MR, CT, and PET imaging in pericardial disease - Springer Link

Heart Fail Rev (2013) 18:289–306 DOI 10.1007/s10741-012-9309-z

MR, CT, and PET imaging in pericardial disease Peter Alter • Jens H. Figiel • Thomas P. Rupp Georg F. Bachmann • Bernhard Maisch • Marga B. Rominger

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Published online: 25 March 2012 Ó Springer Science+Business Media, LLC 2012

Abstract Although echocardiography remains the standard diagnostic tool for identifying pericardial diseases, procedures with better delineation of morphology and heart function are often required. The pericardium consists of an inner visceral (epicardium) and outer parietal layer (pericardium), which constitute for the pericardial cavity. Pericardial effusion can occur as transudate, exudate, pyopneumopericardium, or hemopericardium. Potential causes are inflammatory processes, that is, pericarditis due to autoimmune or infective reasons, neoplasms, irradiation, or systemic disorders, chronic renal failure, endocrine, or metabolic diseases. Pericardial fat can mimic pericardial effusion. Using various image-acquisition sequences, MRI allows identifying and separating fluid and solid structures. Fast spin-echo T1-weighted sequences with black-blood preparation are favourably used for morphological evaluation. Fast spin-echo T2-weighted sequences, particularly with fat saturation, and short-tau inversion-recovery sequences are useful to visualize oedema and inflammation. For further tissue characterization, delayed inversionrecovery imaging is used. Therefore, image acquisition is performed at 5–20 min subsequent to contrast agent administration, the so-called technique of late gadolinium

P. Alter (&)
T. P. Rupp
B. Maisch Internal Medicine—Cardiology, Philipps University, Baldingerstrasse, 35033 Marburg, Germany e-mail: [email protected] J. H. Figiel
M. B. Rominger Department of Radiology, Philipps University, Marburg, Germany G. F. Bachmann Department of Radiology, Kerckhoff Heart Center, Bad Nauheim, Germany

enhancement. Ventricular volumes and myocardial mass can be assessed accurately by steady-state free-precession sequences, which is required to measure cardiac function and ventricular wall stress. Constrictive pericarditis usually results from chronic inflammatory processes leading to increased stiffness, which impedes the slippage of both pericardial layers and thereby the normal cardiac filling. CT imaging can favourably assess pericardial calcification. Thus, MR and CT imaging allow a comprehensive delineation of the pericardium. Superior to echocardiography, both methods provide a larger field of view and depiction of the complete chest including abnormalities of the surrounding mediastinum and lungs. PET provides unique information on the in vivo metabolism of 18-fluorodeoxyglucose that can be superimposed on CT findings and is useful for identifying inflammatory processes or masses, for example neoplasms. These imaging techniques provide advanced information of anatomy and cardiac function to optimize the pericardial access, for example by the AttachLifter system, for diagnosis and treatment. Keywords Pericardial disease
Pericarditis
Pericardial effusion
Constrictive pericarditis
Restrictive cardiomyopathy
Magnetic resonance imaging
Computed tomography
Positron emission tomography
Ventricular wall stress
Pericardiocentesis
AttachLifter

Normal anatomy, function, physiology The pericardium covers the heart and expands to the pulmonary trunk, the upper caval vein, and the ascending aorta. The pericardial sac consists of an inner visceral and outer parietal layer, which constitute for the pericardial cavity. The parietal pericardium localizes the heart in the

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thoracic cavity. Several studies including computed tomography (CT) and magnetic resonance imaging (MRI) as well as autopsy findings examined the normal pericardial thickness, which varies among different regions, being thinnest adjacent to the left ventricle. A normal thickness appeared to be 0.7 mm at the thinnest part when using high-resolution CT (HRCT) and 1.2 mm when using 10 mm CT slices [1]. The upper limit of normal pericardium did not exceed 2 mm [2–5]. Physiologically, the pericardial sac can contain few millilitres of clear fluid.

Technical aspects of MR, CT, and PET imaging Due to its ease of use and widespread availability, echocardiography emerged as first-line imaging modality for visualizing the pericardium with focus on pericardial effusion. MR and CT imaging is judged as second-line modality, positron emission tomography (PET) imaging as third-line diagnostic tool. It should, however, be noted that echocardiography can be misleading when pericardial fat mimics an effusion [6]. Using various image-acquisition sequences, MRI could be helpful in substantiating the diagnosis and avoiding inappropriate potentially harmful procedures. Details of the favourable use of several imaging modalities in perimyocardial disease are summarized in Table 1. MRI Because of the method-inherent favourable imaging contrast among different anatomic structures and tissues as well as unique functional information, MRI provides Table 1 Favourable use of several imaging modalities in perimyocardial disease

accurate information in addition to echocardiography. Usually, ECG-triggered imaging is required to visualize the pericardium. In particular, in patients with pericardial effusion, trigger artefacts have to be taken into account due to low-voltage ECG pattern. Respiratory artefacts can be reduced by using breath-hold techniques. High-resolution images were obtained using dedicated phased array coils and fast-imaging techniques. Depending on the preparation pulse, blood, and fluctuating pericardial fluid, the effusion can be shown as either bright or dark signal. Fast spin-echo T1-weighted sequences with black-blood preparation are favourably used for morphological evaluation of the cardiac chambers and great vessels. Fast spinecho T2-weighted sequences, particularly with fat saturation, are useful to visualize oedema and inflammation that appear as hyperintense area. Therefore, also short-tau inversion-recovery (STIR) sequences are appropriate. The normal pericardium is depicted by a thin rim of low signal at both T1- and T2-weighted images. Cine steady-state free-precession (SSFP) sequences accurately delineate myocardium from the ventricular cavity. Thus, SSFP sequences are used to measure ventricular volume and myocardial mass as well as global and regional ventricular function and wall thickening during the cardiac cycle [7, 8]. This type of bright blood technique can also visualize a fluctuating pericardial effusion in bright exposition. For further tissue characterization, delayed inversionrecovery imaging is used. Therefore, image acquisition is performed at 5–20 min subsequent to administration of the contrast agent, usually a gadolinium-based compound (0.1–0.2 mmol/kg). It is required to choose a time of inversion that leads to signal-nulling of the normal Chest X-ray

Echo

MRI

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Hemopericardium

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Pericardial thickness

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Pericardial anatomy and morphology Pericardial effusion

Pericardial calcification Pericardial constriction

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Restrictive cardiomyopathy Pericardial gas, for example pyopneumopericardium

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Perimyocardial inflammation

Subjective suggestion of the authors taking into account several modality-inherent features and sequences of image acquisition, temporal and spatial resolution, and exposure to radiation

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Inflammation of adjacent structures

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Cardiac volumes, mass, and function

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Flow measurements

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Assessment of myocardial tagging

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myocardium or pericardium. Areas with a remaining signal due to a prolonged interstitial contrast agent deposition that causes T1 shortening exhibit the so-called late gadolinium enhancement, also referred to as delayed hyperenhancement. Causes of late gadolinium enhancement vary among different cardiac diseases. In infarcted areas, postischemic fibrotic remodelling is assumed to be crucial [9–11]. In cardiomyopathies, several mechanisms have to be taken into account [12, 13]. Of particular note, increased ventricular wall stress and mass were associated with the occurrence of late gadolinium enhancement [14]. Further MRI techniques involve velocity-encoded cine imaging that is used to quantify flow, for example transvalvular flow or shunt measurement [15, 16]. The method of tagging uses a grid-like pattern of saturated areas and allows studying deformation of the grid over time. Therefore, a myocardial tagging sequence can be used to show the lack of slippage in constrictive pericarditis [17]. CT CT imaging visualizes the pericardium as thin line of fibrous tissue, whereas the visceral layer cannot be depicted separately. Using CT imaging, the higher pericardial X-ray absorption provides sufficient contrast to distinguish pericardium from surrounding fatty tissue, for example mediastinal or epi-/pericardial fat. These fat volumes appear to be of relevance for cardiovascular risk stratification and monitoring [18]. Of note, a particular advantage of CT imaging is the ability to delineate pericardial calcification accurately and comprehensively, which can be decisive to differ between constrictive pericarditis and restrictive ventricular filling pattern. PET In contrast to CT and MR imaging relying on anatomic structure and function, PET imaging reflects the in vivo metabolism of 18-fluorodeoxyglucose (FDG). Both methods were combined with PET imaging to associate metabolic findings with anatomy, the so-called cardiac hybrid imaging. Usually, inflammatory processes involving the pericardium show a mild-to-moderate FDG uptake, but also no increased FDG uptake can be observed. In contrast, proliferative neoplastic disorders commonly exhibit a markedly increased FDG uptake that is often congruent with a localized mass of tissue.

Pericarditis and pericardial effusion Two pericardial layers, the visceral and parietal sheet, constitute for the pericardial space in between. Normally,

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Gas

Pus

Fig. 1 CT scan of a pyopneumopericardium in a 60-year-old male [19]

few millilitres of fluid reduce the friction rub of the moving heart during physiological action. Pericardial effusion can occur as transudate, exudate, pyopneumopericardium [19] (Fig. 1), or hemopericardium [20]. Potential causes of pericardial effusion are inflammatory processes, that is, pericarditis due to autoimmune or infective reasons, neoplasms, irradiation, or systemic disorders, for example autoimmune diseases, chronic renal failure (uraemia), endocrine, or metabolic diseases [21]. Pericardial fat can mimic pericardial effusion [6, 22]. According to its temporal occurrence, pericarditis is divided into acute, chronic (at least 3 months), and recurrent pericarditis. Presence of a pericardial effusion, also when occurring as small pericardial separation only, is a sensitive, but unspecific finding in perimyocarditis [23–25]. The causes of infectious pericarditis are various agents, for example viruses, bacteria, mycobacteria, fungi, protozoa, and autoimmune diseases [26]. Neoplastic pericardial effusion occurs frequently in lung and breast cancer as well as in leukaemia and lymphoma. Finally, a large proportion of cases remain of the so-called idiopathic origin. The extent of pericardial effusion is highly variable (Figs. 2,3,4). Even few millilitres of acute effusion can cause cardiac tamponade [27]. On the other hand, chronic development of pericardial effusion can occur up to more than two litres without any symptoms. The key determinant is the pressure in the pericardial sac, which results from the volume of the parietal pericardium and the amount of fluid. Increased pressure tends to impress the heart [28]. Since the intracavitary pressure is lowest in the right heart, cardiac tamponade is commonly initiated by right heart compression. Every decrease of the intracardiac pressure

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Fig. 2 Small pericardial effusion (arrows) in a 44-year-old male at early systole in 4-chamber (a), long-axis (b), 3-chamber (c), and short-axis (d) views (cine steady-state free-precession sequences). In this condition, MR cine imaging can be particularly helpful to

distinguish the mobile bright pericardial effusion from solid structures, for example pericardial fat. In addition, a mild mitral valve regurgitation jet is visible (c)

leads to an increase of the transmural gradient between pericardial and intracardiac pressure and thus should be avoided, since tamponade could be evoked. Clinical signs are an increase of the venous pressure and decrease of the arterial pulse pressure (paradoxical pulse) during inspiration [29]. Of note, the latter is not indicative of pericardial tamponade, but also occurs in other conditions, for example constrictive pericarditis. Echocardiography is the standard imaging technique to detect pericardial effusion. Presence of a large effusion or cardiac tamponade can be safely assessed or excluded in the vast majority of patients. However, there are also limitations [30]. Smaller effusions localized at the posterior

or inferior wall incidentally are not detectable by echocardiography. Also, discrimination of a surrounding pleural effusion is challenging (Fig. 5). Although MRI can detect a small pericardial effusion, there is no strong relationship between the measured width of the pericardial separation, that is, distance of both pericardial layers, and the total fluid volume since the effusion can be distributed inhomogenously. Regions with a pericardial width greater than 4 mm can be regarded as abnormal. A moderate pericardial effusion (between 100 and 500 ml of fluid) is usually associated with more than 5 mm of pericardial separation anterior to the right ventricle [31]. Thus, CT and MR imaging allow a comprehensive delineation of pericardial

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Fig. 3 Moderate pericardial effusion (arrows) without signs of cardiac tamponade in a 67-year-old female in 4-chamber (a), long-axis (b), 3-chamber (c), and short-axis (d) views (cine steady-state free-precession sequences)

effusion [32–34]. By using cine imaging, also the hemodynamic relevance of an effusion can be judged. Superior to echocardiography, CT- and MR-based methods provide a larger field of view and thus allow imaging of the complete chest including abnormalities of the mediastinum and lungs [35], which can be required when, for example, pneumonia or a neoplastic origin of the pericardial effusion is taken into account [36–38].

Constrictive pericarditis Constrictive pericarditis usually results from chronic inflammatory processes of the pericardium leading to increased stiffness that impedes the normal filling of all

four cardiac chambers [20, 39]. The visceral (one layer of mesothelial cells) and parietal part (B2 mm thickness) of the pericardium can be involved and adhesions between both layers, that is, concretion and constriction, limit the normal slippage [17]. Fibrosis and frequently calcification occur. Rarely, only the visceral layer can be involved, for example in patients with remote pericardiectomy [40], and also combined effusive-constrictive types are known [41– 43]. Causes of the inflammation are unspecific, but viral and autoimmune processes have to be taken into account (Table 2). Frequently, the presence of hemopericardium of various etiologies is followed by constriction [44]. Before effective treatment was available, tuberculosis was the most common cause of pericardial constriction with marked calcification, the so-called pericarditis calcarea.

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Fig. 4 Large pericardial effusion causing cardiac tamponade in a 49-year-old female in 4-chamber (a), long-axis (b), 3-chamber (c), and shortaxis (d) views (cine steady-state free-precession sequences). All chambers are comprised. Cine imaging shows the typical ‘swinging heart’

More recently, previous therapeutic chest irradiation is a frequent cause, which usually requires a delay of several years until constriction occurs [20]. Patients with constrictive pericarditis present with signs of right-sided or global heart failure. Thus, abdominal complaints, aggravated after large meals, hepatic congestion, and finally cirrhosis as well as ascites can occur. Initially, these signs and symptoms are often misleading and prevent an early diagnosis. The basic underlying pathophysiological mechanism causing all symptoms is the impaired cardiac filling [39], which frequently is associated with a dilated inferior caval vein [45]. In the majority of cases, constrictive pericarditis is associated with marked pericardial thickening (Fig. 6). Constriction following fibrosis without marked thickening

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is rarely observed [5]. The standard method to assess cardiac and pericardial function and morphology is transthoracic and transesophageal echocardiography. In addition to real-time assessment of function, typical transmitral and tricuspid flow patterns can be assessed (E- and A-wave). Similar to a solid capsule covering the heart, constrictive pericarditis prevents influences of the negative intrathoracic pressure on the heart chambers during inspiration, which leads to reduced pulmonary venous flow into the left atrium. Therefore, during inspiration, the transmitral flow decreases, the tricuspid flow increases, and the ventricular septum shifts to the left. Contrary effects occur during expiration. However, echocardiography also has several limitations to delineate the complete pericardium, in particular when the echo window is limited. Thus, CT and MR

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Fig. 5 75-year-old patient with pleural (arrows), but not pericardial effusion in 4-chamber (a), long-axis (b) and short-axis (c) CT views. Of note, previous echocardiography led to the false diagnosis of

pericardial effusion surrounding the left atrium. In addition, two right ventricular pacemaker leads (circle) are shown (c)

Table 2 Causes of constrictive pericarditis

imaging provide an excellent depiction of the complete pericardium [32, 46–51]. In particular, CT imaging is sufficient to delineate pericardial calcification. Physiologically, the pericardial thickness is less than 2 mm [1, 52, 53]. Increased thickening [4 mm is suggestive of constriction. In a small series of patients with surgically proven constrictive pericarditis, a mean pericardial thickness of 9.2 ± 7.0 mm was found in patients with calcification and 4.6 ± 2.1 in patients without calcification [45]. An abnormal septal motion (‘bounce’) caused by the impaired filling was found in 86 % of patients with constriction. Occurrence of pericardial late gadolinium enhancement seems to be an infrequent sign. Recently, it was shown that pericardial late gadolinium enhancement in patients with constrictive pericarditis was associated with histological features of organizing pericarditis and, of note, less fibrosis [54]. In several studies, an opposite correlation has been assumed for myocardial late gadolinium enhancement in cardiomyopathy [55–61]. It has been assumed that constrictive pericarditis with ongoing inflammatory processes is potentially reversible in few cases. In a small pilot study, the response to anti-inflammatory therapy was evaluated to predict LGE-based pericardial thickness [62]. Up to now,

Infectious peri- (myo-) carditis

Various viruses Bacteria Mycobacteria Fungi

Autoimmune peri(myo-) carditis

Protozoa Autoimmune cardiac disease Postmyocardial infarction (Dressler syndrome) Postcardiotomy syndrome Systemic autoimmune processes, for example connective tissue disease, rheumatic diseases

Hemopericardium

After trauma (acute) myocardial infarction Procedure related, for example ICD or pacemaker implant Haemorrhagic effusion of any origin

Irradiation Other systemic diseases

Chronic renal failure Sarcoidosis etc.

Idiopathic

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Fig. 6 Pericardial effusion in 58-year-old man visualized by CT at initial presentation (a). One year later, the patient exhibited signs of constrictive pericarditis. The pericardium was thickened markedly (b) and the diagnosis was ascertained by typical flow and pressure

pattern. Echocardiography (c) shows the transmitral inflow (left) that typically decreases during inspiration (right) as characterized by the yellow bars (E- and A-wave)

the diagnostic significance of LGE remains uncertain in these entities. The final diagnosis of constrictive pericarditis is not based on imaging techniques only (Fig. 6). Of note, occurrence of pericardial thickening or calcification is indicative, but is no proof of constrictive pericarditis [63]. To ascertain constrictive pericarditis, simultaneous measurement of left and right ventricular pressure is required to reveal equation of the diastolic pressure and to assess the typical square-root-shaped pressure curve. For the

treatment of constrictive pericarditis, surgical pericardiectomy can be performed [39] (Fig. 7). Since epicardial coronary arteries can be involved in the constriction, the procedure has a remarkable perioperative risk.

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Restrictive cardiomyopathy Restrictive cardiomyopathy bears some similarities, but must be strictly differentiated from constrictive pericarditis

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Fig. 7 Constrictive pericarditis in a 63-year-old patient. The pericardium is thickened markedly and an effusion is present (a). Postoperative result (b) after partial surgical pericardiectomy (both: T1-weighted turbo spin-echo sequences, single slices, dark blood preparation)

[64]. Both entities are characterized by impaired diastolic filling pattern, whereas systolic disturbances are not required. Despite some hemodynamic similarities, marked differences occur as regards the aetiology, cardiac function, and treatment. From the macroscopic view, restrictive cardiomyopathy typically exhibits a hypertrophic phenotype [65], but does not belong to the hypertrophic cardiomyopathies. Typically, ventricular wall thickening and restrictive filling pattern are evoked by a substance deposition or marked fibrosis, for example infiltrative or storage diseases such as cardiac sarcoidosis, amyloidosis [66], Fabry’s disease [67], hemochromatosis, Loeffler’s [68, 69], or hypereosinophilic Churg–Strauss syndrome [70]. Acromegaly was related to non-constrictive filling pattern caused by cardiomyocyte hypertrophy and interstitial fibrosis [71] (Fig. 8). Also, the so-called idiopathic forms of restrictive cardiomyopathies are known. Either of both ventricles can be involved. Due to increased ventricular filling pressures, biatrial enlargement is a typical finding, which belongs to the diagnostic criteria of restrictive cardiomyopathy [72]. Pulmonary hypertension is common, and the pericardium is not involved. Gadolinium-based compounds used as contrast agents for MR imaging are of small molecular weight and thus can leave the vasculature into the interstitial space [58, 59]. An increase of the interstitial space is commonly associated with a prolonged contrast agent deposition, an impaired redistribution or clearance. Due to the prolonged contrast agent accumulation in storage diseases, occurrence of diffusely spread and marked late gadolinium enhancement is typical [73–75]. It was previously shown by us that occurrence of late gadolinium enhancement is also associated

with increased left ventricular wall stress and mass in patients with non-ischaemic dilated cardiomyopathy [14, 76]. In sum, CT and MR imaging can be favourably used to distinguish constrictive pericarditis from restrictive cardiomyopathy [49, 77, 78]. In particular, the ability to delineate myocardium from pericardium is helpful in this condition.

Mechanical properties Ventricular wall stress is a seminal physiological determinant crucially involved in the pathophysiology of various cardiac diseases [8, 79]. Wall stress is mainly determined by pressure, myocardial mass, and ventricular volume [80–82]. The effective pressure transmitting distending forces on the myocardium is the transmural pressure gradient, which is the difference of heart cavity and surrounding pressure, for example thoracic and pericardial pressure [83, 84]. The pericardium has a constraining effect on the heart and thus can influence the transmural pressure gradient. The pressure–volume or stress–strain relation of the anisotropic pericardium is initially flat, which means the pericardium is compliant to small distending forces, but followed by steep increase of stress, when the normal filling is exceeded [85]. That means that a small pericardial effusion is tolerated without cardiac compression, but beyond a critical degree, cardiac tamponade occurs rapidly. In chronic cardiac dilatation, the pericardial sac adapts by enlargement and also by an increased mechanical compliance, that is, the stress–strain relation shifts to the right and flattens a little [86–89].

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Time of cardiac cycle [ms] Fig. 8 Short-axis views (cine steady-state free-precession sequences) of a patient with acromegaly showing pericardial effusion and nonconstrictive diastolic dysfunction at enddiastole (a) and endsystole (b) [71]. Histology revealed mild cardiomyocyte hypertrophy and

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interstitial fibrosis (c) when compared with a control (d). Left ventricular volumes and diastolic filling were markedly reduced when compared with normal pattern. Of note, the pericardial effusion with potential hemodynamic influences was drained before (e)

Heart Fail Rev (2013) 18:289–306 Fig. 9 Left-sided heart dislocation following hemipneumonectomy c in a.p. chest radiography (a), in a transversal thoracic CT view (b), and depicted as 3-D reconstruction (c) showing entrapment of the heart between the ascending and descending aorta with consecutive left atrial compression [91] (with permission of Georg Thieme Verlag KG, Stuttgart, Germany). Therefore, immediate surgical repositioning was required. LA left atrium, LV left ventricle, RV right ventricle

It can be assumed that chronic pericardial constriction, for example in constrictive pericarditis, influences myocardial wall stress. Increased enddiastolic left ventricular wall stress was shown to precede hypertrophy in dilative heart failure. Cardiac growth is required to cope with the increased wall stress [82]. It was shown in patients who underwent thoracotomy and pericardiotomy for bypass surgery that an increase of left ventricular enddiastolic volume was associated with increased myocardial mass, which supports the hypothesis of ceased pericardial-constraining effects [90]. In turn, it can be assumed that the prevention of normal distending forces by pericardial constriction leads to a decrease of myocardial mass. Thus, surgical pericardiectomy can lead to acute cardiac dilatation, when the myocardial mass is inadequate to cope with an increased wall stress. We recommend assessing ventricular wall stress when the corresponding MRI data are available. As routine parameter, the wall stress index based on a thick-walled sphere model can be used, which does not require invasive pressure measurements [7, 8]. The MR imaging–based method was shown to be superior to an echocardiography-based approach, which underestimated the ventricular wall stress [81].

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Pericardial trauma Posttraumatic and postoperative cardiac luxation represents a serious complication of pericardial rupture, and early diagnosis is required [91]. Although conventional chest X-ray can be helpful, CT has a key role for an early diagnosis (Fig. 9) [91]. Dislocation of the heart, potential entrapment of the left atrium or ventricle, and the occurrence of a pneumocardium associated with pneumothorax are most important CT findings [92].

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Pericardial masses and neoplasms Pericardial cysts are filled with fluid and are not connected to the pericardial space. Their origin is congenital as encapsulated cysts, subsequent to inflammation or ecchinococcal affection. The most common localization is anterior at the cardiophrenic sulcus, but also occurrence adjacent to the left ventricle is known [32, 93]. In contrast

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Fig. 10 53-year-old female with not-otherwise-specified sarcoma (NOS, arrows) at the pericardium involving the lung and mitral valve in T1-weighted 4-chamber (a, T2-weighted single-slice turbo spinecho sequence without fat saturation), 3-chamber (b) and fat-saturated and contrast-enhanced long-axis (c) views (both: T2-weighted single-

slice turbo spin-echo sequence with fat saturation). PET imaging shows the moderate cardiac (around die mitral valve) and the marked pulmonary FDG uptake (d, arrows). PET images are superimposed to CT findings (e). In addition, multiple liver and kidney cysts are visible

to metastases, primary pericardial tumours, for example mesotheliomas, fibrosarcomas, angiosarcomas, and teratomas, are rare [94–96] (Figs. 10,11). Pericardial metastases are found in breast carcinoma, leukaemias, and lymphomas [97, 98].

Insight from imaging applied to pericardial access with the AttachLifter

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Various pericardial diseases require access to the pericardial sac either for diagnostic purposes or for treatment [21].

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Fig. 11 Pericardial sarcoma (arrows) with pericardial effusion in a 65-year-old female in contrast CT (a) and MR images (b, T1weighted fast low-angle shot-2-D sequence, without contrast agent).

Subsequent to contrast agent administration, the sarcoma exhibits a typical enhancement pattern of intensively vascularized tumours (c, inversion-recovery fast low-angle shot 3-D)

In a standard approach, the pericardium is punctured by a needle under fluoroscopic guidance [20]. In order to reduce the risk of cardiac tamponade, the pericardium must be adequately separated from the epicardium. For accessing the pericardial sac with less separation but nonetheless minimized injury risk, a tool (AttachLifter) has been developed, which provides safety features not present in a bare needle [84]. In the AttachLifter approach, adequate separation is achieved by mechanically lifting the pericardium off the epicardium. During this manoeuvre, the pericardium should not become detached from the device. While a suction head was used previously in a number of tools for grasping and moving objects, it turned out that for the pericardial lifting, the suction head required flexible

clamps. A small part of the pericardium is sucked by vacuum into the head and is securely held within the suction head by clamps made from flexible material. This permits a rotation of the suction head by about 90°, thereby lifting the pericardium away from the epicardium. The needle is pushed through the attached pericardium whereby guidance in the form of a ridge prevents any contact of the needle with the epicardium. The crucial safety features of this approach are shown (Fig. 12). For demonstrating the efficacy of the flexible clamps, the suction head was turned by 180° and not by 90° as in the regular approach. Even under this condition, the pericardium remains attached to the suction head, and the needle can be pushed through the pericardium into the pericardial space. The suction head

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Flexible clamp

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Fig. 12 Access to the pericardial space with the AttachLifter. An approach is shown for a pericardium of normal thickness, whereby a safety ridge prevents injury to the epicardium (a). A thickened pericardium can be entered by a relatively stiff wire guided by a

rotatable 90° side tube (b). Contrary to the standard subxiphoidal needle approach, the pericardium is entered nearly parallel to the heart surface that reduces risk of cardiac injury (from H. Rupp et al. unpublished; (b) modified from patent WO 2008/071367 A1)

was designed for a normal pericardial thickness. Based on high-resolution CT slices, the upper limit of the thinnest portion of normal pericardium was 0.7 mm [1]. The width of the thickest portion varied widely between subjects. It was concluded that localized expansions represent small pockets of physiological pericardial fluid. The mean maximum was 2.8 mm. Measurement of the thickest portion of the pericardium was, however, not found useful for diagnosing a generally thickened pericardium. When accessing the pericardial sac in obese persons with visceral fat accumulation, increased intrathoracic fat has to be taken into account. Thoracic fat refers to adipose

tissue outside the pericardium [18, 99]. The term pericardial fat refers to adipose tissue enclosed by the pericardium, including the epicardial fat surrounding the coronary arteries. Both fat volumes correlate with abdominal visceral fat and are strongly associated with the presence of coronary calcium and the metabolic syndrome [18]. As regards the AttachLifter procedure, it is expected that the presence of thoracic fat does not interfere with reaching the pericardial surface. Nonetheless, a technique was developed for thickened pericardium potentially overlaid with a small fat layer. During this procedure, the pericardium remains attached to the suction head, a rotatable 90° bend

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side tube is directed towards the pericardial sac and a relatively stiff guidewire is pushed through the firmly attached thickened tissue into the pericardial space. The procedures available with the AttachLifter differ from a previous approach with the PerDUCER where the pericardium was sucked into the head portion of the tool, and the penetrating needle had to puncture the pericardium within the suction head. If the suction head was filled out by thickened pericardium, the pericardial space could, however, not be accessed [100]. Further insight from high-resolution imaging of the pericardium and surrounding tissues is expected to optimize the design of the AttachLifter.

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Conclusion Although echocardiography remains the standard diagnostic tool for identifying pericardial diseases, procedures with better tissue characterization are often needed to substantiate diagnosis and further treatment. With MRI, various acquisition sequences are available to obtain cardiac function and tissue morphology. Contrary to MRI, CT requires radiation. Besides cardiac function and morphology, in particular, pericardial calcification can be depicted by CT. PET provides unique information on metabolism that can be superimposed to CT findings and is useful for identifying inflammatory processes or masses, for example neoplasms. These imaging techniques can be used for optimizing access to the pericardial space.

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