Circulation, Vol 78, 186-201, Copyright © 1988 by American Heart Association
HF Weisman, DE Bush, JA Mannisi, ML Weisfeldt and B Healy
Infarct expansion is acute regional dilatation and thinning of the infarct
zone. There are several possibilities for the mechanism of this alteration
in cardiac shape: thinning could be caused by 1) cell rupture, 2) a
reduction in the intercellular space, or 3) stretching of myocytes or 4)
slippage of groups of myocytes so that less cells are distributed across
the wall. To determine the relative contributions of these cellular
mechanisms of wall thinning and dilatation, detailed study of transverse
histological sections of rat hearts with infarct expansion was performed 1,
2, and 3 days after coronary ligation. The number of cells across the wall
was determined in six regions within, adjacent to, and remote from the
infarct. Cell counting was performed so that the total number of cells
across the wall and the number of cells per unit length (cell density)
across the wall were determined. The transmural cell count and the cell
density were correlated with the wall thickness in each region. Myocyte
cross-sectional areas and sarcomere lengths were also measured. The results
from the infarct expansion hearts were compared with those of sham-operated
control hearts that had been similarly analyzed. To ensure that mechanisms
identified in the rat were applicable to human infarct expansion, five
hearts from patients who died within 3 days of infarction and two hearts
from patients without coronary disease were studied histologically in a
similar fashion. Wall thinning occurred in all regions of the rat infarct
expansion hearts compared with controls (p less than 0.0001) but, as
expected, was most pronounced in the infarct zone. A decrease in the number
of cells across the wall accompanied the wall thinning at each site (p less
than 0.0001), and this change in cell number was highly correlated with the
changes in wall thickness (r = 0.915, p less than 0.001). Cell density
increased from controls only within the infarct zone (p less than 0.001)
and accounted for at most 20% of the thinning in that region. The change in
cell density was attributable to both cell stretch (measured by increased
sarcomere length and decreased myocyte cross-sectional area) and a decrease
in the intercellular space. A similar strong correlation between wall
thinning and decreased number of cells across the wall was identified in
the human hearts (r = 0.94, p less than 0.001).(ABSTRACT TRUNCATED AT 250
WORDS)
ARTICLES
Cellular mechanisms of myocardial infarct expansion
Peter Belfer Laboratory for Myocardial Research, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland.
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