Key result
NSAIDs, hormonal therapies, anticoagulants, and antipsychotics can trigger MI via endothelial dysfunction, coronary spasm, and thrombosis.
Why the study?
Myocardial infarction can arise from various etiological factors, including pharmacological triggers, requiring exploration of the diverse drugs involved and their pathophysiological mechanisms.
This review highlights the pathophysiological mechanisms by which various common medications can trigger myocardial infarction, emphasizing the need for healthcare professional awareness to mitigate risks.
Myocardial infarction (MI) is a significant cardiovascular event caused by the decrease in or complete cessation of blood flow to a portion of the myocardium. It can arise from a variety of etiological factors, including pharmacological triggers. This review aims to explore the diverse drugs and substances that might lead to drug-induced myocardial infarction, focusing on their mechanisms of action and the pathophysiological processes involved. Various established and emerging pharmacological agents that could elevate the risk of myocardial infarction, such as nonsteroidal anti-inflammatory drugs, hormonal therapies, anticoagulants, and antipsychotic medications, are discussed. The role of drug-induced endothelial dysfunction, coronary artery spasm, and thrombosis are presented in order to highlight the underlying mechanisms. This review emphasizes the need for increased awareness among healthcare professionals to mitigate the risks associated with different pharmacological therapies to improve patient outcomes.
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Boarescu et al. (2024) conducted a review in Drug-induced myocardial infarction. Pharmacological agents (NSAIDs, hormonal therapies, anticoagulants, antipsychotics) was evaluated. Pharmacological agents including NSAIDs, hormonal therapies, anticoagulants, and antipsychotics can trigger myocardial infarction via endothelial dysfunction, coronary artery spasm, and thrombosis.
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