Dual-isotope myocardial SPECT in patients with redefined myocardial infarction.
BACKGROUND
According to the redefinition of myocardial infarction (MI) by the ESC/ACC Committee, patients with unstable angina (UA) without significant elevation of creatine kinase (CK) but with elevation of troponin T should be diagnosed as MI.


METHODS
One hundred and forty-six consecutive patients formerly diagnosed as UA, with peak CK levels<twice upper normal level, who underwent myocardial Thallium-201 (Tl; perfusion tracer) and (123)I-15-iodophenyl 3-methyl pentadecanoic acid (BMIPP; metabolism tracer) dual isotope single-photon emission computed tomography (SPECT), were retrospectively reclassified into redefined MI and UA groups according to the redefinition (troponin T: rapid bedside assay positive or quantitative level >0.10 ng/ml). Dual SPECT findings were analyzed qualitatively and quantitatively in blinded manner.


RESULTS
Forty-seven patients (32%) were redefined as MI and 99 patients (68%) were redefined as UA. On admission, there were small but statistically significant elevations in laboratory parameters such as white blood cell count, C-reactive protein, CK and CK-MB in the redefined MI group compared with the redefined UA group. The proportion of patients with perfusion and metabolic abnormalities was significantly higher in the redefined MI group (Tl defect 36% vs. 4%, odds ratio: 13.5, p<0.001; BMIPP defect 64% vs. 23%, odds ratio: 5.8, p<0.001). Semi-quantitative evaluation revealed that the total Tl and BMIPP scores were significantly higher in the redefined MI patients (p<0.001).


CONCLUSIONS
In the redefined MI patients, perfusion and metabolic abnormalities occurred frequently and more extensively. However, Tl/BMIPP dual SPECT had limited ability to detect minor myocardial infarcts classified as redefined MI. A more sensitive stratification combined with troponin T directed assignment should be established to incorporate the ongoing minor infarcts which could not be assessed by serial dual-scintigraphic evaluations.
Fukushima
Masato
M
First Department of Internal Medicine, Nippon Medical School, 1-1-5, Sendagi, Bunkyo-ku, 113-8603 Tokyo, Japan.
Seino
Yoshihiko
Y
Kumita
Shin-ichiro
S
Nakajo
Hidenobu
H
Cho
Keiichi
K
Takano
Teruo
T
D000368:Aged; D000789:Angina, Unstable / Q000097:blood / Q000000981:diagnostic imaging; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D017023:Coronary Angiography; D023921:Coronary Stenosis / Q000097:blood / Q000000981:diagnostic imaging; D052279:Creatine Kinase, MB Form / Q000097:blood; D003937:Diagnosis, Differential; D004452:Echocardiography; D004562:Electrocardiography; D005227:Fatty Acids; D005260:Female; D006801:Humans; D007462:Iodobenzenes; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000000981:diagnostic imaging* / Q000628:therapy; D009204:Myocardial Revascularization; D019275:Radiopharmaceuticals; D012107:Research Design; D012189:Retrospective Studies; D013794:Thallium Radioisotopes; D015899:Tomography, Emission-Computed, Single-Photon / Q000379:methods; D020107:Troponin T / Q000097:blood* / Q000378:metabolism
D015415:Biomarkers; D005227:Fatty Acids; D007462:Iodobenzenes; D019275:Radiopharmaceuticals; D013794:Thallium Radioisotopes; D020107:Troponin T; C049338:iodofiltic acid; D002097:C-Reactive Protein; D052279:Creatine Kinase, MB Form