Circulation, Vol 69, 409-417, Copyright © 1984 by American Heart Association
RJ Bache, CE Arentzen, AB Simon and TR Vrobel
This study tested the hypothesis that in the chronically hypertrophied left
ventricle pacing stress may cause abnormalities of perfusion that result in
myocardial ischemia. Left ventricular hypertrophy (LVH) was produced by
banding the ascending aorta of 10 dogs at 6 weeks of age, and studies were
carried out after the animals had reached adulthood and when mean left
ventricular/body weight ratio was 74% greater than in eight control dogs.
Myocardial blood flow was measured with microspheres during pacing at 100,
200, and 250 beats/min, while aortic and coronary sinus blood samples were
obtained for determination of concentrations of lactate and the adenosine
metabolites inosine and hypoxanthine. In the control dogs, increasing heart
rates were associated with an increase in mean myocardial blood flow while
subendocardial flow was maintained at a level equal to or greater than
subepicardial flow. Myocardial lactate uptake ranged from +60% to -5%, and
adenosine metabolites were not detected in coronary sinus blood (less than
0.5 microM/l). In four dogs that underwent aortic banding no production of
lactate or adenosine metabolites was observed at any heart rate; in these
animals subendocardial flow was maintained at a level equal to or greater
than subepicardial flow at all pacing rates. The remaining six dogs with
LVH demonstrated net lactate production significantly greater than control
during pacing at 250 beats/min; five of these six animals also produced
adenosine metabolites.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Abnormalities in myocardial perfusion during tachycardia in dogs with left ventricular hypertrophy: metabolic evidence for myocardial ischemia
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