Author + information
- Received March 23, 1995
- Revision received June 21, 1995
- Accepted July 10, 1995
- Published online November 15, 1995.
- Rob S.B. Beanlands, MD, FRCP(C)a,b,c,1,*,
- Otto Muzik, PhDa,b,c,
- Pierre Melon, MDa,b,c,
- Ronald Sutor, MDa,b,c,
- Steve Sawada, MDa,b,c,
- David Muller, MDa,b,c,
- Diane Bondie, RNa,b,c,
- Gary D. Hutchins, PhDa,b,c and
- Markus Schwaiger, MD, FACCa,b,c
- ↵*Address for correspondence:Dr. Rob S. B. Beanlands, Division of Cardiology, University of Ottawa Heart Institute, 1053 Carling Avenue, Ottawa, Ontario KIY 4E9, Canada.
Objectives. The aim of this study was to evaluate patients with coronary artery disease to 1) determine the relation between flow reserve measured by nitrogen-13 (N-13) ammonia kinetic modeling and stenosis severity assessed by quantitative angiography, and 2) examine whether flow reserve is impaired in regions supplied by vessels without significant angiographic disease.
Background. With the advent of new therapeutic approaches for coronary disease, an accurate noninvasive approach for absolute quantification of flow and flow reserve is needed to evaluate functional severity and extent of atherosclerosis. Nitrogen-13 ammonia kinetic modeling may permit such evaluation.
Methods. Twenty-seven subjects were classified into three groups: group 1= 5 young volunteers; group 2= 7 middle-aged volunteers; and group 3= 15 patients with coronary artery disease. Dynamic N-13 ammonia positron emission tomographic imaging was performed at rest and during adenosine infusion. A three-compartment model was fit to regional N-13 ammonia kinetic data to determine myocardial flow. Group 3 patients underwent quantitative coronary angiography.
Results. The regional blood flow results in patients with coronary disease were classified into four subgroups: no significant detectable disease and mild (50% to 69.9% area stenosis), moderate (70% to 94.9% area stenosis) or severe (95% to 100% area stenosis) coronary disease. Flow reserve was 2.95 ± 0.65; 2.09 ± 0.47; 2.02 ± 0.51; 1.3 ± 0.32, respectively (p ≤ 0.01 except mild vs. moderate). Flow reserve was correlated with percent area stenosis (r = −0.56) and minimal lumen diameter (r = 0.75). In volunteers (groups 1 and 2), flow reserves were greater than in segments without detectable disease in group 3 patients (4.10 ± 0.71 and 3.79 ± 0.42, respectively, vs. 2.88 ± 0.56, p ≤ 0.02).
Conclusions. The functional severity of coronary disease measured by N-13 ammonia positron emission tomography varied for a given stenosis but was significantly related to angiographic severity. Among patients with coronary disease, myocardial regions without significant angiographic stenoses displayed reduced flow reserve than did regions in control subjects, indicating that vascular reactivity was more diffusely impaired in group 3 than was suggested by angiography. Noninvasive quantification of myocardial flow reserve using dynamic N-13 ammonia positron emission tomography yields important functional data that permit definition of the extent of disease even when disease is not apparent by angiography.
↵1 Dr. Rob Beanlands was a Research Fellow supported by the Centennial Fellowship Award, of the Medical Research Council of Canada, Ottawa, Ontario, Canada and is currently a Research Scholar for the Medical Research Council of Canada at the University of Ottawa Heart Institute.
This work was carried out during the tenure of Dr. Schwaiger as an Established Investigator of the American Heart Association, Dallas, Texas, and was supported in part by Grant ROI HL41047-01 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.
This work was presented in abstract form in two separate parts at the 65th Annual Scientific Sessions of the American Heart Association, Dallas, Texas, November 1992 (Circulation 1992; 86 Suppl 1: 1–185) and the Young Investigator Award Competition for the Cardiovascular Council of the Society of Nuclear Medicine (J Nucl Med 1992; 33: 826).
- Received March 23, 1995.
- Revision received June 21, 1995.
- Accepted July 10, 1995.
- American College of Cardiology