How to differentiate from restrictive cardiomyopathy -- Recognizing constrictive pericarditis as a cause of shortness of breath

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Author: Yashvir Sangwan
Date: Feb. 1, 2007
From: Journal of Respiratory Diseases(Vol. 28, Issue 2)
Publisher: CMP Medica, LLC
Document Type: Article
Length: 2,838 words
Lexile Measure: 1880L

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Byline: YASHVIR SANGWAN, MD, TIMOTHY J. BARREIRO, DO, and DAVID J. GEMMEL, PhD

ABSTRACT: In the past, constrictive pericarditis was most often caused by tuberculosis. Today, however, it is more likely to be preceded by injury or trauma, infection, or previous cardiac surgery. Most patients with constrictive pericarditis present with dyspnea and have elevated jugular venous pressure. Other potential symptoms and signs include peripheral edema, abdominal fullness, hepatomegaly, ascites, and chest pain. Electrocardiography demonstrates nonspecific ST-segment and T-wave changes and generalized T-wave inversion or flattening. In many cases, chest radiography and CT reveal pericardial calcification, and echocardiography shows increased pericardial thickness and calcification. Treatment may include NSAIDs, corticosteroids, antibiotics, angiotensin-converting enzyme inhibitors, and diuretics. Surgery is the treatment of choice for chronic disease, and pericardiectomy is typically effective.

(J Respir Dis. 2007;28(2):49-56)

KEY WORDS: Constrictive pericarditis, Pericardial calcification

Constrictive pericarditis (CP) is a rare condition characterized by nonspecific symptoms, including dyspnea, abdominal distention, and generalized edema. It frequently is misdiagnosed as chronic liver or renal disease or is confused with restrictive cardiomyopathy.1,2 Correct diagnosis is vital, since pericardiectomy can dramatically improve patients' symptoms. CP should be suspected in any patient who has signs and symptoms of right-sided heart failure that are disproportionate to pulmonary disease or right-sided heart disease.3

The underlying pathology of CP is chronic inflammation of the pericardial sac, leading to variable thickening, fibrosis, and pericardial calcification. This eventually leads to impaired filling of the cardiac chambers.4 Pericardium thickness exceeds normal in 80% of cases, and pericardial calcifications are observed in 25% of patients who have chronic CP. The symptoms of CP arise as the thickened and fibrotic pericardium interferes with normal diastolic cardiac filling.

Traditionally, increased pericardial thickness and calcification were considered important in the diagnosis of CP; many patients had significant calcifications of the entire pericardium, secondary to tuberculosis.5 Today, other causes of CP predominate and a calcified pericardium is uncommon. Recent reports have indicated that patients with calcifications have longer duration of symptoms, larger atria, and more atrial arrhythmias, suggesting calcification is a nonspecific response to inflammation. Calcifications are a marker of poor postoperative outcome in some studies.6,7 Pericardial calcification can occur in the absence of CP, but it is usually patchy and less dense.

In this article, we discuss the pathophysiology, diagnosis, and treatment of CP.

Epidemiology

Today, CP is rare. It is seen in 25% to 44% of patients with a surgically resected pericardium in developed countries and in up to 79% of patients undergoing pericardiectomy in countries in which tuberculosis is prevalent.8-12 It primarily affects adults and has a male preponderance of 2:1 to 3:1.

The rate of calcification among patients with CP has declined. In a 1959 study, calcification was present in 90% of patients with CP, usually after tuberculous pericarditis.13 A Mayo Clinic study of 231 patients followed for 40 years found only a 40% incidence of calcific disease.14 Because CP is now less likely to be caused by tuberculosis, the incidence of calcific disease in patients with CP in...

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Gale Document Number: GALE|A160025067