Bimei Jiang

Background Despite the advent of new pharmacotherapies, statins remain a cornerstone in the secondary prevention of myocardial infarction (MI). However, the cardiac adverse events (AEs) linked to statins are not well-documented. Aim This pharmacovigilance study used data from the FDA Adverse Event Reporting System (FAERS) to investigate the association between statin use and cardiac AEs in MI patients. Method Reports from the FAERS database (2004–2023) identifying statins as the primary suspect in MI patients were analyzed. The study evaluated seven types of statins: atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, and simvastatin. Disproportionality analysis using four major indices, Reporting Odds Ratio (ROR), Proportional Reporting Ratio (PRR), Bayesian Confidence Propagation Neural Network (BCPNN), and Multi-Item Gamma-Poisson Shrinker (MGPS), was conducted to detect signals of statin-related cardiac AEs. Results Of the 20,346,289 reports reviewed, 150 identified statins as the primary suspect drug in MI patients. The most common cardiac AEs were recurrent MI (50 reports), acute MI (14 reports), followed by tachycardia (10), angina pectoris (8), coronary artery occlusion (6), cardiac failure (6), and arrhythmia (6). The analysis revealed no significant signals of statin-induced cardiac AEs. Conclusion The findings confirm that statin use in MI patients does not significantly increase the risk of cardiac adverse effects, supporting their safety profile in this context.

Background: Despite the advent of new pharmacotherapies, statins remain a cornerstone in the secondary prevention of myocardial infarction (MI). However, the cardiac adverse events (CAEs) linked to statins are not well-documented. Aim: This pharmacovigilance study used data from the FDA Adverse Event Reporting System (FAERS) to investigate the association between statin use and CAEs in MI patients. Method: Reports from the FAERS database (2004-2023) identifying statins as the primary suspect in MI patients were analyzed. The study evaluated seven types of statins: atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, and simvastatin. Disproportionality analysis using four major indices, Reporting Odds Ratio (ROR), Proportional Reporting Ratio (PRR), Bayesian Confidence Propagation Neural Network (BCPNN), and Multi-Item Gamma-Poisson Shrinker (MGPS), was conducted to detect signals of statin-related CAEs. Results: Of the 20,346,289 reports reviewed, 150 identified statins as the primary suspect drug in MI patients. The most common CAEs were recurrent MI (50 reports), acute MI (14 reports), followed by tachycardia (10), angina pectoris (8), coronary artery occlusion (6), cardiac failure (6), and arrhythmia (6). The analysis revealed no significant signals of statin-induced CAEs. Conclusion: The findings confirm that statin use in MI patients does not significantly increase the risk of cardiac adverse effects, supporting their safety profile in this context.

Background Sepsis-induced myocardial injury, as one of the important complications of sepsis, can significantly increase the mortality of septic patients. Our previous study found that nucleolin affected mitochondrial function in energy synthesis and had a protective effect on septic cardiomyopathy in mice. During sepsis, glucose metabolism disorders aggravated myocardial injury and had a negative effect on septic patients. Objectives We investigated whether nucleolin could regulate glucose metabolism during endotoxemia-induced myocardial injury. Methods The study tested whether the nucleolin cardiac-specific knockout in the mice could affect glucose metabolism through untargeted metabolomics, and the results of metabolomics were verified experimentally in H9C2 cells. The ATP content, lactate production, and oxygen consumption rate (OCR) were evaluated. Results The metabolomics results suggested that glycolytic products were increased in endotoxemia-induced myocardial injury, and that nucleolin myocardial-specific knockout altered oxidative phosphorylation-related pathways. The experiment data showed that TNF-α combined with LPS stimulation could increase the lactate content and the OCR values by about 25%, and decrease the ATP content by about 25%. However, interference with nucleolin expression could further decrease ATP content and OCR values by about 10–20% and partially increase the lactate level in the presence of TNF-α and LPS. However, nucleolin overexpression had the opposite protective effect, which partially reversed the decrease in ATP content and the increase in lactate level. Conclusion Down-regulation of nucleolin can exacerbate glucose metabolism disorders in endotoxemia-induced myocardial injury. Improving glucose metabolism by regulating nucleolin was expected to provide new therapeutic ideas for patients with septic cardiomyopathy.