Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024 Dec 18;11(12):406.
doi: 10.3390/jcdd11120406.

Drug-Induced Myocardial Infarction: A Review of Pharmacological Triggers and Pathophysiological Mechanisms

Ioana Boarescu  1 , Paul-Mihai Boarescu  2   3
Affiliations
Review

Drug-Induced Myocardial Infarction: A Review of Pharmacological Triggers and Pathophysiological Mechanisms

Ioana Boarescu et al. J Cardiovasc Dev Dis. .

Abstract

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.

Keywords: drugs; myocardial infarction; pathophysiological mechanisms; pharmacological triggers.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Pathophysiological mechanisms of drug-induced myocardial infarction.
See this image and copyright information in PMC

References

    1. Reimer K.A., Jennings R.B., Tatum A.H. Pathobiology of acute myocardial ischemia: Metabolic, functional and ultrastructural studies. Am. J. Cardiol. 1983;52:72–81. doi: 10.1016/0002-9149(83)90180-7. - DOI - PubMed
    1. Thygesen K., Alpert J.S., Jaffe A.S., Simoons M.L., Chaitman B.R., White H.D. Third universal definition of myocardial infarction. Circulation. 2012;126:2020–2035. doi: 10.1161/CIR.0b013e31826e1058. - DOI - PubMed
    1. Thygesen K., Mair J., Giannitsis E., Mueller C., Lindahl B., Blankenberg S., Huber K., Plebani M., Biasucci L.M., Tubaro M., et al. How to use high-sensitivity cardiac troponins in acute cardiac care. Eur. Heart J. 2012;33:2252–2257. doi: 10.1093/eurheartj/ehs154. - DOI - PubMed
    1. Thygesen K., Mair J., Katus H., Plebani M., Venge P., Collinson P., Lindahl B., Giannitsis E., Hasin Y., Galvani M., et al. Recommendations for the use of cardiac troponin measurement in acute cardiac care. Eur. Heart J. 2010;31:2197–2204. doi: 10.1093/eurheartj/ehq251. - DOI - PubMed
    1. Apple F.S., Jaffe A.S., Collinson P., Mockel M., Ordonez-Llanos J., Lindahl B., Hollander J., Plebani M., Than M., Chan M. IFCC educational materials on selected analytical and clinical applications of high sensitivity cardiac troponin assays. Clin. Biochem. 2015;48:201–203. doi: 10.1016/j.clinbiochem.2014.08.021. - DOI - PubMed

LinkOut - more resources