High-resolution quantitative stress perfusion CMR to assess the impact of blood pressure and hypertension on global myocardial blood flow (RF_FR_392)

A number of factors are thought to have an effect on myocardial blood flow (MBF), including blood pressure (BP). It has previously been demonstrated that coronary blood flow is directly proportional to coronary perfusion pressure during hyperaemia.1 However, patients with longstanding hypertension have been shown to have reduced myocardial perfusion reserve (MPR).² Quantitative stress perfusion cardiovascular magnetic resonance (CMR) is increasingly used to assess MBF. The aim of this study was to assess whether there was a relationship between BP and MBF in patients without obvious myocardial ischaemia.

Methods:

Patients receiving clinical stress perfusion CMR were recruited at St Thomas’ Hospital between January 2022 and May 2023. All those with arrhythmia, inducible regional or subendocardial hypoperfusion, or presence of late-gadolinium enhancement were excluded. Imaging was performed at both hyperaemia and rest using a high-resolution stress perfusion sequence with automated quantitative MBF map generation.^3,4 Haemodynamic measurements were recorded at baseline and at regular intervals after the commencement of vasodilator administration. Mean arterial pressure (MAP) was calculated using systolic and diastolic BP measurements. Global whole-myocardium MBF values were established and used to calculate MPR. Only patients receiving adenosine were included in rest MBF and MPR analysis. Pearson correlation coefficient and Mann Whitney-U testing were utilised to establish statistical relationships.

Results:

248 patients were included in the analysis (55.2% male, mean age 55.5±12.7 years, mean LVEF 59.6±7.6%). 45.2% patients had known hypertension prior to scanning. Those with known hypertension tended to be older (median age 60 [50-66] years vs. 55 [42-64] years, p=0.006). No significant correlation was seen between either stress MBF or MPR with baseline MAP (stress MBF: R=0.045, p=0.483; MPR: R=-0.125, p=0.081) [Figure 1]. Similarly, no linear correlation was seen between stress MBF or MPR compared with hyperaemic MAP (stress MBF: R=0.014, p=0.824; MPR: R=-0.023, p=0.753).

Those patients with known hypertension had lower stress MBF values compared with those without (2.37 [2.01-2.75] ml/min/g vs. 2.62 [2.23-3.05] ml/min/g, p=0.001) [Figure 2]. Additionally, MPR was significantly reduced in those with known hypertension (2.32 [2.04-2.68] vs. 2.60 [2.26-2.96], p< 0.001). However, no significant difference was observed for rest MBF (0.95 [0.80-1.19] ml/min/g vs. 1.00 [0.84-1.21] ml/min/g, p=0.854).

Conclusion:

No significant correlation was observed between stress MBF and baseline or hyperaemic MAP. Similarly, there was no correlation between baseline / hyperaemic MAP and MPR. Despite this, patients with longstanding hypertension did have reduced stress MBF and MPR values compared with patients without hypertension, suggestive that hypertension leads to chronic changes affecting MBF.