Outcome Predictors in Patients Presenting With Acute Aortic Dissection

ObjectiveTo investigate the role of thyroid hormones and other factors in acute aortic dissection and an association with in-hospital adverse events.DesignA retrospective analysis.SettingA university-affiliated cardiac center.ParticipantsA total of 151 patients with aortic dissection admitted to the authors’ hospital between January 2011 and May 2015.InterventionNone.Measurements and ResultsThe 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.ConclusionT3 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

Anti-Fibrosis Effect of Relaxin and Spironolactone Combined on Isoprenaline-Induced Myocardial Fibrosis in Rats via Inhibition of Endothelial–Mesenchymal Transition

Background: The effect of relaxin and spironolactone combined on myocardial fibrosis has not been reported. Thus, we investigated the effect of the combined therapy on isoprenaline-induced myocardial fibrosis and the mechanism. Methods: Rats were injected subcutaneously with isoprenaline to induce myocardial fibrosis and underwent subcutaneous injection with relaxin (2 µg·kg-1·d-1) and given a gavage of spironolactone (30 mg·kg-1·d-1) alone or combined for 14 days. In vitro, the endothelial–mesenchymal transition was induced with transforming growth factor β (TGF-β) in human umbilical vein endothelial cells (HUVECs) pretreated with relaxin, 200 ng/ml, and/or spironolactone, 1uM. Results: Relaxin and spironolactone used alone or combined improved cardiac function and decreased cardiac weight indices; reduced fibrous tissue proliferation; reduced levels of type I and III collagen; decreased the expression of α–smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1), and increased the expression of cluster of differentiation-31 (CD31) in rats with isoprenaline-induced myocardial fibrosis. In vitro, compared with TGF-β treatment, relaxin and spironolactone used alone or combined with TGF-β decreased cell mobility, α-SMA and vimentin levels but increased vascular endothelial cadherin (VE-cadherin) and endothelial CD31levels. Especially, combined therapy had more remarkable effect than relaxin and spironolactone used alone both in vitro and in vivo. Conclusion: Relaxin and spironolactone combined affected isoprenaline-induced myocardial fibrosis in rats that the mechanism might be inhibition of the cardiac endothelial–mesenchymal transition

Anti-Fibrosis Effect of Scutellarin via Inhibition of Endothelial–Mesenchymal Transition on Isoprenaline-Induced Myocardial Fibrosis in Rats

Scutellarin (SCU) is the major active component of breviscapine and has been reported to be capable of decreasing myocardial fibrosis. The aim of the present study is to investigate whether SCU treatment attenuates isoprenaline-induced myocardial fibrosis and the mechanisms of its action. Rats were injected subcutaneously with isoprenaline (Iso) to induce myocardial fibrosis and rats in the SCU treatment groups were intraperitoneally infused with SCU (10 mg·kg−1·d−1 or 20 mg·kg−1·d−1, for 14 days). Post-treatment, cardiac functional measurements and the left and right ventricular weight indices (LVWI and RVWI, respectively) were analysed. Pathological alteration, expression of type I and III collagen, Von Willebrand factor, α-smooth muscle actin, cluster of differentiation-31 (CD31), and the Notch signalling proteins (Notch1, Jagged1 and Hes1) were examined. The administration of SCU resulted in a significant improvement in cardiac function and decrease in the cardiac weight indices; reduced fibrous tissue proliferation; reduced levels of type I and III collagen; increased microvascular density; and decreased expression of α-smooth muscle actin and increased expression of CD31, Notch1, Jagged1 and Hes1 in isoprenaline-induced myocardial fibrosis in rats. Our results suggest that SCU prevents isoprenaline-induced myocardial fibrosis via inhibition of cardiac endothelial-mesenchymal transition potentially, which may be associated with the Notch pathway