Background: Dynamic 15O-water PET is used to quantify myocardial blood flow. For clinical use however, additional information regarding left ventricular performance is often required but is not obtained from standard tracer kinetic modelling. The aim of this study was to explore the use of a novel index, the central circulatory turnover (CCT) which represents the fractional exchange of blood per stroke within the cardiopulmonary blood pool and can be measured from any dynamic PET scan.
Methods: Data from 111 clinical patients were analysed retrospectively. Patients underwent a 6-min 15O-water scan during rest and adenosine-induced stress. Patients were categorized into 4 groups based on stress myocardial blood flow (MBF, in mL/g/min): all segments >2.3 (group 1, n=53), one vessel <2.3 (group 2, n=18), global <2.3 (group 3, n=25) or global <1.3 (group 4, n=15). Using automated software, LV and RV time-activity curves were extracted after which their first-pass peaks were isolated and the centroid of each peak was obtained. Mean pulmonary transit time (MPTT, min) was defined as the difference between the LV centroid and the RV centroid and CCT was defined as 1/(MPTT*heart rate).
Results: MPTT progressively increased with disease severity during stress (mean MPTT±SD of 0.142±0.051 min, 0.176±0.042 min, 0.186±0.040 min and 0.248±0.077 min for groups 1 to 4, ANOVA p<0.001). Similar results were obtained during rest (MPTT of 0.175±0.035 min, 0.205±0.043 min, 0.201±0.033min and 0.237±0.059 min for groups 1 to 4, ANOVA p<0.001). CCT decreased with increasing disease severity both during stress (CCT of 0.082±0.028, 0.077±0.027, 0.075±0.015 and 0.056±0.014 for groups 1 to 4, ANOVA p<0.001) and rest (CCT of 0.089±0.014, 0.076±0.025, 0.081±0.014 and 0.061±0.017 for groups 1 to 4, ANOVA p<0.001). Decrease of CCT was especially pronounced in severely ischemic patients already at rest
Conclusion: Pulmonary transit times and central circulatory turnover can be measured automatically using dynamic PET. Since both are correlated with severity of myocardial ischemia already at rest, they appear to reflect manifest adverse cardiopulmonary remodelling. Both measures add information to standard tracer kinetic approaches and may play a future role in diagnosing and evaluating heart failure.