(Circulation. 1998;97:2297-2298.)
© 1998 American Heart Association, Inc.
Load-Dependent Myocyte Dysfunction
William H. Barry, MD
From the Division of Cardiology, University of Utah Health Sciences
Center, Salt Lake City.
Correspondence to William H. Barry, MD, Division of Cardiology, University of Utah Health Sciences Center, 50 N Medical Dr, Salt Lake City, UT 84132. E-mail whbarry@med.utah.edu
Key Words: Editorials • myocytes • ventricles
The term
"cardiomyopathy of overload" was coined by
Arnold Katz in 1990.1 As he pointed out, it has
been recognized since the time of Osler that in patients with chronic
pressure or volume overload of the heart, a syndrome of progressive
ventricular dysfunction can develop.
Hypertrophy initially normalizes wall
stress,2 but eventually ventricular
dilation occurs, resulting in a secondary increase in wall stress
because of ventricular remodeling and associated increase
in the radius of curvature of the ventricle. This increase in wall
stress is proposed to cause further deterioration of
ventricular function by a progressive sequence of
hypertrophy
decreased ventricular
functiondilationincreased wall
stresshypertrophydecreased ventricular
function. This sequence of events may also account for the progressive
nature of the ventricular enlargement and remodeling that
can occur after loss of a significant component of functioning
myocardium, or reduction in the number of myocytes as
caused, for example, by myocardial infarction or myocarditis. Indeed,
the well-recognized influence of depressed ventricular
function and cardiac dilation on prognosis in patients with
valvular disease, cardiomyopathy, and
ischemic heart disease may in part be due to this process.
The potential causes of ventricular chamber
dysfunction in patients with advanced hypertrophy were well
summarized by Katz1 and include altered
energetics, myocyte "drop out" caused by necrosis and/or
apoptosis, alterations in the ventricular
connective tissue matrix, and hypertrophy-induced changes
in expression of myocyte genes and resulting alterations in myocyte
protein constituents that lead to a decrease in myocyte function. Work
from many laboratories has shown . . . [Full Text of this Article]
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