CHAPTER 70 Constrictive Pericarditis
PREVALENCE AND EPIDEMIOLOGY
Constrictive pericarditis is uncommon. It is more commonly seen in patients with a preexisting episode of pericarditis, prior surgery, or prior radiation therapy, although many patients have no documented antecedent pericardial disease. In a prospective assessment of the outcome of acute pericarditis, 56% of patients with tuberculous pericarditis, 35% of patients with purulent pericarditis, and 17% of patients with neoplastic pericardial disease developed constrictive pericarditis.1 Only 1% of patients with idiopathic pericarditis developed constrictive pericarditis in this series. In contrast, transient constrictive pericarditis (see later) was more commonly seen in patients with idiopathic pericarditis, occurring in approximately 20% of cases.2
ETIOLOGY AND PATHOPHYSIOLOGY
In the United States, the most common causes of constrictive pericarditis are idiopathic or postviral pericarditis, prior cardiac surgery, and radiation therapy (Table 70-1). The scarred pericardium inhibits the ability of the cardiac chambers to dilate during diastolic filling, acting as a cage covering the heart. As a result of the inability to dilate, the intracardiac pressures of each chamber are elevated and equalized. This elevated pressure is transmitted to the pulmonary and systemic veins. Because the atrial pressures are elevated, there is rapid filling of the ventricles early in ventricular diastole. This ventricular filling rapidly ceases when the ventricle can no longer expand to accept the incoming volume. Systemic venous hypertension results in hepatomegaly, ascites, and peripheral edema.
Data from Bertog SC, Thambidorai SK, Parakh K, et al. Constrictive pericarditis: etiology and cause-specific survival after pericardiectomy. J Am Coll Cardiol 2004; 43:1445-1452.
MANIFESTATIONS OF DISEASE
Clinical Presentation
Patients with constrictive pericarditis present with signs and symptoms of right heart failure. Patients may complain of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea, abdominal fullness secondary to ascites, and pedal edema. On physical examination, there is distention of the neck veins, peripheral edema, and hepatomegaly. In a patient without pericardial constriction, there is a decrease in jugular venous pressure during inspiration because of decrease in intrathoracic pressure. In patients with constrictive pericarditis, because the intrapericardial pressure is dissociated from the intrathoracic pressure, there is an increase in jugular venous pressure during inspiration (Kussmaul sign).3 A pericardial knock, which corresponds to the rapid cessation of ventricular filling, can be heard along the cardiac apex and left sternal border.
Imaging Techniques and Findings
Ultrasonography
The classic finding of constrictive pericarditis is the equalization of the end-diastolic pressure in all four cardiac chambers with early rapid diastolic filling. Paradoxical motion of the interventricular septum may also be seen. Pericardial thickening may be missed on transthoracic echocardiography, particularly if it is located in the near field, or if there is localized involvement.4,5 Transesophageal echocardiography has been found to be more sensitive in detecting pericardial thickening compared with transthoracic echocardiography.6 Dilation of the atria, inferior vena cava, and hepatic veins may be noted.
