Constrictive Pericarditis

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CHAPTER 70 Constrictive Pericarditis

In constrictive pericarditis, the interpreting physician is consulted to establish the presence or absence of pericardial thickening or calcification or both. Documentation of abnormal pericardial thickening or calcification and characteristic alterations of cardiac structures, coupled with the appropriate hemodynamic changes, establishes the diagnosis of constrictive pericarditis in most cases.

DEFINITION

Constrictive pericarditis is a disease state in which previous insult to the pericardium results in pericardial scarring leading to constriction and compression of the underlying cardiac chambers.

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.

TABLE 70-1 Etiologies of Constrictive Pericarditis

Idiopathic or viral

Postsurgical (e.g., coronary artery bypass graft surgery, valvular surgery)

Radiation therapy

Miscellaneous causes (tuberculosis, connective tissue disease, bacterial pericarditis, Wegener granulomatosis, blunt chest trauma, neoplasm)

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 Indications and Algorithm

Patients suspected to have constrictive pericarditis based on history, physical examination, and echocardiographic findings are referred for CT or MRI to evaluate for thickening or calcification within the pericardium.

Imaging Techniques and Findings

A subset of patients with constrictive physiology may have no detectable pericardial thickening yet would benefit from pericardiectomy.⁷^,⁸ In a series of 26 patients who underwent pericardiectomy despite the absence of pericardial thickening or calcification, on pathologic examination, all showed areas of either focal fibrosis or calcification.⁷ In these patients without demonstrable pericardial thickening, the constrictive physiology is thought to be the result of pericardial adhesions.⁵ If ECG gated images are obtained, abnormal septal motion can be evaluated. The myocardium can also be assessed for myocardial thinning because this finding has been associated with increased mortality after pericardiectomy.⁹

Magnetic Resonance Imaging

Although it cannot differentiate between calcified and thickened pericardium, MRI can be used to detect pericardial thickening and the associated cardiac deformities typically seen in patients with constrictive pericarditis (Fig. 70-2). MRI is better than CT in distinguishing small pericardial effusions from pericardial thickening. In patients who have constrictive pericarditis without associated pericardial thickening, myocardial tagging techniques can be used to document the lack of normal movement between the myocardium and pericardium.¹⁰ Just as pericardial thickening can exist without constrictive pericarditis, pericardial adhesions identified with myocardial tagging can also occur in the absence of constrictive physiology. Septal motion can be evaluated using cine MRI sequences. As with echocardiography, paradoxical diastolic motion (“septal bounce”) may be present.¹¹ The myocardium can also be assessed for myocardial thinning because this finding has been associated with increased mortality after pericardiectomy.⁹