Impaired ovarian function and risk factors for atherosclerosis in premenopausal women

Punnonen, R.; Jokela, Hannu; Aine, Risto; Teisala, Klaus; Salomäki, Anne; Uppa, Helena

doi:10.1016/s0378-5122(97)00040-6

Cited by 40 publications

(19 citation statements)

References 18 publications

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“…175,176 A third study has shown that irregularly menstruating women, in comparison with normally cycling control women, have elevated plasma fibrinogen concentrations (a risk factor for CAD) and a thickened arterial intima. 177 The possibility that these observations might reflect the reduced concentrations of endogenous estrogen characteristic of ovary-impaired women is supported by the finding that premenopausal women with angiographically confirmed CAD have significantly lower plasma estradiol concentrations than do control subjects and that such levels resemble those observed in subordinate female monkeys. 173,178 Notably, many premenopausal women may experience ovarian compromise at some time during their reproductive years.…”

Section: Sex Differencesmentioning

confidence: 97%

“…174 Nonetheless, surrogate measures (eg, a history of menstrual irregularity) are associated with premature CAD or elevated CAD risk factors. 176,177 Hence, the percentage of premenopausal women who experience accelerated atherosclerosis may be much larger than the number diagnosed as amenorrheic or otherwise ovary-impaired. At present, however, atherosclerosis progression has not been studied prospectively in premenopausal women in conjunction with ovarian function.…”

Section: Sex Differencesmentioning

confidence: 99%

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Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

1999

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Abstract-Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis.Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys.Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. ...

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Section: Sex Differencesmentioning

confidence: 97%

Section: Sex Differencesmentioning

confidence: 99%

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

1999

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“…26 In efforts to determine mechanisms underlying the higher in-hospital mortality of younger women with MI, genetic and hormonal pathways have been hypothesized, including abnormalities of the estrogen receptor, 27 ovarian dysfunction, 28,29 premature menopause, 30 and proinflammatory properties of hormone replacement therapy. 31 Although it has been shown that estrogen has numerous protective effects on the cardiovascular system, 32 a proinflammatory effect of exogenous hormone therapy has been described.…”

Section: Possible Mechanismsmentioning

confidence: 99%

Sex Differences in Hospital Mortality After Coronary Artery Bypass Surgery

et al. 2002

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Background-Data are conflicting over whether women have higher mortality than men after coronary artery bypass graft (CABG) surgery. Younger but not older women hospitalized for acute myocardial infarction have higher in-hospital mortality rates than men. We hypothesized that younger women also have higher in-hospital mortality rates after CABG. Methods and Results-We studied 51 187 patients (30% women) included in the National Cardiovascular Network database who received CABG at 23 clinical centers between October 1993 and December 1999. Compared with men, fewer women were white and more women had risk factors and comorbidities. These differences were more apparent in younger patients. In all age groups, however, women had higher left ventricular ejection fraction and fewer diseased vessels. Women had higher in-hospital mortality rates than men, but sex differences in mortality were more marked among younger patients. Women Ͻ50 years of age were 3 times more likely to die than men (3.4% versus 1.1%), and women 50 to 59 years of age were 2.4 times more likely to die than men (2.6% versus 1.1%). In the older age categories, the sex difference in in-hospital mortality was less marked (PϽ0.001 for the interaction between sex and age). Adjustment for preoperative risk factors only slightly decreased the strength of this interaction. Conclusions-Younger women undergoing CABG surgery are at a higher risk of in-hospital death than men, but this difference in risk decreases with advancing age. Additional investigation is needed to determine why in-hospital mortality is higher in women after CABG, with particular focus on younger women.

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“…2 Indeed, the risk of atherosclerosis is increased when estrogen production stops, either naturally or after surgery 3 or in woman with impaired ovarian function. 4 The time since menopause is a major risk factor for the development and progression of atherosclerotic lesions, as well as the development of hypertension. 5 In fact, cardiovascular disease has claimed the lives of more females than males in every year since 1984, although women develop CAD Ϸ10 years later than men.…”

mentioning

confidence: 99%