Constrictive pericarditis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Muhammad Umer Tariq, M.D., Atif Mohammad, M.D. Huda A. Karman, M.D.

Pericardial constriction occurs when a fibrotic, adherent pericardium restricts diastolic filling of the heart. Variants of constrictive pericarditis have been described such as transient, subtle, effusive and chronic, depending on the course of the disease. The disease process typically begins with pericardial inflammation that progresses onto fibrosis. (Pathophysiology)It may occasionally follow an episode of acute pericarditis. There is fibrous scarring of the pericardium and usually fusion of the visceral and parietal pericardium. The pericardium is composed of a double-layered sac that surrounds the heart and the roots of the great vessels. The serous layer (smooth visceral) and a fibrous layer (tough parietal) of the pericardium encloses the pericardial cavity which contains pericardial fluid.The pericardium function is to protect the heart against infection and to provide it with lubrication. Constrictive pericarditis is a chronic inflammation that leads to the thickening, fibrosis, and scarring of the pericardial sac. The thickened fibrotic pericardium restricts the normal late diastolic filling in constrictive pericarditis and results in significant respiratory variation in blood flow in the ventricles. This is known as ventricular interdependence, where the amount of blood flow into one ventricle is dependent on the amount of blood flow into the other ventricle.The intrapericardial space contains 50 mL of plasma ultrafiltrate that minimize friction during cardiac motion. pericarditis causes that can trigger the development of constrictive pericarditis are tuberculosis, viral infection, radiation therapy, trauma, post-cardiac surgery. Constrictive pericarditis is most commonly caused by conditions or events that cause inflammation to develop around the heart, including idiopathic, infectious (viral, bacterial, tuberculous, fungal, parasitic ) and purulent pericarditis. It can also occur post MI (Dressler syndrome), post surgical (CABG), post radiation therapy. Constrictive pericarditis can also be caused by or associated with connective tissue disease, pulmonary asbestosis, chronic renal failure, neoplasm (mesothelioma). Constrictive pericarditis must be differentiated from restrictive cardiomyopathy. The evaluation of ventricular interdependence between the two ventricles is the best objective method to distinguish the two syndromes. Constrictive pericarditis should also be differentiated from cardiac tamponade, right-sided atrial tumors, such as myxomas, superior vena cava syndrome, right-sided valvular abnormalities (tricuspid stenosis or tricuspid regurgitation), systolic or diastolic congestive heart failure( pressure-overload and myocardial, valvular, or atherosclerotic disease causes)

• In 1989, Hatle et al reported the two characteristic features in constrictive pericarditis:
  • First, they showed dissociation between intrathoracic and intracardiac pressures
  • Second, enhanced ventricular interaction can also occur
    
    

The pericardium is composed of a double-layered sac that surrounds the heart and the roots of the great vessels. The serous layer (smooth visceral) and a fibrous layer (tough parietal) of the pericardium encloses the pericardial cavity which contains pericardial fluid.The pericardium function is to protect the heart against infection and to provide it with lubrication. Constrictive pericarditis is a chronic inflammation that leads to the thickening, fibrosis, and scarring of the pericardial sac. The thickened fibrotic pericardium restricts the normal late diastolic filling in constrictive pericarditis and results in significant respiratory variation in blood flow in the ventricles. This is known as ventricular interdependence, where the amount of blood flow into one ventricle is dependent on the amount of blood flow into the other ventricle.The intrapericardial space contains 50 mL of plasma ultrafiltrate that minimize friction during cardiac motion. pericarditis causes that can trigger the development of constrictive pericarditis are tuberculosis, viral infection, radiation therapy, trauma, post-cardiac surgery.

Constrictive pericarditis is most commonly caused by conditions or events that cause inflammation to develop around the heart, including idiopathic, infectious (viral, bacterial, tuberculous, fungal, parasitic ) and purulent pericarditis. It can also occur post MI (Dressler syndrome), post surgical (CABG), post radiation therapy. Constrictive pericarditis can also be caused by or associated with connective tissue disease, pulmonary asbestosis, chronic renal failure, neoplasm (mesothelioma).

Constrictive pericarditis must be differentiated from restrictive cardiomyopathy as they are treated very differently. Multi-modality imaging including echocardiography with flow and tissue doppler imaging, cardiac MRI and heart catheterization are used to differentiate between the two conditions that may present with similar clinical signs and symptoms. The finding of ventricular interdependence (respiratory variation of mitral and tricuspid flows) as demonstrated by different imaging modalities is key in differentiating the two syndromes.

Constriction can occur after almost any pericardial process. Historically, the most common etiology was tuberculosis, but in the modern age, this cause now accounts for <2% of cases. In a study of 95 patients undergoing pericardiectomy at Stanford, no cause could be found in 42% of patients. 31% occurred after radiotherapy, particularly following high dose mantle radiation for Hodgkin’s disease. Pericardial constriction occurred a mean of 85 months after radiotherapy, but occurred as early as 1 month and as late as 244 months. It also occurred post-operatively in 11% of cases. Connective tissue disorders accounted for 4%, neoplasm 3%, uremia 2% and sarcoidosis for 1% of cases. The likelihood of a constrictive pericarditis diagnosis is less than 10 in 100,000 hospital admissions considering only 9% of acute pericarditis patients develop pericardial constriction. This disease is more prevalent in males with a male-to-female ratio of 3:1. Constrictive pericarditis has been documented in people 8-70 years of age, with a median of 61 years of age.

Constrictive pericarditis (CP) is rare and is usually developed as a complication of acute pericarditis. Although there are no established risk factors for constrictive pericarditis, prospective studies have shown an increased risk after long-term follow-up of acute pericarditis.

Constrictive pericarditis is when there is scarring of the sac (the pericardium) around the heart, which may require surgical stripping of the scar. Failure to diagnose or treat constrictive pericarditis could result with severe complications that include cardiac tamponade, damage to the coronary arteries, heart failure, pulmonary edema, scarring of the heart muscle.

The diagnosis of constrictive pericarditis is based on the clinical findings (symptoms and signs) of right heart failure, and diastolic filling impairment due to pericardial constriction. The diagnostic imaging methods include echocardiography, CT, CMR, cardiac catheterization.

The clinical history of pericardial constriction cannot be solely used to make a diagnosis due to the multiple symptoms this disease presents. The symptoms may not be recognizable to the patients considering they develop slowly and over time. The early symptoms of pericardial constriction are often more consistent with liver disease and the patient may be erroneously referred for imaging studies of the liver.

Physical findings of patients with constrictive pericarditis may include general, cardiovascular and other organ systemic findings. General findings could be indistinct or could include muscle wasting, cachexia, or jaundice. Cardiovascular Findings include sinus tachycardia, distant or muffled heart sounds, pericardial knock, cardiac murmur, pulsus paradoxicum (paradoxus), kussmaul sign (elevation of systemic venous pressures with inspiration). Other systemic findings include hepatomegaly, spider angiomata, palmar erythema, peripheral edema.

Constrictive pericarditis lab findings can show evidence of congestive heart failure, or associated protein losing enteropathy, nephrotic syndrome, and LFT abnormalities consistent with hepatic congestion and chylous ascites

Electrocardiographic signs of constrictive chronic pericarditis are usually inconsistent and non specific. It includes left atrial enlargement, frequent atrial arrhythmias, right axis deflection, possible reduction in voltages, diffuse negative T-waves. Typical findings are normal QRS axis, low voltage, and generalized T wave flattening or inversion. Evidence of right ventricular hypertrophy or right axis deviation can present which is usually an unexplained finding (cardiac rotation and distortion), or due to the presence of severe fibrotic annular subpulmonic constriction

Plain chest radiographs in patients with constrictive pericarditis may show pericardial calcification, small cardiac silhouette (uncomplicated CP), large cardiac silhouette (if CP coexist with cardiomyopathy). Less reliable plain radiographic findings include an abnormal cardiac contour, such as straightening of the right atrial border and, more rarely, straightening of the right and left cardiac borders, with obliteration of the normal curves, on frontal images. The absence of calcification does not exclude the diagnosis of constrictive pericarditis.

Constrictive pericarditis can present with typical echocardiographic findings, such as normal systolic function, a plethoric inferior vena cava, a restrictive mitral inflow pattern with respiratory variation, reversal of expiratory hepatic vein flow, a septal motion suggestive of enhanced ventricular interaction, or an elevated early diastolic mitral annular velocity (E′) detected by tissue Doppler imaging

Per ESC guidelines, CT and/or CMR are indicated as second-level imaging techniques to assess calcifications (CT), pericardial thickness, degree and extension of pericardial involvement.

MRI has been included in the multi-modality imaging guidelines for the diagnosis of constrictive pericarditis. It is of great value when echocardiography is non diagnostic of constrictive pericarditis and the suspicion remains high. MRI delineates two essential components of the evaluation: pericardial anatomy and functional imaging demonstrating ventricular interdependence. It also can be used to rule out restrictive cardiomyopathy. MRI is especially useful with the use of late gadolinium enhancement as it identifies pericardial inflammation when suspected in the context of a short duration of symptoms and elevated inflammatory markers.

There are no other imaging findings associated with constrictive pericarditis.

Cardiac Catheterization can be used for the diagnosis of constrictive pericarditis. Typically, there is equalization of diastolic pressures in all four chambers. These filling pressures are typically elevated. RVSP is usually moderately elevated but rarely exceeds 60 mmHg.

Pericardial constriction is a progressive disease without spontaneous reversal of the pericardial thickening. Some patients can be medically managed for several years. Edema can be controlled with diuretics and slowing of the heart rate can maximize the diastolic filling time. Most patients eventually develop significant debility from impaired cardiac output and elevated right and left sided filling pressures.

Pericardiectomy is the only definitive management of chronic constrictive pericarditis. Effort should be made to remove as much of the pericardium as possible. Extensive penetration of the myocardium by fibrosis and calcification is associated with poor outcome. Operative mortality ranges from 55% to 10%.

There are no established measures for the primary prevention of constrictive pericarditis.

There are no established measures for the secondary prevention of constrictive pericarditis.

nl:Pericarditis constrictiva sr:Констриктивни перикардитис

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Huda A. Karman, M.D.

• There is limited information about the historical perspective of constrictive pericarditis. In 1989, Hatle et al reported the two characteristic features in constrictive pericarditis. First, they showed dissociation between intrathoracic and intracardiac pressures. Second, enhanced ventricular interaction can also occur

• There is limited information about the historical perspective of constrictive pericarditis.
• In 1989, Hatle et al reported the two characteristic features in constrictive pericarditis:
  • First, they showed dissociation between intrathoracic and intracardiac pressures
  • Second, enhanced ventricular interaction can also occur ^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Atif Mohammad, M.D. Huda A. Karman, M.D.

The pericardium is composed of a double-layered sac that surrounds the heart and the roots of the great vessels. The serous layer (smooth visceral) and a fibrous layer (tough parietal) of the pericardium encloses the pericardial cavity which contains pericardial fluid.The pericardium function is to protect the heart against infection and to provide it with lubrication. Constrictive pericarditis is a chronic inflammation that leads to the thickening, fibrosis, and scarring of the pericardial sac. The thickened fibrotic pericardium restricts the normal late diastolic filling in constrictive pericarditis and results in significant respiratory variation in blood flow in the ventricles. This is known as ventricular interdependence, where the amount of blood flow into one ventricle is dependent on the amount of blood flow into the other ventricle.The intrapericardial space contains 50 mL of plasma ultrafiltrate that minimize friction during cardiac motion. pericarditis causes that can trigger the development of constrictive pericarditis are tuberculosis, viral infection, radiation therapy, trauma, post-cardiac surgery.

The pathophysiology of constrictive pericarditis is ^{[1] [2] [3]}. The pericardium is composed of a double-layered sac that surrounds the heart and the roots of the great vessels. The serous layer (smooth visceral) and a fibrous layer (tough parietal) of the pericardium encloses the pericardial cavity which contains pericardial fluid.The pericardium function is to protect the heart against infection and to provide it with lubrication. The intrapericardial space contains 50 mL of plasma ultrafiltrate that minimize friction during cardiac motion.

Constrictive pericarditis is a chronic inflammation that leads to the thickening, fibrosis, and scarring of the pericardial sac. The thickened fibrotic pericardium restricts the normal late diastolic filling in constrictive pericarditis and results in significant respiratory variation in blood flow in the ventricles^[4]

Chronic constrictive pericarditis characterized by obliteration of pericardial cavity by granulation tissue during healing of:^[5]

• An acute episode of fibrinous or serofibrinous pericarditis
• A resorption of chronic pericardial effusion.

The heart becomes encased by the granulation tissue which gradually contracts may get calcified. The rigid thickened pericardium limits the normal elasticity of the pericardium and hence limits the ventricular filling. Ventricular filling in early diastole is not affected as it is impeded only when the pericardium elastic limit is reached.

During inspiration, the negative pressure in the thoracic cavity will cause increased blood flow into the right ventricle (increased intrathoracic pressure). This increased volume in the right ventricle will cause the interventricular septum to bulge towards the left ventricle, leading to decreased filling of the left ventricle. Due to the Frank-Starling law, this will cause decreased pressure generated by the left ventricle during systole. Because constrictive pericarditis limits the ability of the ventricles to expand, the intracardiac pressure variation during respiratory cycle occurs only between right and left ventricles.

The intrathoracic and intracardiac pressures dissociation leads to the following during inspiration:

• Pulmonary venous pressure decreases
• Venous return decreases
• Left atrial pressure doesn’t change
• Pulmonary veins to left atrial (LA) flow decreases

During expiration, the amount of blood entering the right ventricle will decrease, allowing the interventricular septum to bulge towards the right ventricle, and increased filling of the left ventricle and subsequent increased pressure generated by the left ventricle during systole.

This is known as ventricular interdependence, since the amount of blood flow into one ventricle is dependent on the amount of blood flow into the other ventricle.

The impairment of diastolic filling uniformly affects both ventricles, especially during the latter third of diastole. The symmetrical constricting effect of the pericardium results in elevation and equilibration of diastolic pressures in all four chambers of the heart. As a result of this constriction and elevated venous filling pressure, most diastolic filling occurs rapidly and early in diastole. This filling abruptly halts when the myocardium encounters the noncompliant pericardium.

Triggers:

The following are pericarditis causes that can trigger the development of constrictive pericarditis:

• Tuberculosis
• Viral infection
• Radiation therapy
• Trauma
• Post-cardiac surgery

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Huda A. Karman, M.D.

Constrictive pericarditis is most commonly caused by conditions or events that cause inflammation to develop around the heart, including idiopathic, infectious (viral, bacterial, tuberculous, fungal, parasitic ) and purulent pericarditis. It can also occur post MI (Dressler syndrome), post surgical (CABG), post radiation therapy. Constrictive pericarditis can also be caused by or associated with connective tissue disease, pulmonary asbestosis, chronic renal failure, neoplasm (mesothelioma).

Constrictive pericarditis is most commonly caused by conditions or events that cause inflammation to develop around the heart, including:

• Coronary artery bypass graft surgery: In patients who have undergone coronary artery bypass surgery with pericardial sparing, there is danger of tearing a bypass graft while removing the pericardium. If any pericardium is not removed, it is possible for bands of pericardium to cause localized constriction which may cause symptoms and signs consistent with constriction.
• Radiation therapy to the chest ^[1]
• Tuberculosis. This is the most frequent cause of constriction in Africa and Asia.
• Post viral pericarditis
• Post-surgical
• Prior mediastinal radiation therapy
• Chronic renal failure (uremic pericarditis) ^[2]
• Connective tissue disorders
• Neoplastic pericardial infiltration
• Incomplete drainage of purulent pericarditis
• Fungal and parasitic infections
• Following pericarditis associated with ST elevation myocardial infarction (Dressler’s syndrome)
• In association with pulmonary asbestosis
• Mesothelioma
• Bacterial, viral, or surgical infections that cause abnormal buildup in the covering of the heart

Cardiovascular	Chylopericardium, Rheumatic pericarditis, Coronary artery bypass graft surgery, Post mediastinal surgery, Post viral pericarditis, Neoplastic pericardial infiltration, Dressler’s syndrome
Chemical / poisoning	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	Bromocriptine, Hydralazine, Methysergide, Procainamide
Ear Nose Throat	No underlying causes
Endocrine	No underlying causes
Environmental	No underlying causes
Gastroenterologic	No underlying causes
Genetic	Mulibrey nanism
Hematologic	No underlying causes
Iatrogenic	Coronary artery bypass graft surgery, Implantation of an automated implantable cardiac defibrillator, Implantation of an epicardial pacemaker, Incomplete drainage of purulent pericarditis, Orthopedic heart transplant, Post mediastinal surgery, Prior mediastinal radiation therapy, Radiation therapy, Sclerotherapy for esophageal varices.
Infectious Disease	Adenovirus, Bacterial infections, Coxsackievirus, Echovirus, Fungal infections, Hepatitis viruses, Pneumococcal pneumonia, Post viral pericarditis, Tuberculosis
Musculoskeletal / Ortho	No underlying causes
Neurologic	No underlying causes
Nutritional / Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	Mesothelioma, Neoplastic pericardial infiltration
Opthalmologic	No underlying causes
Overdose / Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	In association with pulmonary asbestosis, Pneumococcal pneumonia, Mesothelioma
Renal / Electrolyte	Chronic renal failure, Uremia
Rheum / Immune / Allergy	Connective tissue disorders, Dressler’s syndrome, Rheumatoid arthritis, Sarcoidosis, Systemic sclerosis
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Dental	No underlying causes
Miscellaneous	No underlying causes

• Adenovirus
• Bacterial infections
• Chronic renal failure
• Chylopericardium
• Connective tissue disorders
• Coronary artery bypass graft surgery
• Coxsackievirus
• Dressler’s syndrome
• Echovirus
• Fungal infections
• Hepatitis viruses
• Hydralazine
• Implantation of an automated implantable cardiac defibrillator
• Implantation of an epicardial pacemaker
• In association with pulmonary asbestosis
• Incomplete drainage of purulent pericarditis
• Mesothelioma
• Methysergide
• Mulibrey nanism
• Neoplastic pericardial infiltration
• Orthopedic heart transplant
• Pneumococcal pneumonia
• Post mediastinal surgery
• Post viral pericarditis
• Prior mediastinal radiation therapy
• Procainamide
• Radiation therapy
• Rheumatic pericarditis
• Rheumatoid arthritis
• Sarcoidosis
• Sclerotherapy for esophageal varices.
• Systemic sclerosis
• Tuberculosis
• Uremia

http://www.nlm.nih.gov/medlineplus/ency/article/001103.htm Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Huda A. Karman, M.D.

Constrictive pericarditis must be differentiated from restrictive cardiomyopathy. The evaluation of ventricular interdependence between the two ventricles is the best objective method to distinguish the two syndromes. Constrictive pericarditis should also be differentiated from cardiac tamponade, right-sided atrial tumors, such as myxomas, superior vena cava syndrome, right-sided valvular abnormalities (tricuspid stenosis or tricuspid regurgitation), systolic or diastolic congestive heart failure( pressure-overload and myocardial, valvular, or atherosclerotic disease causes)

Both syndromes are associated with abnormalities in left ventricular filling. In patients with constriction, this is due to constriction of filling of the left ventricle by the pericardium. In restriction, there is impaired relaxation of the left ventricle.

Ventricle interdependence is the effect of the size, shape and compliance of one ventricle on the size, shape and compliance of the other ventricle. These effects are most apparent with respiration or with sudden postural changes. Whereas diastolic ventricular interdependence is mainly mediated through the pericardium, systolic ventricular interdependence is mediated through the interventricular septum as well as through the pericardium.

The clinical importance of ventricular interdependence is in the differentiation between constrictive pericarditis and restrictive myocarditis as both of them present with symptoms of right heart failure.

Ventricular interdependence is assessed in the cardiac catheterization laboratory. In this test, the systolic pressure generated in the left ventricle is compared to that in the right ventricle during inspiration. During inspiration, there is negative intrathoracic pressure, and increased filling of the right ventricle.

Among patients with constrictive pericarditis, with inspiration, there is increased filling of the right ventricle and given that it is constrained by the pericardium, the systolic pressure in the right ventricle rises. There is bulging of the septum into the left ventricle, and reduced filling of the left ventricle, and therefore the pressure drops in the left ventricle. The RV enlarges, and the LV gets smaller during inspiration.

Shown below is an image illustrating the changes in the size of the left and right ventricles during respiration in the case of constrictive pericarditis.

Among patients with restrictive cardiomyopathy, there is an equal decline in LV and RV systolic pressures during inspiration.

Shown below is an image illustrating the changes in the size of the left and right ventricles during respiration in the case of restrictive cardiomyopathy.

Both syndromes are associated with abnormalities in left ventricular filling. In patients with constriction, this is due to constriction of filling of the left ventricle by the pericardium. In restriction, there is impaired relaxation of the left ventricle.

The E prime velocity is normal as there is no impediment to relaxation of the left ventricle.

The E prime velocity is low (5 or below) in restriction due to impaired filling of the ventricle due to impaired relaxation.

• History of radiation, breast cancer, Hodgkins disease, prior heart surgery
• When there are signs and symptoms of heart failure out of proportion to myocardial or valve abnormalities
• There is respiratory variation on Doppler ultrasound
• There is septal shift with inspiration
• BNP is not very elevated
• The left atrium is not enlarged

• Large or giant atrium due to impaired left ventricular filling.

In many cases, constrictive pericarditis is a late sequela of an inflammatory condition of the pericardium. The inflammatory condition is usually an infection that involves the pericardium, but it may be after a heart attack or after heart surgery.

Almost half the cases of constrictive pericarditis in the developing world are idiopathic in origin. In regions where tuberculosis is common, it is the cause in a large portion of cases.

Several conditions produce signs and symptoms that are similar to those generated by pericarditis, including life threatening conditions such as myocardial infarction, aortic dissection and pulmonary embolism. The conditions with similar symptoms to constrictive pericarditis include:

• Amyloidosis
• Atrial myxoma
• Cardiac cirrhosis
• Primary cardiac neoplasms
• Cardiac sarcoma
• Cardiac tamponade
• Cardiomyopathy, Dilated
• Restrictive Cardiomayopathy
• Hemochromatosis
• Nephrotic syndrome
• Ovarian cancer
• Pericardial effusion
• Pericarditis, Acute
• Pericarditis, Constrictive-Effusive
• Pericarditis, Uremic
• Sarcoidosis
• Superior vena cava syndrome
• Tricuspid regurgitation
• Tricuspid stenosis
• Uremia

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Atif Mohammad, M.D.; Huda A. Karman, M.D.

Constriction can occur after almost any pericardial process. Historically, the most common etiology was tuberculosis, but in the modern age, this cause now accounts for <2% of cases. In a study of 95 patients undergoing pericardiectomy at Stanford, no cause could be found in 42% of patients. 31% occurred after radiotherapy, particularly following high dose mantle radiation for Hodgkin’s disease. Pericardial constriction occurred a mean of 85 months after radiotherapy, but occurred as early as 1 month and as late as 244 months. It also occurred post-operatively in 11% of cases. Connective tissue disorders accounted for 4%, neoplasm 3%, uremia 2% and sarcoidosis for 1% of cases. The likelihood of a constrictive pericarditis diagnosis is less than 10 in 100,000 hospital admissions considering only 9% of acute pericarditis patients develop pericardial constriction. This disease is more prevalent in males with a male-to-female ratio of 3:1. Constrictive pericarditis has been documented in people 8-70 years of age, with a median of 61 years of age.

Constriction can occur after almost any pericardial process. Historically, the most common etiology was tuberculosis, but in the modern age, this cause now accounts for <2% of cases. In a study of 95 patients undergoing pericardiectomy at Stanford, no cause could be found in 42% of patients. 31% occurred after radiotherapy, particularly following high dose mantle radiation for Hodgkin’s disease. Pericardial constriction occurred a mean of 85 months after radiotherapy, but occurred as early as 1 month and as late as 244 months. It also occurred post-operatively in 11% of cases. Connective tissue disorders accounted for 4%, neoplasm 3%, uremia 2% and sarcoidosis for 1% of cases.

The likelihood of a constrictive pericarditis diagnosis is less than 10 in 100,000 hospital admissions considering only 9% of acute pericarditis patients develop pericardial constriction. This disease is more prevalent in males with a male-to-female ratio of 3:1. Constrictive pericarditis has been documented in people 8-70 years of age, with a median of 61 years of age.

In a prospective study, 500 patients with acute pericarditis were followed over 8 years. At a median follow-up of 6 years, 9 patients developed constrictive pericarditis among whom 2 patients had viral/idiopathic etiology.^[1] Incidence rates of constrictive pericarditis per person years observed were as follows:

Incidence rates^[1]

Idiopathic/viral pericarditis	76 cases per 100,000 person years
Connective tissue disease/pericardial injury	440 cases per 100,000 person years
Malignant pericarditis	633 cases per 100,000 person years
Tuberculous pericarditis	3165 cases per 100,000 person years
Purulent pericarditis	5274 cases per 100,000 person years

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Huda A. Karman, M.D.

Constrictive pericarditis (CP) is rare and is usually developed as a complication of acute pericarditis. Although there are no established risk factors for constrictive pericarditis, prospective studies have shown an increased risk after long-term follow-up of acute pericarditis.

Constrictive pericarditis (CP) is rare and is usually developed as a complication of acute pericarditis. Although there are no established risk factors for constrictive pericarditis, prospective studies have shown an increased risk after long-term follow-up of acute pericarditis. Acute pericarditis can be developed due to the following:

• Idiopathic
• Viral
• Connective tissue disease
• Pericardial injury syndromes
• Neoplastic pericarditis
• Tuberculosis pericarditis.
• Purulent pericarditis
  All these factors or etiologies can result in the development of constrictive pericarditis eventually^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Huda A. Karman, M.D.

Constrictive pericarditis is when there is scarring of the sac (the pericardium) around the heart, which may require surgical stripping of the scar. Failure to diagnose or treat constrictive pericarditis could result with severe complications that include cardiac tamponade, damage to the coronary arteries, heart failure, pulmonary edema, scarring of the heart muscle.

Constrictive pericarditis is when there is scarring of the sac (the pericardium) around the heart, which may require surgical stripping of the scar.

Failure to diagnose or treat constrictive pericarditis could result with severe complications such as: ^[1]

• Cardiac tamponade
• Damage to the coronary arteries
• Heart failure
• Pulmonary edema
• Scarring of the heart muscle

Constrictive pericarditis may be life threatening if left untreated. However, surgery to treat the condition is associated with a relatively high complication rate and is usually reserved for patients who have severe symptoms.

The long-term outcome of patients who have undergone the surgery have been adverse due to these factors:^[2]

• Advanced age
• Poor renal function
• Abnormal left ventricular systolic function
• High pulmonary artery systolic pressure
• Lower serum sodium level
• Postradiation cause
• Worsening NYHA classification

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: Pericardial stripping; pericardial excision

Pericardiectomy is the surgical removal of part or most of the pericardium. This operation is performed to relieve constrictive pericarditis or to remove a pericardium that is calcified and fibrous. Constrictive pericarditis is a progressive disease without spontaneous reversal of pericardial thickening. Some patients can be medically managed for several years. Edema can be controlled with diuretics and slowing the heart rate can maximize the diastolic filling time. Many patients eventually develop significant debility from impaired cardiac output and elevated right and left sided filling pressures. The definitive treatment for constrictive pericarditis is pericardiectomy which is also known as pericardial stripping. This is a surgical procedure where the entire pericardium is peeled away from the heart. Due to the significant risks involved with pericardial stripping, many patients are treated medically, with judicious use of diuretics.

The procedure begins when the surgeon makes an incision in the skin over the sternum and divides it to expose the pericardium. During the surgery, the surgeon will grasp the pericardium surrounding the heart, and will remove the fibrous, calcified or infected tissue covering of the heart. Once the pericardium is removed, the surgeon will wire the sternum back together, the incision is closed, and the procedure is completed.

The procedure has significant risks involved,^[1] with mortality rates of 6%-12% in major referral centers.^[2][3] The procedure can be complicated by perforation or tearing of the heart muscle if the heart muscle is tightly adherent to the pericardium. Stated simply, removal of the pericardium can remove the densely adherent heart muscle itself which is a catastrophic complication.

The high risk of the procedure is attributed to adherence of the thickened pericardium to the myocardium and coronary arteries. In patients who have undergone coronary artery bypass surgery with pericardial sparing, there is danger of tearing a bypass graft while removing the pericardium. Given the thin wall of the right ventricle, this can be a dangerous procedure and should only be undertaken if the patient’s symptoms are incapacitating.

If any pericardium is not removed, it is possible for bands of pericardium to cause localized constriction which may cause symptoms and signs consistent with constriction. Some patients do not have complete relief of symptoms and up to 60% will have at least echocardiographic evidence of a restrictive filling pattern at approximately 2 years. Radiation induced disease seems to have a worse prognosis for improvement in functional class. The 5 and 10-year survival after pericardiectomy is 78% and 57% respectively, but is obviously highly correlated with the underlying illness.

Pericardiectomy may be used in treatment of recurrent pericardial efussion due to TB, in tuberculous constrictive pericarditis, or if there is no hemodynamic and general improvement after 4-8 weeks following antituberculosis chemotherapy.^[4] If it is performed in the early stages of TB pericardial constriction, pericardiectomy has a low mortality rate when compared to advanced stages of the disease where pericardiectomy is poorly tolerated. Mortality rate secondary to this procedure is 3-16%.^[5][6] This surgery should be undertaken under the coverage of antitubercular drugs.

Treatment of effusive constrictive pericarditis is challenging because pericardiocentesis does not relieve the impaired filling of the heart, and surgical removal of the fibrinous exudate coating the visceral pericardium may not be possible. Patients should be started on antitubercular drugs and serial echocardiography should be performed to monitor the changes of pericardium and to make a decision regarding its surgical stripping.^[4]

• Hemopericardium
• Pneumopericardium
• Chylopericardium
• Pericardial effusion
• Congenital absence of the pericardium
• Pericardial window
• Pericardial sac
• Pericardial friction rub
• Pericardiocentesis
• Pericardium

• National Guideline Clearinghouse

The content on this page was first contributed by C. Michael Gibson, M.S., M.D.

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