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It's my pleasure to be with you. And I'm excited to talk about menopause and the heart. I have no conflicts of interest. Our learning objectives today will be to counsel on cardiovascular health risks associated with the menopause transition. And specifically to discuss changes in cardiovascular risk across the menopause transition and explain a personalized risk reduction strategy. The menopause transition is really an opportunity for cardiovascular disease prevention. We know women develop heart disease a decade later than men with a notable increase in midlife. The mean expectancy for a woman now is 81 years and women will live about half of their adult lives in menopause. The menopause transition is a period of accelerated cardiovascular disease risk. We know that this transition is characterized by dynamic changes in estradiol and follicle stimulating hormone levels. Not all women experience a uniform pattern of estradiol decline or follicle stimulating hormone rise over the menopause transition. But we know about 44% of midlife women have a steep early decline almost one year before their final menstrual period. Approximately 6000 w women enter menopause in the United States every day. That's more than 2 million women every year just in the US alone. This is the stages of reproductive aging workshop or the straw criteria. So I just wanna point your attention to the words menopause transition and perimenopause and red. So we can level set about what we're talking about here. So the menopause transition begins right after the late reproductive stage. And what is characterized by is when menstrual length starts to vary by seven days or more. So that means you could have a 21 day cycle, one month and a 35 day cycle the next month. That's, that means you've entered the menopause transition, the menopause transition ends when you have your final menstrual period. But here's the kicker. You don't know you're in menopause for a whole 12 months after that. So, perimenopause includes the menopause transition and the 1st 12 months of no menstrual cycles at that point when that's over, you know, you're post menopause. What does the evidence show for cardiovascular risk factors and menopause? I frequently have patients coming in, they're complaining they're saying they're gaining weight. I've never had issues with my BP and my cholesterol. Now everything's going south. Is this related to menopause? So let's talk about menopause characteristics related to cardiovascular disease risk. This is the Framingham study. Uh the relation bet the relationship between menopause and cardiovascular disease instance was examined in this Framingham cohort, which consisted of nearly 3000 women. Cardiovascular disease incidence was defined as the occurrence of coronary heart disease, stroke or congestive heart failure. You'll see here, there was a trend for a 2 to 6 fold higher incidence of disease in postmenopausal women compared to premenopausal women in the same age range. These data demonstrate that there's also an age associated increase in the incidence of cardiovascular disease for both premenopausal and postmenopausal women. In addition, these and other data indicate that the loss of estrogen in menopause is associated with an increased risk for heart disease. Above that seen for premenopausal women. This increase in cardiovascular disease risk is also seen in women who undergo a bilateral oophorectomy at a younger age, know if there was little to no association between bilateral salpingo oophorectomy and cardiovascular disease risk when the BSO occurred around the time of natural menopause. So that over 45 group. And importantly, you'll note that hysterectomy without BSO was not associated with increased cardiovascular disease risk. And that's noted in the Dark Navy bars here. Now switching to other signs and symptoms of menopause. It has been shown that vasomotor symptoms reported midlife are associated with adverse lipid profiles and greater incidence of hypertension. In this longitudinal cohort study of 3300 women. This is a Swan study. These mid were midlife women and they were followed up for over 20 years. Uh The investigators found that frequent or persistent menopausal vasomotor symptoms. So hot flashes and night sweats were associated with a 50% increased risk of future cardiovascular disease events and these associations were not explained by standard cardiovascular risk factors or by endogenous estradiol levels. This is important because almost 80% of women experience vasomotor symptoms during the menopause transition. So, again, increased, um vasomotor symptom frequency was associated with greater CBD risk and CBD mortality. So this showed that the same thing was found with persistent BMS. So frequent and persistent BMS were found to be associated um with cardiovascular disease, rest down the line. So, what are the clinical implications? Here, we know that vasomotor symptoms may represent a novel female specific cardiovascular disease risk factor, midlife and older women with frequent or persistent vasomotor symptoms warrant particular attention for cardiovascular disease, risk reduction and prevention. And it really does beg the question whether vasomotor symptoms are a manifestation of neurovascular dysfunction that we need to be aware of. Ok. So the summary here, we know an earlier age at natural menopause is associated with increased CBD risk. We know that bilateral salpingo oophorectomy during the premenopausal period is associated with increased cardiovascular disease risk. We know that hysterectomy regardless of ovarian status is pretty neutral in terms of risk. And then vasomotor symptoms are linked with increased cardiovascular disease, risk factors, CBD and endothelial dysfunction. Let's talk about the cardiometabolic changes during menopause and let's discuss whether it's ovarian aging. So menopause related or is it chronological aging just getting older? So, body composition and fat distribution, we know that weight weight gain, pinching an inch is a very common complaint at the time of menopause. It's actually one of the most bothersome uh issues for women during this time. And this is what brings women in, in tears m more than hot flashes is this weight gain in menopause. However, we know that is more about aging than ovarian aging. So we know men and women gain weight in midlife. This is most likely due to reduced energy expenditure and a lower basal metabolic rate. However, um we notice there's a shift from lean mass to fat mass, that's probably both ovarian aging as well as chronological aging. Whereas the bottom bullet, greater visceral adipose tissue in the abdomen related to me that is related to menopause, that fat gain, that persistent irritating fat gain in the midsection. That's a menopause phenomenon. Ok. This is the Swan study and it showed us that fat mass increases across the menopause transition, lean mass decreases. And if you look at that far, right panel, the Swan investigators looked at visceral adipose tissue longitudinally and they identified three distinct trajectories. So the change in vat so vat is visceral adipose tissue was relatively modest for women who were more than two years before their last menstrual period. So that slope there is not that great. This was followed by a significant increase in vat by 8% per year during the menopause transition. That's from two years before the final menstrual period to the final menstrual period and then that continues to increase after that, but it slows down to about 5% per year after the final menstrual period. So we see an accelerated rate of visceral fat accumulation during the menopause transition. So this is related to ovarian aging. All right, these data show that increases in abdominal fat v at um in perimenopause are associated with log increases in carotid intima media thickness. So, carotid disease, we don't see much of a change premenopause. We see this accelerated increase perimenopause and postmenopause. Um it continues but the curve is less steep. These models are just for age race, steady sight smoking. LDL cholesterol, systolic BP and BM I and we believe the shift is due to the loss of estrogen, which influences lipoprotein lipase activity. Lower estrogen is associated with decreased gluteofemoral lipoprotein lipase.