The authors ascertained cardiovascular events (myocardial infarction and angina pectoris) in 498 women with systemic lupus erythematosus seen at the University of Pittsburgh Medical Center from 1980 to 1993 (3,522 person-years). Subjects were stratified by age, and cardiovascular event incidence rates were determined. The authors compared these rates with cardiovascular event rates were determined. The authors compared these rates with cardiovascular event rates occurring over the same time period in 2,208 women of similar age participating in the Framingham Offspring Study (17,519 person-years). Age-specific rate ratios were computed to determine whether the cardiovascular events in the lupus cohort were greater than expected. The risk factors associated with cardiovascular events in women with lupus were determined. There were 33 first events (11 myocardial infarction, 10 angina pectoris, and 12 both angina pectoris and myocardial infarction) after the diagnosis of lupus: two thirds were under the age of 55 years at the time of event. Women with lupus in the 35- to 44-year age group were over 50 times more likely to have a myocardial infarction than were women of similar age in the Framingham Offspring Study (rate ratio = 52.43, 95% confidence interval 21.6-98.5). Older age at lupus diagnosis, longer lupus disease duration, longer duration of corticosteroid use, hypercholesterolemia, and postmenopausal status were more common in the women with lupus who had a cardiovascular event than in those who did not have an event. Premature cardiovascular disease is much more common in young premenopausal women with lupus than in a population sample. With the increased life expectancy of lupus patients due to improved therapy, cardiovascular disease has emerged as a significant threat to the health of these women. The impact of this problem has been underrecognized, with little focus placed on aggressive management of hypercholesterolemia and other possible risk factors.
The authors measured the relation between C-reactive protein, alpha 1 acid glycoprotein and albumin, an acute phase protein, and subsequent risk of myocardial infarction and coronary heart disease death in a nested case-control study among the Multiple Risk Factor Intervention Trial (MRFIT) participants. There were 98 myocardial infarction cases, 148 coronary heart disease deaths, and 491 controls. The cases and controls were followed for up to 17 years for deaths and 6-7 years for myocardial infarction cases and controls. There was a significant association between available distribution of C-reactive protein and subsequent coronary heart disease mortality. For smokers at baseline, the risk of coronary heart disease deaths in quartile 4 of C-reactive protein as compared with quartile 1 was 4.3 (95% confidence interval 1.74-10.8). The association persisted when adjusted for characteristics related to smoking and smoking cessation during the trial and to pulmonary function. There was no relation between alpha 1 acid glycoprotein and either myocardial infarction or coronary heart disease death. Albumin was inversely related to coronary heart disease death only for deaths that occurred between 7 and 13 years after baseline, consistent with previous MRFIT analyses. This is the first prospective study in "healthy but high risk individuals" to document the relation between C-reactive protein and coronary heart disease mortality.
Postmenopausal women are believed to have a higher risk of coronary artery disease than premenopausal women. In this study, we prospectively determined changes in coronary risk factors that were attributable to natural menopause in 541 healthy, initially premenopausal women 42 to 50 years of age. After approximately 2 1/2 years, 69 women had spontaneously stopped menstruating for at least 12 months, and 32 women had stopped natural menstruation and received hormone-replacement therapy for a period of at least 12 months. An equal number of age-matched premenopausal women in the study group served as controls. In women who had a natural menopause and did not receive hormone-replacement therapy, serum levels of high-density lipoprotein (HDL) cholesterol declined as compared with those of premenopausal controls (-0.09 vs. 0.00 mmol per liter; P = 0.01), and levels of low-density lipoprotein (LDL) cholesterol increased (+0.31 vs. +0.14 mmol per liter; P = 0.04). In menopausal women who received hormone-replacement therapy, HDL and LDL cholesterol levels did not change, but the levels of triglycerides (+0.42 vs. -0.04 mmol per liter; P less than 0.001), apolipoprotein A-I (+0.18 vs. +0.03 g per liter; P less than 0.01), and apolipoprotein A-II (+0.05 vs. -0.03 g per liter; P less than 0.05) increased as compared with premenopausal controls. Natural menopause did not affect blood pressure, plasma glucose or insulin levels, body weight, the total number of kilojoules consumed in the diet, or the total number of kilojoules expended in physical activity. These results suggest that a natural menopause has an unfavorable effect on lipid metabolism, which may contribute to an increase in the risk of coronary disease. Hormone-replacement therapy may prevent some of these changes.
The authors prospectively studied the effect of demographic, reproductive, stress-related, and health behavior factors measured at study entry on age of natural menopause in 185 healthy US women. At study entry, women were 42.5-47.5 years old and premenopausal. After a baseline examination (1983-1985), women were followed for 7-9 years, during which time they reported on a monthly basis their menstrual status and whether they were taking hormones. Menopausal age was defined as age at the last menstrual period prior to stopping menstruation for 12 months (and not taking hormones). Estimated median age at menopause was 51.5 years for the whole sample. Median age at menopause was earlier for women who reported irregular menstrual cycles at study entry (50.2 years), were African-American (49.3 years), were smokers (50.6 years), or were currently on a weight reduction diet (50.5 years). Psychosocial stress was predictive of an even earlier median age at menopause in African Americans (48.4 years) and in those with irregular cycles at baseline (49.4 years). Results suggest that premenopausal women in their forties who are experiencing irregular menstrual cycles, are smokers, are dieting, or are African-American are likely to reach menopause earlier than their contemporaries. African-American women may have a different "biological clock" than white women, especially when under stress, or they may experience more stress of longer duration.
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