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July 1, 1978Circulation Research190 citationsOpen Access

Coronary blood flow in experimental canine left ventricular hypertrophy.

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DODennis D. O’KeefeJHJulien I.E. HoffmanRCR Cheitlin

Key Points

  • This study aims to understand how left ventricular hypertrophy affects coronary blood flow and resistance in dogs.
  • Inflation of a balloon around the ascending aorta in nine dogs; six served as controls.

Structured PICO

Does left ventricular hypertrophy alter total and regional coronary blood flow and resistance in a canine model?

P
Population
21 dogs (9 with balloon inflated around ascending aorta to induce left ventricular hypertrophy, 6 acute controls, 6 sham-operated controls)
I
Intervention
Induction of left ventricular hypertrophy via balloon inflation around the ascending aorta for 6 weeks
C
Comparator
Acute controls and sham-operated controls
O
Outcome
Total and regional coronary blood flow and coronary vascular resistance at rest and during maximal vasodilationsurrogate

In a canine model, left ventricular hypertrophy increases minimal coronary vascular resistance during maximal vasodilation, potentially predisposing to stress-induced subendocardial ischemia.

Limitations

  • Arterial capacity could not be estimated
  • Changes noted might have been due to coronary arterial responses to raised coronary pressures rather than to hypertrophy itself

Abstract

To determine whether left ventricular hypertrophy LVH altered total and regional coronary blood flow, we inflated a balloon around the ascending aorta of nine dogs; six acute and six sham-operated dogs were controls. After 6 weeks, all dogs were studied with an open chest under anesthesia; the balloons were deflated. There was moderate LVH as shown by increased left ventricular weight and fiber diameter. At rest there were no major differences of coronary flow or resistance per gram of muscle. With maximal coronary vasodilation due to adenosine or carbochrome, mean coronary vascular resistance was 84% higher in LVH than in normal hearts; with isoproterenol, resistance was 54% higher in LVH. These changes were similar in right and left ventricles. Minimal coronary resistance at end diastole also was higher in LVH--64% and 94% for the two sets of vasodilators, respectively. There were no significant differences in capillary or large vessel proportional volumes in LVH and control dogs, but arterial capacity could not be estimated. The raised minimal coronary resistance suggests the possibility that, with stress, coronary flow, especially to subendocardial muscle, might be inappropriate and perhaps cause ischemic damage. However, the changes noted might have been due to coronary arterial responses to raised coronary pressures rather than to hypertrophy itself.

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Cite This Study

O’Keefe et al. (1978) studied this question.

synapsesocial.com/papers/6a1757bf3510de12de8d7cd0https://doi.org/10.1161/01.res.43.1.43
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