolization from the peripheral venous system. In situ right thrombi are usually associated with structural heart disease, AF, indwelling vascular catheters [Figure 8], pacemaker leads, or a prosthetic tricuspid valve. Other rare causes include conditions such as right ventricular (RV) infarction, endomyocardial fibrosis [Figure 9], arrhythmogenic RV cardiomyopathy, or antiphospholipid antibody syndrome. Compared to LAA, the RAA has wider and shallow anatomy, making it less likely to be a site for thrombus formation; it can however occur in AF or hypercoagulable states. It is important to diagnose a right heart thrombus because it can cause pulmonary embolism or paradoxical embolization across the patent foramen ovale, which would then require emergency hospitalization. The overall mortality rate in patients with right heart thrombi has been reported as 28% and as high as 100% in untreated patients.[2],[3],[6]{Figure 8}{Figure 9}
Cardiac Magnetic Resonance Findings in Thrombus Mimics
Anatomic variants
Eustachian valve
It is a thin flap-like structure at the inferior cavo–atrial junction at the orifice of inferior vena cava (IVC) into RA. Embryologically, it helps direct blood to the foramen ovale. It has a typical location, linear shape, and lacks contrast enhancement.[18]
Crista terminalis
It is a C-shaped fibromuscular projection into RA extending along its posterolateral wall between the orifices of the superior vena cava and IVC. Embryologically, it is the remnant of septum spurium, and anatomically, it is closely associated with the sinoatrial node and artery. It has a typical location and lacks contrast enhancement[2],[19] [Figure 10].{Figure 10}
Warfarin/coumadin ridge
It is the ridge separating the LAA and left upper pulmonary vein. Historically, it was confused with thrombus, and the patients were often prescribed heparin for anticoagulation and hence named warfarin (coumadin) ridge. It has a typical location and matches signal characteristics of myocardial tissue without significant enhancement[20] [Figure 11].{Figure 11}
Non-neoplatic
Caseous degeneration of mitral annulus
It is a chronic degenerative process of the fibrous skeleton of the mitral annulus commonly seen in elderly hypertensive patients or patients with renal failure. It is characterized by the development of mitral annular calcification typically at the posterior annular ring, which can seldom show circumferential involvement. Owing to its calcific nature, it appears hypointense on both T1 and T2 without contrast enhancement [Figure 12]. The peripheral fibrous ring may occasionally show rim enhancement. Rarely, the center may show liquefactive necrosis showing T1 and T2 hyperintense signals with postcontrast enhancement.[21]{Figure 12}
Endocarditis and vegetations
Cardiac valvular vegetation can be infective [Figure 13] as well as nonbacterial thrombotic (Libman-Sacks endocarditis) [Figure 14] and [Video 3]. Vegetations are commonly attached to the valvular apparatus and their supporting structures at the site of jet injury. However, they can arise in any cardiac chamber or even in the aortopulmonary trunk. Vegetations can be easily missed on cardiac MRI due to their small size and chaotic motion. If large, the vegetations appear isointense to hypointense on cine sequences. They move chaotically and are independent of the motion of the valve to which they are attached. Postcontrast imaging may show variable contrast enhancement patterns with occasional peripheral rim LGE.[22],[23]{Figure 13}{Figure 14}
[SUPPORTING:4]
Video 3: 2C cine SSFP images show a mobile, pedunculated polypoidal lesion attached to the anterior mitral leaflet. An inferiorly directed mitral regurgitant jet is seen. 2C: Two-chamber, SSFP: Steady-state free precession.
Benign neoplasms
Myxoma
It is the most common primary cardiac tumor in adults. Myxomas appear as well-defined round to oval, spherical, or lobulated mobile, pedunculated, or sessile masses frequently located in the LA with attachment to the fossa ovalis. They appear hyperintense to the myocardium on cine images, isointense on T1, and hyperintense on T2 and STIR images. Hemorrhagic areas may have a high signal on T1; conversely, calcifications appear low on both T1 and T2. They may show some weak heterogeneous enhancement on first-pass perfusion with more heterogeneous LGE.[24],[25] The native T1 values, T2 values, and extracellular volume are also elevated[12] [Figure 15]. It is often a diagnostic dilemma to differentiate atrial myxomas from thrombi. Salient features are shown in [Figure 16] and [Table 1].{Figure 15}{Figure 16}{Table 1}
Papillary fibroelastoma
It is the most common cardiac valvular tumor. The most common locations are the atrial side of the mitral valve and the aortic surface of the aortic valve. They are highly mobile, pedunculated, and have multiple fronds. They appear isointense on T1 and T2 and often show homogeneous LGE. Native T1 and T2 values are also elevated[12],[14],[26] [Figure 17] and [Video 4].{Figure 17}
[SUPPORTING:5]
Video 4: 2C cine SSFP image shows mobile lesion involving the posterior mitral leaflet extending up to the free margin. Mitral regurgitation jet is seen. 2C: Two-chamber, SSFP: Steady-state free precession.
Malignant neoplasms
The incidence of secondary malignant tumors is much higher than the primary malignant tumors of the heart. Common intracardiac primary malignancies include sarcomas and lymphoma, whereas secondary malignancies may arise from lung, breast, liver, kidney, or melanoma. Signal characteristics vary, are usually heterogeneous, and may show necrotic areas. They are usually large, multiple, infiltrating in the myocardium with indistinct borders, involving the right heart more than the left, and often associated with pericardial effusion. They show intense first-pass gadolinium enhancement due to hypervascularity.[14],[27]
Conclusion
Precise identification of intracardiac thrombus over other mimics is vital for appropriate management and prevention of complications. CMR can accurately distinguish between thrombi and other mimics as well as identify the risk factors for thrombus formation.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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