Propofol in a Cardiac Setting: Recent Findings in Clinical Applicability and Protective Mechanisms

Researchers: Nizam Ali Karim B.S. Justin Viet Quang Le B.S.A. Zahir Malik Amin B.S. Harmandeep Singh B.S. Winston Tawiah B.S. The University of Texas Medical Branch (UTMB) John Sealy School of Medicine, Galveston, TX

Background: Propofol is a widely used intravenous anesthetic agent known for its rapid onset and short duration of action. Beyond its primary anesthetic role, propofol has been found to possess cardioprotective properties. This study aims to investigate the mechanisms underlying these cardioprotective effects and evaluate their clinical applicability in cardiac medicine.

Methods: A systematic review was conducted using PubMed to ascertain published studies in the English language over the period of 2021-2024 using the appropriate search terms. The primary papers of interest were those that examined the cardioprotective effect of the intravenous anesthetic propofol. The search criteria yielded a total of 26 articles, which were then examined by three researchers for inclusion in the study. A total of 15 articles met the inclusion criteria and were included.

Results: The systematic review evaluated the cardioprotective effects of propofol in various preclinical and clinical settings. The studies reviewed included experiments on H9c2 rat-derived cardiac cells subjected to hypoxia/reoxygenation conditions, animal models of myocardial ischemia/reperfusion (I/R) injury, and clinical trials involving cardiac surgery patients. Propofol postconditioning (P-PostC) significantly reduced hypoxia/reoxygenation-induced apoptosis and autophagy in H9c2 cells. This effect was mediated by the upregulation of forkhead transcription factors FoxO1 and FoxO3a. Silencing these transcription factors reversed the cardioprotective effects, indicating their critical role in propofol's mechanism. Additionally, propofol alleviated oxidative stress, as evidenced by decreased reactive oxygen species (ROS) levels. In rat models, propofol pretreatment reduced myocardial infarct size, improved cardiac function, and decreased markers of myocardial injury such as lactate dehydrogenase (LDH) and creatine kinase (CK). Propofol also inhibited mast cell degranulation by reducing calcium influx through store-operated Ca2+ channels (SOCs) and activated the PI3K/AKT/Bcl-2 pathway, enhancing cell survival. Furthermore, in patients undergoing off-pump coronary artery bypass grafting (OPCABG), both volatile anesthetics and propofol demonstrated cardioprotective effects. However, volatile anesthetics slightly outperformed propofol in reducing myocardial injury markers such as troponin. Despite this, no significant difference in overall mortality or major morbidity was observed between these anesthetics.

Conclusion: Propofol exhibits significant cardioprotective effects through multiple mechanisms, including modulation of molecular pathways, inhibition of mast cell degranulation, activation of survival pathways, antioxidant activity, modulation of calcium homeostasis, and reduction of ischemia-reperfusion injury. Utilizing these effects, propofol can improve the quality of care in patients with cardiovascular conditions. Although its benefits in cardiac surgery are well-documented, further clinical research is warranted to optimize its use in non-surgical cardiac interventions.