Relation of myocardial perfusion at rest and during pharmacologic stress to the PET patterns of tissue viability in patients with severe left ventricular dysfunction.
BACKGROUND
Stress perfusion imaging can assess effectively the amount of jeopardized myocardium, but its use for identifying underperfused but viable myocardium has yielded variable results. We evaluated the relation between measurements of myocardial perfusion at rest and during pharmacologic stress and the patterns of tissue viability as determined by positron emission tomographic (PET) imaging.


RESULTS
We studied 33 patients with coronary artery disease and left ventricular (LV) dysfunction (LV ejection fraction, 30%+/-8%). PET imaging was used to evaluate regional myocardial perfusion at rest and during pharmacologic stress with [13N]-ammonia as a flow tracer, and to delineate patterns of tissue viability (i.e., perfusion-metabolism mismatch or match) using [18F]-deoxyglucose (FDG). We analyzed 429 myocardial regions, of which 229 were dysfunctional at rest. Of these, 30 had normal perfusion and 199 were hypoperfused. A severe resting defect (deficit >40% below normal) predicted lack of significant tissue viability; 31 of 35 regions (89%) had a PET match pattern denoting transmural fibrosis. Although regions with mild or moderate resting defects (deficit <40% below normal) showed evidence of metabolic activity, perfusion measurements alone failed to identify regions with PET mismatch (reflecting hibernating myocardium). Reversible stress defects were observed with slightly higher frequency in regions with a PET mismatch (10 of 37) than in those with a PET match (36 of 162) pattern of viability. A reversible stress defect was a specific (78%) marker, but was a relatively insensitive marker (27%) of viable myocardium as defined by the PET mismatch pattern.


CONCLUSIONS
In patients with LV dysfunction, the severity of regional contractile abnormalities correlates with the severity of flow deficit at rest. Severe reductions in resting blood flow in these dysfunctional regions identify predominantly nonviable myocardium that is unlikely to have improved function after revascularization. Although dysfunctional myocardium with mild to moderate flow reductions contains variable amounts of viable tissue (as assessed by FDG uptake), flow measurements alone do not distinguish between regions with PET mismatch (potentially reversible dysfunction) and PET match (irreversible dysfunction). The presence of an irreversible defect on stress imaging is a relatively specific (78%) marker of PET match, whereas a reversible stress defect is a rather insensitive (27%) marker of viability, as defined by the PET mismatch pattern.
Di Carli
M F
MF
Department of Medical and Molecular Pharmacology, UCLA School of Medicine, Los Angeles, Calif, USA. mdicarli@pet.wayne.edu
Asgarzadie
F
F
Schelbert
H R
HR
Brunken
R C
RC
Rokhsar
S
S
Maddahi
J
J
D000368:Aged; D000641:Ammonia; D003326:Coronary Circulation / Q000187:drug effects*; D003327:Coronary Disease / Q000150:complications; D004176:Dipyridamole / Q000494:pharmacology; D005260:Female; D019788:Fluorodeoxyglucose F18; D006321:Heart / Q000000981:diagnostic imaging; D006801:Humans; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology*; D009590:Nitrogen Radioisotopes; D019275:Radiopharmaceuticals; D014022:Tissue Survival; D014055:Tomography, Emission-Computed; D014665:Vasodilator Agents / Q000494:pharmacology; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology
D009590:Nitrogen Radioisotopes; D019275:Radiopharmaceuticals; D014665:Vasodilator Agents; D019788:Fluorodeoxyglucose F18; D004176:Dipyridamole; D000641:Ammonia