In patients with chronic myocardial infarction, myocardial viability is unlikely when basal regional myocardial blood flow is < 0.25 ml/min per g. Average basal flow in segments with normal or nearly normal wall motion is 0.78 +/- 0.35 ml/min per g. Thus, positron emission tomographic measurement of regional myocardial blood flow is helpful in identifying nonviable myocardium in these patients.
In humans with ischemic heart disease, myocardial blood flow responses to dobutamine and adenosine are linearly correlated over a wide range. The hyperemic response to dobutamine is in excess of that predicted by rate-pressure product and reflects the unmeasured inotropic, oxygen-wasting, and beta2-agonist effects of the drug. Dobutamine induces coronary steal with a frequency approaching that of adenosine.
This review focuses on several related issues concerning positron emission tomography measurements of regional myocardial blood flow using 13-N-ammonia in humans. The effect of partial volume correction on estimates of K1, the model parameter describing myocardial blood flow, is considered. In addition a new method for computing K1 images of myocardial flow distribution is briefly described and compared to a standard method. Potential differences between K1 and equilibrium levels of 13-N-ammonia in the myocardium for estimation of myocardial blood flow are discussed also. The issue of heterogeneity of myocardial blood flow and flow reserve in normal volunteers is considered from the clinical point of view in terms of evaluation of patients with ischemic heart disease. Finally, the use of absolute measurement of adenosine-stimulated myocardial blood flow to assess physiological significance of coronary artery stenoses is addressed.
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