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From the Department of Anatomy and Structural Biology, University of
South Dakota, Vermillion (T.O., T.T., S.S., A.M.G.), and the South Dakota
Cardiovascular Research Institute, Sioux Falls (T.T., S.S., A.M.G.), SD; and
the Department of Food Science and Technology, Ohio State University,
Columbus, Ohio (S.A.M.).
Correspondence to A. Martin Gerdes, PhD, South Dakota Cardiovascular Research Institute, 1400 W 22nd St, Sioux Falls, SD 57105. E-mail mgerdes{at}usd.edu
Abstract—Progression to failure
in hypertension is associated with ventricular dilation,
excessive myocyte lengthening, and an increase in myocyte length/width
ratio. The temporal development of these changes in relation to
impaired pump performance is unknown. We examined isolated
myocytes from 1- to 12-month-old spontaneously hypertensive heart
failure (SHHF) rats who develop heart failure at approximately 24
months of age. Left ventricular myocyte cross-sectional
area reached a maximum of
© 1998 American Heart Association, Inc.
Scientific Contributions
Maladaptive Remodeling of Cardiac Myocyte Shape Begins Long Before Failure in Hypertension
350 to 400 µm2 at 3
months of age and did not change significantly thereafter. Nonetheless,
LV systolic wall stress, a known stimulus for myocyte
transverse growth, increased progressively between 3 and 12 months of
age. Unlike the situation in normally aging rats with stable body mass,
myocyte length in SHHF rats continued to increase with aging
(P<0.05 from 9 to 12 months of age). In summary, (1)
left ventricular myocyte transverse growth reaches an upper
limit by 3 months of age although systolic wall stress
continues to rise; and (2) cell length is significantly increased by 12
months of age. This study suggests that maladaptive remodeling of
cardiac myocyte shape begins long before pump failure in hypertension.
Additionally, it appears that the left ventricle may be robbed of an
important adaptive mechanism to normalize wall stress (eg, myocyte
transverse growth) early in the progression to failure.
Key Words: heart failure • ventricular remodeling • myocytes
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