Background: The normal pericardial sac accommodates a 250-350 gram heart an
d 15-50 ml of pericardial fluid. Cardiac enlargement and/or increases in fl
uid must be accompanied by an increase in pericardial volume and a concomit
ant expansion of the pericardial sac. The mechanism of such expansion has b
een debated, but theoretical considerations include fibroblastic proliferat
ion with new connective tissue deposition versus remodeling of the pre-exis
tent connective tissue. Design. Nineteen pericardia were obtained from cons
ecutive 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 hematoxyl
in-eosin (H&E), Masson's trichrome, and Verhoeffs elastin stain (EVG). An a
dditional 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 histolo
gic evidence of fibroblastic proliferation, Parameters indicative of collag
en stretching or damage were evaluated. The greatest correlative factor in
identifying an enlarged pericardium was the average of foul measurements of
the greatest distance between elastic fibers surrounding obliquely oriente
d collagen layers. Five of six cases with a cardiac score >450 showed an av
erage measurement of less than 15 mu, and 10 of 14 cases with a cardiac sco
re less than or equal to 450 showed an average measurement of >15 mu (p = 0
.0498). Histologic and ultrastructural evidence of collagen damage was iden
tified in the pericardium from the 900-g heart with the 1,000-ml effusion.
Conclusions. We propose that collagen stretching and slippage of oblique or
iented collagen layers contribute to the increased surface area needed to a
ccommodate larger volumes. When these limits are exceeded, collagen damage
ensues, Cardiovasc Pathol 2000:9:9-15 (C) 2000 by Elsevier Science Inc.