In an experimental rat myocardial infarction model, gastrointestinal dysfunction (manifested as increased gastric retention rate etc) after myocardial infarction has been reported, involving abnormal tryptophan-5-hydroxytryptamine metabolism.

https://pubmed.ncbi.nlm.nih.gov/28212441/

Somewhat relevant reports in humans

https://pubmed.ncbi.nlm.nih.gov/16259436/

https://pubmed.ncbi.nlm.nih.gov/2290328/

This is a bit different question, but there is also a debate over associations between proton pump inhibitors (gastric acid-suppressing agents) and cardiovascular risks including myocardial infarction, including effects of such inhibitors on myocardial H+/K+–ATPase.

https://pubmed.ncbi.nlm.nih.gov/28321021/

https://pubmed.ncbi.nlm.nih.gov/27607343/

Hi. Yes, I think it affects the secretion of epinephrine, which causes blood vessels to constrict and reduce blood flow to the stomach, and is considered stressful in itself, and gastric acid secretion increases under stress.

Panax quinquefolius saponins combined with dual antiplatelet drug therapy alleviate gastric mucosal injury and thrombogenesis through the COX/PG pathway in a …

Na Kou, Mei Xue, Lin Yang, Ming-Xuan Zang, Hua Qu, Ming-Ming Wang, Yu Miao, Bin Yang, Da-Zhuo Shi

PloS one 13 (3), e0194082, 2018

Nonvariceal upper GI hemorrhage after percutaneous coronary intervention for acute myocardial infarction: a national analysis over 11 months

Mohammad Bilal, Ronald Samuel, Mazen K Khalil, Shailendra Singh, Sreeram Parupudi, Marwan S Abougergi

Gastrointestinal endoscopy 92 (1), 65-74. e2, 2020

1.Stess incited by myocardial infarction can have dual effect. Increase in acid secretion in response to the stress induced increase norepinephrine. The other is protective by reducing the prostaglandins. 2.The haemodynamic changes that may occur following myocardial infarction can also increase the acid secretion.