Value of Splenic Switch-Off sign in adenosine stress CMR

Aparna Irodi MD, FRCR (Vellore) reviewing Patriki, D., von Felten, E., Bakula, A. et al. Splenic switch-off as a predictor for coronary adenosine response: validation against 13N-ammonia during co-injection myocardial perfusion imaging on a hybrid PET/CMR scannerJ Cardiovasc Magn Reson 23, 3 (2021).
https://doi.org/10.1186/s12968-020-00696-y

https://jcmr-online.biomedcentral.com/articles/10.1186/s12968-020-00696-y

Study Questions:
What is the value of splenic switch-off (SSO) in predicting adenosine response during stress cardiac MRI (CMR)?

Background

  • Adenosine is a safe and widely used vasodilator for myocardial perfusion imaging (MPI). Diagnostic performance of MPI (i.e. ability to predict ischemia) depends on achieving maximum vasodilatation. Commonly used hemodynamic markers (like increase in heart rate and fall in BP) to assess whether maximum vasodilatation is achieved, are not always reliable.
  • Recently, the splenic switch-off (SSO) sign (defined as a visible decrease in splenic signal intensity during adenosine stress as compared to rest, presumably due to reactive sympathetic splenic vasoconstriction after adenosine-induced hypotension) has been proposed as a more objective and direct marker of adequate adenosine response during stress CMR.
  • The authors sought to test the hypothesis that SSO constitutes a reliable predictor of adequate coronary adenosine response by comparing the SSO with myocardial flow reserve measured on adenosine stress PET study. 

Methodology

  • Prospective study of 64 patients who simultaneously underwent 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. 
  • The stress protocol consisted of 6 min of adenosine infusion at a dose of 140 μg/kg/min. A body mass index adapted dose of 13N-ammonia (i.e., 200–600 megabecquerels (MBq) and 0.1 mmol/kg of Gadolinium based contrast agent was simultaneously injected 3 min into adenosine stress.
  • Resting perfusion imaging was performed using an identical acquisition protocol after a minimum of 15 min following the stress acquisition.
  • Summed semi-quantitative myocardial PET tracer uptake and quantitative MBF was obtained from stress and rest scans and analyzed using QPET (Version 2015, Cedars-Sinai Medical Center, Los Angeles, California, USA). Datasets were examined in consensus by two experienced readers regarding the presence of ischemia and/or scar.
  • CMR stress and rest perfusion scans were acquired using three left ventricular short-axis slices per cardiac cycle (basal, mid, and apical levels) each of 10 mm slice thickness and ECG-gated breath-hold protocol.
  • Myocardial flow reserve (MFR) of > 1.5 or the presence of ischemia on PET was taken as markers for adequate coronary adenosine response.
  • Hemodynamic response was assessed as increase in heart rate by 10bpm.
  • Visual analysis for SSO was performed independently by two readers in a blinded fashion.

Results:

    • 64 patients included
    • Three (5%) patients with an MFR ≤ 1.5 and without any signs of ischemia neither in PET nor CMR were classified as adenosine non-responders. i.e 95% were responders
    • While 95% of the patients were coronary adenosine responders, SSO was absent in 28% of the patients. i.e. some of the responders did not show the SSO sign.
    • There was only a weak correlation between splenic signal intensity ratio and MFR as well as between splenic to myocardial signal intensity ratio and MFR.
    • Only 45% patients had a positive HR increase of ≥ 10 bpm. There was a trend towards higher MFR in patients with vs. patients without a positive HR response (3.2 vs 2.7 ml/min/g; p = 0.053) but there was no difference in the proportion of patients with and without a positive HR response among patients with or without SSO (p = 0.23).

Limitations:

  • Binary system was used to classify patients as responders and non-responders and graded response was not considered.
  • Results were not correlated with angiography findings.

Conclusions:

While presence of SSO is a strong marker for adequate coronary adenosine response, the absence of SSO does not necessarily imply that a patient failed to respond to adenosine.

Perspective:
  • Presence of SSO increases readers’ confidence in case of a normal CMR myocardial perfusion scan. But, its absence does not always mean that adequate vasodilatation has not been achieved, as some of the responders also may not show SSO.
  • Increasing usage of vasodilators such as regadenoson (which are more specific to A2A receptors), will reduce the clinical value of SSO in the future.