MiRNA‐mediated pyroptosis play crucial effects in the development of myocardial ischaemia/reperfusion (I/R) injury (MIRI). Piperine (PIP) possesses multiple pharmacological effects especially in I/R condition. This study focuses on whether PIP protects MIRI from pyroptosis via miR‐383‐dependent pathway. Rat MIRI model was established by 30 minutes of LAD ligation and 4 hours of reperfusion. Myocardial enzymes, histomorphology, structure and function were detected to evaluate MIRI. Recombinant adenoviral vectors for miR‐383 overexpression or miR‐383 silencing or RP105 knockdown were constructed, respectively. Luciferase reporter analysis was used to confirm RP105 as a target of miR‐383. Pyroptosis‐related markers were measured by Western blotting assay. The results showed that I/R provoked myocardial injury, as shown by the increases of LDH/CK releases, infarcted areas and apoptosis as well as worsened function and structure. Pyroptosis‐related mediators including NLRP3, cleaved caspase‐1, cleaved IL‐1β and IL‐18 were also reinforced after MIRI. However, PIP treatment greatly ameliorated MIRI in parallel with pyroptotic repression. In mechanistic studies, MIRI‐caused elevation of miR‐383 and decrease of RP105/PI3K/AKT pathway were reverted by PIP treatment. Luciferase reporter assay confirmed RP105 as a miR‐383 target. miR‐383 knockdown ameliorated but miR‐383 overexpression facilitated pyroptosis and MIRI. Moreover, the anti‐pyroptotic effect from miR‐383 silencing was verified to be relied on the RP105/PI3K/AKT signalling pathway. Additionally, our present study further indicated the miR‐383/RP105/AKT‐dependent approach resulting from PIP administration against pyroptosis in MIRI. Therefore, PIP treatment attenuates MIRI and pyroptosis by regulating miR‐383/RP105/AKT pathway, and it may provide a therapeutic manner for the treatment of MIRI.

Background: The monocyte-to-lymphocyte ratio (MLR) has emerged as a novel marker of inflammation. Nevertheless, its potential utility in predicting the development of left ventricular aneurysm (LVA) remains unexplored. This study aims to investigate the association between MLR and the risk of LVA in patients presenting with acute ST segment elevation myocardial infarction (STEMI). Methods: A total of 551 patients were enrolled in the first cohort, and 471 patients were included in the validation cohort. To evaluate the predictive value of MLR for LVA, multivariable logistic regression analysis, restricted cubic splines (RCS) analysis, and receiver operating characteristic (ROC) analysis were employed. Results: The prevalence of LVA was 14.5% in the first cohort and 13.6% in the validation cohort. The multivariable logistic regression analysis revealed that individuals in the highest quartile of MLR (Q4) exhibited a significantly increased risk of LVA formation compared to those in the lowest quartile (Q1) in both cohorts (first cohort: OR = 3.07, 95% CI = 1.33–7.08, P = 0.009; validation cohort: OR = 3.55, 95% CI = 1.34–9.42, P = 0.011). The RCS analysis identified a positively nonlinear association in the first cohort and a positively linear association in the validation cohort between MLR and the risk of LVA (overall P < 0.05). Furthermore, the discriminative ability of MLR for LVA is 0.69 in the first cohort and 0.71 in the validation cohort, exceeding that of both monocyte and lymphocyte alone. The subgroup analyses further substantiated the robustness of our findings. Conclusion: An elevated MLR was independently linked to an increased risk of LVA development in patients with STEMI who received primary PCI. This readily available inflammatory index may offer supplementary prognostic information and could be considered for inclusion in future risk stratification models.

The C-reactive protein (CRP) to albumin ratio (CAR) has emerged as a novel marker of inflammation. However, its potential predictive value for the development of left ventricular aneurysm (LVA) has not yet been evaluated. This study aims to explore the association between CAR and the risk of LVA in patients experiencing acute ST-segment elevation myocardial infarction (STEMI). This study recruited 551 patients in the first cohort and 471 patients in the validation cohort. Multivariable logistic regression analysis, restricted cubic splines (RCS) analysis, and receiver operating characteristic were conducted to assess the predictive value of CAR for LVA. The prevalence of LVA were 14.5% in the first cohort and 13.6% in the validation cohort. Multivariable logistic regression analysis indicated that individuals in the highest quartile of CAR (Q4) were significantly associated with the risk of LVA formation compared to those in the lowest quartile (Q1) in both cohorts (First cohort: OR = 3.26, 95% CI = 1.51–7.05, P = 0.003; Validation cohort: OR = 4.05, 95% CI = 1.71–9.60, P = 0.002). RCS analysis demonstrated a positive and nonlinear association between CAR and the risk of LVA (overall P < 0.05, nonlinear P < 0.05). Furthermore, the discriminative ability of CAR for LVA is 0.72 in the first cohort and 0.74 in the validation cohort, exceeding that of both CRP and albumin alone. Subgroup analyses further corroborated the robustness of our findings. Elevated CAR was independently linked to an increased risk of LVA development in patients with STEMI who received primary PCI. This finding may hold considerable significance for clinical practice and could aid in the development of a personalized prevention strategy that incorporates the monitoring of CAR.