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Assessing myocardial perfusion in heart failure - are we achieving adequate stress?

Session Poster session 1

Speaker Louise Brown

Congress : EuroCMR 2019

  • Topic : imaging
  • Sub-topic : Cardiac Magnetic Resonance: Systolic and Diastolic Function
  • Session type : Poster Session
  • FP Number : P152

Authors : L Brown (Leeds,GB), CED Saunderson (Leeds,GB), A Das (Leeds,GB), T Craven (Leeds,GB), H Xue (Bethesda,US), K Knott (London,GB), E Levelt (Leeds,GB), E Dall'armellina (Leeds,GB), PP Swoboda (Leeds,GB), J Moon (London,GB), JP Greenwood (Leeds,GB), P Kellman (Bethesda,US), S Plein (Leeds,GB)

L Brown1 , CED Saunderson1 , A Das1 , T Craven1 , H Xue2 , K Knott3 , E Levelt1 , E Dall'armellina1 , PP Swoboda1 , J Moon3 , JP Greenwood1 , P Kellman2 , S Plein1 , 1University of Leeds - Leeds - United Kingdom of Great Britain & Northern Ireland , 2National Institutes of Health - Bethesda - United States of America , 3Barts Health NHS Trust - London - United Kingdom of Great Britain & Northern Ireland ,

European Heart Journal - Cardiovascular Imaging ( 2019 ) 20 ( Supplement 2 ), ii102


Adenosine stress perfusion CMR is frequently used in the assessment of heart failure (HF) of unknown, or suspected ischaemic, aetiology. However, patients with HF have been shown to have a decreased response to adenosine which may hamper the diagnostic utility of CMR using the standard adenosine protocol. With the potential increase in clinical use of quantitative perfusion, it is important to establish an optimal stress perfusion protocol to provide accurate assessment and minimise unnecessary referral for invasive tests. 


We aimed to assess whether a higher dose of adenosine would be a more effective protocol in patients with HF to achieve maximal stress myocardial blood flow (MBF). 


We prospectively recruited 28 patients with HF and 20 patients with coronary artery disease (CAD) to undergo adenosine stress perfusion CMR. All patients underwent two stress perfusion acquisitions during their scan, with rates of 140µg/kg/min (standard dose) and 210µg/kg/min (high dose) in a random order, each given for 4 minutes. Haemodynamic markers of response were recorded; inline quantitative myocardial perfusion mapping allowed assessment of stress myocardial blood flow (MBF) with each adenosine dose. 


Other than ejection fraction, baseline characteristics were similar between groups. Both showed comparable degrees of haemodynamic response to adenosine, and numbers of non-responders (those with a heart rate rise of less than 10% from rest). 

No significant difference was seen in stress MBF in the CAD group (mean difference -0.02ml/g/min, p=0.82). Within the HF group, MBF was significantly higher with high dose adenosine (mean difference 0.15ml/g/min, p=0.03). 


A high-dose adenosine protocol (210 µg/kg/min) is well tolerated and in HF patients induces significantly higher stress MBF. A lower threshold for using high-dose adenosine in these patients should be considered in clinical practice.

Coronary Artery Disease


Heart Failure


Female (%) 20 36 0.5
Age (years) 64.6±8.7 62.7±12.2 0.6
Ejection fraction (%) 52.6±12.7 34.6±13.2 0.02
Heart rate increase with standard dose (%) 19.2±17.8 11.7±17.0 0.2
Heart rate increase with high dose (%) 21.6±15.1 17.9±21.2 0.5
Proportion of non-responders at standard dose (%) 30 39 0.8
Baseline characteristics and haemodynamic response to adenosine. High dose = 210µg/kg/min, standard dose = 140µg/kg/min

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