Key result
Plasma LDH levels ≥450 U/L independently predicted in-hospital mortality in patients with acute aortic syndromes (OR 2.28), with mortality rates of 32.6% compared to 16.8% in those with lower levels.
Why the study?
Do elevated plasma lactate dehydrogenase (LDH) levels predict in-hospital mortality in patients with acute aortic syndromes?
Cohort (n=999)
Yes
Do elevated plasma lactate dehydrogenase (LDH) levels predict in-hospital mortality in patients with acute aortic syndromes?
Odds Ratio: 2.28 (95% CI 1.11–4.66)
Absolute Event Rate: 32.6% vs 16.8%
p-value: p=0.025
Elevated plasma LDH (≥ 450 U/L) at presentation is an independent predictor of in-hospital mortality in patients with acute aortic syndromes.
May aid risk stratification in acute aortic syndromes; leaves open whether LDH improves models or guides therapy.
In acute aortic syndromes (AAS), organ malperfusion represents a key event impacting both on diagnosis and outcome. Increased levels of plasma lactate dehydrogenase (LDH), a biomarker of malperfusion, have been reported in AAS, but the performance of LDH for the diagnosis of AAS and the relation of LDH with outcome in AAS have not been evaluated so far.This was a bi-centric prospective diagnostic accuracy study and a cohort outcome study. From 2008 to 2014, patients from 2 Emergency Departments suspected of having AAS underwent LDH assay at presentation. A final diagnosis was obtained by aortic imaging. Patients diagnosed with AAS were followed-up for in-hospital mortality.One thousand five hundred seventy-eight consecutive patients were clinically eligible, and 999 patients were included in the study. The final diagnosis was AAS in 201 (20.1%) patients. Median LDH was 424 U/L (interquartile range [IQR] 367-557) in patients with AAS and 383 U/L (IQR 331-460) in patients with alternative diagnoses (P < 0.001). Using a cutoff of 450 U/L, the sensitivity of LDH for AAS was 44% (95% confidence interval [CI] 37-51) and the specificity was 73% (95% CI 69-76). Overall in-hospital mortality for AAS was 23.8%. Mortality was 32.6% in patients with LDH ≥ 450 U/L and 16.8% in patients with LDH < 450 U/L (P = 0.006). Following stratification according to LDH quartiles, in-hospital mortality was 12% in the first (lowest) quartile, 18.4% in the second quartile, 23.5% in the third quartile, and 38% in the fourth (highest) quartile (P = 0.01). LDH ≥ 450 U/L was further identified as an independent predictor of death in AAS both in univariate and in stepwise logistic regression analyses (odds ratio 2.28, 95% CI 1.11-4.66; P = 0.025), in addition to well-established risk markers such as advanced age and hypotension. Subgroup analysis showed excess mortality in association with LDH ≥ 450 U/L in elderly, hemodynamically stable and in nonsurgically treated patients.Plasma LDH constitutes a biomarker of poor outcome in patients with AAS. LDH is a rapid and universally available assay that could be used to improve risk stratification and to individualize treatment in patient groups where options are controversial.
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Morello et al. (2016) conducted a cohort in Acute Aortic Syndromes (n=999). Plasma Lactate Dehydrogenase (LDH) ≥ 450 U/L vs. Plasma LDH < 450 U/L was evaluated on In-hospital mortality (OR 2.28, 95% CI 1.11-4.66, p=0.025). Plasma LDH levels ≥450 U/L independently predicted in-hospital mortality in patients with acute aortic syndromes (OR 2.28), with mortality rates of 32.6% compared to 16.8% in those with lower levels.
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