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Web-based lecture series under development
Drug & Innovation Update
Is Minimally Invasive Hemodynamic Monitoring Ready for Cardiac Surgery?
Literature Reviews
Emerging Role of Candida in Deep Sternal Wound Infection
Outcomes following endovascular vs open repair of abdominal aortic aneurysm: a randomized trial
Drug-Eluting Stents vs. Coronary-Artery Bypass Grafting in Multivessel Coronary Disease
Ketamine attenuates delirium after cardiac surgery with cardiopulmonary bypass
Foundation Update
New FOCUS sites sought; SCA Foundation Reception
SCA Bulletin - Printable Version
The Society of Cardiovascular Anesthesiologists (SCA) publishes the SCA Bulletin bimonthly. The information presented in the SCA Bulletin has been obtained by the editors. Validity of opinions presented, drug dosages, accuracy and completeness of content are not guaranteed by SCA.
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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.
J Am Coll Cardiol Vol.54 No.25, 2366-2377. 2009
Reviewers: F. Ahmad Ghaffori, MD
Resident in Anesthesia
Beth Israel Deaconess Medical Center
Harvard Medical School
Boston, MA
Feroze Mahmood, MD
Assistant Professor
Beth Israel Deaconess Medical Center
Harvard Medical School
Boston, MA
Abstract Excerpt
A causal link between increased rates of coronary heart disease (CHD) in women and the postmenopausal state has been established in numerous studies. It remains unclear however whether this risk is due to alterations in endogenous hormone levels, as a result of the onset of increasing age or menopause (either natural onset or surgically-induced) (1-6). Adding to the complexity of this debate, some investigators have suggested that heart disease risk might determine menopausal age rather then the reverse (7, 8). Studies which have examined these issues have been limited by one or more of the following: predominantly Caucasian participants and therefore a lack of diversity in the patient population, insufficient precision in the definition of pre, peri and postmenopausal periods, concomitant changes in independent risk factors that parallel the different periods studied, an incomplete inclusion of all risk markers known to be associated with CHD, and failure to adjust for non-menopausal related cardiovascular risk factors such as lifestyle and pharmacological interventions. The aim of the current study was to describe the change in cardiovascular risk factors, independent of age and other confounding variables, in a multi-ethnic group of women before, during and after their final menstrual period (FMP). The investigators further sought to ascertain whether changes in these risk factors were related to ovarian aging or chorological aging (9).
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.
Reviewers' Comments
The present study is the first to conduct a careful, prospective analysis of covariate adjusted risk factors with precisely defined transitional periods: prior, during and immediately after FMP. Furthermore, the investigators included a large number of patients from multiple institutions, and their diverse patient cohort included multiple ethnicities. The results from this study have important clinical implications because a specific time period has been identified in which known and measurable cardiovascular risk factors can be assessed. Consequently, the clinician is able to identify and closely monitor modifiable risk factors in the appropriate time period. Ultimately, this understanding could lead to lifestyle changes and therapeutic interventions aimed at minimizing the cardiovascular risks associated with menopause.
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.
References
1. Tracy RE. Sex difference in coronary disease: two opposing views. J Chronic Dis 1966;19:1245–51.
2. Colditz GA, Willet WC, Stampfer MJ, Rosner B, Speizer FE, Hennekens CH. Menopause and the risk of coronary heart disease in women. N Engl J Med 1987;316:1105–10.
3. Tunstall-Pedoe H. Myth and paradox of coronary risk and the menopause. Lancet 1998;351:1425–7.
4. Barrett-Connor E. Sex differences in coronary heart disease. Why are women so superior? Circulation 1997;95:252– 64.
5. Howard BV, Kuller L, Langer R, et al. Risk of cardiovascular disease by hysterectomy status, with and without oophorectomy: the Women’s Health Initiative Observational Study. Circulation 2005;111:1462–70.
6. Bittner V. Menopause, Age, and Cardiovascular Risk: A complex Relationship. J Am Coll Cardiol 2009; 54: 2374-2375
7. Kok HS, van Asselt KM, van der Schouw YT, et al. Heart disease risk determines menopausal age rather than the reverse. J Am Coll Cardiol 2006;47:1976–84.
8. Bittner V. Menopause and cardiovascular risk: cause or consequence? J Am Coll Cardiol 2006;47:1984–6.
9. Matthews KA, Crawford SL, Chae CU, et al. Are changes in cardiovascular disease risk factors in midlife women due to chronological aging or to the menopausal transition? J Am Coll Cardiol 2009;54:2366 –73.