Constrictive pericarditis is characterized by the inflammation and stiffening of the pericardium. The pericardium consists of an outer fibrous layer and an inner serous layer, which produces a small amount of lubricating fluid to reduce friction between the heart and the surrounding structures. In addition to its protective function, the pericardium plays a pivotal role in shaping cardiac hemodynamics.
Constrictive pericarditis is marked by the development of granulation tissue within the pericardial sac, causing a decline in its elasticity. This, in turn, results in an impediment to the filling of the ventricles. Typically, a chronic ailment, there are also subacute, transient, and occult variations of this condition that have been documented.
Epidemiology
Around 9% of individuals experiencing acute pericarditis develop constrictive physiology, with infectious causes remaining the primary culprits in the developing world. This condition is relatively uncommon in adults and even rarer in children.
It is more frequently observed in individuals who have undergone cardiac surgery, and there is a notable male predominance with a ratio of 3:1. Notably, there are no known racial preferences associated with this condition.
Anatomy
Pathophysiology
The pathophysiology of chronic constrictive pericarditis implicates the gradual closure of the pericardial cavity due to the formation of granulation tissue, which occurs during the healing process of an acute episode of fibrinous through the absorption of a chronic pericardial effusion. Over time, this granulation tissue contracts and encapsulates the heart, occasionally becoming calcified. This thickened and inflexible pericardium restricts ventricular filling, as its ability to stretch is significantly reduced compared to a normal pericardium. During the early diastole phase, ventricular filling remains unaffected; it is only impeded when the pericardium’s limited elasticity is reached.
This contrasts with cardiac tamponade, where the ventricular filling is hindered throughout the entire diastole. Due to chronic constrictive pericarditis, there is a decrease in end-diastolic volume and, subsequently, a reduction in cardiac output and stroke volume. Furthermore, the thickened and scarred pericardium interferes with the normal decrease in intrathoracic pressure during inspiration, preventing this pressure change from transmitting to the heart chambers.
In cases of chronic constrictive pericarditis, there is a notable disparity between intrathoracic and intracardiac pressures. This leads to a reduction in venous return during inspiration, reducing pulmonary venous pressure. Importantly, the pressure within the left atrium remains relatively stable, and as a consequence, the flow of blood from the pulmonary veins to the left atrium decreases during inspiration. This disconnect between intracardiac, and intrathoracic pressures is a key distinguishing characteristic compared to cardiac tamponade.
In cardiac tamponade, changes in intrathoracic pressure are effectively transmitted to the heart, causing an increase in systemic venous return during inspiration. In both chronic constrictive pericarditis and cardiac tamponade, there is a convergence of pressures in the right ventricle (RV), right atrium (RA), left ventricle (LV), and pulmonary wedge pressure. However, the critical difference lies in how these pressures respond to inspiration. In cardiac tamponade, the pressures decrease with inspiration, whereas in constrictive pericarditis, the RA pressure remains relatively steady while the pulmonary wedge pressure declines.
Etiology
On a global scale, tuberculosis is the primary cause of constrictive pericarditis, contributing to approximately 50% of cases in individuals with tuberculous pericardial effusion, even when undergoing antitubercular treatment. In more developed regions, the leading causes are typically idiopathic or result from post-viral infections, accounting for 40% to 60% of all cases.
Additionally, constrictive pericarditis can emerge as a complication following cardiac surgery and is relatively common in patients who have received mediastinal radiation therapy, with an incidence rate ranging from 2% to 30%.
This condition has also been associated with connective tissue disorders like rheumatoid arthritis and systemic lupus erythematosus. While diagnosing constrictive pericarditis may be relatively straightforward in some instances, establishing a precise cause can often be challenging. In many cases, the origin remains unidentified, attributed to an asymptomatic episode of viral pericarditis.
Genetics
Prognostic Factors
Clinical History
Constrictive pericarditis often presents with a history of prior pericardial inflammation or injury. Patients may have a history of tuberculosis, viral infections, cardiac surgery, mediastinal radiation therapy, or connective tissue disorders.
Patients may complain of reduced exercise tolerance. Some individuals may experience chest discomfort or pain. Symptoms of right-sided heart failure, such as jugular venous distension, hepatomegaly, and ascites, can be present. Constrictive pericarditis typically develops gradually over time. Symptoms may progress over months or years.
Physical Examination
During a physical examination, it is common to observe elevated jugular venous pressure in individuals with constrictive pericarditis. However, in the early stages, JVP may still be within the normal range. Notably, the JVP remains unchanged during inspiration. It’s worth noting that Kussmaul’s sign can also be present in conditions such as tricuspid valve disease and right-sided heart failure.
While the presence of pulsus paradoxus (defined as a drop in systolic blood pressure of more than 10 mm Hg during inspiration) can be seen in constrictive pericarditis, it is more commonly associated with patients experiencing cardiac tamponade. Another characteristic finding during examination is the detection of an accentuated heart sound that occurs earlier in the cardiac cycle than the third heart sound.
This sound is referred to as a pericardial knock and can be heard in roughly half of patients with constrictive pericarditis. Additionally, on abdominal examination, signs such as ascites or hepatomegaly may be present, and peripheral edema can also be observed in some cases. These clinical findings, when considered collectively, can provide valuable clues for diagnosing constrictive pericarditis.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Cardiac Sarcoma
Cardiac Tamponade
Nephrotic Syndrome
Ovarian Cancer
Pleural Effusion
Sarcoidosis
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Diuretics can serve as a means to alleviate edema or elevated venous pressures prior to surgery or provide symptom relief for patients who may not be suitable candidates for surgical intervention. Sometimes, a specific group of patients might experience spontaneous recovery or respond well to medical management, referred to as transient constrictive pericarditis.
Individuals newly diagnosed with constrictive pericarditis who exhibit hemodynamic stability and lack indications of chronic constriction may be considered for treatment with anti-inflammatory medications for up to three months under vigilant supervision. However, if these patients subsequently exhibit signs of chronic constriction and hemodynamic instability, it is imperative to pursue surgical intervention promptly.
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Pericardiectomy stands as the sole conclusive approach to address chronic constrictive pericarditis, necessitating diligent efforts to maximize pericardial removal. Deterioration of myocardial function due to extensive fibrosis and calcification is linked to unfavorable prognoses.
The surgical procedure is associated with a wide-ranging mortality rate from 10% to 55%. Consequently, careful consideration is essential for patients with mild symptoms or advanced disease and other medical conditions, given the significant mortality risk associated with this intervention.
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Constrictive pericarditis is characterized by the inflammation and stiffening of the pericardium. The pericardium consists of an outer fibrous layer and an inner serous layer, which produces a small amount of lubricating fluid to reduce friction between the heart and the surrounding structures. In addition to its protective function, the pericardium plays a pivotal role in shaping cardiac hemodynamics.
Constrictive pericarditis is marked by the development of granulation tissue within the pericardial sac, causing a decline in its elasticity. This, in turn, results in an impediment to the filling of the ventricles. Typically, a chronic ailment, there are also subacute, transient, and occult variations of this condition that have been documented.
Around 9% of individuals experiencing acute pericarditis develop constrictive physiology, with infectious causes remaining the primary culprits in the developing world. This condition is relatively uncommon in adults and even rarer in children.
It is more frequently observed in individuals who have undergone cardiac surgery, and there is a notable male predominance with a ratio of 3:1. Notably, there are no known racial preferences associated with this condition.
The pathophysiology of chronic constrictive pericarditis implicates the gradual closure of the pericardial cavity due to the formation of granulation tissue, which occurs during the healing process of an acute episode of fibrinous through the absorption of a chronic pericardial effusion. Over time, this granulation tissue contracts and encapsulates the heart, occasionally becoming calcified. This thickened and inflexible pericardium restricts ventricular filling, as its ability to stretch is significantly reduced compared to a normal pericardium. During the early diastole phase, ventricular filling remains unaffected; it is only impeded when the pericardium’s limited elasticity is reached.
This contrasts with cardiac tamponade, where the ventricular filling is hindered throughout the entire diastole. Due to chronic constrictive pericarditis, there is a decrease in end-diastolic volume and, subsequently, a reduction in cardiac output and stroke volume. Furthermore, the thickened and scarred pericardium interferes with the normal decrease in intrathoracic pressure during inspiration, preventing this pressure change from transmitting to the heart chambers.
In cases of chronic constrictive pericarditis, there is a notable disparity between intrathoracic and intracardiac pressures. This leads to a reduction in venous return during inspiration, reducing pulmonary venous pressure. Importantly, the pressure within the left atrium remains relatively stable, and as a consequence, the flow of blood from the pulmonary veins to the left atrium decreases during inspiration. This disconnect between intracardiac, and intrathoracic pressures is a key distinguishing characteristic compared to cardiac tamponade.
In cardiac tamponade, changes in intrathoracic pressure are effectively transmitted to the heart, causing an increase in systemic venous return during inspiration. In both chronic constrictive pericarditis and cardiac tamponade, there is a convergence of pressures in the right ventricle (RV), right atrium (RA), left ventricle (LV), and pulmonary wedge pressure. However, the critical difference lies in how these pressures respond to inspiration. In cardiac tamponade, the pressures decrease with inspiration, whereas in constrictive pericarditis, the RA pressure remains relatively steady while the pulmonary wedge pressure declines.
On a global scale, tuberculosis is the primary cause of constrictive pericarditis, contributing to approximately 50% of cases in individuals with tuberculous pericardial effusion, even when undergoing antitubercular treatment. In more developed regions, the leading causes are typically idiopathic or result from post-viral infections, accounting for 40% to 60% of all cases.
Additionally, constrictive pericarditis can emerge as a complication following cardiac surgery and is relatively common in patients who have received mediastinal radiation therapy, with an incidence rate ranging from 2% to 30%.
This condition has also been associated with connective tissue disorders like rheumatoid arthritis and systemic lupus erythematosus. While diagnosing constrictive pericarditis may be relatively straightforward in some instances, establishing a precise cause can often be challenging. In many cases, the origin remains unidentified, attributed to an asymptomatic episode of viral pericarditis.
Constrictive pericarditis often presents with a history of prior pericardial inflammation or injury. Patients may have a history of tuberculosis, viral infections, cardiac surgery, mediastinal radiation therapy, or connective tissue disorders.
Patients may complain of reduced exercise tolerance. Some individuals may experience chest discomfort or pain. Symptoms of right-sided heart failure, such as jugular venous distension, hepatomegaly, and ascites, can be present. Constrictive pericarditis typically develops gradually over time. Symptoms may progress over months or years.
During a physical examination, it is common to observe elevated jugular venous pressure in individuals with constrictive pericarditis. However, in the early stages, JVP may still be within the normal range. Notably, the JVP remains unchanged during inspiration. It’s worth noting that Kussmaul’s sign can also be present in conditions such as tricuspid valve disease and right-sided heart failure.
While the presence of pulsus paradoxus (defined as a drop in systolic blood pressure of more than 10 mm Hg during inspiration) can be seen in constrictive pericarditis, it is more commonly associated with patients experiencing cardiac tamponade. Another characteristic finding during examination is the detection of an accentuated heart sound that occurs earlier in the cardiac cycle than the third heart sound.
This sound is referred to as a pericardial knock and can be heard in roughly half of patients with constrictive pericarditis. Additionally, on abdominal examination, signs such as ascites or hepatomegaly may be present, and peripheral edema can also be observed in some cases. These clinical findings, when considered collectively, can provide valuable clues for diagnosing constrictive pericarditis.
Cardiac Sarcoma
Cardiac Tamponade
Nephrotic Syndrome
Ovarian Cancer
Pleural Effusion
Sarcoidosis
Diuretics can serve as a means to alleviate edema or elevated venous pressures prior to surgery or provide symptom relief for patients who may not be suitable candidates for surgical intervention. Sometimes, a specific group of patients might experience spontaneous recovery or respond well to medical management, referred to as transient constrictive pericarditis.
Individuals newly diagnosed with constrictive pericarditis who exhibit hemodynamic stability and lack indications of chronic constriction may be considered for treatment with anti-inflammatory medications for up to three months under vigilant supervision. However, if these patients subsequently exhibit signs of chronic constriction and hemodynamic instability, it is imperative to pursue surgical intervention promptly.
Pericardiectomy stands as the sole conclusive approach to address chronic constrictive pericarditis, necessitating diligent efforts to maximize pericardial removal. Deterioration of myocardial function due to extensive fibrosis and calcification is linked to unfavorable prognoses.
The surgical procedure is associated with a wide-ranging mortality rate from 10% to 55%. Consequently, careful consideration is essential for patients with mild symptoms or advanced disease and other medical conditions, given the significant mortality risk associated with this intervention.
medtigo
Constrictive pericarditis
Updated :
September 8, 2023
Constrictive pericarditis is characterized by the inflammation and stiffening of the pericardium. The pericardium consists of an outer fibrous layer and an inner serous layer, which produces a small amount of lubricating fluid to reduce friction between the heart and the surrounding structures. In addition to its protective function, the pericardium plays a pivotal role in shaping cardiac hemodynamics.
Constrictive pericarditis is marked by the development of granulation tissue within the pericardial sac, causing a decline in its elasticity. This, in turn, results in an impediment to the filling of the ventricles. Typically, a chronic ailment, there are also subacute, transient, and occult variations of this condition that have been documented.
Around 9% of individuals experiencing acute pericarditis develop constrictive physiology, with infectious causes remaining the primary culprits in the developing world. This condition is relatively uncommon in adults and even rarer in children.
It is more frequently observed in individuals who have undergone cardiac surgery, and there is a notable male predominance with a ratio of 3:1. Notably, there are no known racial preferences associated with this condition.
The pathophysiology of chronic constrictive pericarditis implicates the gradual closure of the pericardial cavity due to the formation of granulation tissue, which occurs during the healing process of an acute episode of fibrinous through the absorption of a chronic pericardial effusion. Over time, this granulation tissue contracts and encapsulates the heart, occasionally becoming calcified. This thickened and inflexible pericardium restricts ventricular filling, as its ability to stretch is significantly reduced compared to a normal pericardium. During the early diastole phase, ventricular filling remains unaffected; it is only impeded when the pericardium’s limited elasticity is reached.
This contrasts with cardiac tamponade, where the ventricular filling is hindered throughout the entire diastole. Due to chronic constrictive pericarditis, there is a decrease in end-diastolic volume and, subsequently, a reduction in cardiac output and stroke volume. Furthermore, the thickened and scarred pericardium interferes with the normal decrease in intrathoracic pressure during inspiration, preventing this pressure change from transmitting to the heart chambers.
In cases of chronic constrictive pericarditis, there is a notable disparity between intrathoracic and intracardiac pressures. This leads to a reduction in venous return during inspiration, reducing pulmonary venous pressure. Importantly, the pressure within the left atrium remains relatively stable, and as a consequence, the flow of blood from the pulmonary veins to the left atrium decreases during inspiration. This disconnect between intracardiac, and intrathoracic pressures is a key distinguishing characteristic compared to cardiac tamponade.
In cardiac tamponade, changes in intrathoracic pressure are effectively transmitted to the heart, causing an increase in systemic venous return during inspiration. In both chronic constrictive pericarditis and cardiac tamponade, there is a convergence of pressures in the right ventricle (RV), right atrium (RA), left ventricle (LV), and pulmonary wedge pressure. However, the critical difference lies in how these pressures respond to inspiration. In cardiac tamponade, the pressures decrease with inspiration, whereas in constrictive pericarditis, the RA pressure remains relatively steady while the pulmonary wedge pressure declines.
On a global scale, tuberculosis is the primary cause of constrictive pericarditis, contributing to approximately 50% of cases in individuals with tuberculous pericardial effusion, even when undergoing antitubercular treatment. In more developed regions, the leading causes are typically idiopathic or result from post-viral infections, accounting for 40% to 60% of all cases.
Additionally, constrictive pericarditis can emerge as a complication following cardiac surgery and is relatively common in patients who have received mediastinal radiation therapy, with an incidence rate ranging from 2% to 30%.
This condition has also been associated with connective tissue disorders like rheumatoid arthritis and systemic lupus erythematosus. While diagnosing constrictive pericarditis may be relatively straightforward in some instances, establishing a precise cause can often be challenging. In many cases, the origin remains unidentified, attributed to an asymptomatic episode of viral pericarditis.
Constrictive pericarditis often presents with a history of prior pericardial inflammation or injury. Patients may have a history of tuberculosis, viral infections, cardiac surgery, mediastinal radiation therapy, or connective tissue disorders.
Patients may complain of reduced exercise tolerance. Some individuals may experience chest discomfort or pain. Symptoms of right-sided heart failure, such as jugular venous distension, hepatomegaly, and ascites, can be present. Constrictive pericarditis typically develops gradually over time. Symptoms may progress over months or years.
During a physical examination, it is common to observe elevated jugular venous pressure in individuals with constrictive pericarditis. However, in the early stages, JVP may still be within the normal range. Notably, the JVP remains unchanged during inspiration. It’s worth noting that Kussmaul’s sign can also be present in conditions such as tricuspid valve disease and right-sided heart failure.
While the presence of pulsus paradoxus (defined as a drop in systolic blood pressure of more than 10 mm Hg during inspiration) can be seen in constrictive pericarditis, it is more commonly associated with patients experiencing cardiac tamponade. Another characteristic finding during examination is the detection of an accentuated heart sound that occurs earlier in the cardiac cycle than the third heart sound.
This sound is referred to as a pericardial knock and can be heard in roughly half of patients with constrictive pericarditis. Additionally, on abdominal examination, signs such as ascites or hepatomegaly may be present, and peripheral edema can also be observed in some cases. These clinical findings, when considered collectively, can provide valuable clues for diagnosing constrictive pericarditis.
Cardiac Sarcoma
Cardiac Tamponade
Nephrotic Syndrome
Ovarian Cancer
Pleural Effusion
Sarcoidosis
Diuretics can serve as a means to alleviate edema or elevated venous pressures prior to surgery or provide symptom relief for patients who may not be suitable candidates for surgical intervention. Sometimes, a specific group of patients might experience spontaneous recovery or respond well to medical management, referred to as transient constrictive pericarditis.
Individuals newly diagnosed with constrictive pericarditis who exhibit hemodynamic stability and lack indications of chronic constriction may be considered for treatment with anti-inflammatory medications for up to three months under vigilant supervision. However, if these patients subsequently exhibit signs of chronic constriction and hemodynamic instability, it is imperative to pursue surgical intervention promptly.
Pericardiectomy stands as the sole conclusive approach to address chronic constrictive pericarditis, necessitating diligent efforts to maximize pericardial removal. Deterioration of myocardial function due to extensive fibrosis and calcification is linked to unfavorable prognoses.
The surgical procedure is associated with a wide-ranging mortality rate from 10% to 55%. Consequently, careful consideration is essential for patients with mild symptoms or advanced disease and other medical conditions, given the significant mortality risk associated with this intervention.
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