Pericardial Disease

HomeCirculationVol. 113, No. 12Pericardial Disease Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBPericardial Disease William C. Little and Gregory L. Freeman William C. LittleWilliam C. Little From the Cardiology Section, Wake Forest University School of Medicine, Winston-Salem, NC (W.C.L.); and Departments of Medicine and Physiology, University of Texas Health Science Center–San Antonio, South Texas Veteran’s Health Care System, San Antonio, Tex (G.L.F.). Search for more papers by this author and Gregory L. FreemanGregory L. Freeman From the Cardiology Section, Wake Forest University School of Medicine, Winston-Salem, NC (W.C.L.); and Departments of Medicine and Physiology, University of Texas Health Science Center–San Antonio, South Texas Veteran’s Health Care System, San Antonio, Tex (G.L.F.). Search for more papers by this author Originally published28 Mar 2006https://doi.org/10.1161/CIRCULATIONAHA.105.561514Circulation. 2006;113:1622–1632is corrected byCorrectionIn contrast to coronary artery disease, heart failure, valvular disease, and other topics in the field of cardiology, there are few data from randomized trials to guide physicians in the management of pericardial diseases. Although there are no American Heart Association/American College of Cardiology guidelines on this topic, the European Society of Cardiology has recently published useful guidelines for the diagnosis and management of pericardial diseases.1 Our review focuses on the current state of knowledge and the management of the most important pericardial diseases: acute pericarditis, pericardial tamponade, pericardial constriction, and effusive constrictive pericarditis.The Normal PericardiumThe pericardium is a relatively avascular fibrous sac that surrounds the heart. It consists of 2 layers: the visceral and parietal pericardium. The visceral pericardium is composed of a single layer of mesothelial cells that are adherent to the cardiac epicardium.2,3 The parietal pericardium is a fibrous structure that is <2 mm thick and is composed primarily of collagen and a lesser amount of elastin. The 2 layers of the pericardium are separated by a potential space that can normally contain 15 to 35 mL of serous fluid distributed mostly over the atrial-ventricular and interventricular grooves.The pericardium surrounds the heart and attaches to the sternum, the diaphragm, and the anterior mediastinum and is invested around the great vessels and the venae cavae, serving to anchor the heart in the central thorax. Because of its location, the pericardium may also function as a barrier to infection.The pericardium is well innervated such that pericardial inflammation may produce severe pain and trigger vagally mediated reflexes. The pericardium also secretes prostaglandins that modulate cardiac reflexes and coronary tone.4As a result of its relatively inelastic physical properties, the pericardium limits acute cardiac dilatation and enhances mechanical interactions of the cardiac chambers.5 In response to long-standing stress, the pericardium dilates, shifting the pericardial pressure-volume relation substantially to the right (Figure 1).6–8 This allows a slowly accumulating pericardial effusion to become quite large without compressing the cardiac chambers and for left ventricular remodeling to occur without pericardial constriction. Download figureDownload PowerPointFigure 1. Pericardial pressure-volume relations determined in pericardium obtained from a normal experimental animal and from an animal with chronic cardiac dilation produced by volume loading. The pericardial pressure-volume relation is shifted to the right in the volume-loaded animal, demonstrating that the pericardium can dilate to accommodate slowly increasing volume. Reproduced with permission from Freeman and LeWinter.6 Copyright 1984, American Heart Association.Despite the known important functions of the normal pericardium, congenital absence or surgical resection of the pericardium does not appear to have any major untoward effects.9Acute PericarditisEtiologyAcute inflammation of the pericardium with or without an associated pericardial effusion can occur as an isolated clinical problem or as a manifestation of systemic diseases.1,10–13 Although as many as 90% of isolated cases of acute pericarditis are idiopathic or viral, the list of other potential causes is extensive (Table 1). Although formerly common, tuberculous and bacterial infections have become rare causes of pericarditis.14 Other causes of acute pericarditis include uremia,15 collagen vascular diseases,16 neoplasms, and pericardial inflammation after an acute myocardial infarction or pericardial injury.17TABLE 1. Causes of Acute PericarditisIdiopathicInfections (viral, tuberculosis, fungal)UremiaAcute myocardial infarction (acute, delayed)NeoplasmPost–cardiac injury syndrome (trauma, cardiothoracic surgery)Systemic autoimmune disease (systemic lupus erythematosus, rheumatoid arthritis, ankylosing spondylitis, systemic sclerosing periarteritis nodosa, Reiter’s syndrome)After mediastinal radiationPericarditis after an acute myocardial infarction most commonly occurs 1 to 3 days after transmural myocardial infarction presumably because of the interaction of the healing necrotic epicardium with the overlying pericardium. A second form of pericarditis associated with myocardial infarction (Dressler’s syndrome) typically occurs weeks to months after a myocardial infarction. It is similar to the pericarditis that may occur days to months after traumatic pericardial injury, after surgical manipulation of the pericardium, or after a pulmonary infarction.18 This syndrome is presumed to be mediated by an autoimmune mechanism and is associated with signs of systemic inflammation, including fever, and polyserositis. The frequency of pericarditis after myocardial infarction has been reduced by the use of reperfusion therapy.19Clinical ManifestationsMost patients with acute pericarditis experience sharp retrosternal chest pain that can be quite severe and debilitating. In some cases, however, pericarditis may be asymptomatic, as is often the case with the pericarditis accompanying rheumatoid arthritis. Pericardial pain is usually worse with inspiration and when supine and is relieved by sitting forward. Typically, pericardial pain is referred to the scapular ridge, presumably due to irritation of the phrenic nerves, which pass adjacent to the pericardium.12 The chest pain of acute pericarditis must be differentiated from that of pulmonary embolism and myocardial ischemia/infarction (Table 2).10TABLE 2. Differentiation of Pericarditis From Myocardial Ischemia/Infarction and Pulmonary EmbolismMyocardial Ischemia or InfarctionPericarditisPulmonary EmbolismAdapted with permission from Lange and Hillis.10 Copyright 2004, Massachusetts Medical Society.Chest pain CharacterPressure-like, heavy, squeezingSharp, stabbing, occasionally dullSharp, stabbing Change with respirationNoWorsened with inspirationIn phase with respiration (absent when the patient is apneic) Change with positionNoWorse when supine; improved when sitting up or leaning forwardNo DurationMinutes (ischemia); hours (infarction)Hours to daysHours to days Response to nitroglycerinImprovedNo changeNo changePhysical examination Friction rubAbsent (unless pericarditis is present)Present in 85% of patientsRare; a pleural friction rub is present in 3% of patientsECG ST-segment elevationLocalized convexWidespread concaveLimited to lead III, aVF, and V1 PR-segment depressionRareFrequentNone Q wavesMay be presentAbsentMay be present in lead III or aVF or both T wavesInverted when ST segments are still elevatedInverted after ST segments have normalizedInverted in lead II, aVF, or V1 to V4 while ST segments are elevatedThe pericardial friction rub is the classic finding in patients with acute pericarditis. It is a high-pitched, scratchy sound that can have 1, 2, or 3 components. These components occur when the cardiac volumes are most rapidly changing: during ventricular ejection, during rapid ventricular filling in early diastole, and during atrial systole. Thus, patients with atrial fibrillation have only 1 or 2 component rubs. The pericardial friction rub can be differentiated from a pleural rub, which is absent during suspended respiration, whereas the pericardial rub is unaffected. Although it is easy to imagine that the pericardial rub arises from the inflamed visceral and parietal layers of the pericardium rubbing together, most patients with acute pericarditis (including those with audible rubs) have at least a small pericardial effusion, which should lubricate the interaction of the 2 layers of the pericardium.12Early in the course of acute pericarditis, the ECG typically displays diffuse ST elevation in association with PR depression (Figure 2).12 The ST elevation is usually present in all leads except for aVR, but in post–myocardial infarction pericarditis, the changes may be more localized. Classically, the ECG changes of acute pericarditis evolve through 4 progressive stages: stage I, diffuse ST-segment elevation and PR-segment depression; stage II, normalization of the ST and PR segments; stage III, widespread T-wave inversions; and stage IV, normalization of the T waves.12 Patients with uremic pericarditis frequently do not have the typical ECG abnormalities.19Download figureDownload PowerPointFigure 2. ECG demonstrating typical features seen on presentation of acute pericarditis. There is diffuse ST elevation and PR depression except in aVR, where there is ST depression and PR elevation.Patients with acute pericarditis usually have evidence of systemic inflammation, including leukocytosis, elevated erythrocyte sedimentation rate, and increased C-reactive protein. A low-grade fever is common, but a temperature >38°C is unusual and suggests the possibility of purulent bacterial pericarditis.10,20Troponin is frequently minimally elevated in acute pericarditis, usually in the absence of an elevated total creatine kinase.21,22 Presumably, this is due to some involvement of the epicardium by the inflammatory process. Although the elevated troponin may lead to the misdiagnosis of acute pericarditis as a myocardial infarction, most patients with an elevated troponin and acute pericarditis have normal coronary angiograms.22 An elevated troponin in acute pericarditis typically returns to normal within 1 to 2 weeks and is not associated with a worse prognosis.10Echocardiography usually demonstrates at least a small pericardial effusion in the presence of acute pericarditis. It is also helpful in excluding cardiac tamponade (see below). Pericardiocentesis is indicated if the patient has cardiac tamponade (see below) or in suspected purulent or malignant pericarditis.1,10,23 In the absence of these situations, when the cause of the acute pericarditis is not apparent on the basis of routine evaluation, pericardiocentesis and pericardial biopsy rarely provide a diagnosis and thus are not indicated.23,24TreatmentIf acute pericarditis is a manifestation of an underlying disease, it often responds to the treatment of the primary condition. For example, uremic pericarditis usually resolves with adequate renal dialysis.15 Most acute idiopathic or viral pericarditis is a self-limited disease that responds to treatment with aspirin (650 mg every 6 hours) or another nonsteroidal antiinflammatory agent (NSAID). The intravenous administration of ketorolac, a parenteral NSAID, was effective in relieving the pain of acute pericarditis in 22 consecutive patients.25 Aspirin may be the preferred nonsteroidal agent to treat pericarditis after myocardial infarction because other NSAIDs may interfere with myocardial healing.10 Indomethacin should be avoided in patients who may have coronary artery disease.If the pericardial pain and inflammation do not respond to NSAIDs or if the acute pericarditis recurs, colchicine has been observed to be effective in relieving pain and preventing recurrent pericarditis.26 The routine use of colchicine is supported by recently reported results of the Colchicine for Acute Pericarditis (COPE) Trial.27 One hundred twenty patients with a first episode of acute pericarditis (idiopathic, acute, postpericardiotomy syndrome, and connective tissue disease) entered a randomized, open-label trial comparing aspirin plus colchicine (1.0 to 2.0 mg for the first day followed by 0.5 to 1.0 mg/d for 3 months) with treatment with aspirin alone. Colchicine reduced symptoms at 72 hours (11.7% versus 36.7%; P≤0.03) and recurrence at 18 months (10.7% versus 36.7%; P=0.004; number needed to treat=5). Colchicine was discontinued in 5 patients because of diarrhea. No other adverse events were noted. Importantly, none of 120 patients developed cardiac tamponade or progressed to pericardial constriction.28Although acute pericarditis usually responds dramatically to systemic corticosteroids, their use early in the course of acute pericarditis appears to be associated with increased incidence of relapse after tapering the steroids.28,29 An observational study strongly suggests that use of steroids increases the probability of relapse in patients treated with colchicine.30 Furthermore, in the COPE Trial, steroid use was an independent risk factor for recurrence (odds ratio=4.3).27 Accordingly, systemic steroids should be considered only in patients with recurrent pericarditis unresponsive to NSAIDs and colchicine or as needed for treatment of an underlying inflammatory disease. If steroids are to be used, an effective dose (1.0 to 1.5 mg/kg of prednisone) should be given, and it should be continued for at least 1 month before slow tapering.31 Experts have suggested that a detailed search for the cause of recurrent pericarditis should be undertaken before steroid therapy is initiated in resistant or relapsing cases of pericarditis.1,28The intrapericardial administration of steroids has been reported to be effective in acute pericarditis without producing the frequent reoccurrence of pericarditis that complicates the use of systemic steroids, but the invasive nature of this procedure limits its utility.29,32 A very few patients with frequent, highly symptomatic recurrences of pericarditis despite intensive medical therapy may require surgical pericardiectomy.32 However, painful relapses can occur even after pericardiectomy, especially if the pericardium is not completely removed.28Most patients with acute pericarditis recover without sequelae. Predictors of a worse outcome include the following: fever >38°C, symptoms developing over several weeks in association with immunosuppressed state, traumatic pericarditis, pericarditis in a patient receiving oral anticoagulants, a large pericardial effusion (>20 mm echo-free space or evidence of tamponade), or failure to respond to NSAIDs.20 In a recent series of 300 patients with acute pericarditis, 254 (85%) did not have any of the high-risk characteristics and had no serious complications.20 Of these low-risk patients, 221 (87%) were managed as outpatients, and the other 13% were hospitalized when they did not respond to aspirin.20On the basis of these considerations, we manage patients presenting with acute pericarditis in the following manner. Patients are hospitalized but are discharged in 24 to 48 hours if they have no high-risk factors and their pain has improved. Initial therapy includes aspirin (650 to 975 mg every 6 to 8 hours) and colchicine (2 g initially followed by 1 g/d). In addition, we use a proton pump inhibitor in most patients to improve the gastric tolerability of the aspirin. We advise against exercise until after the chest pain completely resolves. Even if the pain responds promptly, we continue aspirin for 4 weeks and colchicine for 3 months to minimize the risk of recurrent pericarditis. If pericarditis reoccurs, we reload with colchicine and use intravenous ketorolac (30 mg every 6 hours) and then continue an oral NSAID and colchicine for at least 3 more months. We make every effort to avoid the use of steroids, reserving steroids for patients who cannot tolerate aspirin and other NSAIDs or who have a recurrence not responsive to colchicine and intravenous NSAIDs.It is important to recognize that there are no clear data to guide this set of recommendations. In general, if a recurrence of pericarditis is mild it can be treated with intensification of NSAID therapy; various combinations of aspirin, NSAIDS, and colchicine have been successfully applied in such cases.Cardiac TamponadePathophysiologyCardiac tamponade occurs when fluid accumulation in the intrapericardial space is sufficient to raise the pressure surrounding the heart to the point where cardiac filling is altered. Ultimately, compression of the heart by a pressurized pericardial effusion results in markedly elevated venous pressures and impaired cardiac output producing shock; if untreated, it can be rapidly fatal.33Under normal conditions, the space between the parietal and visceral pericardium can accommodate only a small amount of fluid before the development of tamponade physiology. It is not surprising, therefore, that cardiac perforation quickly results in tamponade. With a gradually accumulating effusion, however, as is often the case in malignancy, very large effusions can be accommodated without tamponade (Figure 1). The key concept is that once the total intrapericardial volume has caused the pericardium to reach the noncompliant region of its pressure-volume relation, tamponade rapidly develops.Because of its lower pressures, the right heart is most vulnerable to compression by a pericardial effusion, and abnormal right heart filling is the earliest sign of a hemodynamically significant pericardial effusion. Under these conditions, adequate filling of the right heart requires a compensatory increase in systemic venous pressure, which results from venoconstriction and fluid retention. Of note, when cardiac tamponade results from hemorrhage into the pericardium, there can be rapid circulatory collapse because not only does pericardial pressure rapidly rise but intravascular volume falls, preventing a compensatory increase in venous pressure.The increased pericardial pressure in cardiac tamponade accentuates the interdependence of the cardiac chambers as the total cardiac volume is limited by the pericardial effusion.33–36 The volume in any cardiac chamber can only increase when there is an equal decrease in the volume in other chambers. Thus, venous return and atrial filling predominantly occur during ventricular systole as the ejection of blood out of the right and left ventricles lowers cardiac volume and allows blood to enter the atria. Moreover, the normal effects of respiration are accentuated such that venous return and right-sided filling occur during inspiration as intrathoracic pressures fall, providing a pressure gradient from the systemic veins to the right atrium. Because the total intrapericardial volume is fixed by the pressurized effusion, this increased inspiratory right ventricular filling crowds the left ventricle and impairs its filling. Thus, in tamponade, left heart filling occurs preferentially during expiration when there is less filling of the right heart. The small normal respiratory variation in left ventricular stroke volume and systolic arterial pressure is markedly accentuated in cardiac tamponade, resulting in the clinical finding of “paradoxical pulse” (see below).Clinical PresentationCardiac tamponade is a treatable cause of cardiogenic shock that can be rapidly fatal if unrecognized. As such, cardiac tamponade should be considered in the differential diagnosis of any patients with shock or pulseless electric activity.1Patients with impending or early tamponade are usually anxious and may complain of dyspnea and chest pain.33 The increased venous pressure is usually apparent as jugular venous distension. The X descent (during ventricular systole) is typically the dominant jugular venous wave with little or no Y descent. In rapidly developing cardiac tamponade, especially hemorrhagic cardiac tamponade, there may not have been time for compensatory increase in venous pressure, and the jugular veins may not be distended. Such “low-pressure” tamponade may also occur in patients with uremic pericarditis who have been volume depleted.37 The heart sounds are classically soft or muffled, especially if there is a large pericardial effusion.The hallmark of cardiac tamponade is a paradoxical pulse. This is defined as a >10-mm Hg drop in systolic arterial pressure during inspiration.1 When severe, the paradoxical pulse can be apparent as an absence of a palpable brachial or radial pulse during inspiration. A paradoxical pulse can also occur when there are wide swings in intrathoracic pressure and in other conditions such as pulmonary embolism and hypovolemic shock. It is important to recognize that the paradoxical pulse may be difficult to recognize in the presence of severe shock and may be absent in cardiac tamponade if there is coexisting aortic insufficiency, atrial septal defect, or preexisting elevated left ventricular end-diastolic pressure due to left ventricular hypertrophy or dilatation.33,38EchocardiographyEchocardiography is an important part of the evaluation in patients with cardiac tamponade and should be performed without delay in any patient who is suspected of having this condition.39 Echocardiography visualizes pericardial effusions as an echo-free space around the heart (Figure 3). Patients with acute hemorrhagic effusions may have pericardial thrombus apparent as an echo-dense mass.40 Small pericardial effusions are only seen posteriorly. Pericardial effusions large enough to produce cardiac tamponade are almost always circumferential (both anteriorly and posteriorly).2Download figureDownload PowerPointFigure 3. A, Two-dimensional echocardiogram in 4-chamber view from a patient with cardiac tamponade. There is a large pericardial effusion apparent as an echo-free space around the heart. In diastole, there is collapse of the right atrium (arrow). B, Doppler measurement of mitral valve and tricuspid flow velocities in a patient with cardiac tamponade. There is marked reciprocal respiratory variation: during inspiration, mitral valve flow velocity decreases, and tricuspid valve flow velocity increases.Echocardiography can also provide information on the significance of the pericardial effusion.41 In the presence of cardiac tamponade, there is diastolic collapse of the free walls of the right atrium and/or right ventricle.42,43 This is due to compression of these relatively low-pressure structures by the higher-pressure pericardial effusion. The collapse is exaggerated during expiration when right heart filling is reduced. Right atrial collapse is more sensitive for tamponade, but right ventricular collapse lasting more than one third of diastole is a more specific finding for cardiac tamponade. Of note, right ventricular collapse may also be present with large pleural effusions in the absence of pericardial effusion or cardiac tamponade.44There are other echo-Doppler findings that are indicative of the hemodynamic consequence of cardiac tamponade.41,45 Distention of the inferior vena cavae that does not diminish with inspiration is a manifestation of the elevated venous pressure in tamponade,46 whereas venous flow predominantly occurs in systole, not diastole, because of the limited cardiac volume.47 In addition, there can be marked reciprocal respiratory variation in mitral and tricuspid flow velocities reflecting the enhanced ventricular interdependence that is the mechanism of the paradoxical pulse (Figure 3).48 Collapse of right-sided chambers is a sensitive indicator of tamponade, but abnormalities of cardiac filling are a more specific finding.47Thus, echocardiography demonstrates the presence and size of the pericardial effusion and reflects its hemodynamic consequences. Right atrial and ventricular collapse indicates cardiac compression, whereas enhanced respiratory variation of ventricular filling is a manifestation of increased ventricular interdependence. Although echocardiography provides important information, it must be emphasized that cardiac tamponade is ultimately a clinical diagnosis (see below).47TreatmentThe treatment of cardiac tamponade is drainage of the pericardial effusion. Medical management is usually ineffective and should be used only while arrangements are made for pericardial drainage. Fluid resuscitation may be of transient benefit if the patient is volume depleted (hypovolemic cardiac tamponade). The use of inotropic agents is usually ineffective because there is already intense endogenous adrenergic stimulation. The initiation of mechanical ventilation in a patient with tamponade may produce a sudden drop in blood pressure because the positive intrathoracic pressure will contribute to a further impairment of cardiac filling.39In the absence of clinical evidence of tamponade, echocardiographic findings of right-sided diastolic collapse do not mandate emergency pericardiocentesis. For example, we do not recommend emergency pericardial drainage in a patient who has a nontraumatic pericardial effusion with right-sided collapse if there is an adequate stable blood pressure (>110 mm Hg systolic) without a paradoxical pulse (ie, <10 mm respiratory variation in systolic pressure). However, the patient must be observed carefully because the development of only a small additional amount of pericardial fluid can result in tamponade. In some patients, the echocardiographic signs of cardiac compression will resolve within a few days, and pericardiocentesis can be avoided if there is no other indication.Traditionally, nonemergent pericardiocentesis has been performed in the cardiac catheterization laboratory under fluoroscopic guidance with invasive hemodynamic monitoring.1 Performing pericardiocentesis in this setting provides the option of utilizing right heart catheterization before and after the procedure to confirm the diagnosis, if necessary, and to detect effusive-constrictive pericardial disease (see below). More recently, echocardiographic-guided pericardiocentesis has been demonstrated to be a safe and effective procedure that can be performed at the bedside.49 During this procedure the ideal entry site (minimal distance from skin to pericardial fluid without intervening structures) can be defined. Continued drainage of the pericardial fluid through an indwelling catheter minimizes the risk of reoccurrence of the effusion. If pericardial tissue is required for diagnosis or in the case of purulent pericarditis or recurrent effusions, surgical drainage may be the preferred treatment. Surgery is also the treatment for traumatic hemopericardium.1Surgical drainage of a pericardial effusion is usually performed through a limited subxiphoid incision. This allows direct visualization and biopsy of the pericardium. The diagnosis accuracy can be improved by inserting a pericardioscope.50 This provides direct visualization of a much larger area of the pericardium and the ability to obtain multiple biopsies. Recently, a flexible pericardioscope has been developed that can be inserted percutaneously.51Malignant pericardial effusions frequently reoccur. Such recurrent pericardial effusions may necessitate the surgical creation of a pericardial window that allows the effusion to drain into the pleural space, preventing reoccurrence of cardiac tamponade. An attractive alternative in these patients, especially if their overall prognosis is poor from the malignancy, is the percutaneous creation of a pericardial window by balloon dilation.52,53Pericardial Effusion Without TamponadeAcute pericarditis is often accompanied by a small pericardial effusion that does not produce tamponade.20 If there is no hemodynamic compromise and the diagnosis can be established by other means, pericardiocentesis may not be necessary.1,23,54 If it accumulates slowly, a large pericardial effusion of a liter or more can be present without cardiac tamponade. However, nearly 30% of a series of 28 patients with large idiopathic pericardial effusions developed cardiac tamponade unexpectedly.55 In this series, pericardiocentesis with catheter drainage alone resulted in resolution of the effusion without reoccurrence in about half of the patients. Thus, pericardiocentesis may be advisable in patients with very large pericardial effusions (>20 mm on echocardiography), even in the absence of tamponade. In contrast, Merce et al47 demonstrated that none of 45 patients with large pericardial effusions managed without pericardial drainage subsequently developed tamponade. It must be recognized that pericardiocentesis will not yield a diagnosis in most patients, and therefore the reason for draining large effusions is to avoid potential progression to tamponade.47 We believe that the risk of progression to tamponade is greatest in patients with the recent development of large effusions or who have evidence of diastolic right-sided collapse. Some experts have recommended routine drainage of pericardial effusions that persist for >3 months.54 We do not believe that this is necessary. A potential algorithm for the management of pericardial effusions is shown in Figure 4. Download figureDownload PowerPointFigure 4. Potential algorithm for managing patients with a moderate to large pericardial effusion. See the text for a discussion of methods to drain the pericardial effusion. Adapted and redrawn with permission from Hoit.54 Copyright 2002, American Heart Association.Pericardial ConstrictionPathophysiologyPericardial constriction occurs