Uu. Nkere et al., PERICARDIAL TRAUMA AND ADHESIONS IN RELATION TO REOPERATIVE CARDIAC-SURGERY, The thoracic and cardiovascular surgeon, 43(6), 1995, pp. 338-346
In an attempt to appreciate the changes that favour adhesion formation
we compared the morphological and fibrinolytic changes that occur in
human primary and reoperative pericardium. Ten patients undergoing pri
mary elective open heart surgery and ten undergoing first time reopera
tive open heart surgery were studied. Pericardial samples were taken a
t four time points. At 0 (time A) and 30 (time B) minutes from the tim
e of pericardiotomy (before the commencement of CPB), 30-50 minutes (t
ime C) after the commencement of CPB, and then finally 10 minutes (tim
e D) after the patient had been rewarmed. The fibrinolytic activity, a
s measured by the plasminogen activating activity (PAA), in the perica
rdial samples of the ten primary cases was compared with that in 5 of
the reoperative cases. For the primary group, the PAA after 30 minutes
of exposure (median 6.65 IU/cm(2), range 3.85-11.89 IU/cm(2), p=0.14,
n=10) was not significantly reduced when compared to the initial acti
vity (median 8.74 IU/cm(2), range 2.22-17.68 IU/cm(2), n=10). After 30
-50 minutes CPB the PAA was significantly reduced (median 3.93 IU/cm(2
), range 1.5-13.24 IU/cm(2), p=0.028, n=10) and still reduced after re
warming for 10 minutes (median 3.12 IU/cm(2), range 0.88-19.93 IU/cm(2
), P=0.047, n=10). The simultaneous plasma tissue-type plasminogen act
ivator activity showed a significant (p<0.05) increase after 30-50 min
utes bypass with a later decline. The changes in the reoperative peric
ardial PAA were similar. in addition, the degree of PAA in reoperative
pericardium was consistently lower than that observed in primary tiss
ue. The extent of primary pericardial mesothelial damage at times B, C
, and D compared with that at time A showed a significant (P<0.01 for
times B, C, and D) increase. Similarly there was a significant worseni
ng of the degree of inflammation . Compared with primary pericardium,
the reoperative samples showed a significant (p<0.01 for times A, B, a
nd C) preponderance of damaged mesothelium at the earlier stages of th
e oepration. It appears that, following the initial bypass surgery, th
e processes that cause pericardial and mesothelial healing with recove
ry of PAA compete with those leading to pericardial adhesions and fibr
osis. The histological and biochemical outcome seen in reoperative per
icardium is the result of these competitive actions.