Volume 17, Issue 7 , Pages 457-464, November 2006
Constrictive pericarditis: A reminder of a not so rare disease
Article Outline
- Abstract
- 1. Introduction
- 2. Pathophysiology
- 3. Etiology and pathology
- 4. Clinical features
- 5. Additional examinations
- 6. Learning points
- Acknowledgements
- References
- Copyright
Abstract
Constrictive pericarditis is a rare condition characterized by clinical signs of right heart failure subsequent to loss of pericardial compliance. The etiology of constrictive pericarditis has changed during the last decades in developed countries. While, in the past, tuberculosis and idiopathic pericardial constriction were the prevalent causes of the disease, cardiac surgery has become one of the main reasons for its development in recent years. However, cases defined as idiopathic constrictive pericarditis are still observed. In addition to the classical chronic and subacute forms, new presentations, such as effusive-constrictive, localized, transient, occult, and constrictive pericarditis with normal pericardial thickness, have been described. Although conservative treatment may alleviate the patient's symptoms, pericardiectomy remains the only definitive treatment for the disease. It is worth noting that the sooner the diagnosis of pericardial constriction is established, the better the outcome is. The pathophysiological features, clinical findings, diagnostic tools, and therapeutic approach to constrictive pericarditis are detailed in this review.
Keywords: Constrictive pericarditis, Pericardium, Constriction
1. Introduction
Dyspnea and peripheral edema are common dilemmas, and detecting the cause of their appearance should not present difficulties for an experienced physician. The main diagnostic possibilities to be considered are the frequent causes of right heart failure. However, the differential diagnosis should comprise rare conditions accompanied by diseases of the pericardium, including constrictive pericarditis [1]. The description of constrictive pericarditis designated as concretio cordis dates back more than 300 years [2]. It presents mostly as chronic fibrous pericardial thickening, calcification of the pericardium, or both. However, in atypical forms, heart constriction may develop with a pericardium that is normal in thickness [3]. According to Hancock [4], compressive pericardial disease may be the sequel of tamponade, as well as either subacute (fibroelastic) or chronic (rigid shell) constriction. We review herein the natural history of this progressive and debilitating pericardial disease.
2. Pathophysiology
In the classical form of constrictive pericarditis, the rigid, heavily fibrosed, or even calcified pericardium causes restriction of the myocardium, preventing adequate ventricular filling after an initial expansion [2], [5]. Because of decreased pericardial compliance and increased venous pressure, the early diastolic filling occurs very rapidly and stops when the intracardiac volume and pressure reach their maximum limits. Since the myocardium in constrictive pericarditis is essentially not affected, relaxation of the left ventricle is usually normal, indicating that the abnormal compliance of the myocardium that results in elevated diastolic pressure equilibrium in all four chambers is due to the rigid pericardium [2], [6]. Consequently, the atrial waves on the jugular veins show a prominent and deep diastolic Y descent. The systolic X descent that reflects a fall in the right atrial pressure throughout early ventricular systole may create an M or W pattern of the venous wave [6].
The hallmarks of constrictive pericarditis are the hemodynamic changes observed during respiration. As a consequence of a diminished gradient between the pressure in the pulmonary veins and the left atrium during inspiration, the left-side flow decreases while the right-side flow increases. These alterations are due to pericardial rigidity that limits transmission of decreased intrathoracic pressure to the pericardial space [2], [5]. The existence of hemodynamic alterations in this condition may also be explained by the rigidity of the pericardium that limits heart relaxation during diastole with a subsequent increase in the right heart volume, causing higher pressure on the intraventricular septum. Subsequently, the septum moves to the left and the left-side volume decreases. Occasionally, the increased venous return from the overfilled splanchnic system elevates the abdominal and right atrial pressures during inspiration, resulting in an inspiratory distention of the jugular veins, a phenomenon designated as Kussmaul's sign [7]. Pulsus paradoxus, i.e., disappearance of the peripheral pulse during inspiration, is another clinical sign that can be found in patients with constrictive pericarditis. This interesting phenomenon is explained by impaired filling of the left ventricle with an enhanced decrease in the systolic pressure during inspiration caused either by fibrosed and calcified pericardium or by the accumulation of pericardial fluid [8]. Shabetai et al. [9] have shown that patients with constricted pericardium are not able to increase the flow velocity in either the vena cava or the pulmonary artery during inspiration, a finding that may be one of the mechanisms for the appearance of pulsus paradoxus. Pooling of blood in the pulmonary bed and filling competition of the ventricles in the presence of a fixed pericardial sac may serve as an additional cause for appearance of pulsus paradoxus [8].
3. Etiology and pathology
The common forms of constrictive pericarditis are the subacute “elastic” constriction and the classical, chronic “rigid” constrictive pericarditis. The elastic form of constrictive pericarditis, described by Hancock [4], presents with clinical features of tamponade, although the actual cause of the disease is pericardial constriction. While, in the past, the main cause of constrictive pericarditis was tuberculosis [2], [6], the etiology of the disease has changed during recent decades [10]. Nowadays, the most frequent causes of the illness in developed countries are prior cardiac surgery, irradiation therapy, and idiopathic pericarditis, while tuberculosis remains the main etiology of the disease in developing countries [11]. Bertog et al. [12] examined 163 patients who underwent pericardiectomy because of constrictive pericarditis over a 24-year period. Forty-six percent of the patients suffered from the idiopathic form, 37% underwent heart surgery, in 9% the disease developed after mediastinal irradiation, mostly for Hodgkin's disease, and in 3.5% the causative agent was tuberculosis. Rheumatoid arthritis, systemic lupus erythematosus, prior chest trauma, Wegener's granulomatosis, and purulent pericarditis were the reason for the disease in the remaining patients.
Ling et al. [13] compared two cohorts of patients after radical pericardiectomy, one who underwent surgery during the years 1936–1962 and the second during the years 1985–1995. The results showed that in patients undergoing surgery in the last 10 years, open-heart surgery and chest irradiation emerged as the most frequent causes of heart constriction. It is worth noting that in 12–18% of patients with constrictive pericarditis undergoing pericardiectomy, the pericardium was of a histologically proven normal thickness [3], [14]. The time interval between heart surgery and appearance of constrictive pericarditis ranges from 3 to 24 months, although it may be as short as 4 weeks [15]. Several factors, such as residual blood elements within the pericardial sac, trauma during the surgical procedure, pericardial irrigation with povidone-iodine solution, and low-grade infection may be implicated in the link between surgery and the development of heart constriction. The role of drugs and chemical substances as an additional cause of constrictive pericarditis should not be ignored. Hydralazine, procainamide, penicillin, minoxiline, isoniazide, and pergolide mesylate have been reported to be causative agents. Rare diseases, such as Mulibrey nanism, porphyria, asbestosis, and Whipple's disease, have been reported to be complicated by constrictive pericarditis [2], [16]. Before the era of renal dialysis and transplantation, when the mortality rate in patients with chronic renal failure was high, constriction was a rare complication of uremic pericarditis. However, the incidence of chronic constrictive pericarditis increased after the introduction of renal dialysis and kidney transplantation, probably as a result of improved patient survival. Patients with renal failure who are treated by dialysis may develop a peculiar form of pericarditis designated as “dialysis pericarditis”, which appears approximately 8 weeks or more after the initiation of dialysis and may progress to constriction [17].
4. Clinical features
The classical presentation of constrictive pericarditis consists of symptoms and signs of debilitating chronic right-side heart failure. Lower leg edema and mild hepatic congestion appear in the early stage of the disease. Later on, the hepatic congestion becomes aggravated, with subsequent development of ascites, anasarca, and jaundice. Dyspnea and orthopnea appear during the advanced stages of the illness. Muscle wasting, severe fatigue, and cachexia may be observed in the end stage of constriction [6].
On physical examination, the most important clinical sign is increased jugular venous pressure, presented as a rapidly collapsing, negative wave of the diastolic Y descent. An X descent wave may appear in addition to the Y descent [6]. One should keep in mind that dyspnea, tachypnea, arrhythmia, or tachycardia limit one's ability to observe the changes in the jugular veins. Kussmaul described a peculiar sign representing increased jugular venous pressure during inspiration [7], [18]. However, this sign is difficult to observe at the bedside [6]. Ling et al. [13] detected the presence of Kussmaul's sign in 28 out of 135 patients with constrictive pericarditis referred for pericardiectomy. The arterial pulse may be normal. Kussmaul has described an additional sign designated as pulsus paradoxus, a “pulse simultaneously slight and irregular, disappearing during inspiration and palpated upon expiration” [7], [18]. It has been named “paradoxus” because of the absence of a radial pulse in the presence of a corresponding heartbeat [8]. Evaluation of pulsus paradoxus may be achieved by measuring systolic blood pressure during inspiration. A decrease in blood pressure by more than 10 mm Hg during inspiration suggests the existence of pulsus paradoxus. Paradoxical pulse may also be observed in patients with cardiac tamponade, pericardial effusion, restrictive cardiomyopathy, acute myocardial infarction, severe pulmonary embolism, bronchial asthma, and tension pneumothorax. Extreme obesity, anaphylactic shock, stomach volvulus, and superior vena cava obstruction may play a role in its appearance [8]. Ling et al. [13] detected pulsus paradoxus in 19% of their patients who underwent surgery because of pericardial constriction. It should be remembered that finding a pulsus paradoxus that exceeds 10 mm Hg during inspiration is uncommon in constrictive pericarditis in the absence of excessive pericardial fluid [6].
Chest examination may reveal systolic retraction of the apex. Diastolic pericardial knock, i.e., the presence of early diastolic sound, is detected 0.06–0.12 s after the aortic component of the second heart sound (A2) (4). S3 was found in 46% of the patients described by the Mayo Clinic group [13] and in 18% of those described by Bertog et al. [12]. Although the presence of S3 is typical for the rigid form of constrictive pericarditis, it can occasionally be heard in patients with the fibroelastic variety of the disease [6], [18]. Hepatomegaly has been described in 63% of the patients, ascites in 45%, and peripheral edema in 76% [12]. In addition to hepatomegaly, prominent hepatic pulsations have been noticed [19]. Older patients may present with huge ascites and massive edema of the lower extremities with signs of muscle wasting and cachexia of the upper extremities. Peripheral edema may be absent in younger patients [20].
5. Additional examinations
5.1. Chest X-ray
Although chest X-rays are not of great help in the diagnosis of constrictive pericarditis, certain findings suggest the existence of heart constriction. In the classical form of the disease, the cardiac silhouette is not enlarged, whereas in other forms of constrictive pericarditis an accumulation of pericardial effusion may contribute to heart-size extension. Occasionally, the left atrium and superior vena cava may be dilated [21]. Signs of pericardial calcification are suggestive of constrictive pericarditis but, as stated by Lorell [6], “ Calcified pericardium is not necessarily a constricted one”. A lateral chest X-ray may reveal pericardial calcification over the right atrium and ventricle, as well as atrioventricular grooves. Ling et al. [22] reported on roentgenological signs of pericardial calcification in 36 out of 135 patients with constrictive pericarditis who underwent pericardiectomy. In 97% of them, the calcifications were found on the inferior, diaphragmatic surface of the heart, in 76% on the anterior right ventricular area, and in 62% on the left atrioventricular groove. Following X-ray examination, Bertog et al. [12] detected pericardial calcifications in 55% of patients with idiopathic constrictive pericarditis, in 10% of individuals who underwent open heart surgery, and in 6.7% of those in whom constrictive pericarditis appeared post-irradiation.
5.2. Electrocardiography
Typical electrocardiographic changes in patients with pericardial constriction include low QRS voltage, left or right bundle branch block, atrial arrhythmia or fibrillation, and the presence of “mitral P” wave. In single cases, the electrocardiogram tracing could be normal [2], [6], [12]. However, one should keep in mind that electrocardiographic findings are usually non-specific and are only suggestive for the diagnosis.
5.3. Echocardiography
The echocardiographic findings observed in patients with heart constriction are summarized in excellent reviews by Nishimura [5] and Troughton et al. [19]. In short, at two-dimensional echocardiogram, a thickened pericardium (mostly on the RV and on the RA-free walls) may be visualized, as well as an unusual motion of the interventricular septum, designated as septal bounce, accompanied by an inspiratory septal shift to the left. The presence of a dilated, non-collapsing inferior caval vein is suggestive of constrictive pericarditis. On the other hand, a normal-sized collapsing inferior caval vein at inspiration almost rules out heart constriction (Fig. 1).
Fig. 1.
Echocardiographic findings in a patient with the classical form of constrictive pericarditis. (A) Parasternal short axis view showing hyper-reflective, thickened posterior pericardium. (B) Doppler mitral flow demonstrating increased respiratory changes. (C) Doppler flow in the left ventricular outflow tract. Note the increased respiratory changes presenting the Echo equivalent of pulsus paradoxus. (D) Subcostal view of the inferior caval vein. There is an absence of normal inspiratory collapse, presenting the Echo equivalent of dilated jugular veins.
The hallmark of constrictive pericarditis on Doppler echocardiography is the increased respiratory flow variation through the heart valves, expressed as a decreased flow through the left-side valves during inspiration and its increase with expiration, while on the right-side valves the reverse phenomenon occurs. This sign is significant in cases in which the decrease in height at the mitral E wave is at least 25%, and it is highly specific for heart constriction. It should be noted that cardiac tamponade, due to a similar pathophysiological mechanism, and severe COPD, due to increased intrathoracic pressure variations, can create the same echocardiographic changes. The flow alterations observed during respiration may be explained by two mechanisms. One, known as “enhanced ventricular interdependence”, is due to suction of venous blood to the right heart at inspiration. Since the heart in constrictive pericarditis is confined in a rigid shell, the only way for the right heart to react to the increased inspiratory volume is by a shift of the interventricular septum to the left with a subsequent decrease in left ventricular volume. The second mechanism proceeds through dissociation between the intrathoracic and intracardiac pressures. Normally, the inspiratory decrease in intrathoracic pressure is transmitted to all intrathoracic organs including the pulmonary veins and heart chambers. In constrictive pericarditis, the transmission of the inspiratory negative pressure to the pulmonary veins is normal and, therefore, does not affect the pressure in the left atrium. The decreased pressure gradient between the pulmonary veins and the left atrium leads to a lesser flow into the left atrium and left ventricle through the mitral valve.
The differentiation between constrictive pericarditis and restrictive cardiomyopathy is a common echocardiographic problem since, in both conditions, right heart failure is the predominant clinical feature. In the classical forms, the enlarged left and right atria on 2D echocardiography, with thickened ventricular walls and normally appearing pericardium, facilitates the diagnosis of restrictive cardiomyopathy. If the 2D picture is equivocal for the diagnosis of restrictive cardiomyopathy, two other distinctive signs may be helpful for the differential diagnosis between restriction and constriction. In restrictive cardiomyopathy, respiratory flow changes are absent, whereas in heart constriction they are present. In addition, while in restrictive cardiomyopathy the relaxation of the myocardium is abnormal, it is normal in constrictive pericarditis since it is not a myocardial disease. On the other hand, the so-called “mixed cases” may present a difficult diagnostic problem. When the chronic inflammation aggressively involves the visceral pericardium and the epicardial layer of the myocardium, mixed diagnostic signs may be observed.
5.4. Heart catheterization and angiography
In cases of constrictive pericarditis, heart catheterization shows a nearly equal increased end-diastolic pressure in the four chambers, the difference between the right and left ventricular end-diastolic pressures being less than 5 mm Hg [2], [25]. Atrial pressure traces show rapid X (systolic) and Y (diastolic) descents. Ventricular tracing shows a dip-and-plateau pressure pattern [2]. The discrepancy between the decreased pulmonary capillary wedge pressure and the end-diastolic pressure in the left ventricle during inspiration reflects a dissociation between intrathoracic and intracardial pressures [19]. The diagnosis of heart constriction is suggestive in cases with right ventricular pressure less than 50 mm Hg and a ratio between the right ventricular end-diastolic pressure to the right ventricular systolic pressure being more than 1:3 [2]. However, some of these findings can also be observed in patients with restrictive cardiomyopathy.
5.5. Computed tomography (CT) and magnetic resonance imaging (MRI)
CT and MRI allow direct visualization of the pericardium and are presently the standard methods for accurate measurement of pericardial thickness (Fig. 2). On MRI T1 imaging, pericardium with a thickness of more than 2–3 mm appears as a thin, low-signal band bordered by a high-intensity signal produced by the surrounding pericardial and epicardial fat [23]. Further options, such as measurement of atrial and ventricular size, the possibility of assessing the diastolic filling pattern, visualization of a dilated vena cava inferior, the presence of hepatomegaly and ascites, are of additional diagnostic value. Moreover, cardiac MRI allows differentiation between transudate and exudate. While transudate generates a low signal on T1-weighted images and a high signal on T2-weighted and gradient-echo images, exudate emits an intermediate signal on both sequences. In cases of hemorrhagic effusion, different signal intensities on spin-echo images may be observed, depending on the effusion duration [23]. It is notable that in chronic constriction, the thickened pericardium shows lower signal intensity than in acute cases [24]. It should be mentioned that pericardial thickening detected on MRI examination is not necessarily diagnostic for constrictive pericarditis [21]. On the other hand, normal pericardial thickness does not rule out the diagnosis of constrictive pericarditis.
Fig. 2.
CT image of the heart of a patient with constrictive pericarditis, showing a thickened pericardium.
5.6. Differential diagnosis
Constrictive pericarditis should be suspected in patients with clinical features of right-side heart failure, such as systemic edema, pleural effusion, ascites, and increased jugular venous pressure without signs of ventricular dysfunction. Other cardiac diseases, in particular right atrial myxoma, tricuspid valve dysfunction, and restrictive cardiomyopathy, must be ruled out [6]. Nephrotic syndrome, obstruction of the superior vena cava, hepatic diseases, and abdominal malignancies should be considered in the differential diagnosis. A previous medical history of pericarditis, open-heart surgery, chest trauma, and radiotherapy suggest the existence of pericardial constriction. Preceding radiotherapy can be one of the reasons for both constrictive pericarditis and restrictive cardiomyopathy. The differentiation between these two conditions may present certain difficulties, a subject thoroughly reviewed by Hancock [25]. Restrictive cardiomyopathy may develop in patients with amyloidosis, Gaucher's or other storage diseases, and endomyocardial fibrosis. Sarcoidosis may be complicated with heart restriction but rarely with constrictive pericarditis. On auscultation, heart restriction usually presents with sounds compatible with mitral and tricuspid regurgitation. In addition, low-pitched, late S3 and occasionally S4 are indicative of restrictive cardiomyopathy. In cases with heart restriction and impaired myocardial relaxation, the early mitral annular velocity and propagation of initial ventricular inflow are decreased [18], [25]. Since heart catheterization cannot always distinguish between constrictive pericarditis and restrictive cardiomyopathy, the differential diagnosis may be problematic [25], [26]. In restrictive cardiomyopathy, the equilibrium of the end-diastolic pressure usually exceeds 5 mm Hg. Endomyocardial biopsy is indicated in difficult cases of restrictive cardiomyopathy. On rare occasions, there is a need for explorative thoracotomy to establish the correct diagnosis [6]. Additional examinations, such as X-rays, CT, MRI, and echocardiography, are important for the definitive diagnosis of constrictive pericarditis [27].
5.7. Treatment
The treatment of constrictive pericarditis consists of the administration of diuretics, salt restriction, and supportive therapy for underlying conditions. Since sinus tachycardia often appears as a compensatory process, careful administration of negative chronotropic drugs, such as beta- and calcium-channel blockers, may be considered. In patients with atrial fibrillation and rapid ventricular response, the recommended drug of choice is digoxin, taking care that the patient's heart rate remains between 80 and 90 beats per minute [20]. In patients with transient constrictive pericarditis, anti-inflammatory agents or steroids are indicated [28], given that in 15% of cases tuberculosis might be the underlying disease [29]. The use of steroids in the prevention of constriction is one of the controversial issues in the treatment of tuberculous pericarditis. Chowdhury et al. [30] recommend prolonged anti-tuberculosis treatment for tuberculous pericarditis and stress that steroid administration is not always able to prevent pericardial constriction.
5.8. Surgical treatment
In advanced cases, pericardiectomy is the definitive treatment [13], [31], and it is recommended for most patients with a central venous pressure between 12 and 15 mm Hg. Higher pressures and liver dysfunction as a result of passive congestion are indications for urgent surgery [10]. It has been reported that patients' survival following pericardiectomy is higher than that of individuals with chronic constrictive pericarditis without surgery [29]. However, choosing the right time for surgical intervention is an important issue: the presence of early constriction and advanced disease with myocardial damage, as well as signs of severe heart failure, limit the benefits of the operation and may present a serious surgical risk. The clinical course of constrictive pericarditis is usually progressive, and deciding the degree of pericardial constriction and myocardial restriction is not an easy task for the cardiologist. However, this distinction is important since, if myocardial involvement dominates, pericardiectomy is not indicated. In such cases, a useful rule is: the more significant respiratory flow variations expressed on echocardiography or heart catheterization, the more likely a constrictive dominance is present, and the better the surgical prognosis is.
5.9. Rare forms of constrictive pericarditis
In addition to classical chronic (rigid shell, calcific) and subacute (elastic) forms, new presentations, such as effusive-constrictive, localized, transient, occult, and constrictive pericarditis with normal pericardial thickness, have been described [3], [28], [32], [33], [34], [35], [36]. Effusive-constrictive pericarditis is a variant of pericardial constriction with a presence of large pericardial effusion. In 1968, Spodick and Kulmar [2] described a form of effusive-constrictive pericarditis that presents as coexisting tamponade and heart constriction. Three years later, Hancock characterized the hemodynamic alterations observed in this entity. According to Sagrista-Sauleda et al. [32], it develops as cardiac tamponade, evolving into constriction and failure of the right atrial pressure to decrease by 50% or more to a level below 10 mm Hg after removal of the pericardial fluid. According to the authors, the presenting signs are right heart failure, distention of the jugular veins and liver enlargement, the presence of pulsus paradoxus in 66% of the patients, and lack of pericardial calcification. The etiology in this series was idiopathic, postsurgical, post-irradiation, or the presence of neoplasms. The pericardial effusion may be treated conservatively or by applying invasive procedures such as pericardiocentesis, balloon pericardiostomy, thoracoscopic pericardiostomy, or even pericardiectomy [33]. The peculiarity of this variant is the involvement of visceral pericardium and the need for its removal. In another report, Sagrista-Sauleda et al. [34] described an entity defined as transient constrictive pericarditis. Their patients showed signs of effusive acute idiopathic pericarditis with cardiac constriction that disappeared spontaneously in less than 3 months after resolution of the pericardial effusion. This form of constrictive pericarditis may appear after pericardiotomy, viral and bacterial infections, collagen vascular diseases, or idiopathic pericarditis [28], [34]. Transient constrictive pericarditis occurred in 10 out of 11 Korean patients with tuberculosis in whom clinical improvement was observed after 2 months of anti-tuberculosis treatment [29]. Occult constrictive pericarditis [35] is another rare form of pericardial constriction presenting with non-specific complaints, such as dyspnea and fatigue. In these patients, rapid fluid administration may provoke clinical and hemodynamic features of heart constriction. However, this is a poorly standardized test, difficult to interpret and, therefore, of limited use [36].
In summary, the diagnosis of constrictive pericarditis should be seriously considered in patients with signs of chronic right-side heart failure with exertional dyspnea, lower limb edema, and mild liver congestion in the presence of normal ventricular contraction. The correct diagnosis should be established before the development of ascites or anasarca which, progressing to muscle wasting and fatigue, indicate the end stage of constriction. For the experienced physician, the finding of distended jugular veins, pulsatile hepatomegaly, pericardial knock, pulsus paradoxus, or the presence of Kussmaul sign can be of great diagnostic help. However, the use of additional diagnostic tools, such as echocardiography and heart visualization, is important and may save patients anguish and complications. It should be remembered that the sooner the diagnosis is established, the better the outcome is. In other words, the heart, in order to keep its secrets, does not have to be armored.
6. Learning points
Acknowledgements
We would like to thank Prof. M. Djaldetti for his help in preparing the manuscript.
References
- . Undercover and overlooked. N Engl J Med. 2004;351:1014–1019
- . Constrictive pericarditis: clinical and pathophysiologic characteristics. Am Heart J. 1999;138:219–232
- Constrictive pericarditis in 26 patients with histologically normal pericardial thickness. Circulation. 2003;108:1852–1857
- . On the elastic and rigid forms of constrictive pericarditis. Am Heart J. 1980;100:917–923
- . Constrictive pericarditis in the modern era: the diagnostic dilemma. Heart. 2001;86:619–623
- . Pericardial diseases. In: Braunwald E editors. Heart disease. Philadelphia: W.B. Saunders Company; 1997;p. 1496–1505
- . Paradoxical physical findings described by Kussmaul: pulsus paradoxus and Kussmaul's sign. Lancet. 2002;359:1940–1942
- . Clinical signs in medicine: pulsus paradoxus. J Postgrad Med. 2002;48:46–49
- . Pulsus paradoxus. J Clin Invest. 1965;44:1882–1898
- . In: The pericardium. Boston: Kluwer Academic; 2003;p. 191–251
- . Surgical pathology of the parietal pericardium: a study of 344 cases (1993–1999). Cardiovasc Pathol. 2001;10:157–168
- Constrictive pericarditis: etiology and cause-specific survival after pericardiectomy. J Am Coll Cardiol. 2004;43:1445–1452
- Constrictive pericarditis in the modern era. Evolving clinical spectrum and impact on outcome after pericardiectomy. Circulation. 1999;100:1380–1386
- Seifert F.C., Miller D.C., Oesterle S.N., et al. Surgical treatment of constrictive pericarditis: analysis of outcome and diagnostic error. Circulation 1985; 72(3 Pt 2): II 264–73.
- . Early development of severe constrictive pericarditis after coronary bypass grafting. Eur J Emerg Med. 2005;12:245–247
- . Mulibrey heart disease. Clinical manifestations, long-term course and results of pericardiectomy in a series of 49 patients born before 1985. Circulation. 2003;107:2810–2815
- . Pericardial involvement in end-stage renal disease. Am J Med Sci. 2003;325:228–236
- . In: Pericarditis and the paradox pulse. vol. 38:Berl Klin Wochenschr; 1873;
- . Pericarditis. Lancet. 2004;363:717–727
- . Pericardial diseases. In: Zipes D editors. Braunwald's heart disease: a textbook of cardiovascular medicine. Elsevier W.B. Saunders Company; 2004;p. 1757–1779
- . Imaging of the pericardium. J Thorac Imaging. 2001;16:47–54
- Calcific constrictive pericarditis: is it still with us?. Ann intern Med. 2000;132:444–450
- . Role of MRI in clinical cardiology. Lancet. 2004;363:2162–2171
- . Clinical use of cardiovascular magnetic resonance. Circulation. 2003;108:647–653
- . Differential diagnosis of restrictive cardiomyopathy and constrictive pericarditis. Heart. 2001;86:343–349
- . Constrictive pericarditis versus restrictive cardiomyopathy: a reappraisal and update of diagnostic criteria. Am Heart J. 1991;122:1431–1441
- . Constrictive pericarditis and restrictive cardiomyopathy: evaluation with MR imaging. Radiology. 1992;182:369–373
- . Transient constrictive pericarditis: causes and natural history. J Am Coll Cardiol. 2004;43:271–275
- Clinical characteristics of constrictive pericarditis diagnosed by echo-Doppler technique in Korea. J Korean Med Sci. 2001;16:558–566
- Pericardiectomy for constrictive pericarditis: a clinical, echocardiographic, and hemodynamic evaluation of two surgical techniques. Ann Thorac Surg. 2006;81:522–529
- Guidelines on the diagnosis and management of pericardial diseases. Executive summary: The task force on the diagnosis and management of pericardial diseases of the European Society of Cardiology. Eur Heart J. 2004;25:587–610
- . Effusive-constrictive pericarditis. N Engl J Med. 2004;350:469–475
- . A clearer view of effusive-constrictive pericarditis. N Engl J Med. 2004;350:435–437
- . Transient cardiac constriction: an unrecognized pattern of evolution in effusive acute idiopathic pericarditis. Am J Cardiol. 1987;59:961–966
- . Occult constrictive pericardial disease. Diagnosis by rapid volume expansion and correction by pericardiectomy. Circulation. 1977;56:924–930
- . Pericardial constriction: uncommon patterns. Heart. 2004;90:257–258
PII: S0953-6205(06)00186-5
doi:10.1016/j.ejim.2006.07.006
© 2006 European Federation of Internal Medicine. Published by Elsevier Inc. All rights reserved.
Volume 17, Issue 7 , Pages 457-464, November 2006
