The significance of post-stress decrease in left ventricular ejection fraction in patients undergoing regadenoson stress gated SPECT myocardial perfusion imaging.

BACKGROUND: The significance of post-stress decrease in left ventricular ejection fraction (LVEF) with regadenoson stress gated SPECT (GSPECT) myocardial perfusion imaging (MPI) has not been studied. METHODS AND RESULTS: Consecutive patients who underwent rest/regadenoson stress GSPECT-MPI followed by coronary angiography within 6 months were analyzed. Change in LVEF by GSPECT-MPI was calculated as stress LVEF minus rest LVEF; a significant decrease was tested at 5% and 10% thresholds. In a diagnostic cohort of 793 subjects, LVEF change was not predictive of severe/extensive coronary artery disease (area under the curve, 0.50; 95% confidence interval, 0.44-0.57; P = 0.946). There was no significant difference in the rates of severe/extensive coronary artery disease in patients with or without a decrease in LVEF, irrespective of MPI findings. In an outcome cohort of the 929 subjects followed for 30 ± 16 months, post-regadenoson stress decrease in LVEF was not associated with increased risk of the composite endpoint of cardiac death or myocardial infarction or in the risk of coronary revascularization. CONCLUSIONS: In patients selected to undergo coronary angiography following regadenoson stress GSPECT-MPI, a decrease in LVEF after regadenoson stress is not predictive of severe/extensive CAD or adverse clinical outcomes, irrespective of MPI findings.

The significance of automatically measured transient ischemic dilation in identifying severe and extensive coronary artery disease in regadenoson, single-isotope technetium-99m myocardial perfusion SPECT.

BACKGROUND: The critical threshold and clinical significance of transient ischemic dilation (TID) for regadenoson, single-isotope (99m)Tc SPECT myocardial perfusion imaging (MPI) are not defined. METHODS: From 100 patients with low likelihood of CAD, we derived the abnormal TID threshold (mean + 2 SD). We validated the threshold in a cohort of 547 patients who received one-day, rest/regadenoson-stress, (99m)Tc-tetrofosmin SPECT-MPI followed by coronary angiography within 6 months. Patients were classified into three CAD severity strata: no significant CAD, mild to moderate CAD, and severe and extensive CAD. RESULTS: The abnormal TID threshold was determined to be 1.31. Though mean TID ratios were different between the three CAD severity groups and the derivation cohort (P < .001), there was no difference in the mean TID ratios between the categories of CAD severity or in the prevalence of severe CAD between TID+ and TID- groups (P = .74). By ROC analysis, TID had a poor discriminatory capacity in identifying severe and extensive CAD [AUC of 0.55 (95% CI 0.47-0.62, P = .25)]. Stepwise multivariate logistic analysis demonstrated that adding TID to clinical and perfusion data did not provide incremental diagnostic value (P = .87). CONCLUSIONS: The clinical utility of TID with regadenoson-stress MPI in this era of declining CAD burden is questionable.

Diagnostic and prognostic significance of ischemic electrocardiographic changes with regadenoson-stress myocardial perfusion imaging.

BACKGROUND: The diagnostic and prognostic value of regadenoson-induced ST-segment depression (ST↓) is not defined. Due to the low incidence of ST↓ ≥1.0 mm with vasodilator stress, a lower threshold to define ischemic ECG response may provide improved clinical utility. METHODS: We conducted a retrospective cohort study of patients who underwent regadenoson-stress SPECT myocardial perfusion imaging (MPI) followed by coronary angiography within 6 months. Ischemic ST↓ was defined as ≥0.5 mm. The prevalence of angiographically severe coronary artery disease (CAD) and the rates of major adverse cardiac events (MACE) including cardiac death, myocardial infarction, and coronary revascularization were determined. RESULTS: In a diagnostic cohort of 629 subjects, 117 (18.6%) had ST↓ ≥0.5 mm. Severe CAD was more prevalent in the ST↓ ≥0.5 vs ST <0.5 group (13.7% vs 5.3%, P = .001). Among patients with normal MPI (n = 229), the prevalence of severe CAD was higher in the ST↓ ≥0.5 group (8.2% vs 2.2%, P = .04). Adjusting for clinical and imaging covariates, ST↓ ≥0.5 mm was independently predictive of severe CAD [odds ratio = 3.37, 95% confidence interval (CI) = 1.67-6.83, P = .001], and provided incremental diagnostic value (Chi square increment = 10.3, P = .001). In an outcome cohort of 748 subjects, after adjusting for clinical and imaging covariates, ST↓ ≥0.5 mm was associated with increased MACE rate in the entire cohort [hazard ratio = 1.41, CI 1.01-1.96, P = .04] and in the subgroup of patients with normal MPI [hazard ratio = 2.2, CI 1.11-4.39, P = .02], and provided incremental prognostic value (Chi square increment = 3.9, P = .049). A diagnostic ST↓ threshold of 0.5 mm provided greater discriminatory capacity than a 1.0 mm cutoff (P = .03). CONCLUSIONS: Among patients selected to undergo coronary angiography, regadenoson-induced ST↓ ≥0.5 mm was associated with higher rates of severe CAD and MACE, irrespective of MPI finding.