Stimulation of the hepatic arterial buffer response using exogenous adenosine: hepatic rest/stress perfusion imaging

Objectives The hepatic arterial buffer response is a mechanism mediated by adenosine whereby hepatic arterial perfusion (HAP) increases when portal flow decreases, and is implicated in liver disease. The first study aim was to measure HAP in patients undergoing myocardial perfusion imaging (MPI), thus developing hepatic arterial rest/stress perfusion imaging (HAPI). The second aim was to compare adenosine-induced changes in splenic perfusion (SP) and HAP with corresponding changes in myocardial blood flow (MBF). Methods Patients had MPI with 82 Rb PET/CT using adenosine ( n = 45) or regadenoson ( n = 33) for stressing. SP and HAP were measured using a first-pass technique that gives HAP rather than total hepatic perfusion. Renal perfusion (RP) was also measured. Results Mean MBF and HAP increased after both adenosine ([stress-rest]/rest 1.1 and 0.8) and regadenoson (1.4 and 0.6), but the respective changes did not correlate. After adenosine, SP (− 0.48) and RP (− 0.26) both decreased. The change in SP correlated positively with the change in MBF ( r = 0.36; p = 0.015) but did not correlate with change in HAP. After regadenoson, SP (0.2) and RP (0.2) both increased. The changes in SP correlated with the changes in MBF ( r = 0.39; p = 0.025) and HAP ( r = 0.39; p = 0.02). Changes in RP correlated with changes in HAP ( r = 0.51; p = 0.0008) but not MBF. Resting SP ( r = 0.32; p = 0.004), but not resting HAP, correlated with hepatic fat burden. Adenosine-induced change in HAP also correlated with hepatic fat ( r = 0.29; p = 0.05). Conclusion HAPI could be a useful new hepatic function test. Neither splenic ‘switch-off’ nor hepatic arterial ‘switch-on’ identifies adequacy of stress in MPI. Key Points • This article describes a new method for assessing arterial perfusion of the liver and its capacity to respond to an infusion of adenosine, a substance that normally ‘drives’ hepatic arterial flow. • Hepatic arterial flow increased in response to adenosine, sometimes dramatically. Adenosine is already used clinically to stimulate myocardial blood flow in patients with suspected coronary disease, but the increase in flow did not correlate with the corresponding increase in hepatic arterial flow. • Analogous to the use of adenosine in the myocardium, the increase in hepatic arterial flow in response to adenosine has the potential to be a new clinically useful method for the evaluation of hepatic arterial haemodynamics in liver disease.