scholarly journals Splenic switch-off as a novel marker for adenosine response in nitrogen-13 ammonia PET myocardial perfusion imaging: Cross-validation against CMR using a hybrid PET/MR device

Author(s):  
Adam Bakula ◽  
Dimitri Patriki ◽  
Elia von Felten ◽  
Georgios Benetos ◽  
Aleksandra Sustar ◽  
...  

Abstract Background No methodology is available to distinguish truly reduced myocardial flow reserve (MFR) in positron emission tomography myocardial perfusion imaging (PET MPI) from seemingly impaired MFR due to inadequate adenosine response. The adenosine-induced splenic switch-off (SSO) sign has been proposed as a potential marker for adequate adenosine response in cardiac magnetic resonance (CMR). We assessed the feasibility of detecting SSO in nitrogen-13 ammonia PET MPI using SSO in CMR as the standard of reference. Methods and Results Fifty patients underwent simultaneous CMR and PET MPI on a hybrid PET/MR device with co-injection of a gadolinium-based contrast agent and nitrogen-13 ammonia during rest and adenosine-induced stress. In CMR, SSO was assessed visually (positive vs negative SSO) and quantitatively by calculating the ratio of the peak signal intensity of the spleen during stress over rest (SIR). In PET MPI, the splenic signal activity ratio (SAR) was calculated as the maximal standard uptake value of the spleen during stress over rest. The median SIR was significantly lower in patients with positive versus negative SSO in CMR (0.57 [IQR 0.49 to 0.62] vs 0.89 [IQR 0.76 to 0.98]; P < .001). Similarly, median SAR in PET MPI was significantly lower in patients with positive versus negative SSO (0.40 [IQR 0.32 to 0.45] vs 0.80 [IQR 0.47 to 0.98]; P < .001). Conclusion Similarly to CMR, SSO can be detected in nitrogen-13 ammonia PET MPI. This might help distinguish adenosine non-responders from patients with truly impaired MFR due to microvascular dysfunction or multivessel coronary artery disease.

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Bakula ◽  
D Patriki ◽  
E Von Felten ◽  
G Benetos ◽  
A Sustar ◽  
...  

Abstract Background Positron emission tomography myocardial perfusion imaging (PET MPI) is a robust and excellent tool for assessing ischemia. So far, however, no methodology has been established to distinguish truly reduced MFR due to microvascular dysfunction or three-vessel coronary disease (CAD) from seemingly impaired MFR due to inadequate adenosine response. Conversely, for cardiac stress magnetic resonance (CMR) the adenosine induced splenic switch-off (SSO) sign has been proposed as a potential marker for adequate adenosine response. Purpose We assessed the feasibility of detecting SSO in adenosine stress 13N-ammonia PET MPI using SSO in CMR as the standard of reference. Methods 50 patients underwent simultaneous PET MPI and CMR on a hybrid PET/MR device with co-injection of 13N-ammonia and a gadolinium-based contrast agent during rest and adenosine-induced stress. In CMR, SSO was assessed qualitatively and quantitatively by calculating the ratio of the peak signal intensity of the spleen during stress over rest (SIR). Similarly, in PET MPI the splenic signal activity ratio (SAR) was calculated as the proportion of the maximal standard uptake value of the spleen in stress and rest. Additionally, MFR was quantified in PET MPI. Results Visual SSO in CMR was present in 37 (74%) patients, whereas 13 patients had no SSO. The median SIR in CMR was significantly lower in patients with visual SSO compared to patients without visual SSO (0.57 [IQR 0.49–0.62] vs. 0.89 [IQR 0.76–0.98]; p&lt;0.001). Similarly, median SAR in PET was significantly lower in patients with visual SSO in CMR compared to patients without visual SSO (0.4 [IQR 0.32–0.45] vs. 0.8 [IQR 0.47–0.98]; p&lt;0.001). SIR correlated significantly with SAR (r=0.4, p&lt;0.05). Mean MFR was significantly higher in patients with visual SSO compared to patients without visual SSO (3.38±0.86 vs. 2.53±0.84; p&lt;0.05). Conclusion Similarly to CMR, SSO can be detected in 13N-ammonia PET MPI. This might help distinguish adenosine non-responders from patients with truly impaired MFR due to microvascular dysfunction or multivessel CAD. Figure 1. Splenic switch off (*) illustrated on transaxial 13N-ammonia PET MPI stress (A) compared to rest perfusion images (B) and similarly in stress (C) and rest (D) short axis CMR (**) in the same patient during adenosine induced stress and co-injection of 13N-ammonia and a gadolinium based contrast agent, acquired on a hybrid PET/MR device. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Swiss National Science Foundation (SNSF)


2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Dimitri Patriki ◽  
Elia von Felten ◽  
Adam Bakula ◽  
Andreas A. Giannopoulos ◽  
Christel H. Kamani ◽  
...  

Abstract Background Inadequate coronary adenosine response is a potential cause for false negative ischemia testing. Recently, the splenic switch-off (SSO) sign has been identified as a promising tool to ascertain the efficacy of adenosine during vasodilator stress cardiovascular magnetic resonance imaging (CMR). We assessed the value of SSO to predict adenosine response, defined as an increase in myocardial blood flow (MBF) during quantitative stress myocardial perfusion 13 N-ammonia positron emission tomography (PET). Methods We prospectively enrolled 64 patients who underwent simultaneous CMR and PET myocardial perfusion imaging on a hybrid PET/CMR scanner with co-injection of gadolinium based contrast agent (GBCA) and 13N-ammonia during rest and adenosine-induced stress. A myocardial flow reserve (MFR) of  > 1.5 or ischemia as assessed by PET were defined as markers for adequate coronary adenosine response. The presence or absence of SSO was visually assessed. The stress-to-rest intensity ratio (SIR) was calculated as the ratio of stress over rest peak signal intensity for splenic tissue. Additionally, the spleen-to-myocardium ratio, defined as the relative change of spleen to myocardial signal, was calculated for stress (SMRstress) and rest. Results Sixty-one (95%) patients were coronary adenosine responders, but SSO was absent in 18 (28%) patients. SIR and SMRstress were significantly lower in patients with SSO (SIR: 0.56 ± 0.13 vs. 0.93 ± 0.23; p < 0.001 and SMRstress: 1.09 ± 0.47 vs. 1.68 ± 0.62; p < 0.001). Mean hyperemic and rest MBF were 2.12 ± 0.68 ml/min/g and 0.78 ± 0.26 ml/min/g, respectively. MFR was significantly higher in patients with vs. patients without presence of SSO (3.07 ± 1.03 vs. 2.48 ± 0.96; p = 0.038), but there was only a weak inverse correlation between SMRstress and MFR (R = -0.378; p = 0.02) as well as between SIR and MFR (R = -0.356; p = 0.004). Conclusions The presence of SSO implies adequate coronary adenosine-induced MBF response. Its absence, however, is not a reliable indicator for failed adenosine-induced coronary vasodilatation.


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