CONSTRICTIVE PERICARDITIS



Constrictive pericarditis results from pericar­dial thickening and fibrosis occurring long after acute episodes of pericarditis. It is less common since the advent of antituberculous therapy but can occur after bacterial, fungal, viral, neoplastic, or uremic pericarditis. The fundamental hemo­dynamic abnormality is abnormal diastolic fill­ing. Eventually the underlying myocardial tissue may atrophy and decreased systolic function may result. Pericardial effusion and constriction may occur together (effusive-constrictive pericarditis), in which case pericardiocentesis may only par­tially relieve the symptoms. Occasionally con­striction can be localized to only certain chambers of the heart.

Symptoms of dyspnea, peripheral edema, ab­dominal swelling, and fatigue usually develop gradually. On physical examination, the jugular veins are distended with a prominent y descent (corresponding to early rapid ventricular filling). Tachycardia, hepatomegaly, ascites, and periph­eral edema are common. Splenomegaly may occur. The pulse pressure is usually normal, and pulsus paradoxus is usually not present. Kuss-maul’s sign may be present. The apical impulse sometimes is not palpable or may retract with sys­tole. An early diastolic apical sound termed a per­icardial knock is often present and can be con­fused with an S3 gallop.
Electrocardiographic findings include low volt­age and nonspecific T wave changes. The chest x-ray reveals clear lungs and normal or only slightly increased heart size. Pericardial calcification is most common in tuberculous constriction. Ech­ocardiography sometimes can suggest constrictive pericarditis but is usually not diagnostic. At car­diac catheterization the right and left ventricular pressures may demonstrate an early diastolic dip with a subsequent rise termed a square root sign. The right atrial pressure tracings may show sharp x and y descents, generating a typical M-shaped contour. There is equalization of end diastolic pressures in all four chambers and the pulmonary artery. Occasionally these findings become evi­dent only after an infusion of saline (occult con­striction).

It is sometimes difficult to distinguish constric­tive pericarditis from restrictive cardiomyopathy. Left ventricular ejection fraction is more likely to be decreased in patients with restrictive cardio­myopathy than constrictive pericarditis. Com-erized tomography is the procedure of choice to demonstrate the thickened pericardium. Endo­cardial biopsy or even surgical exploration is sometimes necessary.

Constrictive pericarditis is slowly progressive. Patients may be managed conservatively with mild sodium restriction and diuretics; however, the mortality and morbidity of pericardiectomy is less when performed early than after progressive calcification and fibrosis have occurred. There­fore, pericardiectomy should probably not be per­formed in patients with very mild, early disease or elderly patients with severe disease and a fi-brotic, calcified pericardium. Improvement oc­curs in about 75 per cent of patients who survive the operation but may be delayed for several weeks or months postoperatively. Cardiac func­tion may not normalize after pericardiectomy either because of inability to completely remove the pericardium or fibrosis and atrophy of the un­derlying myocardium.