The prognostic value of regadenoson stress: Has the case been made?

Journal of Nuclear Cardiology, May 2015

Rami Doukky

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The prognostic value of regadenoson stress: Has the case been made?

Received May The prognostic value of regadenoson stress: Has the case been made? Rami Doukky 1 MSc 1 FACC 1 FASNC 1 2 3 0 3620 , Chicago, IL , 60612; rami_doukky @rush.edu J Nucl Cardiol 1071-3581/$34.00 Copyright 2015 American Society of Nuclear Cardiology 1 Reprint requests: Rami Doukky , MD, MSc, FACC , FASNC Division of Cardiology, John H. Stroger, Jr. Hospital of Cook County , 1901 W. Harrison St., Suite 2 Division of Cardiology, Rush University Medical Center , Chicago, IL 3 Division of Cardiology, John H. Stroger, Jr. Hospital of Cook County , Chicago, IL Since its approval by the Food and Drug Administration in April of 2008, regadenoson has enjoyed a wide implementation by nuclear cardiology laboratories. Presently, it is the preferred vasodilator stress agent in the United States, being used in 8 out of 10 pharmacologic stress SPECT myocardial perfusion imaging (MPI) studies.1 The initial approval of regadenoson was based on two phase 3 ADVANCE-MPI trials, in which regadenoson was demonstrated to produce perfusion defects similar to those induced by standard 6 minute adenosine infusion.2,3 Although diagnostic noninferiority of regadenoson was effectively demonstrated, prognostic noninferiority was beyond the scope of the ADVANCE-MPI trials. Nonetheless, given the similarity in perfusion images, the prognostic value of regadenoson stress was presumed to parallel that of adenosine. In nuclear cardiology, a field that prides itself on vast wealth of outcomes data, extending the prognostic utility of adenosine to regadenoson is just not good enough. In recent years, several studies have investigated the prognostic value of regadenoson stress MPI. Iqbal et al compared the 2-year outcome of patients with normal regadenoson MPI (n = 1,000) to those with normal adenosine MPI (n = 1,000) for the composite endpoint of cardiac death, myocardial infarction, and coronary revascularization.4 The annual event rate was - 1.1% in the regadenoson group and 1.7% in the adenosine group (P = 0.090) and the annual cardiac death rate was 0.9% and 1.15% (P = 0.404), respectively. In propensity score matched analysis of 505 patients from each group, the respective annual event rates in the regadenoson and adenosine groups were 0.7% and 1.3% (P = 0.257) for the primary outcome, and 0.5% and 0.7% (P = 0.763) for cardiac death. Thus, the study effectively demonstrated that, as with normal adenosine MPI, a normal regadenoson MPI predicts very low event rates.4 More recently, Hage et al evaluated the prognostic value of regadenoson stress in 1,400 subjects (700 consecutive normal MPI and 700 consecutive abnormal MPI).5 Based on the quantitative perfusion defect size (percentage of left ventricular myocardium), the cohort was divided into four groups: Group 1, normal (\5%); Groups 2, small defect (\10%); Group 3, moderate sized defect (10%-20%); Group 4, large defect ([20%). During a mean follow-up of 4 years, the composite endpoint of cardiac death, myocardial infarction, and late coronary revascularization ([90 days after MPI) occurred in 10, 27, 31, and 43% (P \ 0.001); while early revascularization (\90 days) occurred in 0.4, 9, 17, and 17% in Groups 1-4, respectively (P \ 0.001). The authors demonstrated a step-wise increase in event rates commensurate with the size of regadenoson-induced defect. The study showed that, as with other stress agents, regadenoson MPI provides powerful prognostic information which can guide clinical decision-making.5 In this issue of the journal, Farzaneh-Far et al compared the prognostic value of regadenoson and adenosine MPI in 3,698 consecutive patients (1,737 adenosine and 1,961 regadenoson) followed for 1 year.6 The cohort included patients with normal and abnormal MPI, unlike the study by Iqbal et al which analyzed patients with normal MPI. The investigators used inverse probability weighted Cox proportional hazards regression modeling to balance the baseline characteristics associated with each vasodilator agent. Irrespective of the vasodilator choice, the Summed Stress Score (SSS) remained a significant predictor of the composite endpoint of cardiovascular death or myocardial infarction (hazard ration [HR], 1.36 per 5% increment; 95% confidence interval [CI] 1.28-1.46; P \ 0.0001) and cardiovascular death (HR, 1.38 per 5% increment; CI 1.28-1.49; P \ 0.0001). Similarly, the Summed Difference Score (SDS) was a significant predictor of the composite of cardiovascular death and myocardial infarction (HR, 1.61 per 5% increment; CI 1.38-1.88; P \ 0.001) and cardiovascular death (HR 1.46 per 5% increment; CI 1.22-1.75; P \ 0.001). Importantly, there was no significant interaction between SSS and stress agent or between SDS and stress agent as determinants of any of the study endpoints. In other words, SSS and SDS derived from adenosine or regadenoson MPI rendered similarly significant prognostic value. This is an important finding; it affirms comparable prognostic significance of perfusi (...truncated)


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Rami Doukky. The prognostic value of regadenoson stress: Has the case been made?, Journal of Nuclear Cardiology, 2015, pp. 608-610, Volume 22, Issue 4, DOI: 10.1007/s12350-015-0179-3