Pulse pressure and coronary atherosclerosis progression in postmenopausal women
Girish V Nair1, David Waters, William Rogers
1Department of Internal Medicine/Cardiology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Insights
High pulse pressure in postmenopausal women with coronary disease significantly predicts faster progression of coronary atherosclerosis. Hormone replacement therapy (HRT) did not impact pulse pressure or disease progression in this study.
Area of Science:
- Cardiovascular Medicine
- Arterial Physiology
- Gerontology
Background:
- Pulse pressure, a marker of large artery stiffness, is linked to coronary events, but underlying mechanisms are not fully understood.
- Postmenopausal women with existing coronary artery disease represent a key population for studying arterial stiffness and atherosclerosis progression.
Purpose of the Study:
- To investigate the association between pulse pressure and the progression of coronary atherosclerosis in postmenopausal women.
- To evaluate the effect of hormone replacement therapy (HRT) on pulse pressure in this patient group.
Main Methods:
- Analysis of data from the Estrogen Replacement in Atherosclerosis (ERA) trial involving 309 postmenopausal women with coronary disease.
- Quantitative coronary angiography used to measure minimal diameter of epicardial segments at baseline and after 3.2 years.
- Mixed-model analysis of covariance employed to assess pulse pressure's impact on coronary stenosis progression and HRT's effect on pulse pressure.
Main Results:
- A significant, graded increase in coronary stenosis progression was observed with higher quartiles of baseline pulse pressure, even after adjusting for confounders.
- Women in the highest quartile of pulse pressure showed a 5-fold greater rate of progression compared to those in the lowest quartile.
- Hormone replacement therapy (estrogen or estrogen plus progestin) demonstrated no detectable effect on pulse pressure levels.
Conclusions:
- Elevated baseline pulse pressure is a significant predictor of subsequent coronary atherosclerosis progression in postmenopausal women with established coronary disease.
- The findings suggest pulse pressure is a clinically relevant indicator of arterial stiffness contributing to coronary disease advancement.
- HRT did not alter pulse pressure in this cohort, indicating it may not be a viable strategy to mitigate pulse pressure-related atherosclerosis progression.
Abstract:
Pulse pressure, an index of large artery stiffness, has been associated with coronary events. However, mechanisms for this association remain unclear. In this study, we examined the relationship between pulse pressure and the progression of coronary atherosclerosis and the effects of hormone replacement therapy (HRT) on pulse pressure in postmenopausal women with angiographically confirmed coronary disease followed for 3.2 years in the Estrogen Replacement in Atherosclerosis (ERA) trial. In the ERA trial, 309 postmenopausal women (mean age 66+/-7 years) with coronary disease were randomized to estrogen, estrogen plus progestin, or placebo, and followed for 3.2 years. Ten standardized epicardial segments were measured for minimal diameter values at baseline and follow-up using quantitative coronary angiography. For this study, mixed-model analysis of covariance was used to: (1) test the association between pulse pressure and change in mean minimum diameter (MMD) adjusted for baseline MMD and (2) the effect of HRT on follow-up pulse pressure. After adjustment for potential confounders, there was a significant graded increase in progression of coronary stenosis with increasing quartiles of baseline pulse pressure (P test for trend=0.0001). The progression rate in women with the highest quartile of baseline pulse pressure was 5-fold higher than in women in the lowest quartile (P<0.01). In postmenopausal women with coronary disease, increased levels of baseline pulse pressure are associated with subsequent progression of coronary atherosclerosis in postmenopausal women. HRT had no detectable effect on pulse pressure.
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