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Published on: August 13, 2019
Post-menopausal hormone therapy and cardiovascular events: a new paradigm based on pharmacogenetics?
1The Ohio State University, 235 Davis Heart and Lung Research Institute, 473 W. 12th Ave, Columbus, OH 43210-1252, USA. glen.cooke@osumc.edu
Insights
Hormone therapy (HT) does not reduce coronary heart disease (CHD) risk in postmenopausal women. Genetic variations in platelet glycoproteins may guide future HT decisions for personalized cardiovascular risk management.
Area of Science:
- Cardiovascular Medicine
- Genetics
- Endocrinology
Background:
- Postmenopausal women face increased coronary heart disease (CHD) risk.
- Hormone therapy (HT) was hypothesized to mitigate this risk.
- However, clinical trials show mixed results, with some indicating no benefit or even increased cardiovascular events.
Purpose of the Study:
- To investigate the role of platelet glycoprotein single-nucleotide polymorphisms (SNPs) in CHD risk.
- To explore the potential of genetic profiling for personalizing HT efficacy and safety.
- To identify patient subgroups who may benefit from or be harmed by HT for CHD prevention.
Main Methods:
- Review of large randomized clinical trials on HT and cardiovascular events.
- Analysis of platelet glycoprotein single-nucleotide polymorphisms (SNPs).
- Exploration of genetic markers for predicting treatment response to HT.
Main Results:
- Large trials failed to show reduced CHD risk with HT in secondary prevention.
- Some primary prevention studies indicated an increased risk of cardiovascular events with HT.
- Platelet glycoprotein SNPs show potential for identifying individual risk and treatment efficacy.
Conclusions:
- HT is not a universally effective strategy for reducing CHD risk in postmenopausal women.
- Genotyping for platelet glycoprotein SNPs could enable personalized medicine approaches.
- Future clinical practice may involve genetic screening to guide HT decisions, optimizing benefits and minimizing harm.
Abstract:
The risk of coronary heart disease (CHD) events increases in women after menopause and it was thought that hormone therapy (HT) would decrease this risk. However, numerous large randomized clinical trials have not demonstrated decreased risk in secondary prevention and some have actually shown increased risk of cardiovascular events with HT in primary prevention. Platelets are involved in CHD events and platelet glycoprotein single-nucleotide polymorphisms may help to identify risk and treatment efficacy. It may become a plausible strategy in the future for clinicians to identify, by genotyping, high-risk patients who would benefit from HT to reduce CHD risk as well as to identify patients with neutral risk for whom HT could be harmful.
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