The effects of proton pump inhibitors on the development of post-stenting major adverse cardiovascular events in patients with acute coronary syndrome

Abstract

Proton pump inhibitors (PPIs) are recommended for the prevention of gastrointestinal bleeding in acute coronary syndrome (ACS) patients who receive dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) but have been associated with an increased risk of major adverse cardiovascular events (MACE) in these patients. We aimed to investigate the relationship between serum asymmetric dimethylarginine (ADMA) and copeptin levels and MACE in those who started on imminent DAPT and PPI therapy after PCI. 90 patients with ACS were included in this prospective observational study and divided into three groups lansoprazole (n=30), rabeprazole (n=31), and pantoprazole (n=29). The serum ADMA and copeptin levels were examined at the time of diagnosis, at the end of 1st and 6th month. MACE was defined as mortality, recurrent AMI (acute myocardial infarction), and CST (coronary stent thrombosis) development after PCI. MACE developed in two patients in the first month and eight patients (8.9%) after six months of follow-up. At six months, CST was seen in only two patients (2.2%). At the first-month evaluation, while a significant increase was observed in serum ADMA levels at the time of admission (p<0.001), the copeptin levels decreased significantly in all patients (p<0.001). In the 6th month, the serum ADMA and copeptin levels significantly increased compared to the time of admission and 1st-month evaluation in all groups (p<0.001). PPIs might significantly influence serum ADMA and copeptin levels in patients undergoing coronary stenting due to ACS. Nevertheless, we did not notice clinical extrapolation of the potential effects.

Heartburn’s Hidden Impact: A Narrative Review Exploring Gastroesophageal Reflux Disease (GERD) as a Cardiovascular Disease Risk Factor

“…Due to the concerns about antiplatelet attenuation with PPIs and the increased risk of worse cardiovascular outcomes, many clinicians have explored the use of H2RAs for patients on dual antiplatelet therapy [59]. A study in 2014 by Luo et al found that H2-receptor activation exaggerated myocardial injury by promoting myocardial mitochondrial dysfunction and by increasing cardiac vascular endothelial permeability [60].…”