BVD a risk factor
Overall in-hospital mortality was 10%. A total of 22.3% of patients had LVSD and 11.8% had RVSD; 16.4% had moderate or greater BVD. There was no association between LVSD or RVSD and in-hospital mortality after adjustment for SCAI stage, but there was a significant association for BVD (adjusted hazard ratio, 1.815; P = .0023). When combined with SCAI, BVC led to an improved ability to predict hospital mortality (area under the curve, 0.784 vs. 0.766; P < .001). Adding semiquantitative RVSD and LVSD led to more improvement (AUC, 0.794; P < .01 vs. both).
RVSD was associated with higher in-hospital mortality (adjusted odds ratio, 1.421; P = .02), and there was a trend toward greater mortality with LVSD (aOR, 1.336; P = .06). There was little change when SCAI shock stage A patients were excluded (aOR, 1.840; P < .001).
Patients with BVD had greater in-hospital mortality than those without ventricular dysfunction (aOR, 1.815; P = .0023), but other between-group comparisons were not significant.
The researchers performed a classification and regression tree analysis using left ventricular ejection fraction (LVEF) and semiquantitative RVSD. It found that RVSD was a better predictor of in-hospital mortality than LVSD, and the best cutoff for LVSD was different among patients with RVSD and patients without RVSD.
Patients with mild or greater RVD and LVEF greater than 24% were considered high risk; those with borderline or low RVSD and LVEF less than 33%, or mild or greater RVSD with LVEF of at least 24%, were considered intermediate risk. Patients with borderline or no RVSD and LVEF of at least 33% were considered low risk. Hospital mortality was 22% in the high-risk group, 12.2% in the intermediate group, and 3.3% in the low-risk group (aOR vs. intermediate, 0.493; P = .0006; aOR vs. high risk, 0.357; P < .0001).
The study authors disclosed no relevant financial relationships.
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