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Review
. 2000 Apr;83(4):475-80.
doi: 10.1136/heart.83.4.475.

Positron emission tomography and myocardial imaging

P G Camici  1
Affiliations
Review

Positron emission tomography and myocardial imaging

P G Camici. Heart. 2000 Apr.
No abstract available

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Figures

Figure 1:
Figure 1:
Physics of positron emission, annihilation, and coincidence detection. Adapted from Camici et al.2
Figure 2:
Figure 2:
Myocardial blood flow under baseline conditions and during hyperaemia induced by intravenous dipyridamole in normal subjects (A), in patients with hypertrophic cardiomyopathy (B), and patients with left ventricular hypertrophy secondary to arterial hypertension or aortic stenosis (C). The diffuse blunting of flow reserve in these patients with angiographically normal coronary arteries is suggestive of widespread microvascular dysfunction. Adapted from Choudhury et al.8
Figure 3:
Figure 3:
Coronary vasodilator reserve falls with increasing percent diameter stenosis and is exhausted for stenoses > 80%. Normal control values of coronary vasodilator reserve are shown at zero percent diameter stenosis on the left. CAD, coronary artery disease. Adapted from Uren et al.7
Figure 4:
Figure 4:
Myocardial viability in two patients with coronary artery disease and severe chronic left ventricular dysfunction assessed by PET with 18F labelled FDG during hyperinsulinaemic euglycaemic clamp. Both patients had previous myocardial infarctions. The scan in panel A shows that FDG uptake in the previously infarcted anteroseptal segment is 0.45 µmol/g/min, suggesting the presence of viable myocardium. In the scan in panel B the uptake of FDG in the anterior wall and the interventricular septum is significantly reduced (0.14 µmol/g/min), suggesting absence of viability in this large area. A cut off point of 0.25 µmol/g/min is routinely used in our laboratory to differentiate between viable and non-viable myocardium.13
Figure 4:
Figure 4:
Myocardial viability in two patients with coronary artery disease and severe chronic left ventricular dysfunction assessed by PET with 18F labelled FDG during hyperinsulinaemic euglycaemic clamp. Both patients had previous myocardial infarctions. The scan in panel A shows that FDG uptake in the previously infarcted anteroseptal segment is 0.45 µmol/g/min, suggesting the presence of viable myocardium. In the scan in panel B the uptake of FDG in the anterior wall and the interventricular septum is significantly reduced (0.14 µmol/g/min), suggesting absence of viability in this large area. A cut off point of 0.25 µmol/g/min is routinely used in our laboratory to differentiate between viable and non-viable myocardium.13
Figure 5:
Figure 5:
Mean left ventricular β adrenoceptor density in normal subjects and in patients with hypertrophic cardiomyopathy with preserved systolic function (HC) or with left ventricular dysfunction (HC-LVD). Adapted from Choudhury et al.16
See this image and copyright information in PMC

References

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    1. N Engl J Med. 1994 Jun 23;330(25):1782-8 - PubMed
    1. Cardiovasc Res. 1994 Nov;28(11):1595-612 - PubMed

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