Reduced LV myocardial blood flow.
Author(s) -
Julien I.E. Hoffman
Publication year - 1978
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.58.3.573
Subject(s) - medicine , cardiology , blood flow , coronary circulation , coronary arteries , chest pain , artery
To the Editor: The interesting article on myocardial blood flow in aortic stenosis by Johnson et al.' makes some statements that need further discussion. The authors commented that in their patients the ratio DPTI/SPTI was not related to myocardial blood flow per beat. However, that ratio was never proposed as a predictor of total myocardial blood flow by its originators: In animals, the DPTI/SPTI ratio predicts relative subendocardial blood flow (the inner: outer ratio), not total flow.2' 3 Secondly, the authors state that there is no evidence that long standing, compensated aortic stenosis is associated with ischemia at rest, and add that myocardial lactate production at rest is not encountered in these patients. It is true that there are no measurements of subendocardial blood flow in man, so that evidence of reduced subendocardial flows cannot be provided. Nevertheless, in children with aortic stenosis there is a fairly good correlation between the DPTI/SPTI ratio (or its equivalent) and changes in the resting electrocardiogram that suggest myocardial ischemia.4 Furthermore, patients with severe aortic stenosis usually have well-marked subendocardial fibrosis, and references to this appear in a recent publication.5 It is likely that if there is severe ischemia at rest for more than a short time, muscle cells will die and be replaced by fibrous tissue. Subendocardial blood flow will then be below normal but will be adequate to oxygenate the surviving muscle cells at rest. As a result there is no net myocardial lactate production at rest, but with exercise there may be angina, lactate production, and electrocardiographic signs of subendocardial ischemia due to ischemia of the remaining subendocardial muscle. Finally, replacement of some subendocardial muscle by fibrous tissue will provide mass without a corresponding increment of myocardial oxygen consumption or blood flow. Thus, although Johnson et al. found a reduced myocardial blood flow per unit mass of left ventricle, it is possible that flow per unit mass of muscle might have been within normal limits at rest. JULIEN I. E. HOFFMAN, M.D. University of California, San Francisco San Francisco, California
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