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Heart. 2007 August; 93(8): 993–1000.
PMCID: PMC1994428

Pericardial disease: what the general cardiologist needs to know

Emma L Ivens and Bradley I Munt, Robert R Moss

Pericardial disease remains an important cause of morbidity and mortality, spanning a complex spectrum from asymptomatic and transient to severely symptomatic and life threatening. Knowledge about the presenting symptoms, clinical findings, diagnosis and management is essential for effective clinical management.

This article focuses on the pertinent features of the major pericardial diseases seen in clinical practice and the recommended diagnostic and treatment strategies. In many cases the management of pericardial disease is based on best clinical practice; however, evidence based recommendations are emerging. Published data, gleaned from observing numbers of patients, must be crystallised into an individualised management plan.

THE NORMAL PERICARDIUM

The pericardium consists of two layers that surround the heart and the proximal aorta, pulmonary artery, vena cava and pulmonary veins. The thick fibrous outer layer, which attaches to the adventia of the major vessels, diaphragm, sternum and vertebrae, provides strong structural support for the heart.1 The inner layer is a thin serous membrane composed of only a single row of mesothelial cells which lies both on the surface of the heart, where it is called the visceral pericardium, and by folding back on itself and underlying the fibrous layer, forms the lining of the parietal pericardium. Normally the pericardium is <2 mm thick. The pericardial space is a blind sac contained within the visceral and parietal pericardium and usually contains only a small amount of pericardial fluid. The transverse sinus is the part of the pericardial sac which lies between the great vessels and the oblique sinus lies posteriorly between the pulmonary veins.

Pericardial fluid is produced by the visceral pericardial cells and resembles an ultrafiltrate of plasma that serves to lubricate and reduce friction between the visceral and parietal pericardial surfaces. The pericardial fluid is drained by the thoracic and right lymphatic ducts. Normally there is between 10–50 ml of pericardial fluid.

The pericardium, although not critical for survival, has several important functions including: limiting acute dilatation of the heart and excessive cardiac motion within the chest; optimising cardiac shape; balancing right and left sided ventricular outputs via diastolic and systolic interactions (ventricular coupling); and preventing spread of adjacent infection or neoplasia to the heart.1

Being a relatively inelastic and non‐compliant structure, the pericardium limits the total volume of the contained cardiac chambers and pericardial fluid, which is referred to as pericardial constraint. It is the parietal pericardium, more than the visceral pericardium, that mediates most of this effect. Under normal conditions, this constraint is not particularly pronounced.

Pericardial pressure is normally low and follows intrathoracic (or intrapleural) pressure and right atrial pressure. It is influenced by respiration.

ABNORMAL PERICARDIAL PHYSIOLOGY

Raised intrapericardial pressure can occur by three main mechanisms: (1) increased fluid within the intrapericardial space; (2) increased volume of the cardiac chambers; or (3) increased stiffness of the pericardium. Raised intrapericardial pressure has three potential adverse effects on the heart: (1) a compressive effect which limits diastolic filling of the heart; (2) increased diastolic filling pressures; and (3) reduced stroke volume and cardiac output. Compensatory mechanisms are activated, but severe elevation of pericardial pressure can rapidly lead to death if not treated.

The concept of pericardial compliance is integral to understanding the clinical effects of an accumulating pericardial effusion. In the normal situation, the pericardium has a small capacitance reserve that will accommodate only small increases in cardiac chamber size and/or pericardial fluid volume of about 150–250 ml before significant increases in pericardial pressure occur.1 Once the pericardial capacitance reserve is reached, any further increase in contained volume dramatically increases pericardial pressure as this occurs on the steep incline part of the pressure–volume curve (fig 11).

figure ht86587.f1
Figure 1 Cardiac tamponade. Pericardial pressure–volume (or strain–stress) curves are shown in which the volume increases slowly or rapidly over time. In the left panel, rapidly increasing pericardial fluid first reaches the limit ...

ACUTE PERICARDITIS

Acute pericarditis is a disorder characterised by acute inflammation of the pericardium. There are many different causes (webtable 12,3,4,5,6,7,8,9,10) (to view webtable 1 visit the Heart website—http://heart.bmj.com/supplemental). Primary acute pericarditis, without an obvious underlying cause, is presumably of viral aetiology. Most secondary causes of acute pericarditis are evident before pericardial involvement occurs.

Presentation is usually with pleuritic chest pain in a haemodynamically stable patient. There may be a history of a recent viral illness or another predisposing condition. The duration of symptoms is usually short, and the pain is typically sharp, worse on deep inspiration, coughing and on lying flat. The pain can be intermittent or constant. It can be severe enough for the patient to seek urgent medical assessment. Other symptoms that may be present include a dry cough, dyspnoea, malaise, myalgia and fever.

Examination findings are listed in webtable 22,4,8,11,12,13,14,15,16,17,18,19,20,21,22,23 and usually reveal a stable patient who is normotensive (to view webtable 2 visit the Heart website—http://heart.bmj.com/supplemental). A pericardial friction rub may be audible on auscultation in approximately 35% of patients, although it is often transient.13,14 Some believe it is more likely in those without an effusion, although this has been debated. It is felt to be caused by the two inflamed layers of pericardium moving against each other in atrial systole, ventricular systole and/or rapid diastolic filling. Sinus tachycardia and fever may be present.

Investigations that should be performed and the typical ECG findings are outlined in webtable 2. Elevated cardiac enzymes are not uncommon in acute pericarditis and usually do not imply ischaemic heart disease. In one study of 69 patients with acute pericarditis, cardiac troponin I was detectable in 49% and above 1.5 ng/ml−1 in 22%.24 Approximately half the patients with elevated troponin I levels had coronary angiography performed and no coronary artery disease was detected.24 Elevated troponin values were felt to reflect superficial myocardial inflammation and were not an adverse prognostic marker after a mean follow‐up of 24 months.25

Echocardiography should be performed in all patients with pericarditis, for a number of reasons, and has been given a class 1 indication according to the 2003 taskforce of the American College of Cardiology, the American Heart Association and the American Society of Echocardiography. It is helpful in detecting pericardial effusions that may be present in up to 66% of patients and this finding is, in general, supportive of the diagnosis.14 Echocardiography is also helpful in looking for other complications and for evaluating other differential diagnoses. Regional wall motion abnormalities or global dysfunction may be present and may reflect either myocarditis, or ischaemia/infarction secondary to underlying coronary disease. Echocardiography may also detect pericardial thickening or suggest an alternative cardiac diagnosis.

The diagnosis of acute pericarditis is made by clinical assessment in combination with supportive examination and ECG findings. Many authors recommend two out of the three following criteria for a firm diagnosis: typical pleuritic chest pain; pericardial friction rub; and widespread ST segment elevation on the ECG.2,14

Treatment is symptomatic and consists of anti‐inflammatory medication, predominantly non‐steroidal anti‐inflammatory drugs (NSAIDs) with or without colchicine. Aspirin is the preferred choice at a dose range of 325–650 mg orally four times daily.14 Ibuprofen is the next recommended NSAID due to its low side effects, favourable impact on coronary blood flow, and large dose range of 300–800 mg, 6–8 hourly.15 NSAIDs can be continued until any effusion and/or symptoms have resolved (generally for days to weeks), with the dose being reduced as clinically indicated.15 Many uncomplicated episodes of acute idiopathic pericarditis only require 1–4 days of treatment, although the optimal duration of treatment recommended is unknown. Gastrointestinal protection is recommended for all patients.13,14,15 Colchicine, 500 μg daily, can be given as monotherapy or in combination with an NSAID for symptomatic relief and for the prevention of further episodes.14 Oral steroids are usually reserved for patients with underlying connective tissue disease, uraemia or recurrent disease according to the European Society of Cardiology.15 As these are weaned, colchicine or NSAID treatment is usually introduced. Steroid use should be restricted as it is an independent risk factor for recurrence.14

The COPE trial provides randomised data that further supports and expands the role of colchicine in the primary treatment of acute pericarditis.14 Of 120 patients recruited, 60 received aspirin for 1 month and 60 received combination treatment with aspirin for 1 month and colchicine for 3 months. Results showed a statistically significant reduction in the pericarditis recurrence rate of 32.3% vs 10.7% with combination treatment (p = 0.004, number needed to treat = 5). Colchicine also significantly reduced symptom persistence at 72 h (11.7% vs 36.7%, p = 0.003). Colchicine should therefore be considered in the primary treatment of acute pericarditis.

Diagnostic pericardiocentesis has a low yield in the setting of acute pericarditis and is not routinely recommended unless there is a high clinical suspicion of purulent pericarditis.2,3,4 Therapeutic pericardiocentesis is reserved for those with pericardial effusion and tamponade, or a significant effusion with a poor clinical course after 7–10 days of NSAID treatment, although the latter is controversial.2

Many patients with acute pericarditis do not require hospitalisation and can be followed up after appropriate evaluation as an outpatient. In a recent review of 300 patients, 254 (85%) were managed as outpatients with NSAIDs, if they did not have high risk features on initial clinical and echocardiographic assessment.13 These high risk features were fever >38°C, subacute onset, immunosuppression, trauma, oral anticoagulant treatment, myopericarditis, large pericardial effusion (>2 cm) or tamponade. Outpatient treatment was efficacious in 87% of cases. During the study, 13% of patients were admitted because of failure of NSAIDs to control symptoms. Higher rates of recurrent disease and constriction were seen in NSAID resistant patients. In those treated as an outpatient, there was no incidence of serious complications after a mean follow‐up of 38 months.

Specific types of acute pericarditis may also require additional treatment, such as antimicrobial therapy and surgical drainage for bacterial pericarditis, antituberculous treatment for tuberculosis infection, and haemodialysis for uraemic pericarditis. These are discussed in further details in the reference texts.1,15

After an episode of acute pericarditis, all patients require follow up assessment for complications such as recurrent disease and constriction.

PERICARDIAL EFFUSION

A pericardial effusion is present when there is increased fluid within the pericardial space. This fluid can be serous, serosanguinous, pus, lymph or blood. There are many different possible causes (webtable 1). The reported aetiology varies with the study population and the diagnostic criteria and exclusions used. Routine diagnostic pericardiocentesis has a low yield, particularly in smaller effusions. In large effusions, the diagnostic yield of pericardiocentesis has been reported as between 7–26% and is higher in cardiac tamponade.2,3,4,5,6,26 This supports the notion that routine diagnostic pericardiocentesis in the absence of cardiac tamponade is not indicated. Therapeutic pericardiocentesis may, however, be required for symptoms and/or cardiac tamponade.

The relationship between effusion size and adverse effects is influenced by the time course of accumulation. Many effusions are small, only discovered incidentally and are asymptomatic. Larger effusions that collect slowly may initially be asymptomatic, but cause dyspnoea or tamponade at a late stage. Rapidly accumulating effusions can result in cardiac tamponade and death, even when relatively modest in size. In this instance the pericardial pressure can rise rapidly because there is insufficient time for the non‐compliant pericardium to stretch (fig 11).

Diagnosis of a pericardial effusion is usually achieved by echocardiography and can be circumferential or localised (loculated). Pericardial effusions are usually classified as small (<1 cm), moderate (1–2 cm) or large (>2 cm). The assessment of haemodynamic effect will be discussed in the next section.

The management of small or moderate pericardial effusions, without tamponade, is usually conservative, with clinical and echocardiographic surveillance. If the pericardial effusion is likely to be purulent then it should be drained. If the effusion is felt to be malignant, pericardiocentesis is recommended if confirmation would change management and can be performed safely.

The management of large, idiopathic, chronic pericardial effusions (asymptomatic and present for more than 3 months), without cardiac tamponade, is controversial. Many believe they should be monitored and managed conservatively, unless cardiac tamponade develops, and that they overall have a good prognosis. Merce et al reviewed 71 patients with large pericardial effusions in the absence of tamponade or a suspicion of purulent disease and found a relatively benign course.26 Another study by Sagrista‐Sauleda, however, showed a reasonably high risk of the development of overt tamponade and recommended a more invasive approach.27 Pericardiocentesis will resolve the effusion in a proportion of cases. A risk–benefit assessment needs to be made for each patient, weighing the risk of pericardiocentesis against potential diagnostic and therapeutic benefit.

Pericardial effusions in patients with known malignancy can be neoplastic, idiopathic, or due to radiation, drugs or other conditions. Pericardiocentesis with analysis of cytological fluid is usually positive in 65–85% of patients with malignant effusions.28 Open subxiphoid pericardial biopsy may diagnose many of the remaining patients. The management of large symptomatic malignant effusions, with or without tamponade, is usually by pericardiocentesis which had a success rate of 97% and a complication rate of less than 3%.28 The risk of recurrence varies and is reduced by prolonged initial catheter drainage, and by the addition of systemic chemotherapy and/or radiotherapy in many cases.28 The use of intrapericardial sclerosing agents and intrapericardial chemotherapy has been limited by the side effects of chest pain and atrial arrhythmias. Options for recurrent malignant effusions include repeat pericardiocentesis, subxiphoid window, pleuropericardial window and thoracotomy with pericardectomy.28 A percutaneous technique has also been used to create a pericardial window.28 The overall survival in patients with malignant pericardial effusions is poor and generally in the order of 10–13 months with breast cancer and less than 6 months in patients with other cancers. Survival is worse in patients with positive cytology in the fluid.

The risk of significant pericardial effusion/haematoma requiring treatment, after cardiac surgery, is approximately 1%. The effusion is often localised and the typical echocardiographic findings of tamponade may not be present. Transoesophageal imaging may be required for diagnosis if transthoracic images are suboptimal. If unexplained clinical deterioration occurs in the presence of a significant pericardial effusion/haematoma postoperatively, surgical exploration should be strongly considered even in the absence of echocardiographic markers of tamponade. Postoperative effusion/haematoma with tamponade can be treated with percutaneous or surgical drainage, depending on local experience. Surgical drainage should be particularly considered if there is active bleeding or localised posterior pockets.

CARDIAC TAMPONADE

Cardiac tamponade is a life threatening condition that is diagnosed clinically by elevated jugular venous pressure, hypotension and pulsus paradoxus in the setting of a pericardial effusion. It occurs when an accumulation of fluid within the pericardial space causes a significant rise in intrapericardial pressure. When intrapericardial pressure becomes higher than intracavitary pressure, compression of the heart occurs with reduced diastolic filling. This is first seen on the right side, rather than the left, due to the thinner walls and reduced chamber pressure. For similar reasons, the right atrium usually is compressed before the right ventricle. If the effusion is localised, compression of a single chamber can occur. If diastolic compression becomes too significant to be overcome by elevated filling pressures and other compensatory mechanisms, cardiac output and blood pressure will fall.

Many of the clinical and echocardiographic features are explained by the above findings and the effect of respiration on intracardiac flows and pressures.

The typical causes, and clinical and echocardiographic findings, are shown in webtables 1 and 2 and fig 22.. Treatment is with prompt drainage of pericardial fluid (see Pericardiocentesis key points).

figure ht86587.f2
Figure 2 (A) Transthoracic parasternal long axis echocardiographic image showing a large pericardial effusion. Arrow points to diastolic right ventricular compression. (B and C) Pulsed wave Doppler of the mitral and tricuspid valves showing increased ...

CONSTRICTIVE PERICARDITIS

Constrictive pericarditis is usually characterised by a thickened, adherent pericardium that restricts ventricular filling and limits chamber expansion and maximal diastolic volumes. Elevated filling pressures are required to maintain adequate cardiac output. End‐diastolic pressures in all heart chambers are usually elevated and equalised. Compensatory mechanisms are activated but may ultimately fail, leading to elevated venous pressure, oedema and diminished cardiac output.

The aetiology of pericardial constriction is changing (webtable 1).

Clinical findings are listed in webtable 2 and the presentation is usually with features mimicking right‐sided heart failure with low cardiac output. Typical symptoms are exertional dyspnoea, peripheral oedema, abdominal distension and fatigue. Pulmonary oedema is not normally a feature.

Diagnosis is usually made by a combination of clinical findings, chest x ray, echocardiography, CT or MRI imaging and in many cases invasive haemodynamic studies (webtable 2, fig 33).

figure ht86587.f3
Figure 3 (A) Simultaneous recordings of left ventricular (LV) and pulmonary capillary wedge (PAW) pressures demonstrating dissociation of intrathoracic and intracardiac pressures. Note the fall in early diastolic gradient with inspiration (beat ...

Echocardiography is an important tool for suggesting or supporting the diagnosis. The typical findings are listed in webtable 2.

In patients with notably elevated left atrial pressure, respiratory variation of the Doppler inflows may not be present unless preload is reduced by head‐up tilt or diuretics.29

Not all patients with proven constriction at surgery actually have increased respiratory variation of Doppler inflows. Of 19 patients with surgically confirmed constrictive pericarditis, for example, nine (47%) did not have more than 25% respiratory variation of mitral E wave velocity.30

In patients with atrial fibrillation, changes in mitral E velocity may reflect variations in ventricular filling rather than constriction.

Patients with chronic obstructive pulmonary disease (COPD) without constriction may have increased respiratory variation in mitral and tricuspid inflow velocities and this may occasionally cause diagnostic difficulty. In contrast to constriction, variation is not typically maximal on the first inspiratory beat. In addition, mitral inflow is less restrictive with lower E/A ratios than in patients with constriction and longer deceleration times.31 Analysis of the superior vena cava (SVC) Doppler signal may be useful in this setting. SVC Doppler shows pronounced increases in forward flow with inspiration in patients with COPD which is not usually seen in constriction (mean (SD) respiration variation in COPD of SVC systolic flow velocity 39.5 (18.8) cm/s vs 4.2 (3.4) cm/s in constriction).31 In one study, 95% of patients with COPD had respiratory variation of SVC systolic forward velocity >20 cm/s or a >35% increase with inspiration.31 In addition, COPD patients usually have systolic dominant superior vena caval Doppler flow rather than diastolic dominant in constriction.31

Evaluation of the pericardium by chest radiography and pericardial thickness by CT or MRI provides important supplementary information that often helps in making this diagnosis in the majority of affected patients. Invasive haemodynamic evaluation is particularly important in patients with suggestive clinical features and equivocal non‐invasive tests. Typical catheterisation findings are described in webtable 2 and table 11,, and in fig 33..

Table thumbnail
Table 1 Comparison of constrictive pericarditis and restrictive cardiomyopathy

B‐type natriuretic peptide (BNP) is usually normal or only mildly raised in constrictive pericarditis (128 (52.7) pg/ml) but significantly higher in patients with restrictive cardiomyopathy (825.8 (172.2) pg/ml) (p<0.001).23 A more recent study, however, revealed that a significant difference in BNP values existed only between those patients with idiopathic constrictive pericarditis and patients with restrictive cardiomyopathy. No statistically significant difference was found between patients with secondary constrictive pericarditis (for example, secondary to radiation or post‐cardiac surgery) and restrictive cardiomyopathy.32 This may reflect co‐existent cardiac muscle disease in patients with secondary constrictive pericarditis where certain disease processes may affect both pericardium and cardiac muscle.

Features that would support a diagnosis of restrictive cardiomyopathy rather than constrictive physiology are listed in table 11.

Treatment of established chronic constrictive pericarditis is by radical pericardectomy.

TRANSIENT CONSTRICTION

Transient pericardial constriction has been reported in the following settings: acute pericarditis, cardiac surgery, collagen vascular disease, malignancy, tuberculosis, trauma and idiopathic. Typical patient characteristics and treatment modalities are discussed in detail elsewhere. The mechanism of transient constriction is felt to be secondary to an inflammatory mediated reduction in pericardial compliance; a trial of medical treatment may be appropriate in haemodynamically stable patients with recovery expected at an average of 3 months. It is not clear from the available evidence if medical treatment affects the natural history of this disorder. Treatment should be directed at symptoms while monitoring for clinical and echocardiographic improvement. If deterioration occurs, early surgery should be considered.

EFFUSIVE CONSTRICTIVE PERICARDITIS

Effusive constrictive pericarditis is a condition where a pericardial effusion coexists with constriction of the heart by the visceral layer of the pericardium. The pericardial effusion is usually tense and causes pericardial tamponade. The clinical diagnosis rests on the demonstration that a clinical and haemodynamic picture of constriction persists after drainage. Simultaneous pericardiocentesis and right heart catheterisation will show a persistent elevation of right atrial pressure despite the normalisation of intrapericardial pressure following drainage. A study by Sagrista‐Sauleda et al identified 15 patients who met the criteria for effusive constrictive pericarditis who were followed for a median period of 7 years.9 All 15 patients had clinical manifestations of right heart failure. The underlying aetiology is shown in webtable 1. Pericardectomy was required by seven patients who had persistent constriction and clinical features of severe and persistent heart failure who were operative candidates. Significant thickening and adhesions were found of both the visceral and parietal pericardial layers in all these patients at surgery. Spontaneous resolution occurred in three patients.

Echocardiographically guided pericardiocentesis: key points

In all but emergency cases, echocardiographic guided pericardiocentesis should be performed in an area where the patient can be closely monitored.

Continuous ECG monitoring, invasive or 2 min non‐invasive blood pressure monitoring, and continuous pulse oximetry should all be available.

The best technique in an individual patient depends on the amount and location of the effusion, the patient's clinical status and the operator's experience.

Surgical treatment should be performed in patients with pericardial effusions caused by aortic dissection, a direct puncture wound or ruptured ventricular aneurysm. The steps we employ for non‐emergency echocardiographically guided percutaneous pericardiocentesis are summarised below:

  • The patient's echocardiogram is reviewed. The approach is chosen where the most direct route to the maximum amount of pericardial fluid occurs while avoiding any vital structures.
  • Laboratory tests are ordered or reviewed. Any coagulopathy, electrolyte disturbance (especially hypokalaemia) or severe anaemia should be corrected.
  • Intravenous access is obtained and O2 is delivered to maintain oxygen saturation of >90%.
  • Echocardiography is performed by the bedside. A proposed entry point is marked on the patient's skin where the percutaneous needle should penetrate the chest wall, and the transducer angle is noted as this will need to be replicated by the pericardiocentesis needle. The distance from the chest wall to the effusion and the distance to the nearest cardiac structure is determined as this will determine the maximum distance that the pericardial needle can be safely advanced. If an acoustic window is available, remote to the proposed puncture site, needle puncture can be directly visualised. If not, the imaging probe should be covered with a sterile cover, and available for the physician performing the procedure to use if needed.
  • Local anaesthetic is infiltrated. The pericardiocentesis needle is inserted and advanced along the previously determined pathway. Constant aspiration during needle advancement followed by a slight pause for injection should be performed to make sure that a plug of tissue or clot is not occluding the needle tip.
  • Once the pericardium is entered, fluid should flow freely into the syringe. If there is any doubt, the position of the needle can be confirmed by injecting agitated saline contrast. A guidewire is introduced into the pericardial space and its correct position can usually be verified echocardiographically. Dilators are used to enlarge the guidewire track. A pigtail catheter is thread over the wire into the pericardial space. The pericardial effusion should be drained completely, if possible. Intermittent echocardiographic re‐evaluation of the pericardial fluid volume throughout the aspiration procedure is useful to assess the degree of remaining fluid.

The pericardial catheter is usually left in situ for 12–36 h. Once drainage ceases, the patient is re‐imaged and the catheter is removed when only a minimal amount of fluid remains.

MIXED CONSTRICTION AND RESTRICTION

Mixed constriction and restriction is a disorder characterised by difficulty in making and confirming the diagnosis, less clearly defined treatment options and in general, a poorer outcome. This diagnosis can be suspected on cardiac imaging using three criteria: (1) localised thickening of the pericardium confirmed on CT or MRI; (2) restrictive mitral inflow pattern on echocardiography and/or pulmonary venous inflow; and (3) the absence of significant respiratory variation of early diastolic filling velocity (<25% mitral E velocity variation). Webtable 1 shows the underlying aetiology of 38 patients with mixed constriction and restriction confirmed on cardiac catheterisation and, in some cases, surgical findings.10 Just under half (45%) of the patients underwent pericardial stripping and none were transplanted. Overall 5 and 10 year survival rates were 60 (8)% and 50 (10)%, respectively.10 Survival appears worse in the mixed constriction and restriction group than with constriction alone.10 Of the patients with mixed physiology, there was no significant difference in survival between the surgically treated group and the medically treated group.10 Treatment options in this complex group include medical therapy, pericardectomy and heart transplantation in selected patients.

CONCLUSIONS

Pericardial disease encompasses a complex spectrum of disorders. Correct management requires an integrated approach including sound clinical skills and a good knowledge of cardiac physiology. In addition, skill in the interpretation of a variety of imaging modalities and haemodynamic data is required. Cardiologists should have the skills to perform a needle pericardiocentesis and an awareness of the possibilities and limitations of pericardial surgery. As the understanding of pericardial disease evolves, cardiologists must apply the evidence from clinical studies to individual patients to ensure the best possible outcomes in patient care.

Additional references appear on the Heart website— http://heart.bmj.com/supplemental

INTERACTIVE MULTIPLE CHOICE QUESTIONS

This Education in Heart article has an accompanying series of six EBAC accredited multiple choice questions (MCQs).

To access the questions, click on BMJ Learning: Take this module on BMJ Learning from the content box at the top right and bottom left of the online article. For more information please go to: http://heart.bmj.com/misc/education.dtl Please note: The MCQs are hosted on BMJ Learning—the best available learning website for medical professionals from the BMJ Group.

If prompted, subscribers must sign into Heart with their journal's username and password. All users must also complete a one‐time registration on BMJ Learning and subsequently log in (with a BMJ Learning username and password) on every visit.

To view webtables 1 and 2, and the additional references, visit the Heart website—http://heart.bmj.com/supplemental

Supplementary Material

[web only appendices]

Footnotes

In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. Brad Munt has received grants from the Heart and Stroke Foundation British Columbia and the Yukon and the Diamond Foundation

To view webtables 1 and 2, and the additional references, visit the Heart website—http://heart.bmj.com/supplemental

References

1. Goldstein J A. Cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy. Curr Probl Cardiol 2004. 29503–567.567Comprehensive overview of pericardial disease with clear descriptions and diagrams of pericardial physiology and pathophysiology. [PubMed]
2. Zayas R, Anguita M, Torres F. et al Incidence of specific etiology and role of methods for specific etiologic diagnosis of primary acute pericarditis. Am J Cardiol 1995. 75378–382.382 [PubMed]
3. Permanyer‐Miralda G, Sagrista‐Sauleda J, Soler‐Soler J. Primary acute pericardial disease: A prospective series of 231 consecutive patients. Am J Cardiol 1985. 56623–630.630 [PubMed]
4. Sagrista‐Sauleda J, Merce J, Permanyer‐Miralda G. et al Clinical clues to the causes of large pericardial effusions. Am J Med 2000. 10995–101.101 [PubMed]
5. Corey G R, Campbell P T, Van Trigt P. et al Etiology of large pericardial effusions. Am J Med 1993. 95209–213.213 [PubMed]
6. Levy P Y, Corey R, Berger P. et al Etiologic diagnosis of 204 pericardial effusions. Medicine (Baltimore) 2003. 82385–391.391 [PubMed]
7. Oh J, Hatle L, Seward J. et al Diagnostic role of Doppler echocardiography in constrictive pericarditis. J Am Coll Cardiol 1994. 23154–162.162 [PubMed]
8. Ling L, Oh J K, Schaff H V. et al Constrictive pericarditis in the modern era: evolving clinical spectrum and impact on outcome after pericardectomy. Circulation 1999. 1001380–1386.1386An important large study showing the changing incidence of underlying aetiology of constrictive pericarditis. [PubMed]
9. Sagrista‐Sauleda J, Angel J, Sanchez A. et al Effusive‐constrictive pericarditis. N Engl J Med 2004. 350469–475.475 [PubMed]
10. Yamada H, Tabata T, Jaffer S J. et al Clinical features of mixed physiology of constriction and restriction: echocardiographic characteristics and clinical outcome. Eur J Echocardiogr 2007. 8185–194.194 [PubMed]
11. Appleton C P, Hatle L K, Popp R L. Cardiac tamponade and pericardial effusion: respiratory variation in transvalvular flow velocities studied by Doppler echocardiography. J Am Coll Cardiol 1988. 111020–1030.1030 [PubMed]
12. Borganelli M, Byrd B F. Doppler echocardiography in pericardial disease. Cardiol Clin 1990. 8333–349.349 [PubMed]
13. Imazio M, Demichelis B, Parrini I. et al Day‐hospital treatment of acute pericarditis: a management program for outpatient therapy. J Am Coll Cardiol 2004. 431042–1046.1046A study of 254 low risk patients with acute pericarditis managed as outpatients with a high success rate of outpatient treatment. [PubMed]
14. Imazio M, Bobbio M D, Cecchi E. et al Colchicine in addition to conventional therapy for acute pericarditis. Circulation 2005. 272012–2016.2016A randomised trial of 120 patients with acute pericarditis randomised to aspirin treatment or combination treatment with aspirin and colchicine. Results showed benefit from the addition of colchicine, with reduction of symptom persistence at 72 h and a reduced recurrence rate. [PubMed]
15. Maisch B, Seferovic P M, Ristic A D. et al Guidelines on the diagnosis and management of pericardial diseases. Eur Heart J 2004. 25587–610.610A comprehensive overview of pericardial disease with clinical guidelines. [PubMed]
16. Spodick D. Acute cardiac tamponade. New Engl J Med 2003. 349684–690.690 [PubMed]
17. Reydel B, Spodick D H. Frequency and significance of chamber collapses during cardiac tamponade. Am Heart J 1990. 1191160–1163.1163 [PubMed]
18. Otto C. Textbook of clinical echocardiography, 3rd ed. Philadelphia: Elsevier Sanders, 2004. 259–275.275
19. Hatle L K, Appleton C P, Popp R L. Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography. Circulation 1989. 79357–370.370 [PubMed]
20. Rajagopalan N, Garcia M J, Rodriguez L. et al Comparison of new Doppler echocardiographic methods to differentiate constrictive pericardial heart disease and restrictive cardiomyopathy. Am J Cardiol 2001. 8786–94.94A study of 30 patients, using new Doppler echocardiographic methods, giving sensitivity and specificity in distinguishing constrictive pericarditis from restrictive cardiomyopathy. [PubMed]
21. Talreja D R, Edwards W D, Danielson G K. et al Constrictive pericarditis in 26 patients with histologically normal pericardial thickness. Circulation 2003. 1081852–1857.1857 [PubMed]
22. Hurrel D G, Nishimura R A, Higano S T. et al Value of dynamic respiratory changes in left and right ventricular pressures for the diagnosis of constrictive pericarditis. Circulation 1996. 932007–2013.2013Detailed study of invasive haemodynamic data obtained during cardiac catheterisation for the diagnosis of constrictive pericarditis. [PubMed]
23. Leya F S, Arab D, Joyal D. et al The efficacy of brain natriuretic peptide levels in differentiating constrictive pericarditis from restrictive cardiomyopathy. J Am Coll Cardiol 2005. 451899–1902.1902
24. Bonnefoy E, Godon P, Kirkorian G. et al Serum cardiac troponin I and ST‐segment elevation in patients with acute pericarditis. Eur Heart J 2000. 21832
25. Imazio M, Demichelis B, Cecchi E. et al Cardiac troponin I in acute pericarditis. J Am Coll Cardiol 2003. 422144
26. Merce J, Sagrista‐Sauleda J, Permanyer‐Miralda G. et al Should pericardial drainage be performed routinely in patients that have a large pericardial effusion without tamponade? Am J Med 1998. 105106–109.109 [PubMed]
27. Sagrista‐Sauleda J, Angel J, Permanyer‐Miralda G. et al Long term follow up of idiopathic chronic pericardial effusion. N Engl J Med 1999. 3412055–2058.2058
28. Vaitkus P T, Herrmann H C, LeWinter M M. Treatment of malignant pericardial effusion. JAMA 1994. 27259–64.64Thorough discussion of the management options when treating malignant effusions and their complications. [PubMed]
29. Oh J K, Tajik A J, Appleton C P. et al Preload reduction to unmask the characteristic Doppler features of constrictive pericarditis. A new observation. Circulation 1997. 95796–799.799 [PubMed]
30. Ha J W, Oh J K, Ommen S R. et al Diagnostic value of mitral annular velocity for constrictive pericarditis in the absence of respiratory variation in mitral inflow velocity. J Am Soc Echocardiogr 2002. 151468–1471.1471 [PubMed]
31. Boonyaratavej S, Oh J K, Tajik A J. et al Comparison of mitral inflow and superior vena cava Doppler velocities in chronic obstructive pulmonary disease and constrictive pericarditis. J Am Coll Cardiol 1998. 322043–2048.2048 [PubMed]
32. Babuin L, Alegria J R, Oh J K. et al Brain natriuretic peptide levels in constrictive pericarditis and restrictive cardiomyopathy. J Am Coll Cardiol 2006. 471489–1491.1491 [PubMed]

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