Circulation, Vol 86, 426-430, Copyright © 1992 by American Heart Association
AM Gerdes, SE Kellerman, JA Moore, KE Muffly, LC Clark, PY Reaves, KB Malec, PP McKeown and DD Schocken
BACKGROUND. Chronic ischemic heart disease may lead to ventricular dilation
and congestive heart failure (ischemic cardiomyopathy [ICM]). The changes
in cardiac myocyte shape associated with this dilation, however, are not
known. METHODS AND RESULTS. Left ventricular myocyte dimensions were
assessed in cells isolated from explanted human hearts obtained from
patients with ICM (n = 6) who were undergoing heart transplantation. Cells
were also examined from three nonfailing donor hearts with normal coronary
arteries (NCA). Compared with cells from patients with NCA, myocyte length
was 40% longer in hearts from patients with ICM (197 +/- 8 versus 141 +/- 9
microns, p less than 0.01), cell width was not significantly different, and
cell length/width ratio was 49% greater (11.2 +/- 0.9 versus 7.5 +/- 0.6, p
less than 0.01). Sarcomere length was the same in myocytes from both
groups. The extent of myocyte lengthening is comparable to the increase in
end-diastolic diameter commonly reported in patients with ICM. CONCLUSIONS.
These data suggest that increased myocyte length (an intracellular event),
instead of myocyte slippage (an extracellular event), is largely
responsible for the chamber dilation in ICM. Furthermore, maladaptive
remodeling of myocyte shape (e.g., increased myocyte length/width ratio)
may contribute to the elevated wall stress (e.g., increased chamber
radius/wall thickness) in ICM.
ARTICLES
Structural remodeling of cardiac myocytes in patients with ischemic cardiomyopathy
Department of Anatomy, University of South Florida, College of Medicine, Tampa 33612.
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