Phosphatidylserine Supplementation as a Novel Strategy for Reducing Myocardial Infarct Size and Preventing Adverse Left Ventricular Remodeling

Liu

et al. 2022

BMC Cardiovasc Disord

Introduction To develop and validate clinical evaluators that predict adverse left ventricular remodeling (ALVR) in non-ST-elevation myocardial infarction (NSTEMI) patients after primary percutaneous coronary intervention (PCI). Methods The retrospective study analyzed the clinical data of 507 NSTEMI patients who were treated with primary PCI from the Affiliated Hospital of Xuzhou Medical University and the Second Affiliated Hospital of Xuzhou Medical University, between January 1, 2019 and September 31, 2021. The training cohort consisted of patients admitted before June 2020 (n = 287), and the remaining patients (n = 220) were assigned to an external validation cohort. The endpoint event was the occurrence of ALVR, which was described as an increase ≥ 20% in left ventricular end-diastolic volume (LVEDV) at 3–4 months follow-up CMR compared with baseline measurements. The occurrence probability of ALVR stemmed from the final model, which embodied independent predictors recommended by logistic regression analysis. The area under the receiver operating characteristic curve (AUC), Calibration plot, Hosmer–Lemeshow method, and decision curve analysis (DCA) were applied to quantify the performance. Results Independent predictors for ALVR included age (odds ratio (OR): 1.040; 95% confidence interval (CI): 1.009–1.073), the level of neutrophil to lymphocyte ratio (OR: 4.492; 95% CI: 1.906–10.582), the cardiac microvascular obstruction (OR: 3.416; 95% CI: 1.170–9.970), peak global longitudinal strain (OR: 1.131; 95% CI: 1.026–1.246), infarct size (OR: 1.082; 95% CI: 1.042–1.125) and left ventricular ejection fraction (OR: 0.925; 95% CI: 0.872–0.980), which were screened by regression analysis then merged into the nomogram model. Both internal validation (AUC: 0.805) and external validation (AUC: 0.867) revealed that the prediction model was capable of good discrimination. Calibration plot and Hosmer–Lemeshow method showed high consistency between the probabilities predicted by the nomogram (P = 0.514) and the validation set (P = 0.762) and the probabilities of actual occurrence. DCA corroborated the clinical utility of the nomogram. Conclusions In this study, the proposed nomogram model enabled individualized prediction of ALVR in NSTEMI patients after reperfusion and conduced to guide clinical therapeutic schedules.

Section: Discussionsupporting

confidence: 88%

Development and validation of a predictive model for adverse left ventricular remodeling in NSTEMI patients after primary percutaneous coronary intervention

Liu

et al. 2022

BMC Cardiovasc Disord

“…PS is ordinarily asymmetrically localized to the internal layer of the plasma membrane. If activated or injured, cells expose PS to the external leaflet of their plasmalemma and form a pattern that is subsequently recognized by macrophages and antibodies [ 33 ]. PS externalization of cardiomyocytes occurs after a short ischemic insult in a rabbit model and is associated with apoptosis [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

Coronary Artery Disease with Elevated Levels of HDL Cholesterol Is Associated with Distinct Lipid Signatures

Xia

2023

Metabolites

Levels of high-density lipoprotein cholesterol (HDL-C) are inversely associated with the incidence of coronary artery disease (CAD). However, the underlying mechanism of CAD in the context of elevated HDL-C levels is unclear. Our study aimed to explore the lipid signatures in patients with CAD and elevated HDL-C levels and to identify potential diagnostic biomarkers for these conditions. We measured the plasma lipidomes of forty participants with elevated HDL-C levels (men with >50 mg/dL and women with >60 mg/dL), with or without CAD, using liquid chromatography–tandem mass spectrometry. We analyzed four hundred fifty-eight lipid species and identified an altered lipidomic profile in subjects with CAD and high HDL-C levels. In addition, we identified eighteen distinct lipid species, including eight sphingolipids and ten glycerophospholipids; all of these, except sphingosine-1-phosphate (d20:1), were higher in the CAD group. Pathways for sphingolipid and glycerophospholipid metabolism were the most significantly altered. Moreover, our data led to a diagnostic model with an area under the curve of 0.935, in which monosialo-dihexosyl ganglioside (GM3) (d18:1/22:0), GM3 (d18:0/22:0), and phosphatidylserine (38:4) were combined. We found that a characteristic lipidome signature is associated with CAD in individuals with elevated HDL-C levels. Additionally, the disorders of sphingolipid as well as glycerophospholipid metabolism may underlie CAD.

Oxidative Medicine and Cellular Longevity

“…Previous studies have pointed out a potential cardioprotective role of phosphatidylserine in heart ischemia [ 70 – 73 ], suggesting that the phosphatidylserine signaling pathway is associated with MIRI. Schumacher et al [ 74 ] indicated that phosphatidylserine significantly reduced the infarct size by 30% and improved heart function by 25% in a chronic model of acute myocardial infarction (AMI), suggesting that phosphatidylserine supplementation may be a promising novel strategy to reduce infarct size following AMI and to prevent myocardial injury during myocardial infarction or cardiac surgery. A large number of studies have confirmed that chemokines [ 75 – 77 ], including C-X-C motif chemokine receptor 3 (CXCR3) [ 78 ], are closely related to the ischemia–reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

The Preventive Effect of Cardiac Sympathetic Denervation Induced by 6‐OHDA on Myocardial Ischemia–Reperfusion Injury: The Changes of lncRNA/circRNAs‐miRNA‐mRNA Network of the Upper Thoracic Spinal Cord in Rats

et al. 2021

In this study, we investigated whether chemical 6-hydroxydopamine (6-OHDA) stimuli caused cardiac sympathetic denervation (SD), and we analyzed gene expression profiles to determine the changes in the lncRNA/circRNAs-miRNA-mRNA network in the affected spinal cord segments to identify putative target genes and molecular pathways in rats with myocardial ischemia–reperfusion injury (MIRI). Our results showed that cardiac sympathetic denervation induced by 6-OHDA alleviated MIRI. Compared with the ischemia reperfusion (IR, MIRI model) group, there were 148 upregulated and 51 downregulated mRNAs, 165 upregulated and 168 downregulated lncRNAs, 70 upregulated and 52 downregulated circRNAs, and 12 upregulated and 11 downregulated miRNAs in the upper thoracic spinal cord of the SD-IR group. Furthermore, we found that the differential genes related to cellular components were mainly enriched in extracellular and cortical cytoskeleton, and molecular functions were mainly enriched in chemokine activity. Pathway analysis showed that the differentially expressed genes were mainly related to the interaction of cytokines and cytokine receptors, sodium ion reabsorption, cysteine and methionine metabolism, mucoglycan biosynthesis, cGMP-PKG signaling pathway, and MAPK signaling pathway. In conclusion, the lncRNA/circRNAs-miRNA-mRNA networks in the upper thoracic spinal cord play an important role in the preventive effect of cardiac sympathetic denervation induced by 6-OHDA on MIRI, which offers new insights into the pathogenesis of MIRI and provides new targets for MIRI.