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Abstract Purpose The present study evaluated the efficacy of C-reactive protein (CRP) and D-dimer and the combination of them as prognostic indicators for patients with acute type A aortic dissection (ATAAD). Methods This is a retrospective cohort study. From January 2019 to December 2021, patients with ATAAD admitted to the emergency medicine center of our hospital within 24 h after symptoms (chest pain, back pain, abdominal pain and so on) onset were enrolled in our study. Serum concentration of CRP and D-dimer were measured during hospitalization. Logistic regression was used to evaluate the association between these two biomarkers and in-hospital adverse outcomes (IAO) by adjusting confounding factors. Predictive efficacy was assessed by area under the curve (AUC) of receiver operating characteristic curve. Results A total of 199 patients with ATAAD were finally enrolled. They were categorized as Non-IAO group (n = 146) and IAO group (n = 53) according to postoperative outcomes. After controlling for potentially confounding variables, we found categorized variables that admission CRP > 54.28 mg/L, admission D-dimer > 8.45 mg/L and peak D-dimer > 24.89 mg/L were independent predictors of in-hospital adverse outcomes. Multiple Logistic regression analysis revealed that the odd ratios were 2.9 for admission D-dimer > 8.45 [95% Confidence Interval (CI) 1.11–7.5, p = 0.03], 4.9 for admission CRP > 54.28 (95% CI 1.6–14.9, p = 0.005) and 5.7 for peak D-dimer > 24.89 (95% CI 2.49–13, p 8.45 mg/L, peak D-dimer > 24.89 mg/L and admission CRP > 54.28 mg/L are independent predictors of in-hospital adverse outcomes in patients with ATAAD. Combination of these three markers will improve the predictive efficacy.

Background: Atrial remodeling has emerged as the structural basis for the maintenance and recurrence of atrial fibrillation. Lactate signaling cascade was recently linked to some cardiovascular disorders for its regulatory functions to myocardial structural remodeling. It was hypothesized that lactate signaling cascade was involved in the maintenance and recurrence of atrial fibrillation by regulating atrial structural remodeling. Methods: Biopsies of right atrial appendage and clinical data were collected from sex- and age-matched 30 persistent atrial fibrillation, 30 paroxysmal atrial fibrillation, 30 sinus rhythm patients undergoing isolated mitral valve surgery and 10 healthy heart donors. Results: Atrial fibrillation groups had higher atrial lactate expression and this upregulated expression was positively correlated with regulatory indicators of atrial structural remodeling as reflected by severe oxidative stress injury and mitochondrial control of apoptosis. Conclusions: The present findings suggest a potential role for lactate signaling cascade in the maintenance and recurrence of atrial fibrillation and possibly represent new targets for therapeutic intervention in this disorder. [ABSTRACT FROM AUTHOR]