Hemodynamic response to pharmacologic stress testing with regadenoson

Objectives The selective A2A adenosine receptor agonist regadenoson is approved as a pharmalogical stress agent for detecting reversible myocardial hypoperfusion. Regadenoson has a more rapid onset of action and a different side effect profile than other stress agents like adenosine and dipyridamole. Clinical studies of the hemodynamic response caused by regadenoson are poorly described in the literature.

Methods Prospective analysis of 309 consecutive patients referred to myocardial perfusion imaging (MPI). Prior to the exam we registered age, history of coronary artery disease (CAD) and antihypertensive treatment (AT) in all patients. During the examination we registered changes in systolic blood pressure (SBP) and heart rate (HR).

Results Of 309 consecutive patients, 308 (99.7 %) received regadenoson. Overall, there were significant changes in SBP and HR after 1 and 3 min respectively: (-6 and -8 mm Hg) and (+19 and +14 bpm) (p<0.001). Correlation to age, CAD and AT were analyzed: Age-1min: (<50y: -1 mmHg, 50-69y: -4 mmHg, ≥70y: -11 mmHg (p<0.01)) and (<50y: +28 bpm, 50-69y: +20 bpm, ≥70y: +14 bpm (p<0.001)). Age-3min: (<50y: -8 mmHg, 50-69y: -6 mmHg, ≥70y: -12 mmHg (p<0.05)) and (<50y: +18bpm, 50-69y: +14 bpm, ≥70y: +11 bpm (p<0.001)). CAD-1min: (Yes: -8 mmHg, No: -4 mmHg (p=0.05)) and (Yes: +18 bpm, No: +20bpm (p=0.12)). CAD-3min: (Yes: -8 mmHg, No: -8 mmHg (p=0.70)) and (Yes: +13 bpm, No: +14bpm (p=0.70)) AT-1min (number of drugs): (0: -3 mmHg, 1: -4 mmHg, 2: -8 mmHg, ≥3: -11 mmHg (p<0.05)) and (0: +23 bpm, 1: +21 bpm, 2: +16 bpm, ≥3 +14 bpm (p<0.001)). AT-3min: (0: -7 mmHg, 1: -8 mmHg, 2: -9 mmHg, ≥3: -10 mmHg (p=0.76)) and (0: +15 bpm, 1: +16 bpm, 2: +12 bpm, ≥3 +10 bpm (p<0.001)).

Conclusions Regadenoson resulted in significant changes in SBP and HR after 1 and 3 min during MPI. Older patients and patients with more intensive AT experienced larger blood pressure falls. Interestingly, these patients showed smaller compensatory increments in heart rate. There was no significant correlation between known CAD and hemodynamic response.