Thrombus

This is by far the commonest cardiac filling defect and both atrial and ventricular thrombi are readily visualized by SE, GE and following gadolinium (Figure 5.1). On T1W SE imaging, thrombus has intermediate signal intensity often slightly higher than myocardium and blood. T2W SE shows surrounding slow-flowing blood as having higher signal intensity than the thrombus itself, thereby enhancing differentiation from myocardium. With SSFP cine GE and velocity mapping techniques thrombus has the lowest signal intensity in distinction to blood flow, even where it is diminished, which has a high signal intensity. Injection of gadolinium contrast agent increases diagnostic accuracy and characteristically demonstrates an avascular filling defect by rest perfusion CMR and EGE. In the case of LV thrombus, subsequent LGE images usually reveal an area of infarction which has acted as the substrate for thrombus formation. For atrial thrombi, a dilated LA and LA appendage can be demonstrated as with transoesophageal echocardiography (TOE).

Figure 5.1 Large inferior LV false aneurysm lined by a thick layer of laminated thrombus (black arrows) in a 70-year-old woman with a history of MI.

(a) Two-chamber and (b) mid-ventricular short-axis SSFP GE cines show the thrombus to have much lower signal intensity than the intracavity blood flow above. Equivalent (c) two-chamber and (d) short-axis views obtained using T2W SE imaging demonstrates non-homogenous signal in the thrombus indicative of the differing stages of haemoglobin breakdown within it. (e) Two-chamber EGE confirms an avascular filling defect surrounded inferiorly by LV transmural LGE on the ventricular short-axis view (f; dashed white arrow).

Tumours

Secondary cardiac deposits are more frequent than primary cardiac tumours, but both are rare with a necropsy incidence of 1% and 0.05% respectively. Secondary involvement is usually clinically silent and limited to the epicardium. Presenting cardiac signs, when they occur, are those of a large pericardial effusion or incipient tamponade, arrhythmias, cardiomegaly or heart failure. Locally infiltrating malignancies include carcinoma of the lung or breast and renal cell carcinoma may embolize to the RA (Figure 5.2). Cardiac metastases are seen with malignant melanomas, leukaemias and lymphomas.

Figure 5.2 CMR study from a 63-year-old man with left renal cell carcinoma.

(a) SSFP GE cine image of the RA shows cardiac tumour invasion (white arrow) via the inferior vena cava (IVC). (b) Transaxial SSFP GE cine confirms tumour within the RA (black arrow). (c) Renal CE-MRA demonstrating a 5.5 ×4.0 ×4.5 cm³ mass in the upper half of the left kidney (white circle).

The majority of primary cardiac tumours are benign with the most frequent being atrial myxomas (45%) and cardiac lipomas (20%) (Figure 5.3). Malignant cardiac tumours make up one quarter of primary tumours and the most common are sarcomas (95%). CMR anatomical evaluation of intra- and extracardiac involvement has implications for staging, surgical treatment and surveillance (Figure 5.4). CMR differentiation between malignant and benign tumours uses a combination of general principles applied by other modalities and some more specific features. In general terms, malignancy is more likely with larger masses having a broad-based attachment, involving more than one cardiac chamber or great vessel, and with associated pericardial or extracardiac extension. More specifically, T1W and T2W images use the biochemical composition of masses to assist with diagnosis. High signal intensity on T1W images can be due to cystic lesions with a high protein content, fatty tumours (lipoma, liposarcoma), recent haemorrhage and melanoma. Low signal intensity on T1W is seen in cysts with low protein content, within vascular malformations, in calcified lesions, or if the mass contains air. Subsequent T2W imaging demonstrates cysts as having high signal intensity, and the addition of a fat saturation prepulse distinguishes lipid content. Rest perfusion first-pass CMR shows contrast uptake into vascular tumours (haemangioma, angiosarcoma) and may also identify small vessels. In malignancy, EGE typically demonstrates dark areas with surrounding enhancement from necrotic tissue, while LGE can show enhancement due to expanded interstitial space such as in fibrosis (Figure 5.5). Such enhancement is absent in cystic lesions and most benign tumours, with exceptions being haemangiomas, myxomas and fibromas (Figure 5.6).

Figure 5.3 CMR characterization of a solitary LA myxoma (black arrows) from a 65-year-old man noted to have an LA mass on TTE and TOE. (a) Transaxial SSFP cine GE sequence of the 4.2 ×3.8 ×4.0 cm³ ovoid mass within the LA. The base is attached to the interatrial septum and the mass has a lower signal intensity than the surrounding blood pool. (b) T1W SE imaging in an equivalent plane shows largely intermediate signal intensity but with a central area of increased intensity consistent with haemorrhage. (c) T2W imaging reveals the mass to have predominantly low signal intensity. (d) Four-chamber first-pass perfusion CMR demonstrates a small central core of perfusion compatible with vascularity. (e) Transaxial EGE view is largely negative but with central enhancement. (f) LGE in the same plane demonstrates significant enhancement, probably areas of necrosis or fibrosis.

Figure 5.4 Serial assessment two-chamber SSFP GE cine views from a 44-year-old man with a LA sarcoma before and after treatment (a–c; solid black arrows). CMR was used to accurately evaluate tumour size (a; white cross) and MV function (a; dashed black arrow) at each stage.

Figure 5.5 CMR study from an 82-year-old man with TTE findings of a pericardial effusion and diastolic abnormality.

(a) Transaxial T1W FSE demonstrates a large, irregularly shaped, highly lobulated anterior mediastinal mass (white arrow) infiltrating the sternum and chest wall anteriorly and the pericardium posteriorly. (b) EGE shows the mass to have patchy contrast uptake. (c) Patchy LGE was present. These appearances are highly suggestive of a malignancy such as lymphoma, angiosarcoma or thymic carcinoma.

Figure 5.6 Basal short-axis views from a 34-year-old woman referred for CMR with an echocardiographic finding of localized basal anteroseptal hypertrophy and subsequent normal cardiac biopsy.

Initial SSFP cine readily confirms the TTE findings (a; black arrow), while EGE showed no enhancement within the mass (b) and LGE demonstrated homogenous contrast uptake (c). These CMR appearances are characteristic of a fibroma.

Acute pericarditis and pericardial effusion

Acute pericarditis may be accompanied by symptoms and signs of heart failure or arrhythmias if there is concomitant myocarditis. CMR findings range from no abnormality to regional WMA, pericardial thickening and pericardial effusion. The heart is imaged in different planes to determine the greatest extent of thickening or effusion, especially in cases of loculation. An effusion less than 10 mm wide is considered small whereas large effusions are greater than 20 mm. Both thickened pericardium and effusions can show low signal intensity on T1W SE imaging while GE techniques reveal non-haemorrhagic effusions to have high signal intensity (Figure 5.8). The appearance of haemorrhagic effusions depends on the age of the pericardial haematoma. Acutely, there is high signal intensity on T1W SE and lower signal intensity on GE images, while more chronic haematomas exhibit heterogeneous signal intensities by SE techniques. Differentiation of transudates from exudates and chylous effusions is through T1W SE imaging. Signal intensity is low in transudates but high in chylous collections, with an intermediate appearance in exudates.

Figure 5.8 Four-chamber views from a 42-year-old woman with a large global pericardial effusion (a; white arrow) secondary to metastatic leiomyosarcoma (b; black arrow). The effusion is seen to have intermediate signal intensity by SE imaging (a) and a high signal intensity using the GE technique, which clearly shows the tumour (b).

SSFP GE cine imaging demonstrates diastolic chamber collapse and abnormal septal motion in cardiac tamponade. In the latter, the heart can often have a swinging motion. Other pathological findings include dilated superior and inferior vena cavae and the presence of abnormalities within the mediastinum and lung fields which could provide clues as to aetiology.

Following gadolinium injection, inflamed pericardium shows early enhancement with a smooth contour suggestive of acute pericarditis in contrast to an irregular outline after a more insidious clinical course. Such pericardial contrast enhancement is also seen in malignant infiltration. Contrast enhancement is usually absent in pericardial fluid.

With massive effusion, ECG amplitude may diminish making it difficult to trigger cardiac imaging. CMR assessment can also be limited in patients who are significantly symptomatic since they have a tachycardia and find it difficult to lie flat within the magnet for prolonged periods.

Constrictive pericarditis

Following inflammation or bleeding into the pericardial space, fibrosis and calcification of the pericardium may ensue and the pericardium becomes thickened and stiff. This progressively restricts and impairs the filling of the cardiac chambers. Diastolic pressures are elevated and equalized in all four cardiac chambers. Impaired diastolic function leads to tachycardia and volume expansion, resulting in systemic venous congestion. Systolic function is usually preserved unless there is associated myocardial disease. The heart is insulated from changes in intrathoracic pressure that occur with respiration and atrial and ventricular filling patterns vary significantly with inspiration and expiration, resulting in ventricular interdependence. During inspiration, right-sided filling is increased, the ventricular septum deviates to the left, and left-sided filling correspondingly decreases. The converse occurs at expiration.

The distinction between constrictive pericarditis and restrictive cardiomyopathy is difficult but important clinically and imaging techniques such as CMR and cardiac CT are useful in diagnosis. The diagnostic hallmark of constrictive pericarditis is pericardial thickening with or without calcification in the presence of suggestive symptoms and signs of constriction (Figure 5.9). Care should be taken when evaluating pericardial thickness since oblique views yield falsely high values and several planes must be assessed and used in measurements. The absence of pericardial thickening/calcification does not exclude the presence of constriction and a thickened pericardium does not always equate to constrictive pericarditis. It is therefore crucial to evaluate concomitant functional consequences and CMR is well-suited for this purpose.

Figure 5.9 Four-chamber SSFP GE cine view from an 81-year-old woman with a history of recurrent pericardial effusions requiring surgical drainage and features of constrictive pericarditis at recent cardiac catheterization.

There is bi-atrial dilatation and a thickened pericardium (black arrows), which measured 9 mm in this plane. No pericardial effusion is seen and LVEF was 68% (normal).

A thickened pericardium as well as pericardial effusions can often be identified at the early low-resolution FSE sequence. Pericardial thickness is definitively measured on subsequent T1W FSE views and differentiated from effusion with SSFP cines acquired in these same planes. In the presence of effusion, pericardial thickness can be determined by use of gadolinium which can outline the visceral and parietal layers. Chronic fibrotic pericardium shows late enhancement, which is also seen with associated myocardial fibrosis or infarction. Areas of calcification appear as regions of attenuated signal intensity on CMR but CT is recommended for accurate assessment of this feature. Other findings include typically normal-sized or small ventricles with normal ejection fraction, dilated atria and vena cavae, pleural effusions, plethoric hepatic veins, hepatic enlargement and ascites. The ventricles may assume a tube-like configuration. The presence of epicardial fat separating the epimyocardium from the thickened visceral pericardium is also a useful finding for the surgeon when planning surgical pericardiectomy.

On high temporal resolution SSFP cines, the ventricular septum may be seen to deviate towards the LV in early diastole. Additional real-time cines are useful in demonstrating ventricular interdependence. The patient is instructed to inhale and exhale throughout these cines, which are acquired over approximately 20 s and at least three respiratory cycles. With constrictive physiology, the ventricular septum flattens and deviates towards the LV on inspiration before resuming its normal position on expiration—‘septal bounce’. The technique of myocardial tagging can determine myocardial tethering to the overlying thickened pericardium with persistent concordance of the tag lines between myocardium and pericardium throughout systole and diastole.

In summary, a suggested CMR imaging protocol in significant pericardial effusion/constriction is as follows:

CMR reports include:

Pericardial cyst and diverticula

Pericardial cysts are uncommon remnants of defective pericardial embryologic development. They are benign and occur as round, sharply demarcated, fluid-filled bodies, found most commonly in the right cardiophrenic angle but also in the hilar and mediastinal regions. They do not communicate with the pericardial space. Using T2W SE images they typically exhibit high signal intensity, while on T1W SE images they show intermediate or low signal intensities (Figure 5.10). There is no enhancement with gadolinium contrast.

Figure 5.10 An incidental finding of a small 2.6 ×1.8 ×5 cm³ pericardial cyst (white arrows) discovered in a 71-year-old man referred for coronary MRA showing characteristic high signal intensity by (a) SSFP cine and (b) T2W SE imaging in a transaxial plane at the level of the pulmonary bifurcation.

Pericardial diverticula are rare outpouchings of the pericardial sac and therefore are in communication with the pericardial space.

Congenital absence of the pericardium

Absence of the pericardium is rare and often asymptomatic. The defect is usually left-sided and partial but can be right-sided, diaphragmatic or complete. Associated congenital cardiac anomalies include atrial septal defects (ASDs), patent ductus arteriosus (PDA) and tetralogy of Fallot (TOF). The heart shifts to the left and posteriorly, and with partial left-sided absence the left atrial appendage may be dilated. Herniation of the left atrial appendage through a partial defect may lead to strangulation and sudden death. CMR can reveal the defect, associated cardiac anomalies and displacement, and herniation (Figure 5.11).

Figure 5.11 Four-chamber SSFP GE cine image from a 46-year-old patient demonstrating herniation of both ventricles through a partially absent pericardium at the level arrowed.

There is associated RA and RV dilatation on this image secondary to severe TR which is not shown.