Ventricular remodeling during development and recovery from a
modified tachycardia-induced cardiomyopathy model.
Yamamoto, Kazuhiro, John C. Burnett, Jr., Lane M. Meyer, Lisa
Sinclair, Tracy L. Stevens, Margaret M. Redfield.
The Division of Cardiovascular Diseases and Internal Medicine, Mayo
Clinic, Rochester, MN
APStracts 3:0201R, 1996.
This study was designed to characterize left ventricular (LV) function
and mass in a modified cardiomyopathy model in the dog where right
ventricular pacing rates are gradually increased throughout 38 days.
On the last day of the pacing protocol, ejection fraction was reduced
(25 +/- 3 vs 60 +/- 1%) and LV end-diastolic diameter index (a ratio
of LV end-diastolic diameter to body weight, 2.09 +/- 0.02 vs 1.79
+/- 0.08 mm/kg) and LV mass index (a ratio of LV mass to body weight,
5.2 +/- 0.3 vs 4.3 +/- 0.2 g/kg) were greater than in the normal dogs
(p<0.05, respectively). Cardiac filling pressures increased and
LV diastolic function and coronary blood flow were impaired. After 4
weeks of recovery from the progressive pacing protocol, LV end
-diastolic diameter index (2.12 +/- 0.06 mm/kg) and LV mass index (5.6
+/- 0.2 g/kg) remained increased. Ejection fraction was improved (38
+/- 4%) but still depressed. LV diastolic function, coronary blood
flow and cardiac filling pressures returned to levels seen in the
normal dogs. This modified cardiomyopathy model associated with LV
hypertrophy complements the conventional tachycardia-induced
cardiomyopathy model without LV hypertrophy.
Received 1 March 1996; accepted in final form 1 May 1996.
APS Manuscript Number R127-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 June 96