Mechanism of Pericardial Expansion with Cardiac Enlargement

Abstract 

Background: The normal pericardial sac accommodates a 250–350 gram heart and 15–50 ml of pericardial fluid. Cardiac enlargement and/or increases in fluid must be accompanied by an increase in pericardial volume and a concomitant expansion of the pericardial sac. The mechanism of such expansion has been debated, but theoretical considerations include fibroblastic proliferation with new connective tissue deposition versus remodeling of the pre-existent connective tissue. Design: Nineteen pericardia were obtained from consecutive adult autopsies. Total pericardial fluid was measured; the absolute value of pericardial fluid volume and cardiac weight were added to create a total score. Representative pericardial tissue was stained with hematoxylin-eosin (H&E), Masson's trichrome, and Verhoeff's elastin stain (EVG). An additional archival case with the pericardium from a 900-g heart with 1,000-ml of fluid was also included. Results: None of the sections showed histologic evidence of fibroblastic proliferation. Parameters indicative of collagen stretching or damage were evaluated. The greatest correlative factor in identifying an enlarged pericardium was the average of four measurements of the greatest distance between elastic fibers surrounding obliquely oriented collagen layers. Five of six cases with a cardiac score >450 showed an average measurement of less than 15 μ, and 10 of 14 cases with a cardiac score ⩽450 showed an average measurement of >15 μ (p = 0.0498). Histologic and ultrastructural evidence of collagen damage was identified in the pericardium from the 900-g heart with the 1,000-ml effusion. Conclusions: We propose that collagen stretching and slippage of obliquely oriented collagen layers contribute to the increased surface area needed to accommodate larger volumes. When these limits are exceeded, collagen damage ensues.