Related Experiment Video
Updated: Aug 2, 2026

Routine Screening Method for Microparticles in Platelet Transfusions
Published on: January 31, 2018
Long-term hormone replacement therapy does not cause increased platelet activation
Marlene S Williams1, Dhananjay Vaidya, Thomas Kickler
1Department of Medicine, Johns Hopkins Medical Institute, Baltimore, MD, USA. mswillia@jhmi.edu
Insights
Long-term hormone replacement therapy (HRT) did not increase platelet activation or aggregation in postmenopausal women with coronary artery disease. Early HRT initiation effects on platelet function remain unassessed.
Area of Science:
- Cardiovascular Science
- Endocrinology
- Hematology
Background:
- Observational studies suggested reduced ischemic coronary disease risk with hormone replacement therapy (HRT) in postmenopausal women.
- Recent studies indicated increased ischemic cardiac events with HRT initiation in women with existing coronary artery disease.
- Estrogen's potential role in increasing platelet aggregation was postulated.
Purpose of the Study:
- To evaluate the effect of long-term hormone replacement therapy (HRT) on platelet activation and aggregation in postmenopausal women with coronary artery disease.
- To investigate whether HRT influences platelet function markers, specifically P selectin and PAC1 expression and platelet-rich plasma aggregation.
- To assess platelet function in women on HRT for over two years compared to a placebo group.
Main Methods:
- Platelet activation was measured using flow cytometry with P selectin and PAC1 as markers.
- Platelet aggregation was assessed via standard methods in platelet-rich plasma.
- The study included 27 postmenopausal women from two placebo-controlled angiographic trials, with 17 on HRT and 10 on placebo, all on aspirin therapy.
Main Results:
- No significant differences were observed in platelet aggregation between the HRT and placebo groups across various agonist doses.
- Flow cytometry analysis revealed comparable levels of platelet activation between women receiving HRT and those on placebo.
- These findings suggest long-term HRT does not elevate platelet activation or aggregation in this patient population.
Conclusions:
- Long-term hormone replacement therapy (HRT) does not appear to increase platelet activation and aggregation in postmenopausal women with coronary artery disease.
- The study did not assess potential transient increases in platelet activation during the early period of HRT initiation.
- Further research may be needed to clarify the acute effects of HRT initiation on platelet function.
Background:
Observational studies have shown apparently lower ischemic coronary disease risk in postmenopausal women receiving hormone replacement therapy (HRT). However, several recent studies have shown an increase in ischemic cardiac events when HRT is initiated in postmenopausal women with known coronary artery disease. It is postulated that estrogen may result in increased platelet aggregation.
Methods:
We evaluated platelet activation, as measured by flow cytometric analysis using P selectin and PAC1 as activation markers, and aggregation, as measured by standard platelet aggregation using platelet-rich plasma, in 27 postmenopausal women (17 HRT, 10 placebo) who were participants in 2 placebo-controlled randomized angiographic trials evaluating the effect of HRT on coronary atherosclerosis or saphenous vein graft disease. All women had received HRT or placebo for >2 years and were on aspirin therapy. The estrogen component was either conjugated equine estrogen or 17beta-estradiol.
Results:
Patients on HRT and those on placebo had comparable degrees of platelet aggregation when measured using various doses of agonists (adenosine diphosphate and epinephrine). There were no significant differences in levels of platelet activation measured by flow cytometry.
Conclusion:
We conclude that long-term HRT does not appear to cause increased platelet activation and aggregation in women with coronary artery disease. There may be increased platelet activation in the early period after HRT initiation; however, this was not assessed in this study.
Related Concept Videos
Targeted Cancer Therapies
There are several types of targeted therapies against specific...
Hormones and Bone Tissue
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
Venous Thrombosis III: Interprofessional Care

