Cardiovascular magnetic resonance in pericardial diseases
© Bogaert and Francone; licensee BioMed Central Ltd. 2009
Received: 28 November 2008
Accepted: 04 May 2009
Published: 04 May 2009
The pericardium and pericardial diseases in particular have received, in contrast to other topics in the field of cardiology, relatively limited interest. Today, despite improved knowledge of pathophysiology of pericardial diseases and the availability of a wide spectrum of diagnostic tools, the diagnostic challenge remains. Not only the clinical presentation may be atypical, mimicking other cardiac, pulmonary or pleural diseases; in developed countries a shift for instance in the epidemiology of constrictive pericarditis has been noted. Accurate decision making is crucial taking into account the significant morbidity and mortality caused by complicated pericardial diseases, and the potential benefit of therapeutic interventions. Imaging herein has an important role, and cardiovascular magnetic resonance (CMR) is definitely one of the most versatile modalities to study the pericardium. It fuses excellent anatomic detail and tissue characterization with accurate evaluation of cardiac function and assessment of the haemodynamic consequences of pericardial constraint on cardiac filling. This review focuses on the current state of knowledge how CMR can be used to study the most common pericardial diseases.
Pericardial anatomy and physiology
Although the normal pericardium is a thin, avascular, relatively inelastic, flask-shaped sac enveloping the heart, this structure is an important determinant of cardiac filling [1–3]. In most cases, evaluation of pericardial diseases extends beyond morphologic assessment, and the diagnostic challenge is to determine the impact of abnormal pericardium on cardiac filling. Anatomically, the pericardium is composed of two layers, an inner serous membrane and an outer fibrocollagenous layer . The inner serosal layer, termed the visceral pericardium, is closely attached to the epicardial surface of the heart and covers a subepicardial layer of conjunctive tissue containing fat and coronary vessels. The serosal layer reflects back on itself to become the inner lining of the outer fibrous layer. Together, these layers form the parietal pericardium. The pericardium contains two major pericardial sinuses which are composed of different recesses . The transverse sinus is the connection between the two tubes of pericardium that envelop the great vessels. The aorta and pulmonary artery are enclosed in one anterosuperior tube, and the vena cava and pulmonary veins are enclosed in a more posterior tube. The oblique sinus lies behind the left atrium so that the posterior wall of the left atrium is actually separated from the pericardial space. This explains why a posterior pericardial effusion is seen behind the left atrium only when it is very large. The pericardial virtual cavity normally contains between 10 and 50 ml of an ultrafiltrate of plasma . The fluid is produced by the visceral pericardium and drainage of the cavity is toward both the thoracic duct and the right lymphatic duct.
The pericardium holds the heart within the anterior mediastinum, protecting it form adjacent organs. Its relative inelasticity provides constraint during diastolic filling which limits chamber dilation, particularly of the thin-walled right atrium and ventricle . While acute pericardial dilation is limited because of its exponential pressure-volume relation, chronic pericardial stress, e.g. slowly accumulating pericardial effusion or left ventricular remodeling, in contrast, may occur without pericardial constriction [1, 6, 7]. As the pericardium slowly dilates, the pericardial pressure-volume relation shifts to the right, explaining why chronic pericardial effusion may become quite large without compressing the cardiac chambers . The pericardium, moreover, equalizes compliance between right and thicker walled left ventricle, and produces interdependence of filling between ventricles, a phenomenon also called "ventricular coupling" (see constrictive pericarditis). Though, normally not physiologically important, ventricular coupling is exaggerated and a key diagnostic feature when intrapericardial pressure is increased (as in cardiac tamponade) or when the pericardial cavity is fixed (as in constrictive pericarditis) [2, 6–10]. Finally, the pericardium acts also as a physiological intermediate between the pleural space and heart chambers, and the respiratory changes in intrathoracic pressure are directly transmitted to the subatmospheric pericardial cavity and subsequently to the cardiac chambers. Because of its thinner wall, this interaction is more pronounced on the right than on the left ventricle.
Comprehensive pericardial imaging should provide information on morphologic characteristics of the pericardium and cardiac structures, and assess the impact of pericardial diseases on cardiac function, in particular cardiac filling. Though CMR is traditionally considered together with computed tomography (CT), as the preferred imaging modality to morphologically visualize the pericardium and pericardial space, CMR can substantially aid in clarifying the intricate relation between pericardial constraint and cardiac filling. Black-blood T1-weighted spin-echo CMR, using a fast, segmented sequence, is the best approach to visualize, the heart, pericardium and mediastinum [11, 12]. Use of a small field of view and a saturation block positioned on the frontal chest wall may hereby improve pericardial visualization. Scanning in two perpendicular oriented planes through the heart guarantees optimal depiction of the entire pericardium, for instance, using a set of axial views combined with coronal or cardiac short-axis views. T2-weighted spin-echo CMR, preferably using a short-tau inversion-recovery (STIR) sequence (also called "triple-inversion" spin-echo), highly useful to depict myocardial edema [13, 14], can also be applied to detect pericardial fluid and/or edema of the pericardial layers in patients with inflammatory pericarditis. Use of paramagnetic contrast agents can be recommended in case of pericardial masses, inflammatory pericarditis, to depict concomitant myocardial pathology (e.g. myocarditis) and may be useful to better differentiate between inflammatory and constrictive forms of pericarditis. Either T1-weighted spin-echo CMR or inversion-recovery gradient-echo CMR with late enhancement (LGE CMR) is fit for post-contrast imaging [15–17].
Cine CMR, using balanced steady-state free precession (SSFP) gradient-echo sequences, is today the reference technique to quantify global and regional cardiac systolic function, and is of interest for example to rule out underlying RV or LV dysfunction in patients clinically suspected of constrictive pericarditis. Moreover, the high spatial and temporal resolution of cine CMR can be applied to exploit new applications such as the assessment of pericardial mobility, which can help in depicting a rigid pericardium in patients with a non or minimally thickened constrictive pericarditis. The availability of new real-time cine sequences enabled to study dynamic, fast-changing, physiologic events such as ventricular coupling (see below). CMR tagging techniques may be of use to detect fibrotic adhesion of pericardial layers or to diagnose myocardial involvement in constrictive pericarditis . Assessment of diastolic heart function, though usually obtained with Doppler-echocardiography, can be achieved with velocity-encoded or phase-contrast CMR technique too [11, 20, 21]. Analysis of pulmonary and/or systemic venous pattern in combination with cardiac inflow patterns through the atrioventricular valves can yield findings that are classic for restrictive cardiac filling.
To conclude, improvements in CMR technology have shifted the way this technique can be applied to study the pericardium from basically a static morphologic assessment toward an integrated dynamic morphological-functional approach, raising the hope to improve diagnostic testing to the often complex and intriguing group of pericardial disorders (Appendix 1).
Congenital pericardial anomalies
Congenital pericardial agenesis is an uncommon entity, and is considered to result from an abnormal embryonic development that may be secondary to abnormalities in the vascular supply of the pericardium. Pericardial defects occur in a spectrum ranging from a small defect to total absence of the pericardium. Partial defects (large more common than small partial defects) are far more common than total defects [27, 30]. It may be associated, in at least one-third of cases, with other malformations, particularly malformations of the heart (tetralogy of Fallot, atrial septal defect, patent ductus arteriosus) or other types of abnormalities (bronchogenic cyst or hiatus hernia) [31, 32]. Cardiac structures or portions of the lung can herniate through the defect. The clinical presentation is variable. Patients are often asymptomatic, and the disease may be detected on routine chest radiograph as an abnormal left cardiac contour . Symptoms occur when cardiac structures are transiently entrapped or incarcerated in the defect. Herniation of the left atrial appendage through a small defect may lead to infarction of the appendage or the left coronary artery might be compressed leading to ischaemia especially during exercise .
The diagnosis of a pericardial defect is not always straightforward on CMR, since in normal conditions the pericardium over the lateral side of the left ventricle, corresponding to the most frequent location of pericardial defects, is usually not well depicted because of a paucity of surrounding fat . So, the diagnosis usually relies on other signs such as an abnormal location of cardiac structures with excessive levorotation or cardiac indentation at the location of the defect [35, 36]. Since herniation is often intermittent in time, positional changes such as to positioning the patient in left lateral decubitus can be helpful in diagnosing pericardial defects. Functional examination may be helpful in establishing the diagnosis of congenital pericardial defect. Whereas the normal cardiac apex is essentially stationary in the chest during the cardiac cycle, excessive mobility may be indicative of a pericardial defect .
Pericardial diverticulum is an exceedingly rare condition that can be congenital or acquired. It corresponds to a herniation through a defect in the parietal pericardium that communicates with the pericardial cavity . Congenital diverticula result from a failure in the fusion of one of the mesenchymal lacunae that normally concur to form the pericardial sac. They typically occur in the cardiophrenic angles and have the tendency to change in size over time. CMR is helpful in reaching a preoperative diagnosis. Although it resembles a pericardial cyst, the diagnosis of a diverticulum should be suspected when a complete wall cannot be identified in all parts of the lesion .
Acquired pericardial diseases
Additional file 1: Moderate pericardial effusion with signs of cardiac tamponade. Moderate pericardial effusion with collapse of right atrial and right ventricular wall during the cardiac cycle. (AVI 5 MB)
Analysis of CMR signals enables, at least to some extent, fluid characterization. Transudates typically have a low signal intensity on T1-weighted spin-echo CMR, and a high signal intensity on T2-weighted sequences. Exudates, having a high protein and cell content, increase T1-relaxation (higher signal intensity) and shorten T2-relaxation (lower signal intensity)(Figs. 3, 4). However, because of motion artifacts, pericardial fluid characterization is not always feasible. In particular non-linear motion of pericardial fluid during cardiac motion may falsely cause high signal on T1-weighted spin-echo CMR within the effusion even in the presence of a simple transudate. Moreover characterization of small effusions may be often difficult. The signal intensity of a hemorrhagic pericardial effusion is dependent on the duration of the disease (see pericardial hematoma). With balanced SSFP-gradient-echo techniques, often a better characterization of the pericardial fluid content can be achieved such as the visualization of fibrinous strands or presence of coagulated blood. Other abnormalities helpful in the diagnosis are depiction of thickened pericardial blades with assessment of pericardial inflammation [11, 17].
Inflammation of the pericardium (inflammatory pericarditis) presents in many clinical settings and has a wide range of causes . The acute presentation is an important differential in the assessment of acute chest pain, but pericarditis can also present in subacute or chronic forms. The symptoms are mainly related to the severity of pericardial inflammation. Although the true incidence and prevalence of pericarditis are difficult to measure, a prevalence of 1% in autopsy studies suggests that pericarditis may be subclinical . In up to 30% of patients no cause of pericarditis can be defined (idiopathic). Infections (viral/bacterial/tuberculosis/fungal) are common causes of acute pericarditis. It can be noted that organisms responsible for myocarditis are commonly implicated. In developed countries, tuberculosis has become less common, but should still be considered in immunocompromised hosts [1, 2, 42]. Radiation therapy for treatment of mediastinal tumors and breast cancer is an increasingly important cause of pericarditis and pericardial constriction. Pericarditis can be a manifestation of various systemic diseases (e.g. rheumatoid arthritis, systemic lupus erythematosus, scleroderma); can be secondary to primary or metastatic pericardial disease, and can be found in patients with uremia or following an acute myocardial infarction. The latter occurs early postinfarction and is typically found in transmural infarctions. This condition should be differentiated from late postinfarction pericarditis (Dressler's syndrome). While acute post-infarction pericarditis, also called "epistenocardic pericarditis", has a close temporal relation with the acute event due to the pericardial spread of infarct-related inflammation, Dressler's syndrome has an autoimmune etiology without a close temporal relation with myocardial infarction. Finally, direct or indirect trauma can cause traumatic pericarditis.
In the acute phase, inflammation of the pericardial layers is characterized by formation of young, highly vascularized granulation tissue with fibrin deposition . Usually, a variable amount of pericardial fluid is present, and the fibrin deposition may lead to a fibrinous adhesion of the pericardial layers. Chronic inflammation is characterized by a progressive sclerosing pericarditis with fibroblasts, collagen and a lesser amount of fibrin deposition . This may progress towards an end-stage, chronic fibrosing pericarditis with fibroblasts and collagen. The main feature of this end-stage is a stiff pericardium with constriction of the heart (constrictive pericarditis).
Chronic fibrosing pericarditis is characterized by a thickened, fibrotic and/or calcified pericardium, not infrequently constricting the heart and impairing cardiac filling ("constrictive" pericarditis) . Patients with pericardial constriction typically present with manifestations of elevated systemic venous pressures and low cardiac output . The diagnosis should always be considered in patients presenting with predominant right heart failure symptoms . The pathophysiological hallmarks of pericardial constriction, which are caused by confinement of the cardiac chambers by the rigid, fixed pericardial volume, are equalization of end-diastolic pressures in all 4 cardiac chambers, and increased ventricular coupling which is strongly influenced by respiration [1, 2].
Pericardial constriction is most commonly idiopathic but can be the end result of any cause of inflammatory pericarditis. Tuberculosis has become less frequent, while cardiac surgery and radiation-induced pericarditis have become also important . In non-tuberculous pericarditis pericardial thickening and calcification may be less prominent. In radiation therapy, systolic dysfunction may accompany constriction and is a marker of poor prognosis after pericardiectomy. Pathology typically shows an avascular collagen-rich, fibrotic tissue, often containing areas of calcification. Moreover, in extensive cases the fibrosing process may be adherent or even involve the myocardium.
Today, despite a wide arsenal diagnostic tools, the diagnosis of constrictive pericarditis often remains a challenge, and the diagnostic approach taken should be individualized for each patient. First, all other causes of (right) heart failure (e.g. pulmonary hypertension, LV/RV infarction) should be excluded. Second, it should be determined whether the pericardium is causing constriction hereby impeding cardiac filling, and thirdly whether the patient will benefit of a pericardial stripping. One of the major dilemmas, is that diseases with decreased myocardial compliance, such as restrictive cardiomyopathy, are also characterized by impaired cardiac filling, and may present in a very similar way. Distinction between the two entities is crucial, because constrictive pericarditis patients are potentially successfully treated by early pericardiectomy whilst for restrictive cardiomyopathy medical treatment is recommended [46–50]. Several other factors may hamper straightforward diagnosis of constrictive pericarditis. The morphologic pericardial abnormalities classically found in constrictive pericarditis may be not impressive, be absent or have an atypical presentation. Moreover, increased pericardial thickness does not necessarily imply pericardial constriction, and vice versa . Finally, for instance in patients with a history of radiation therapy, restrictive cardiomyopathy and constrictive pericarditis may simultaneously occur. This makes the diagnosis of constrictive pericarditis, especially in atypical or complex cases, often challenging. Since no one method is completely reliable, information from more than one imaging technique should be considered to provide an assessment of anatomical and physiological function .
Though beyond the scope of this paper, it should be emphasized CMR has an increasingly important role in investigating patients with restrictive cardiomyopathy . Myocardial enhancement patterns on LGE CMR may be strongly indicative of specific myocardial infiltrative or storage diseases, while T2*-weighted CMR may be used to non-invasively depict iron deposition cardiomyopathy .
Functional and Haemodynamic Abnormalities
The consequences of encasement of the heart by a rigid pericardium are basically threefold, (a) dissociation between intrathoracic and intracardiac pressure, isolating the heart from normal respiratory changes in intrathoracic pressure, (b) increased ventricular coupling, (c) increased cardiac filling pressures with pressure equalization in all 4 cardiac chambers. Assessment of these effects is usually performed by echocardiography and cardiac catheterization, [1, 2, 46, 64–67]. CMR, with the exception of intracardiac pressure measurements, may provide valuable information too, and has the intrinsic advantage that findings may be directly linked to morphologic abnormalities. Velocity-encoded CMR typically shows a restrictive filling pattern with an enhanced early filling, and decreased or absent late filling, depending on the degree of pericardial constriction and increased filling pressures. Also the venous flow patterns may show restrictive physiology with diminished or absent forward, or even reversed systolic flow, and increased early diastolic forward flow and late backflow. Constrictive pericarditis, in contrast with restrictive myocarditis, is typically characterized by a strong respiratory-related variation in cardiac filling (i.e., enhanced RV filling on inspiration, enhanced LV filling on expiration)[65, 66]. Real-time velocity CMR is a potential alternative to echo-Doppler to assess the effects of respiration on cardiac filling, though ideally slice-tracking techniques are needed to compensate for through-plane motion .
Assessment of pericardial mobility is another potential application of dynamic CMR, and is appealing to differentiate normal from rigid pericardium (Fig. 8) [see Additional file 3]. The latter exhibits no or at most a limited displacement, while normal pericardium slightly moves during the cardiac cycle, often in synchronicity with the underlying myocardial motion. Moreover, the restricted expansion of the myocardium during cardiac filling abutting against the stiff pericardium can be well appreciated. These issues may be important in diagnosing patients with minimally or non-thickened constrictive pericarditis. CMR tagging may be of help to demonstrate extension of the fibrocalcific process into the underlying myocardium.
Other entities that have a mass-like appearance are pericardial hematoma and pericardial gossypiboma. The appearance and CMR signal characteristics of a pericardial hematoma depends on the age of the collection . Pericardial gossypiboma or foreign body granuloma should be considered in patients with previous cardiac surgery. In the pericardium, it includes surgical sponges in the pericardial space overlooked after pericardiectomy [11, 79].
The added value of CMR compared to the standard techniques used for assessment of patients with pericardial diseases has substantially increased in recent years, questioning whether this technique should not be considered the most appropriate non-invasive modality to study the pericardium. Strong points in favor of CMR are the integration of anatomic and functional information within a single examination, the ability for tissue characterization and to determine the presence and degree of inflammation and activity of disease, and the value of CMR to accurately assess the rest of the heart, in particular the myocardium, helpful in the differential diagnosis, which currently often remains a diagnostic challenge.
CMR strategies to evaluate the pericardium
* Pericardial morphology (spin-echo CMR/cine CMR)
* Pericardial layer/fluid characterization (T1w/T2w spin-echo CMR/cine CMR/gadolinium-enhanced CMR)
* Pericardial function
motion pattern (cine CMR)
fusion of pericardial layers (CMR tagging)
* Cardiac morphology (spin-echo CMR, cine CMR)
size and shape of ventricles and ventricles
myocardial morphology (restrictive cardiomyopathy)
* Cardiac systolic function (cine CMR)
regional and global systolic ventricular function
* Cardiac filling (velocity-encoded CMR)
* Ventricular coupling (real-time cine CMR)
ventricular septal shape and septal motion patterns
respiratory-related septal shift
* Other findings (spin-echo CMR/cine CMR/gadolinium-enhanced CMR)
myocardial enhancement (associated myocarditis? myocardial infiltrative or storage disease?)
caval vein size
The authors would like to thank Steven Dymarkowski MD, PhD, Javier Ganame MD, PhD, and Andrew M. Taylor MD, PhD for their help in preparing this manuscript.
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