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Chapter Summary

This chapter discusses the etiology, presentation, diagnosis and treatment of constrictive pericarditis, a potentially curable form of diastolic heart failure due to inflamed, scarred, or even calcified pericardium limiting diastolic filling of the heart. Effusive or chronic constrictive pericarditis can result from progression of acute pericarditis with pericardial inflammation or pericardial effusion (see Fuster and Hurst's Central Illustration). Traditionally, cardiac catheterization has been the gold standard for diagnosing constrictive pericarditis, but advances in cardiac imaging have allowed diagnostic hemodynamic assessment by echocardiography, delineation of pericardial and cardiac anatomy by computed tomography, and detection of pericardial inflammation by cardiac magnetic resonance imaging. A subset of the patients with constrictive pericarditis predominantly due to pericardial inflammation, as seen in effusive or transient constrictive pericarditis, can be managed medically. Cardiac imaging can identify this subset of the patients. However, therapeutic pericardiectomy is the recommended treatment for symptomatic patients with constrictive pericarditis. Surgical pericardiectomy can cure chronic constrictive pericarditis unless it is mixed with myocardial diseases from radiation, ischemia, or fibrosis. Constriction can recur if pericardiectomy is incomplete.

eFig 55-01 Chapter 55: Constrictive Pericarditis


Constrictive pericarditis (CP) occurs in the setting of inflammation and/or scarring of the pericardium, resulting in impaired cardiac filling.1 Therefore, CP is a form of diastolic heart failure. The importance of its recognition lies in the fact that pericardial constriction is a potentially curable disease and it is still underdiagnosed, carrying a very poor prognosis if left untreated.2


CP develops after an injury to the pericardium triggers ongoing pericardial inflammation and ultimately fibrosis. This process might be acute (over the course of days), subacute, or chronic; in acute cases, inflammation prevails whereas fibrosis tends to be predominant in chronic forms of the disease. Pericardial inflammation may resolve spontaneously or with anti-inflammatory therapy, but the pericardium typically becomes fibrotic or scarred if the inflammatory process is not resolved within 3 months. The reason for which some patients will evolve into CP after an acute event is unclear; however, certain etiologies (for example, tuberculous pericarditis) are associated with higher risk of developing CP.3,4 The disease also appears to favor men (2:1 ratio).1 Although, CP is primarily a pericardial disease, subepicardial myocardial atrophy might be present5 (particularly in long-standing cases), leading to concomitant myocardial systolic and diastolic dysfunction. A mixed pattern with coexistent myocardial disease is also the norm in patients who develop constriction after cardiac surgery or in those with a history of mediastinal irradiation therapy.

Given the abnormal pericardial compliance, diastolic filling is significantly impaired in patients with CP (ie, steeper increase in pressure per change in volume in the pressure–volume curve). As a consequence, cardiac filling pressures increase and cardiac output ...

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