Mmh. Marijianowski et al., REMODELING AFTER MYOCARDIAL-INFARCTION IN HUMANS IS NOT ASSOCIATED WITH INTERSTITIAL FIBROSIS OF NONINFARCTED MYOCARDIUM, Journal of the American College of Cardiology, 30(1), 1997, pp. 76-82
Objectives, This study was specifically designed to evaluate whether n
oninfarcted hypertrophic myocardium in patients with end stage heart f
ailure after myocardial infarction (MI) is associated with an increase
in interstitial fibrous tissue. Background. Postinfarction remodeling
consists of complex alterations that involve both infarcted and nonin
farcted myocardium, The question arises whether ventricular dysfunctio
n is due to physical events, such as inadequate myocardial hypertrophy
to compensate for increased tangential wall stress, or is caused by t
he development of progressive interstitial fibrosis in noninfarcted my
ocardium. Methods. Fifteen hearts were obtained as cardiac explants (n
= 13) or at autopsy (n = 2) from patients with end stage coronary art
ery disease, Sixteen normal hearts served as reference hearts, Samples
were taken from the left ventricular (LV) wall that contained the inf
arcted area, the border area and noninfarcted myocardium remote from s
car areas, Collagen was quantified biochemically and microdensitophoto
metrically. Collagen type I and III ratios were analyzed by using the
cyanogen bromide method and immunohistochemical staining, followed by
microdensitophotometric quantification. Results. In noninfarcted myoca
rdium remote from the scar areas, total collagen levels and collagen t
ype I/III ratios did not differ statistically from those in reference
hearts, These observations contrasted with high total collagen content
and high collagen type I/III ratios in scar and border areas. Conclus
ions. Remodeling of LV myocardium after MI in patients with end stage
heart failure is not necessarily associated with interstitial fibrosis
in noninfected hypertrophic myocardium remote from scar areas, This f
inding raises questions regarding therapeutic interventions designed t
o prevent or retard the development of interstitial fibrosis. (C) 1997
by the American College of Cardiology.