BACKGROUND: We studied the prognostic value of fully automated quantitative analysis software applied to new solid-state, high-speed (HS) SPECT-myocardial perfusion imaging (MPI). METHODS: 1,613 consecutive patients undergoing exercise or adenosine HS-MPI were followed for 2.6 ± 0.5 years for all-cause mortality (ACM). Automated quantitative software was used to compute stress total perfusion deficit (sTPD) and was compared to semi-quantitative visual analysis. MPI was characterized as 0% (normal), 1%-4% (minimal perfusion defect), 5%-10% (mildly abnormal), and >10% (moderately/severely abnormal). RESULTS: During follow-up, 79 patients died (4.9%). Annualized ACM increased with progressively increasing sTPD; 0% (0.87%), 1%-4% (1.94%), 5%-10% (3.10%), and >10% (5.33%) (log-rank P < .0001). While similar overall findings were observed with visual analysis, only sTPD demonstrated increased risk in patients with minimal perfusion defects. In multivariable analysis, sTPD > 10% was a mortality predictor (HR 3.03, 95% CI 1.30-7.09, P = .01). Adjusted mortality rate was substantial in adenosine MPI, but low in exercise MPI (9.0% vs 1.0%, P < .0001). CONCLUSIONS: By quantitative analysis, ACM increases with increasing perfusion abnormality among patients undergoing stress HS-MPI. These findings confirm previous results obtained with visual analysis using conventional Anger camera imaging systems.
BACKGROUND: We studied the prognostic value of fully automated quantitative analysis software applied to new solid-state, high-speed (HS) SPECT-myocardial perfusion imaging (MPI). METHODS: 1,613 consecutive patients undergoing exercise or adenosine HS-MPI were followed for 2.6 ± 0.5 years for all-cause mortality (ACM). Automated quantitative software was used to compute stress total perfusion deficit (sTPD) and was compared to semi-quantitative visual analysis. MPI was characterized as 0% (normal), 1%-4% (minimal perfusion defect), 5%-10% (mildly abnormal), and >10% (moderately/severely abnormal). RESULTS: During follow-up, 79 patients died (4.9%). Annualized ACM increased with progressively increasing sTPD; 0% (0.87%), 1%-4% (1.94%), 5%-10% (3.10%), and >10% (5.33%) (log-rank P < .0001). While similar overall findings were observed with visual analysis, only sTPD demonstrated increased risk in patients with minimal perfusion defects. In multivariable analysis, sTPD > 10% was a mortality predictor (HR 3.03, 95% CI 1.30-7.09, P = .01). Adjusted mortality rate was substantial in adenosine MPI, but low in exercise MPI (9.0% vs 1.0%, P < .0001). CONCLUSIONS: By quantitative analysis, ACM increases with increasing perfusion abnormality among patients undergoing stress HS-MPI. These findings confirm previous results obtained with visual analysis using conventional Anger camera imaging systems.
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