Circulation, Vol 79, 872-883, Copyright © 1989 by American Heart Association
WH Gaasch, MR Zile, PK Hoshino, CS Apstein and AS Blaustein
Serial changes in left ventricular (LV) size and function during the
adaptation to chronic pressure overload and the transition to pump failure
were studied in 16 conscious dogs (aortic bands placed at 8 weeks of age).
Echocardiographic data at baseline and at 3, 6, 9, and 12 months after
banding revealed a progressive increase in LV mass in all dogs. In six dogs
with LV pump failure, there was a progressive decline in circumferential
fiber shortening (29 +/- 4% at 12 months); this was significantly less than
that seen in five littermate controls (38 +/- 3%, p less than 0.05). The
average LV to body weight ratio in this group was 9.8 +/- 2.7 g/kg. In 10
dogs without pump failure (compensated LVH group), shortening exceeded that
seen in the controls (43 +/- 4%, p less than 0.05); the LV to body weight
ratio was 7.7 +/- 1.0 g/kg. At 12 months (cardiac catheterization), the LV
end-diastolic pressure was higher in the failure (25 +/- 15 mm Hg) than in
the compensated group (8 +/- 5 mm Hg, p less than 0.05); mean systolic
stress was also higher in the failure group (313 +/- 67 g/cm2) than in the
compensated group (202 +/- 53 g/cm2, p less than 0.05). The transmural
distribution of myocardial blood flow was measured (at 12 months) with the
radioactive microsphere technique; flow data were then related to an index
of demand (a stress-time index). There was preferential blood flow to the
subendocardial layers in the control (endo/epi = 1.28) and compensated
hearts (endo/epi = 1.10), but in the failure group there was a relative
decrease in subendocardial flow (endo/epi = 0.92). However, the absolute
values for subendocardial flow in the normal, compensated, and failure
groups were 77 +/- 54, 125 +/- 48, and 113 +/- 64 ml/min/100 g; the
stress-time indexes in the subendocardial shell were 38 +/- 11, 74 +/- 19,
and 93 +/- 34 g sec.10(2)/cm2/min. Despite what appears to be a marginal
balance between blood flow and the stress time index in the failure group,
the myocardial high energy phosphates were not depleted and the inoptropic
state was not depressed. In this model of LV hypertrophy, the observed
differences in fiber shortening can be explained on the basis of the
inverse afterload-shortening relation; pump failure was due to an
inadequate LV hypertrophy with afterload excess.(ABSTRACT TRUNCATED AT 400
WORDS)
ARTICLES
Stress-shortening relations and myocardial blood flow in compensated and failing canine hearts with pressure-overload hypertrophy
Department of Medicine (Cardiology), Medical Center of Central Massachusetts/Memorial, Worcester 01605.
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