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Menopausal Age & Cardiovascular Mortality
those incurred when intervention occurs after a diagnostic test reveals an abnormality prior to the patient becoming symptomatic. This was not considered in either their data or conclusions. Guidelines are often not structured adequately to resolve this defiCiency. The bottom line is to improve the quality and efficiency of the care we provide. The danger lies in managed care organizations assuming that studies such as this one represent signs of progress. Lower utilization and standardization alone do not necessarily represent better care.
Menopausal Age & Cardiovascular Mortality van der Schouw YT, van der GraafY, Steyerberg EW, Eijkemans M]C, Banga]D. Age ar menopause as a risk facrot for cardiovascular mortality. Lancet 1996;347:714-8.
Synopsis: For this study, 12,115 postmenopausal women, aged 5065, enrolled in a breast screening project were retrospectively reviewed to determine the effect ofage at menopause on cardiovascular mortality. In the sample, 824 women died of cardiovascular disease. The risk of cardiovascular mortality was higher for women with early menopause than for those with late menopause. For each year's delay in the onset of the menopause, cardiovascular mortality risk decreased by 2%. For example, a woman with menopause beginning at age 45 had a risk of cardiovascular disease .98 times that of a woman 44 years of age. At hysterectomy, age at menopause was not associated with cardiovascular risk. The effect following oophorectomy was somewhat stronger but not statistically significant. Smoking advances the age of natural menopause by 1.5 years. In this study, although a difference was
observed between smokers (1.007) and nonsmokers (.976), the authors believe that the effect of smoking on cardiovascular mortality overrides the effect of early menopause.
• • • Commentary: A woman has a 23% lifetime risk of developing ischemic heart disease. This is in contrast to 4% for breast cancer, 2.5% for osteoporotic fractures, and 2% for genital tract neoplasia. Cardiovascular disease becomes the leading cause of death in men by approximately age 35 and in women by approximately age 70. Because women on the average have a longer life expectancy than men by 7-8 years, ultimately more women than men (52% versus 46%) die of cardiovascular disease. Usual risk factors include obesity, plasma lipids, hypertension, diabetes mellitus, smoking, sedentary lifestyle, increased blood viscosity, and postmenopausal estrogen defiCiency. Women with premature menopause have an increased risk of developing cardiovascular disease compared with premenopausal women of the same age. Late menarche has also been related to an increased risk for cardiovascular disease. Estrogen replacement studies in postmenopausal women indicate a decreased risk of cardiovascular disease in women who receive estrogen when compared with controls. The results of this large study are consistent with expected results in menopausal women with estrogen deficiency.
Genetic Influences on Osteoarthritis Specror TD, Cicuttini F, Baker j, Loughlin ], Hart D. Genetic influences on osteoarthritis in women: a rwin study. BMJ 1996;312:
940-4.
Synopsis: In this study, 130 identical and 120 nonidentical female twins,
age 48-70, were compared for radiological changes at the interphalangeal and first carpometacarpal joints of the hands and the tibiofemoral joint and parellofernoral joint of the knee expressed as intraclass correlations. The intraclass correlation of radiographic osteophytes and narrowing at most sites, the presence of Heberden's nodes, and knee pain were higher in the identical twin group. Correlation was .64 in identical twins compared with .38 in nonidentical twins. The results show for the first time a clear genetic effect for radiographic osteoarthritis of the hands and knees in women with a genetic influence ranging from 39% to 65%, independent of known environmental or demographic confounders.
• • • Commentary: The etiology and pathogenesis of osteoarthritis in women remain largely unknown. Morbidity is well known to every clinician who cares for elderly women. The greatest source of disability is in the knee, which is estimated to result in pain and loss of function in 1015% of women over age 45. Previous studies in the literature have shown that osteoarthritis is more common in twins and first-degree relatives. The nature of the genetic effect is speculative and may en tail a structural defect, ie, collagen, alterations in cartilage, or bone metabolism. It is possible that the turnover or repair ofcartilage and bone is under genetic control with different thresholds and responses in genetically distinct individuals. Up to 65% of the variance can be explained by genetic factors. Specific alleles of the gene for type II procollagen on chromosome 12, the precursor of the major protein of cartilage, may be involved. Osteophytes and narrowing of joint space are the classic features of osteoarthritis. Both probably represent independent markers of the disease. Radiological evaluation is the method of choice in detecting these changes for an epidemiologic study. Pllll085-6862(961oo027-1
Menopausal Age & Cardiovascular Mortality van der Schouw YT, van der GraafY, Steyerberg EW, Eijkemans M]C, Banga]D. Age ar menopause as a risk facrot for cardiovascular mortality. Lancet 1996;347:714-8.
Synopsis: For this study, 12,115 postmenopausal women, aged 5065, enrolled in a breast screening project were retrospectively reviewed to determine the effect ofage at menopause on cardiovascular mortality. In the sample, 824 women died of cardiovascular disease. The risk of cardiovascular mortality was higher for women with early menopause than for those with late menopause. For each year's delay in the onset of the menopause, cardiovascular mortality risk decreased by 2%. For example, a woman with menopause beginning at age 45 had a risk of cardiovascular disease .98 times that of a woman 44 years of age. At hysterectomy, age at menopause was not associated with cardiovascular risk. The effect following oophorectomy was somewhat stronger but not statistically significant. Smoking advances the age of natural menopause by 1.5 years. In this study, although a difference was
observed between smokers (1.007) and nonsmokers (.976), the authors believe that the effect of smoking on cardiovascular mortality overrides the effect of early menopause.
• • • Commentary: A woman has a 23% lifetime risk of developing ischemic heart disease. This is in contrast to 4% for breast cancer, 2.5% for osteoporotic fractures, and 2% for genital tract neoplasia. Cardiovascular disease becomes the leading cause of death in men by approximately age 35 and in women by approximately age 70. Because women on the average have a longer life expectancy than men by 7-8 years, ultimately more women than men (52% versus 46%) die of cardiovascular disease. Usual risk factors include obesity, plasma lipids, hypertension, diabetes mellitus, smoking, sedentary lifestyle, increased blood viscosity, and postmenopausal estrogen defiCiency. Women with premature menopause have an increased risk of developing cardiovascular disease compared with premenopausal women of the same age. Late menarche has also been related to an increased risk for cardiovascular disease. Estrogen replacement studies in postmenopausal women indicate a decreased risk of cardiovascular disease in women who receive estrogen when compared with controls. The results of this large study are consistent with expected results in menopausal women with estrogen deficiency.
Genetic Influences on Osteoarthritis Specror TD, Cicuttini F, Baker j, Loughlin ], Hart D. Genetic influences on osteoarthritis in women: a rwin study. BMJ 1996;312:
940-4.
Synopsis: In this study, 130 identical and 120 nonidentical female twins,
age 48-70, were compared for radiological changes at the interphalangeal and first carpometacarpal joints of the hands and the tibiofemoral joint and parellofernoral joint of the knee expressed as intraclass correlations. The intraclass correlation of radiographic osteophytes and narrowing at most sites, the presence of Heberden's nodes, and knee pain were higher in the identical twin group. Correlation was .64 in identical twins compared with .38 in nonidentical twins. The results show for the first time a clear genetic effect for radiographic osteoarthritis of the hands and knees in women with a genetic influence ranging from 39% to 65%, independent of known environmental or demographic confounders.
• • • Commentary: The etiology and pathogenesis of osteoarthritis in women remain largely unknown. Morbidity is well known to every clinician who cares for elderly women. The greatest source of disability is in the knee, which is estimated to result in pain and loss of function in 1015% of women over age 45. Previous studies in the literature have shown that osteoarthritis is more common in twins and first-degree relatives. The nature of the genetic effect is speculative and may en tail a structural defect, ie, collagen, alterations in cartilage, or bone metabolism. It is possible that the turnover or repair ofcartilage and bone is under genetic control with different thresholds and responses in genetically distinct individuals. Up to 65% of the variance can be explained by genetic factors. Specific alleles of the gene for type II procollagen on chromosome 12, the precursor of the major protein of cartilage, may be involved. Osteophytes and narrowing of joint space are the classic features of osteoarthritis. Both probably represent independent markers of the disease. Radiological evaluation is the method of choice in detecting these changes for an epidemiologic study. Pllll085-6862(961oo027-1