OBJECTIVE:
To investigate the role of thyroid hormones and other factors in acute aortic dissection and an association with in-hospital adverse events.
DESIGN:
A retrospective analysis.
SETTING:
A university-affiliated cardiac center.
PARTICIPANTS:
A total of 151 patients with aortic dissection admitted to the authors’ hospital between January 2011 and May 2015.
INTERVENTION:
None.
MEASUREMENTS AND RESULTS:
The total in-hospital mortality rate was 12.6%. Triiodothyronine (T3) level was lower in nonsurviving than surviving patients (0.8±0.3 v 1.0±0.4 nmol/L, p<0.05). T3 independently predicted in-hospital mortality (hazard ratio [HR] 0.07, 95% CI 0.01-0.43, p<0.01) and in-hospital acute renal failure (HR 0.22, 0.05-0.89, p<0.05) for all patients. Other independent predictors of in-hospital mortality were pericardial effusion (HR 8.18, 2.11-31.67, p<0.01), conservative treatment (HR 82.12, 12.49-540.09, p<0.01) and Stanford type-A aortic dissection (HR 3.86, 1.06-14.09, p<0.05). Inpatient conservative treatment, T3 (HR 0.01, 0.00-0.18, p<0.01) as well as pericardial effusion (HR 11.80, 2.46-56.59, p<0.01), Stanford type-A dissection (HR 22.35, 3.15-158.40, p<0.01), and in-hospital acute renal failure (HR 16.95, 2.04-140.86, p<0.01) were predictors for in-hospital mortality. In nonconservatively treated patients, T3 (HR 0.02, 0.00-0.88, p<0.05) as well as cardiac care unit stay (HR 0.74, 0.59-0.94, p<0.01) and postoperative acute renal failure (HR 21.32, 3.07-147.88, p<0.01) were predictors for in-hospital mortality.
CONCLUSION:
T3 was downregulated in acute aortic dissection. Low T3 level was a risk factor for in-hospital death and acute renal failure in patients with acute aortic dissection.
