Free Online CME

Published: January 1, 2009

Pericardial Disease

Ron Jacob

Richard A. Grimm

Print this Content

Acute pericarditis

Definition

Acute pericarditis is an inflammatory process involving the pericardium that results in a clinical syndrome with the triad of chest pain, pericardial friction rub, and changes in the electrocardiogram (ECG).1

Prevalence

Acute pericarditis is the admitting diagnosis in 0.1% of hospital admissions. It occurs more commonly in men than in women.

Causes

The most common form of acute pericarditis is idiopathic, which accounts for about 90% of cases (Box 1). 2 Other common causes include infection, renal failure, myocardial infarction (MI), 3 malignancy, radiation, and trauma. 4 These are discussed in more detail later.

Signs and Symptoms

Symptoms

The most common symptom of acute pericarditis is severe, sharp, retrosternal chest pain, often radiating to the neck, shoulders, or back. Positional changes are characteristic, with worsening of the pain in the supine position and with inspiration, and improvement with sitting upright and leaning forward. Other symptoms may occur, reflecting the underlying disease.

Physical Examination Findings

A scratchy, grating, high-pitched friction rub (“squeak of leather of a new saddle”) caused by fibrinous deposits in the pericardial space (Fig. 1) with three components—atrial systole, ventricular systole, and early ventricular diastole—is classic. It is best heard during inspiration at the left lower sternal border, with the patient leaning forward. The rub may disappear with the development of an effusion and impending cardiac tamponade.1

 

Box 1: Common Causes of Pericarditis and Pericardial Effusion
Idiopathic
Infectious—bacterial, viral, fungal, HIV
Myocardial infarction
Radiation
Postoperatively after open heart surgery
Chest trauma—blunt, sharp
Malignancy
  • Primary—mesothelioma, angiosarcoma
  • Metastatic—lung, breast, bone, lymphoma, melanoma
Collagen vascular diseases—rheumatoid arthritis, SLE
Metabolic—uremia, hypothyroidism
Pharmacologic—penicillin, phenytoin, procainamide, hydralazine, minoxidil, cromolyn sodium, methysergide, doxorubicin

HIV, human immunodeficiency virus; SLE, systemic lupus erythematosus.

Specific Types of Acute Pericarditis

Idiopathic Pericarditis.

The cause of acute pericarditis is often difficult to establish, and idiopathic pericarditis remains the most common diagnosis.

Viral Pericarditis.

Coxsackievirus B virus and echovirus are the most common viruses, and a fourfold increase in antiviral titers is required for the diagnosis. Patients often experience a prodrome of an upper respiratory tract infection. The prognosis of viral pericarditis is good, the course is usually self limited, and patients may be treated on an outpatient basis.

Purulent Pericarditis.

Before the antibiotic era, pneumonia was the prime cause of purulent pericarditis. Currently, causes include thoracic surgery, chemotherapy, immunosuppression, and hemodialysis. Presentation is usually acute with high fevers, chills, night sweats, and dyspnea, but the classic findings of chest pain or friction rub are rare. Cardiac tamponade occurs frequently (42% to 77% of patients in select series), and mortality is high. If purulent pericarditis is suspected, hospital admission with immediate pericardiocentesis and intravenous broad-spectrum antibiotics are mandatory, followed by early surgical drainage. Findings on pericardial fluid analysis include a high protein level (more than 6 g/dL), low glucose level (lower than 35 mg/dL), and very high leukocyte count (6,000 to 240,000/mm3). 5

Tuberculous Pericarditis.

This occurs in 1% to 2% of cases of pulmonary tuberculosis. Immunocompromised or human immunodeficiency virus (HIV)–positive patients are at increased risk.6 Nonspecific symptoms such as dyspnea, fever, chills, and night sweats develop slowly, and a friction rub or chest pain is often absent. The ECG is usually unrevealing, but the chest radiograph may be most useful when findings of pulmonary tuberculosis are present (Figs. 2 and 3). A patient with suspected or diagnosed pericardial tuberculosis should be hospitalized, and antituberculous therapy (e.g., rifampin, isoniazid, streptomycin, ethambutol) started promptly.

Analysis of the pericardial fluid shows high specific gravity, very high protein level (often more than 6 g/dL), and predominantly lymphocytic cells. A pericardial biopsy with acid-fast bacilli polymerase chain reaction testing is recommended for all patients with suspected tuberculous pericarditis. However, a normal pericardial biopsy does not exclude the diagnosis.

Uremic and Dialysis-Associated Pericarditis.

Uremic pericarditis occurs in 6% to 10% of patients with advanced renal failure before the initiation of hemodialysis; blood urea nitrogen levels usually exceed 60 mg/dL. The typical ST-segment elevation on the ECG usually is absent. A large hemorrhagic effusion caused by impaired platelet function is common, although tamponade is rare. Dialysis-associated pericarditis is caused by fluid overload, and the fluid is usually serous. With both forms, initiation or intensification of hemodialysis is indicated, usually leading to improvement in 1 to 2 weeks.7,8

Postmyocardial Infarction Pericarditis.

This is a common complication (25% to 40% of patients with MI) and occurs early, within 3 to 10 days after the MI. Its development correlates with the extent of necrosis, is more frequent with anterior than inferior infarcts, and is associated with a higher 1-year mortality rate and incidence of congestive heart failure.9

The diagnosis of post-MI pericarditis requires symptoms or a new pericardial friction rub; a pericardial effusion alone is nonspecific. In addition to the typical ST elevation seen with acute pericarditis that may be difficult to differentiate from the actual MI in this setting, findings on the ECG are persistently positive T waves more than 2 days post-MI or normalization of previously inverted T waves.10

Postcardiac Injury Syndrome.

Dressler's syndrome typically occurs 2 to 3 weeks after MI or open heart surgery. An autoimmune component and possibly a latent viral infection are believed to be responsible. The fully expressed syndrome consists of pleuritic chest pain, fever, leukocytosis, and a pericardial friction rub. Pleural effusions or pulmonary infiltrates may be seen.11

Malignancy.

Pericarditis associated with malignancy is caused mostly by metastatic disease. Bronchogenic or breast carcinoma, Hodgkin's disease, and lymphoma are common (Fig. 4); primary mesothelioma and angiosarcoma are rare. Diagnosis is based on analysis of pericardial fluid cytology, which has a sensitivity ranging from 70% to 90% and a specificity of up to 95% to 100%.1

Radiation Pericarditis.

Recent or remote mediastinal radiation may cause pericarditis at any time from weeks to months after the exposure.

Traumatic Pericarditis.

Sharp or blunt trauma (Figs. 5, 9 and 10) and even a minimally invasive procedure such as cardiac diagnostic or interventional catheterizations has been associated with pericardial irritation.

Diagnosis

The diagnosis of acute pericarditis remains a clinical diagnosis based on history, physical examination, and the ECG. Other imaging studies, including computed tomography (CT), magnetic resonance imaging (MRI), and echocardiography, may be used in select cases to investigate the pericardium.

Electrocardiography

The ECG in acute pericarditis has four consecutive stages (Table 1). Stage 1, characterized by diffuse ST elevation, is the most useful stage for the diagnosis of acute pericarditis (Fig. 6). The distinction between pericarditis and acute MI is difficult at times, but there are several clues (Table 2).12 Troponin levels may be elevated in up to 50% of patients with pericarditis but, in the absence of myocarditis, the prognosis remains unchanged.13

 

Table 1: Stages of Acute Pericarditis by Electrocardiography
Stage Time ST Segment T Wave PR Segment
1 Hours Diffuse elevation Upright
  • Leads aVR, V1—elevation
  • All others—depression
2 Days Resolution Flattening Resolution
3 Days-weeks Inversion
4 Days-weeks Upright

 

Table 2: Electrocardiographic Differentiation of Acute Pericarditis and Myocardial Infarction
Parameter Acute Pericarditis Acute Myocardial Infarction
ST elevation Diffuse in I, II, and III

Originating from S wave

Concave

Lead V6—ST-T amplitude >0.24 mm
Focal—vascular territory

Originating from R wave

Convex
ST depression Lead aVR only Present; reciprocal changes to ST elevation according to territory
PR segment Leads aVR, V1—elevation frequent Rare changes if atrial infarction is present
Chest Radiography

The chest radiograph may be entirely normal unless there is a pericardial effusion causing cardiomegaly (Fig. 7) or changes caused by an underlying disease.

Echocardiography

An episode of acute pericarditis that responds well to therapy may be followed clinically. Indications for echocardiography are symptoms persisting for longer than 1 to 2 weeks, the presence of hemodynamic abnormalities, clinical suspicion of a large or increasing pericardial effusion, or recent cardiac surgery.

Treatment

Most cases of acute pericarditis are uncomplicated and self limited and may be treated on an outpatient basis. Indications for an imaging modality, hospital admission, or both include clinical suspicion of a large effusion, hemodynamic instability, severe pain or other symptoms, suspicion of a serious underlying condition, or any other signs or symptoms of clinical instability or impending deterioration.

Medical Management

Treatment of the underlying disease is the mainstay of therapy. 14 Nonsteroidal anti-inflammatory drugs (NSAIDs) can be used for relief of pain, with agents such as indomethacin and aspirin having similar efficacy.15 Ibuprofen may be started at a dose of 400 mg every 8 hours and increased for symptom relief.15 Ketorolac tromethamine may be used as a parenteral agent for relief of symptoms.16 NSAIDs are contraindicated in the early period (less than 7 to 10 days) after MI (may predispose to cardiac rupture), and aspirin should be used instead.

If pericarditis recurs (20% to 30% of patients) or response to NSAIDs is poor, prednisone may be started at high doses and then tapered over 3 weeks. Use of steroids in acute pericarditis may promote a recurrence.17 As with NSAIDs, steroids should be avoided in post-MI pericarditis because there is an increased incidence of myocardial wall rupture.

Colchicine may be effective for persistent or refractory cases of Dressler's syndrome and idiopathic pericarditis.18,19 The COPE trial found that colchicine in addition to aspirin reduces the recurrence of pericarditis from 32.3% to 10.7%.20 If not mandatory, anticoagulants should be avoided during the acute phase of pericarditis to reduce the risks of bleeding and tamponade.

Pericardiectomy

Indications for pericardiectomy include the development of pericardial constriction and, rarely, recurrent pericarditis. Pericardiectomy is the most definitive procedure, with almost no recurrence; the 30-day perioperative mortality rate is about 5%.

Outcomes

Patients with uncomplicated acute pericarditis should have regular follow-up after the initial visit to ensure resolution of symptoms and rule out the development of constrictive symptoms.

Back to Top

Pericardial effusion

Definition

Pericardial effusion is defined as an increased amount of pericardial fluid.

Cause

The most common causes of large pericardial effusions (see Box 1) are malignancy (25% of cases), infection (27%), collagen vascular disease (12%), and chest radiation (14%). 21,22 A pericardial effusion is the most common cardiovascular manifestation of acquired immunodeficiency syndrome and is associated with a worse outcome.23–25

Pathophysiology

The pericardial sac normally contains 15 to 30 mL of fluid; it can hold 80 to 200 mL of fluid acutely and even up to 2 L if the fluid accumulates slowly. The development of tamponade depends on the rate of accumulation rather than on the volume of the effusion. Typically, signs of right ventricular diastolic failure develop first, followed by left-sided symptoms. As the understanding of tamponade has evolved, it has been shown that cardiac hemodynamics can be altered early, because fluid accumulates without clinical evidence of tamponade.26

Signs and Symptoms

Symptoms

Symptoms arise from the compression of surrounding structures (lung, stomach, phrenic nerve) or diastolic heart failure and include chest pressure or pain, dyspnea, and nausea, abdominal fullness, and dysphagia. Phrenic nerve irritation may cause hiccup.

Physical Examination Findings

With a small effusion, the physical examination is unremarkable. Larger effusions cause muffled heart sounds and, rarely, Ewart's sign (dullness to percussion, bronchial breath sounds, and egophony below the angle of the left scapula). With increasing volume of the effusion, signs and symptoms of cardiac tamponade may occur.

Diagnosis

Electrocardiography

Low voltage and electrical alternans (Fig. 8) may be seen if the effusion is large.

Chest Radiography

Cardiomegaly occurs if there is more than 250 mL of fluid in the pericardial sac (see Fig. 7). Displacement of the pericardial lining more than 2 mm away from the lower heart border is best seen on lateral film.27,28

Echocardiography

A pericardial effusion causes an echo-free space between visceral and parietal pericardium; the extent of the space defines the size of the effusion (Table 3). Large effusions may produce the picture of a “swinging heart”. Although echocardiography is the imaging modality of choice for diagnosing a pericardial effusion, it may miss small loculated effusions.

Table 3: Sizing of Pericardial Effusion by Echocardiography
Size Small Medium Large
Volume (mL) <100 100-500 >500
Localization Localized Circumferential Circumferential
Width (cm) <1 1-2 >2
Magnetic Resonance Imaging and Computed Tomography

CT is the best imaging modality for assessing the pericardium itself, being slightly superior to MRI in spatial resolution. Both are superior to echocardiography in detecting loculated effusions.

Laboratory Tests

Laboratory analysis in a patient with a pericardial effusion should include a complete blood count, chemistry panel, and erythrocyte sedimentation rate. Further testing should be done according to clinical suspicion.

Advertisement


Analysis of Pericardial Fluid

Pericardiocentesis should be performed for diagnostic purposes if the cause is unclear or if malignancy, tuberculous, fungal, or bacterial infection is suspected. Therapeutic pericardiocentesis should be performed for large effusions that are increasing in size or those causing pretamponade or tamponade.

The initial inspection should assess whether the fluid is hemorrhagic, purulent, or chylous. A red blood cell count higher than 100,000/mm3 is suggestive of trauma, malignancy, or pulmonary embolism (rare). Chylous fluid implies injury to the thoracic duct by trauma or infiltration. The fluid should be sent for a cell count, Gram stain, culture, cytology, acid-fast bacilli, determination of glucose, protein, and lactate dehydrogenase (LDH) levels, and specific gravity. The parameters listed in Table 4 have a high sensitivity for differentiating exudates versus transudates. An elevated protein level higher than 6.0 g/dL often indicates tuberculous, purulent, or parapneumonic effusion. An isolated increased fluid LDH level (higher than 300 U/dL) with a normal serum LDH level is most likely caused by malignancy. A low pericardial fluid glucose level (lower than 60 to 80 mg/dL) may be caused by parapneumonic, rheumatoid, tuberculous, or malignant effusion. However, no diagnostic test of pericardial fluid is specific for effusion associated with postpericardiotomy syndrome, radiation or uremic pericarditis, hypothyroidism, or trauma. The overall diagnostic yield of pericardial fluid analysis and biopsy is low (about 20%), emphasizing the importance of clinical history and examination.5

Table 4: Pericardial Effusion: Exudate Versus Transudate
Parameter Exudate Transudate
Cause Malignancy Radiation
Infectious, parainfectious Uremia
Postpericardiotomy syndrome Hypothyroidism
Collagen vascular disease Trauma
Specific gravity (g/mL) >1.015 <1.015
Total protein (g/dL) >3.0 <3.0
Fluid-to-serum protein ratio >0.5 <0.5
Fluid-to-serum LDH ratio >0.6 <0.6
Fluid-to-serum glucose ratio <1.0 >1.0

LDH, lactate dehydrogenase

Treatment

The medical management of pericardial effusion is based on treating the underlying cause.29 Diuretics may help decrease the intensity of fluid overload symptoms if present. Effusions causing pretamponade or tamponade require immediate drainage. Volume expansion and inotropic support may be used for hemodynamic stabilization pending drainage. In the immediate postoperative setting, surgical management and open drainage are preferred because of the high incidence of loculated effusions.

Pericardiocentesis

Echocardiographically guided pericardiocentesis is safe and effective. Indications for pericardiocentesis include a large effusion with hemodynamic compromise or tamponade, or for diagnostic purposes.

Surgical Treatment
Percutaneous Balloon Pericardiotomy.

This is the least invasive of the surgical procedures. It is used mostly for neoplastic effusion with a poor prognosis as a palliative treatment option. The success rate for relieving reaccumulation of pericardial fluid is 85% to 92% at 30 days. It may be performed in the catheterization laboratory under fluoroscopy using a balloon-dilating catheter.

Subxyphoid Pericardiostomy.

This procedure, known as a “pericardial window,” may be done under local anesthesia. It has a high success rate, with few complications, and recurrence of fluid accumulation is rare.

Outcomes

After drainage, follow-up echocardiography to rule out reaccumulation and constrictive physiology should be performed in all patients. Cardiac tamponade may develop with large or rapidly accumulating effusions.30

Back to Top

Cardiac tamponade

Definition

Cardiac tamponade occurs when fluid accumulation in the finite pericardial space causes an increase in pressure, with subsequent cardiac compression and hemodynamic compromise.

Prevalence

Of patients with large pericardial effusions, 25% to 30% develop tamponade.31

Pathophysiology

The elevated intrapericardial pressure leads to progressive limitation of mostly early diastolic ventricular filling, resulting in low cardiac output.32,33

Signs and Symptoms

Symptoms

Symptoms resulting from decreased cardiac output and congestion include dyspnea, chest discomfort, weakness, restlessness, agitation, drowsiness, oliguria, and anorexia. If the tamponade develops acutely as a complication of an acute MI (free wall rupture) or trauma, the presentation is usually catastrophic, with sudden death or shock and high mortality (Figs. 9 and 10).

Physical Examination Findings

The combination of the classic findings known as Beck's triad (hypotension, jugular venous distention, and muffled heart sounds) occurs in only 10% to 40% of patients. Tachycardia, tachypnea, and hepa tomegaly are common. Pulsus paradoxus is defined as an inspiratory decline in systolic blood pressure of more than 10 mm Hg resulting from compression and poor filling of the left ventricle caused by increased venous return to the right side of the heart. Pulsus paradoxus is nonspecific and insensitive and may occur with extracardiac disease, such as severe chronic obstructive pulmonary disease or asthma. 34

Diagnosis

Electrocardiography

The ECG may be unremarkable. Abnormal findings on ECG include electrical alternans (see Fig. 8), low voltage, and changes associated with acute pericarditis (see Fig. 6).

Transthoracic Echocardiography

Usually, a moderate-size or large pericardial effusion is present and leads to increasing compression and subsequent diastolic compression of the cardiac chambers, usually in the sequence right atrium–right ventricle–left atrium. The most sensitive finding for tamponade physiology on the echocardiogram is inferior vena cava plethora, with absent inspiratory collapse. Right ventricle inversion is the most accurate finding for diagnosis. Other less specific findings include excessive respiratory variations in diastolic mitral valve inflow, which is analogous to pulsus paradoxus.

Right Heart Catheterization

The most typical finding of right heart catheterization is equalization of mean right atrial, right ventricular and pulmonary artery diastolic, and mean pulmonary capillary wedge pressures.

Differential Diagnosis

The symptoms of pericardial tamponade may mimic those of right-sided heart failure, right ventricle infarction, constrictive pericarditis, and pulmonary embolism. However, with the use of echocardiography and right heart catheterization, these may be easily distinguished.

Treatment

Patients with pretamponade and tamponade require immediate hospital admission and prompt pericardial drainage by pericardiocentesis. The drain catheter may be left in place for up to 48 hours if drainage is slow or re-accumulation likely. If follow-up echocardiography documents fluid re-accumulation, a pericardial window should be considered, because the infection risk associated with a pericardial drain increases after 48 hours.35 Pending drainage, intravenous fluid expansion and inotropic support may be used for hemodynamically unstable patients.

Back to Top

Pericardial constriction

Definition

Constrictive pericarditis refers to an abnormal thickening of the pericardium, resulting in impaired ventricular filling and decreased cardiac output.

Cause

Most cases are idiopathic, although a history of acute or chronic pericarditis may occasionally be elicited.

Pathophysiology

The initiating event causes a chronic inflammatory pericardial process, resulting in fibrinous thickening, calcification of the pericardium (Fig. 11; also see Figs. 2 and 3), and limitation of intrapericardial volume. This leads to impaired ventricular filling and decreased cardiac output. Ultimately, right and then left ventricular heart failure develop. Distinguishing heart failure caused by constrictive physiology from diastolic restrictive physiology is a classic diagnostic dilemma.

Signs and Symptoms

Clinical Symptoms

Symptoms are often vague and their onset is insidious; they include malaise, fatigue, and decreased exercise tolerance. With progression of constriction, symptoms of right-sided heart failure (e.g., peripheral edema, nausea, abdominal discomfort, ascites) become apparent and usually precede signs of left-sided failure (e.g., exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea).

Physical Examination Findings

Increased ventricular filling pressures cause jugular venous distention and Kussmaul's sign, (absent inspiratory decline of jugular venous distention), which is sensitive but nonspecific for constriction.36 Auscultation reveals muffled heart sounds and occasionally a characteristic pericardial knock (60 to 200 milliseconds after the second heart sound), caused by sudden termination of ventricular inflow by the encasing pericardium.

Constrictive Effusive Pericarditis

This entity consists of a tense pericardial effusion in the presence of pericardial constriction, and both tamponade and constrictive signs and symptoms are present. Therapy includes pericardiocentesis initially, followed by pericardiectomy for long-term management.37

Diagnosis

Electrocardiography

The ECG does not show specific findings, but low voltage may be seen.

Laboratory Test Findings

Brain natriuretic peptide (BNP) is a serum biomarker that may help distinguish constrictive pericarditis from restrictive cardiomyopathy. Despite elevated filling pressures in both conditions, levels of BNP are significantly higher in restrictive cardiomyopathy.38

Chest Radiography

Pericardial calcifications (see Figs. 2 and 3), pleural effusions, and biatrial enlargement may be noted on the chest radiograph.

Echocardiography

This is the best imaging modality for assessing hemodynamic parameters noninvasively. M-mode echocardiography is useful to look for flattening of the left ventricular free wall. Two-dimensional echocardiography shows septal bounce and inferior vena cava plethora with absent inspiratory collapse, as well as the effects of increased pericardial pressure on the relatively low-pressure right atrial and right ventricular chambers. Doppler echocardiographic findings have the highest sensitivity and specificity for detecting constrictive physiology. Excessive respiratory variations in transmitral, transtricuspid, pulmonary venous, and hepatic vein flow are characteristic.39,40 More recently developed echocardiographic modalities such as tissue Doppler imaging have enhanced the ability to discriminate between restriction and constriction.41

Right Heart Catheterization

Direct pressure measurements are performed if there is doubt about the diagnosis. M- or W-shaped atrial pressure waveforms and “square root” or “dip-and-plateau” right ventricular pressure waveforms reflect impaired ventricular filling. Because of the fixed and limited space within the thickened and stiff pericardium, end-diastolic pressure equalization (typically within 5 mm Hg) occurs between these cardiac chambers. Pulmonary artery systolic pressures are usually normal in pericardial constriction; higher pulmonary pressures suggest a restrictive cardiomyopathy.

Magnetic Resonance Imaging and Computed Tomography

CT is the imaging modality of choice to evaluate the pericardium, being slightly superior to MRI in spatial resolution. Pericardial calcifications may easily be identified on CT. Although the finding of thickened pericardium on the CT or MRI is specific for constriction, up to 18% of patients with constriction confirmed by other modalities may not have pericardial thickening (see Fig. 11). 42

Treatment

Medical treatment is difficult and does not affect the natural progression or prognosis of the disease. Diuretics and a low-sodium diet may be tried for patients with mild to moderate (New York Heart Association [NYHA] Class I or II) symptoms or contraindications to surgery. 43 For most patients, pericardiectomy is advised, with 80% to 90% of patients experiencing improvement and 50% complete relief of symptoms. The 30-day perioperative mortality rate averages 5% to 10%. 44,45

Outcomes

Recurrence following surgery is caused mainly by incomplete resection. Without surgical treatment, biventricular failure develops.

Transient Constrictive Pericarditis

In a minority of patients, constrictive pericarditis may resolve with medical therapy, without surgical intervention. Although most cases are caused by prior cardiovascular surgery, there may be other causes, with the exception of radiation. In select cases, a trial of medical therapy has been reported to be useful in the early stages of pericardial constriction. 46

Summary

  • Acute pericarditis manifests with the triad of acute chest pain, changes on the ECG, and a pericardial rub. Ninety percent of cases are idiopathic, with troponin levels being elevated in about 50% of cases. NSAIDs should be used for most patients, except post-MI pericarditis, with steroids as an additional option for primary treatment. Steroids may increase the recurrence rate of pericarditis. Colchicine may reduce the recurrence of pericarditis.
  • Cardiac tamponade is a clinical diagnosis made by documenting pulsus paradoxus, jugular venous distention, and muffled heart sounds in the presence of a pericardial effusion. The signs depend on the volume of fluid in the pericardial sac and the rate at which the fluid accumulates. Echocardiography can confirm the diagnosis at an early stage and help with the drainage of the effusion.
  • Pericardial constriction results from an abnormal thickening of the pericardium that causes an impairment of diastolic filling. The diagnosis can be made by noting hemodynamic derangements on echocardiography and a thickening of the pericardium on CT or MRI. About 20% of patients will not demonstrate thickening of the pericardium by CT. The treatment of choice is surgical excision of the pericardium. In a minority of patients, transient constriction can occur, which may respond to medical management.

Back to Top

References

  1. Zipes DP, Libby P , Bonow RO , Braunwald E. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 7th ed. 2005; Philadelphia. WB Saunders, 2005.
  2. Pericardial disease. Circulation. 113: 2006; 1622-1632.
  3. Pericardial effusion in the course of myocardial infarction: Incidence, natural history, and clinical relevance. Circulation. 73: 1986; 294-299.
  4. The incidence and natural history of pericardial effusion after cardiac surgery—an echocardiographic study. Circulation. 69: 1984; 506-511.
  5. The usefulness of diagnostic tests on pericardial fluid. Chest. 111: 1997; 1213-1221.
  6. Tuberculous pericarditis. JAMA. 266: 1991; 99-103.
  7. Pericarditis in end-stage renal disease. Cardiol Clin. 8: 1990; 701-707.
  8. Pericarditis associated with renal failure: Evolution and management. Semin Dial. 14: 2001; 61-66.
  9. Factors associated with pericardial effusion in acute Q wave myocardial infarction. Circulation. 81: 1990; 477-481.
  10. Electrocardiographic diagnosis of postinfarction regional pericarditis. Ancillary observations regarding the effect of reperfusion on the rapidity and amplitude of T wave inversion after acute myocardial infarction. Circulation. 88: 1993; 896-904.
  11. The postcardiac injury syndromes. Clin Cardiol. 15: 1992; 67-72.
  12. Infarction-associated pericarditis. Rarity of diagnostic electrocardiogram. N Engl J Med. 311: 1984; 1211-1214.
  13. Clinical practice. Acute pericarditis. N Engl J Med. 351: 2004; 2195-2202.
  14. Management of malignant pericardial effusion and tamponade. JAMA. 257: 1987; 1088-1092.
  15. Nonsteroidal anti-inflammatory drugs in the treatment of pericarditis. Cardiol Rev. 11: 2003; 211-217.
  16. Rapid resolution of symptomatic acute pericarditis with ketorolac tromethamine: A parenteral nonsteroidal antiinflammatory agent. Am Heart J. 125: 1993; 1455-1458.
  17. Recurrent pericarditis: Recent advances and remaining questions. Circulation. 112: 2005; 1921-1923.
  18. Colchicine treatment for recurrent pericarditis. A decade of experience. Circulation. 97: 1998; 2183-2185.
  19. Recurrent pericarditis. Relief with colchicine. Circulation. 82: 1990; 1117-1120.
  20. Colchicine in addition to conventional therapy for acute pericarditis: Results of the COlchicine for acute PEricarditis (COPE) trial. Circulation. 112: 2005; 2012-2016.
  21. Clinical clues to the causes of large pericardial effusions. Am J Med. 109: 2000; 95-101.
  22. A prospective trial of subxiphoid pericardiotomy in the diagnosis and treatment of large pericardial effusion. A follow-up report. Ann Surg. 218: 1993; 777-782.
  23. Pericardial effusion and AIDS. Circulation. 94: 1996; 2312.
  24. Pericardial effusion in AIDS. Circulation. 96: 1997; 2080-2081.
  25. Pericardial effusion in AIDS. Incidence and survival. Circulation. 92: 1995; 3229-3234.
  26. Cardiac tamponade. Catheter Cardiovasc Interv. 64: 2005; 245-255.
  27. Roentgenograms in pericardial effusion. JAMA. 258: 1987; 1890-1891.
  28. Supine cross-table lateral chest roentgenogram for the detection of pericardial effusion. JAMA. 257: 1987; 3266-3268.
  29. Treatment of malignant pericardial effusion. JAMA. 272: 1994; 59-64.
  30. Long-term follow-up of idiopathic chronic pericardial effusion. N Engl J Med. 341: 1999; 2054-2059.
  31. Etiology of large pericardial effusions. Am J Med. 95: 1993; 209-213.
  32. Cardiac tamponade. Cardiol Clin. 8: 1990; 627-637.
  33. Spectrum of hemodynamic changes in cardiac tamponade. Am J Cardiol. 66: 1990; 1487-1491.
  34. Pulsus paradoxus: Definition and relation to the severity of cardiac tamponade. Am Heart J. 115: 1988; 391-398.
  35. Diagnosis and management (by subxiphoid pericardiotomy) of large pericardial effusions causing cardiac tamponade. Am J Cardiol. 69: 1992; 1075-1078.
  36. Paradoxical physical findings described by Kussmaul: Pulsus paradoxus and Kussmaul's sign. Lancet. 359: 2002; 1940-1942.
  37. Subacute effusive-constrictive pericarditis. Circulation. 43: 1971; 183-192.
  38. The efficacy of brain natriuretic peptide levels in differentiating constrictive pericarditis from restrictive cardiomyopathy. J Am Coll Cardiol. 45: 2005; 1900-1902.
  39. Doppler features of constrictive pericarditis. Circulation. 96: 1997; 3799-3800.
  40. Value of dynamic respiratory changes in left and right ventricular pressures for the diagnosis of constrictive pericarditis. Circulation. 93: 1996; 2007-2013.
  41. Comparison of new Doppler echocardiographic methods to differentiate constrictive pericardial heart disease and restrictive cardiomyopathy. Am J Cardiol. 87: 2001; 86-94.
  42. Constrictive pericarditis in 26 patients with histologically normal pericardial thickness. Circulation. 108: 2003; 1852-1857.
  43. Pericarditis, pericardial effusion, cardiac tamponade, and constriction. Crit Care Clin. 5: 1989; 455-476.
  44. Constrictive pericarditis in the modern era: Evolving clinical spectrum and impact on outcome after pericardiectomy. Circulation. 100: 1999; 1380-1386.
  45. Surgical treatment of constrictive pericarditis: Analysis of outcome and diagnostic error. Circulation. 72: 1985; II264-II273.
  46. Transient constrictive pericarditis: causes and natural history. J Am Coll Cardiol. 43: 2004; 271-275.

Back to Top

Suggested Readings

  • Pericardial effusion and AIDS. Circulation. 94: 1996; 2312.
  • Transient constrictive pericarditis: Causes and natural history. J Am Coll Cardiol. 43: 2004; 271-275.
  • Colchicine in addition to conventional therapy for acute pericarditis: Results of the COlchicine for acute PEricarditis (COPE) trial. Circulation. 112: 2005; 2012-2016.
  • Clinical practice. Acute pericarditis. N Engl J Med. 351: 2004; 2195-2202.
  • The efficacy of brain natriuretic peptide levels in differentiating constrictive pericarditis from restrictive cardiomyopathy. J Am Coll Cardiol. 45: 2005; 1900-1902.
  • Pericardial disease. Circulation. 113: 2006; 1622-1632.
  • The usefulness of diagnostic tests on pericardial fluid. Chest. 111: 1997; 1213-1221.
  • Nonsteroidal anti-inflammatory drugs in the treatment of pericarditis. Cardiol Rev. 11: 2003; 211-217.
  • Constrictive pericarditis in 26 patients with histologically normal pericardial thickness. Circulation. 108: 2003; 1852-1857.
  • Zipes DP, Libby P , Bonow RO , Braunwald E. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 7th ed 2005; Philadelphia. WB Saunders, 2005.