Lysophosphatidic Acid May Be a Novel Biomarker for Early Acute Aortic Dissection

Abstract

Background: Misdiagnosis and delayed diagnosis of acute aortic dissection (AAD) significantly increase mortality. Lysophosphatidic acid (LPA) is a biomarker related to coagulation cascade and cardiovascular-injury. The extent of LPA elevation in AAD and whether it can discriminate sudden-onset of acute chest pain are currently unclear.Methods: We measured the plasma concentration of LPA in a cohort of 174 patients with suspected AAD chest pain and 30 healthy participants. Measures to discriminate AAD from other acute-onset thoracalgia were compared and calculated.Results: LPA was significantly higher in AAD than in the AMI, PE, and the healthy (344.69 ± 59.99 vs. 286.79 ± 43.01 vs. 286.61 ± 43.32 vs. 96.08 ± 11.93, P < 0.01) within 48 h of symptom onset. LPA level peaked at 12 h after symptom onset, then gradually decreased from 12 to 48 h in AAD. LPA had an AUC of 0.85 (0.80–0.90), diagnosis threshold of 298.98 mg/dl, a sensitivity of 0.81, specificity of 0.77, and the negative predictive value of 0.85. The ROC curve of LPA is better than D-dimer (P = 0.041, Delong test). The decision curve showed that LPA had excellent standardized net benefits.Conclusion: LPA showed superior overall diagnostic performance to D-dimer in early AAD diagnosis may be a potential biomarker, but additional studies are needed to determine the rapid and cost-effective diagnostic tests in the emergency department.

Admission Lysophosphatidic Acid Is Related to Impaired Kidney Function in Acute Aortic Dissection: 2-Year Retrospective Follow-Up Study

“…The mechanism of elevated LPA in AAD patients has previously been described in our study ( 10 ). To summarize in brief, the pathophysiology for elevation is platelet activation, thrombosis, ischemia/reperfusion injury, and inflammatory responses, which also underlie the pathogenesis of AAD-related AKI.…”

“…This was a sub-study of a previously conducted retrospective cohort study consisting of 181 patients with suspected AAD treated at the emergency department of the Second Xiangya Hospital of Central South University in Changsha, China from May 2020 and January 2021 ( 10 ). We non-selectively and consecutively collected data for all participants and excluded patients who had unruptured aortic intramural hematoma, acute myocardial infarction, and pulmonary embolism.…”

“…The samples were centrifuged at 1,000 r/min for 15 min, processed into plasma, and stored at −80°C. The human lysophosphatidic acid kit (CSB-EQ028005HU, Huamei Biological Engineering Co., Ltd., Wuhan, China) was used to measure plasma LPA ( 10 ).…”

“…Lysophosphatidic acid (LPA) is a bioactive phospholipid, which can exert diverse biological effects in various diseased states of the kidney by activating at least 6 cognate G-protein coupled receptors and its complex network of heterotrimeric G-proteins ( 9 ). LPA, mainly produced by activated platelets, is an early biomarker of thrombosis and coagulation initiation in AAD, reflecting the extent of tearing and ischemia ( 10 ). Meanwhile, LPA can also increase fibroblast growth factor-23 (FGF23) in acute and chronic kidney injury levels to promote chronic fibrosis, which is closely associated with subsequent CKD and end-stage renal disease ( 11 ).…”

Metabolomic Profiling of Angiotensin-II-Induced Abdominal Aortic Aneurysm in Ldlr−/− Mice Points to Alteration of Nitric Oxide, Lipid, and Energy Metabolisms

“…Also, in damaged endothelium platelet-derived phospholipase A1 (PLA1) activation will release lysophosphatidylcholine and then phosphatidic acid (PA) a potent enhancer of mineralization and osteogenic transformation in the aortic wall [ 36 ]. Indeed, PA has been recently postulated as an early marker of aortic dissection [ 37 ]. The carnitine profile is also reversed compared with blood, showing a decrease in free (C0) and acetyl-carnitine (C2) without an increase in long-chain acyl-carnitines.…”