Clinical Pearls & Morning Reports
Published November 1, 2023
The noncompliant pericardium in constrictive pericarditis impairs ventricular relaxation and leads to a greater increase in ventricular pressures for any given level of venous return. Moreover, the rigid pericardium creates ventricular interdependence, such that increases in filling in the right heart come at the expense of filling in the left heart. Read the NEJM Clinical Problem-Solving Article here.
Q: What are the major causes of constrictive pericarditis?
A: The majority of cases of constrictive pericarditis in the United States are idiopathic, although previous cardiac surgery and radiation treatment are the most common identified causes. Tuberculosis is the leading cause in developing countries.
Q: How is constrictive pericarditis with active inflammation treated?
A: First-line therapy for actively inflamed constrictive pericarditis includes nonsteroidal antiinflammatory drugs and colchicine. If these therapies are unsuccessful, glucocorticoids and interleukin-1 receptor agonist agents such as anakinra or rilonacept may also be considered. In refractory cases, surgical pericardiectomy may be performed, although mortality associated with the procedure remains high.
A: Physical examination findings in constrictive pericarditis may include jugular venous distention, Kussmaul’s sign, pericardial knock (an extra sound heard after S2, resulting from abrupt cessation of early ventricular filling due to the rigid pericardium), peripheral edema, and hepatomegaly. Transthoracic echocardiography should be performed when constriction is suspected. Echocardiographic findings of septal bounce (due to rapid diastolic equilibration of right ventricular and left ventricular pressures), inspiratory respirophasic leftward shift due to ventricular interdependence, increased medial mitral annular velocity, hepatic vein expiratory diastolic flow reversal, exaggerated variation in intracardiac flows, and reversal of the lateral and medial annular velocity pattern (“annulus reversus”) are highly suggestive of constrictive physiological characteristics.
A: Cardiac magnetic resonance (CMR) is useful in further evaluation because it can confirm ventricular interdependence and identify the presence of pericardial inflammation, thickening, and adhesions. Cardiac CT may also be helpful in identifying pericardial calcification and thickening. Catheterization with hemodynamic assessment has a role in selected cases in which the diagnosis remains uncertain after noninvasive testing. On catheterization, constrictive physiological characteristics that may be seen include sharp x and y descents (due to accelerated atrial relaxation and rapid early diastolic filling, respectively), equalization of right and left diastolic pressures, a dip and plateau pattern in ventricular waveforms due to diastolic resistance to filling, and discordance in left and right ventricular pressures with respiration. There is overlap in the echocardiographic, CMR, and hemodynamic features of tricuspid regurgitation, right ventricular dysfunction, and constriction, which may make a definitive diagnosis of constriction challenging.