The impact of heart rate and beta-blockade on myocardial blood flow assessed by high-resolution quantitative stress perfusion CMR in patients without inducible ischaemia (RF_FR_307)

The need for cessation of beta-blockers prior to stress perfusion cardiovascular magnetic resonance (CMR) is unclear. Previous studies have suggested that beta-blocker use is associated with reduced myocardial blood flow (MBF) during hyperaemia, although the degree of heart rate (HR) response may also play a role.^1,2 This study aimed to identify any correlation of hyperaemic MBF with HR response and evaluate MBF in patients taking beta-blockers without inducible ischaemia.

Methods:

All patients received stress perfusion CMR at St Thomas’ Hospital, London, UK between January 2022 and May 2023. Patients were advised to take medications (including beta-blockers) as normal prior to the scan. Those with arrhythmia, inducible regional or subendocardial perfusion defects, or the presence of any late-gadolinium enhancement were excluded. Perfusion imaging was acquired at both hyperaemia and rest using a high-resolution stress perfusion sequence with automated generation of quantitative MBF maps.^3,4 Patients received either adenosine or regadenoson to induce hyperaemia. HR was recorded at baseline and recurrently following vasodilator administration. HR rise was defined as HR at peak hyperaemia minus HR at baseline – only those with HR rise ≥ 10 beats per minute (bpm) were included in analysis. Global MBF values were calculated and used to determine myocardial perfusion reserve (MPR). Only patients who received adenosine were included in rest MBF and MPR analysis. Pearson correlation coefficient and Mann Whitney-U testing were used to evaluate statistical significance.

Results:

Data from 235 patients was analysed (44.3% female, mean age 55.0±12.8 years, mean LVEF 59.9±7.3%). 43.8% patients had hypertension; 15.3% patients had diabetes mellitus. Stress MBF demonstrated a weakly positive but significant correlation with increasing HR rise (R=0.150, p=0.022) [Figure 1]. MPR also correlated weakly, but this was not significant (R=0.123, p=0.092). Additionally, whilst HR rise correlated negatively with increasing patient age (R=-0.350, p< 0.001), age itself did not correlate with stress MBF (R=-0.108, p=0.100).
 

72 (30.6%) patients were taking beta-blockers on the day of the scan. Patients taking beta-blockers were older (mean age 59.3±11.4 years vs. 53.2±13.0 years, p< 0.001). Median stress MBF was reduced in those taking beta-blockers (2.38 [2.12-2.75] ml/min/g vs. 2.60 [2.13-3.01] ml/min/g, p=0.037) [Figure 2]. Similarly, rest MBF was also reduced in patients taking beta-blockers (0.90 [0.76-1.11] ml/min/g vs. 1.01 [0.87-1.22] ml/min/g, p=0.002). However, no significant difference was seen for MPR regardless of beta-blocker use (2.42 [2.19-2.92] vs. 2.47 [2.10-2.85], p=0.532). Median HR rise was not significantly different between the two groups (23.0 [17.0-30.0] bpm vs. 24.0 [18.0-32.0] bpm, p=0.206).

Conclusion:

The increase in heart rate during hyperaemia positively correlates with stress MBF, although this correlation was not significant for MPR. Furthermore, the concomitant use of beta-blockers reduces both stress and rest MBF, whilst MPR is unaffected, highlighting the importance of rest imaging in patients taking beta-blockers.