Rate pressure product corrections of ^sup 82^Rb PET myocardial blood flow computations

Objectives: Previous investigators recommend that resting myocardial blood flow (MBF) should be corrected by the rate pressure product (RPP) (Circulation 1993;88:62-9), but none of the commercially available PET MBF software packages include this correction. Our study was conducted to determine whet...

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Veröffentlicht in:The Journal of nuclear medicine (1978) 2018-05, Vol.59, p.1547
Hauptverfasser: Tosh, Andrew Van, Mathew, Jaison, Cooke, Charles, Palestro, Christopher, Nichols, Kenneth
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Sprache:eng
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Zusammenfassung:Objectives: Previous investigators recommend that resting myocardial blood flow (MBF) should be corrected by the rate pressure product (RPP) (Circulation 1993;88:62-9), but none of the commercially available PET MBF software packages include this correction. Our study was conducted to determine whether RPP corrections contribute to the ability of PET global MBF measurements to identify pts with severe coronary artery disease (CAD). Methods: Data were examined retrospectively for 103 pts with known or suspected CAD, who underwent both coronary angiography & rest/regandoson-stress 82Rb PET. Global MBF values were computed by Emory Cardiac Toolbox v4 algorithms from dynamic first pass curves. Resting MBF was corrected for RPP as MBF x 10,000/((heart rate at rest) x (systolic blood pressure at rest)). Myocardial flow reserve (MFR) was computed both without RPP corrections (MFR1 = stress MBF/uncorrected rest MBF) & with RPP corrections (MFR2 = stress MBF/corrected rest MBF). Digitized angiograms were graded at a core lab (Boston Cardiac Research Institute). Stenoses >70% were considered significant. The number of major arterial territories with stenoses > 70% were tabulated for each pt. Severe CAD was defined as all 3 major territories with stenoses > 70%. We also analyzed pts with no occluded vessels & 1-vessel CAD as one group, & multi-vessel disease (2- & 3-vessel CAD) as another group. Results: Overall, MFR2 values were higher than MFR1 values (2.42±1.41 versus 2.17±1.08, paired Wilcoxon p = 0.0001). Difference between MFR methods was most pronounced for pts with no CAD (2.74±1.56 versus 2.42±1.12, p = 0.001, N = 57) & with 1-vessel CAD (2.17± 1.03 versus 1.93±0.83, p = 0.01, N = 31). Values were similar for pts with 2-vessel CAD (2.12±1.61 versus 2.07±1.48, p = 0.74, N = 8) & 3-vessel CAD (1.29±0.32 versus 1.34±0.40, p = 0.94, N = 7). ROC thresholds for detecting 3-vessel disease were lower for MFR2 (threshold = 1.55, AOC = 89±5%) than for MFR1 (threshold = 1.71, AOC = 83±7%). Sensitivity to detect 3-vessel disease was 100% for both methods, but specificity was higher for MFR2 (78% versus 65%, p = 0.05). For identifying pts with multi-vessel disease, MFR2 & MFR1 had similar ROC AOC (72±7% versus 71±7%, p = 0.81), & similar sensitivity (62% versus 79%, p = 0.60), but MFR2 had higher specificity (79% versus 62%, p = 0.02). Conclusion: On a phenomenological basis, RPP aided in discriminating pts with severe CAD & MVD from those with less severe disease, & imp
ISSN:0161-5505
1535-5667