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Are Changes in Cardiovascular Disease Risk Factors in Midlife Women Due to Chronological Aging or to Menopausal Transition?
Karen A Matthews PhD, Sybil L Crawford PhD, Caludia U Chae MD et al.
Reviewers: F. Ahmad Ghaffori, MD
Feroze Mahmood, MD
The SWAN (Study of Women’s Health Across the Nation) was a longitudinal, multicenter, community-based, prospective cohort study that included 1,054 women of diverse ethnic backgrounds. Risk factors assessed in a serial fashion included: a complete lipid panel, lipoproteins, CRP, glucose, insulin, blood pressure and hemostatic factors. For each risk factor the magnitude of change was evaluated in the pre, peri and postmenopausal time periods. The data were analyzed in order to assess the quality of fit into either a piecewise linear model, representative of changes driven by ovarian age, or into a linear model, reflecting changes in chronological age and independent of FSH levels.
The study results showed that changes in the following risk factors were better described by the piecewise linear model: total cholesterol, LDL-C, apolipoprotein (Apo) B, HDL-C and Apo A-I. Therefore, they concluded that these changes were caused by increasing ovarian age. The greatest increase in total cholesterol, LDL-C and Apo B occurred in the 1-year interval surrounding the FMP. On the other hand, the greatest increase in HDL-C and Apo A-I occurred before the 1-year interval surrounding the FMP, with subsequent levels either staying constant or declining. Changes in levels of glucose, t-PA-ag, PAI-1 and fibrinogen were better described by a linear model and thus interpreted to be independent of ovarian age. Finally, changes in systolic and diastolic blood pressures, Lp(a), insulin, factor VIIc fit equally in either model. Notably, the patterns of change in all these risk factors were independent of ethnicity.
The current study has a number of limitations. Women who had undergone hormone therapy or who had a hysterectomy or bilateral oophorectomy were excluded. Thus, the results cannot be applied to these patient populations. Additionally, by including these patients they could have further demonstrated a chronological age-independent and ovarian age-dependent set of changes in patients that would not normally have natural onset menopause. Long-term follow-up of these patients would have provided valuable insights into the strength of correlation between these risk factors and clinical endpoints of cardiovascular disease. Additionally, a substantial 25% of women were lost to follow-up as a result of administrative reasons.
With regards to the risk factors assessed, apo A-I continues to increase after the final menstrual period while HDL-C levels decline; this trend represents a discrepancy between cholesterol and apoprotein trajectories. In assessing a woman’s cardiovascular risk, computation of the post-menopausal apo B/A-I ratio would convey a lower risk profile than computation of the LDL-C/HDL-C ratio, as eloquently described by Bittner (6). This discrepancy would have profound effects on the validity of using these two different lipid ratios to determine cardiovascular risk in these patients.
Overall the authors of this review conclude that the current study provides valuable insights into the precise timing of specific changes in a subset of known cardiovascular risk factors that have the potential to increase the risk of CHD in postmenopausal women. Further follow-up will be critical in order to determine the true prognostic power of the changes seen in these risk factors during the studied time periods surrounding menopause. Although future studies are needed to further explore some of the discrepant results found in this study in comparison with previously published data, this analysis provides strong evidence to support close monitoring of cardiovascular risk factors of peri-menopausal women. Whether or not interventions based on these practices will lead to reduced CHD events will need to be determined by future clinical trials.
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