|
 
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| PICTORIAL REVIEW |
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| Year : 2022 | Volume
: 6
| Issue : 2 | Page : 116-128 |
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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
| Date of Submission | 09-Jun-2022 |
| Date of Decision | 17-Jul-2022 |
| Date of Acceptance | 21-Jul-2022 |
| Date of Web Publication | 23-Aug-2022 |
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
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/jiae.jiae_33_22
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. Keywords: Cardiac magnetic resonance imaging, cardiac masses, thrombus
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;6:116-28 |
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 Jun 10];6:116-28. Available from: https://jiaecho.org/text.asp?2022/6/2/116/354319 |
| 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: VT consists of three factors that contribute to thrombus formation, namely stasis, endothelial injury, and hypercoagulability. VT: Virchow's triad
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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: Recommended protocol for the detection and characterization of thrombus. After localizer, sequences of precontrast cine images are acquired in routine 2C, 3C, 4C, and SAX planes. Additional cine stacks may be obtained in planes perpendicular to the mass. Precontrast T1W DIR, T2W TIR, and T1 and T2 mapping sequences should be obtained in planes that best document the mass. Dynamic injection of Gd contrast is followed by the acquisition of perfusion images, EGE images, and LGE images in the optimal imaging plane. Optional 3D heart sequences may be performed. 2C: Two-chamber, 3C: Three-chamber, 3D: Three-dimensional, 4C: Four-chamber, EGE: Early gadolinium enhancement, Gd: Gadolinium, LGE: Late gadolinium enhancement, SAX: Short axis, SSFP: Steady-state free precession, T1W DIR: T1-weighted double inversion recovery, T2W TIR: T2-weighted triple inversion recovery, TI: Time to invert
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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 formation
- Contrast 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 images
- The 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: Chamber-wise list of factors predisposing to thrombus formation. ARVC: Arrhythmogenic right ventricular cardiomyopathy, DVT: Deep vein thrombosis, EMF: Endomyocardial fibrosis, LA: Left atrium, LAA: Left atrial appendage, LV: Left ventricle, RA: Right atrium, RV: Right ventricle
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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: A 55-year-old male known diabetic had dyspnea on exertion class III. ECG was suggestive of anterior wall MI. Cardiac MRI was performed for the assessment of myocardial viability. (a) Precontrast 2C cine diastolic image showing dilated LV with globular morphology (dashed yellow line). Apparent thickening along the anterior wall (black arrow) was also noted. (b) 2C LGE demonstrating nonenhancing layered thrombus along the anterior wall (black arrow). Note the transmural LGE along the anterior and inferior walls and LV apex. (c) Short-axis cine images acquired after administration of Gd contrast showed nonenhancing thrombus (asterisk) along the anterior wall as compared with the enhancing myocardium. Excellent contrast between the thrombus and myocardium is achieved following contrast administration. Compare this with precontrast cine in a. (d) Short-axis LGE image shows near-circumferential ischemic scar and nonenhancing thrombus along the anterior wall (asterisk). Final diagnosis: Multivessel ischemic heart disease with a layered mural clot. 2C: Two-chamber, ECG: Electrocardiogram, Gd: Gadolinium, LGE: Late gadolinium enhancement, LV: Left ventricle, MI: Myocardial infarction, MRI: Magnetic resonance imaging
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 | Figure 5: A 16-year-old male presented with dyspnea for 1 week. He had a history of COVID-19 infection 3 months back. Echocardiography was suggestive of dilated cardiomyopathy with severe LV systolic dysfunction. The cardiac MRI was suggested to ascertain the etiology. (a) 2C LGE MAG and (b) 2C LGE PSIR reconstruction images show a thrombus along the mid-anterior segment (yellow arrow). Interestingly, the MAG and PSIR are discordant with opposite LGE patterns of the thrombus. The PSIR shows dark thrombus (b), while the MAG (a) shows the typical “etched out” black rim at the boundary between tissues with opposite magnetizations. Magnitude images are sensitive to the selected TI, whereas PSIR images better depict the thrombus as well as mid-myocardial LGE (red arrow). (c) Precontrast T1 mapping shows lower T1 values of the thrombus compared to the myocardium due to heme products, suggestive of recent thrombus. (d) Postcontrast T1 mapping shows an approximate 10% drop in the T1 values possibly due to the partial volume effect. Other CMR findings (not shown in the images) include four-chamber dilatations with severe LV dysfunction and global hypokinesia. Final diagnosis: Dilated cardiomyopathy (?postmyocarditis sequelae) with LV clot. 2C: Two-chamber, CMR: Cardiac magnetic resonance imaging, LGE: Late gadolinium enhancement, LV: Left ventricle, MAG: Magnitude reconstruction, MRI: Magnetic resonance imaging, PSIR: Phase-sensitive inversion recovery, TI: Time to inversion
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 | Figure 6: A 60-year-old male presented with severe acute chest pain and elevated troponins. 2D echocardiography revealed regional wall motion abnormality in the inferolateral wall and a thin rim of pericardial effusion. There was a suspicious free wall rupture on echocardiography, and hence, CMR was performed, after the patient was stabilized. Catheter angiography revealed 100% occlusion of the left circumflex artery and significant triple vessel disease. (a) Short-axis cine images at midcavity show thinning of the inferolateral segment with subtle signal abnormality (dashed red ellipse). Cine images revealed subtle tear with adjoining pericardial collection. (b) Routine short-axis LGE images (TI ~225 ms) show nonenhancing areas (MVO) within the myocardium with surrounding LGE. Pericardial effusion with a dark signal is also noted. (c) Long TI (~562 ms) LGE images show near-transmural LGE with low-signal intensity within it. Note increased contrast with the nonenhancing area (clot and MVO) and enhancing myocardium. (d) Precontrast T1 mapping shows near-isointense signal with increased signal intensity in adjoining pericardial sac (clot). (e) Postcontrast T1 mapping values show no significant drop in low-signal intensity area (MVO) along with the pericardial sac (clot). However, adjoining myocardium shows a reduced signal. (f) T2 mapping shows increased T2 values in the area of infarction. Final diagnosis: Acute inferolateral MI with free wall rupture and pericardial effusion with clot. These patients should not be given anticoagulants as this will aggravate rupture. Follow-up echocardiography in this patient showed the formation of pseudoaneurysm. 2D: Two-dimensional, CMR: Cardiac magnetic resonance imaging, LGE: Late gadolinium enhancement, MI: Myocardial infarction, ms: Milliseconds, MVO: Microvascular obstruction TI: Time to inversion
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 | Figure 7: A 36-year-old female is a case of chronic ITP on treatment. She has been experiencing dyspnea on exertion for 1 month. Echocardiography revealed a large mass lesion in the LV cavity, causing obliteration of the LV with moderate tricuspid regurgitation, mild mitral regurgitation, and severe pulmonary arterial hypertension. CMR was performed for the evaluation of cardiac mass (asterisk). (a) T1W double inversion recovery shows that the mass (asterisk) is isointense to the myocardium. (b) 2C cine shows near-complete obliteration of LV cavity by the mass. (c) 4C cine shows near-complete obliteration of the LV cavity by the mass. (d) T2W triple inversion recovery shows that the mass appears isointense to the myocardium. (e) 2C LGE images with routine TI ~230 ms show no appreciable enhancement. Note the nulled myocardium appearing dark. (f) 4C LGE image with TI of 600 ms shows no appreciable enhancement. The thrombus persists to appear dark, whereas the myocardium appears brighter. Compare this with the nulled myocardium in e. The patient underwent an emergency mass excision. Histopathological examination was suggestive of an organized thrombus. Revisiting the CMR images, the mass shows typical features of a thrombus. Final diagnosis: LV thrombus in chronic ITP on treatment.[17] 2C: Two-chamber, 4C: Four-chamber, CMR: Cardiac magnetic resonance imaging, ITP: Idiopathic thrombocytopenic purpura, LGE: Late gadolinium enhancement, LV: Left ventricle, MI: Myocardial infarction, TI: Time to inversion, W: Weighted
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[Additional file 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.
[Additional file 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
[Additional file 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: A 26-year-old female is a known case of systemic lupus erythematosus and autoimmune hemolytic anemia on immunosuppressants. She has a history of central line insertion 1 month back. (a) Axial cine image and (b) LGE image show hypointense thrombus within RA (yellow arrow) with no appreciable enhancement. Final diagnosis: Catheter-associated RA thrombus. LGE: Late gadolinium enhancement, RA: Right atrium
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 | Figure 9: A 25-year-old male from Ethiopia was apparently well 5 months back when he developed a cough with mild-grade fever, treated on the lines of typhoid. He developed progressive exertional dyspnea functional class III within a month. No history of chest pain, syncope, or swelling over the limbs or face was noted. Echocardiography was suggestive of an RV tumor. CMR was performed for cardiac mass evaluation. (a) 4C cine images show RV cavity obliteration (green arrow) with dilated RA. (b) 4C LGE images show a typical “double V” sign. It consists of normal outer myocardium, marked subendocardial thickening and enhancement of RV apex (yellow arrow), and overlying nonenhanced thrombus (asterisk). (c and d) Reconstructed 3D SSFP images show nonenhancing thrombus (asterisk) occupying most of the RV cavity extending into the RV outflow tract (blue arrow). Final diagnosis: Right ventricular endomyocardial fibrosis. 3D: Three-dimensional, 4C: Four-chamber, CMR: Cardiac magnetic resonance imaging, LGE: Late gadolinium enhancement, RA: Right atrium, RV: Right ventricle, SSFP: Steady-state free precession
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| 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: A 57-year-old female is a known case of systemic hypertension, type II diabetes mellitus, and dyslipidemia. She suffered acute posterior wall and RV myocardial infarction and underwent primary percutaneous transluminal coronary angioplasty to the right coronary artery. Echocardiography showed ostium secundum atrial septal defect with left-to-right shunt and RA free wall mass. (a) 4C cine systolic image showing thickening (blue arrow) along the lateral wall of the RA. (b) Corresponding 4C LGE shows no appreciable enhancement (blue arrow). Final diagnosis: The typical location and absent enhancement are consistent with crista terminalis. 4C: Four-chamber, LGE: Late gadolinium enhancement, RA: Right atrium, RV: Right ventricle
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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: A 26-year-old male is a known case of acute myeloid leukemia, postallogeneic stem cell transplantation on immunosuppressants. Echocardiography was suggestive of an LA mass. (a) 4C steady-state free precession diastolic image shows thickening along the lateral wall of the left atrium (red arrow). (b) Corresponding T1W transaxial image shows extension of mediastinal fat between the LA appendage and the left upper pulmonary vein (red arrow). Final diagnosis: The typical location is consistent with coumadin ridge. 4C: Four-chamber, LA: Left atrium, W: Weighted
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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: A 78-year-old male went for a routine health checkup. Echocardiography showed a calcified mitral valve lesion. (a) 2C T1W double inversion recovery, (b) 2C T2W triple inversion recovery, (c) 2C cine, and (d) 2C LGE images show a well-defined lesion at the posterior mitral annulus (asterisk). It appears dark on all the MRI sequences with no enhancement. Final diagnosis: Caseous degeneration of the mitral valve. 2C: Two-chamber, LGE: Late gadolinium enhancement, MRI: Magnetic resonance imaging, W: Weighted
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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: A 25-year-old female with no previous comorbidities presented with fever and weight loss of 2-month duration, and dyspnea with palpitations of 1-month duration. Routine investigations revealed elevated ESR with a right atrial mass of size 2 cm × 3 cm on echocardiography. (a) Axial SSFP and (b) sagittal SSFP images show a large sessile mass lesion (blue arrow) involving the right atrial appendage and extending along the lateral wall inferiorly up to inferior vena cava (I) opening. The mass effect over the distal superior vena cava (S) is present. (c) Sagittal LGE images where the center of the mass shows multiple nonenhancing lesions with peripheral intense enhancement. GeneXpert for TB was positive. Final diagnosis: Tuberculous granulomas. ESR: Erythrocyte sedimentation rate, LGE: Late gadolinium enhancement, SSFP: Steady-state free precession, TB: Tuberculosis
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 | Figure 14: A 23-year-old lady presented with first-ever ischemic stroke. The antiphospholipid antibody was elevated. Echocardiography showed a 10 mm mass lesion attached to the mitral valve. Blood cultures were negative. (a) 4C cine image shows low-intensity mobile lesion on the atrial aspect of the mitral valve. The lesion does not involve free margin or annulus. (b) 4C LGE image shows mild contrast enhancement. Final diagnosis: Primary antiphospholipid antibody syndrome with sterile vegetation (Libman-Sacks endocarditis). 4C: Four-chamber, LGE: Late gadolinium enhancement
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[Additional file 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: A 15-year-old boy was an operated case of tetralogy of Fallot on follow-up. Recent echocardiography was suggestive of RA mass. (a) 4C cine, (b) 4C LGE, and (c) 4C T2W triple inversion recovery images show a mobile lobulated RA mass (orange arrow) attached to the interatrial septum. It shows mild central heterogeneous enhancement and appears hyperintense on T2W triple inversion recovery. He underwent surgical excision of the mass with histopathology suggestive of myxoma. Final diagnosis: RA myxoma. 4C: Four-chamber, LGE: Late gadolinium enhancement, RA: Right atrium, W: Weighted
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 | Figure 16: An 84-year-old nondiabetic, nonhypertensive female with known chronic obstructive pulmonary disease complained of worsening dyspnea, intermittent chest pain, cough, and pedal edema. ECG was suggestive of atrial fibrillation with a fast ventricular rate of about 140/min and T inversion in right precordial leads. Echocardiography showed biatrial dilatation and mass lesions. (a) 4C cine images show dilated right and left atria. A broad-based sessile mass was attached to the right anterolateral wall of the right atrium (red arrow) close to its appendage just below the superior vena cava opening. Another well-defined larger hyperintense lesion with a hypointense rim (blue asterisk) was noted within the left atrium attached to the posterior wall. (b) 4C LGE image shows no enhancement of the right atrial mass (red arrow). Left atrial mass (blue asterisk) shows mild central and intense peripheral enhancement. (c) 4C T2W triple inversion recovery image shows that the right atrial mass is iso to slightly hyperintense (red arrow), whereas the left atrial mass is markedly hyperintense (blue asterisk). Final diagnosis: Right atrial thrombus, left atrial myxoma. 4C: Four-chamber, ECG: Electrocardiogram, LGE: Late gadolinium enhancement, W: Weighted
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 | Table 1: Differentiating features of left atrial thrombus versus myxoma[2],[12],[24],[25]
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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: A 56-year-old male presented with occasional palpitations and chest discomfort. Echocardiography was suggestive of a 9 mm-sized mass over the mitral valve. (a) 4C cine and (c) 2C cine image show mobile mass lesion attached to the inferior part of anterior mitral leaflet extending up to the free margin of the valve (yellow arrow). (b) 4C LGE and (d) 2C LGE show intense enhancement of the lesion (yellow arrow). Final diagnosis: Papillary fibroelastoma. 2C: Two-chamber, 4C: Four-chamber, LGE: Late gadolinium enhancement
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[Additional file 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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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16], [Figure 17]
[Table 1]
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