Cardiac Health After Menopause | Recorded Live at The 2026 ACVS

In this insightful session from the 2026 Atlanta Cardiovascular Symposium, Dr. Pavani Kolakalapudi addresses a critical but often overlooked area of medicine: the unique cardiovascular risks women face during and after menopause.

As estrogen levels decline, women experience physiological changes that can significantly impact heart health—from shifts in lipid profiles to increased vascular stiffness. Dr. Kolakalapudi provides a deep dive into the latest 2026 clinical data, emphasizing that "heart health for women is not just a smaller version of heart health for men." This presentation is essential for clinicians and patients alike who are looking to navigate this life transition with a proactive, heart-first approach.

Transcript

SPEAKER_01 0:04

Welcome to put your heart into it. About common clinical scenarios so that we can better treat our patients. Podcasts on this account are made for educational purposes only and should not be used as a substitute for medical diagnoses or advice. If you have any clinical symptoms or medical questions, please consult a licensed healthcare provider.

SPEAKER_00 0:29

Thank you again for everybody for joining us on this Saturday morning. My name is Pav Nicola Galpadi, one of the cardiologists here, and I can't believe we're in the 15th year of this. So thank you for all of you and the community who's been there since day one. Appreciate it. So the title of my talk today is menopause transition. I call it a critical window because that's kind of how I want us to approach this lecture as it is a finite time-sensitive area where we can actually, the actions we take, the things that we measure biomarkers can change the cardiovascular trajectory for half the population. So I hope I'm gonna challenge you to think about cardiovascular or menopause transition not only as a reproductive milestone, but a cardiometabolic event. Alright, so I'll start with my patient. She is very unique. She is very young to have had established cornea atherosclerosis meeting in RCA, PCI tour RCA for unstable angina a few years ago. She is a mom of three kids. She's a teacher, she plays tennis, and tennis is actually what made her feel her shortness of bread symptoms seeking cardiac care. She's done well, you know, by all clinical means. Her LDL is great, she's on high potency statin therapy, she's doing great. Almost in passing, at the end of our visit, she says, Hey, I'm having more fatigue. I'm having, I can't sleep at night, I have some palpitations. Do you think I'm going through perimenopause? So that's the patient I want you to think about as I go through my lecture, because we will see more younger patients with astrophysic disease, so much so that the prevent ASCBD calculator starts at screening at age 30. So that's the patient I want you to think about, and hopefully by the end of the lecture, you'll feel more comfortable answering her question. So the objectives today I have is again challenging you to see menopause transition as a cardiometabolic event, not just a reproductive one, recognizing basomotor symptoms and association with coronary vascular disease, understanding differences, timing of hormone replacement therapy, as well as performing that risk assessment in our perimenopausal patients. So I'll use this as a the straw reproductive aging, and you can see here that towards the end of late perimenopause, you can see that symptoms of variable basomotor symptoms, risk factors can start towards the late perimenopause. So symptoms can start even three years before the final menstrual period in a woman, and sometimes those symptoms can last almost 10 years. But there is a true infliction point where you see that towards the end here, towards the end where you see the FSH increasing at the time of the final menstrual period, shifting that acute change in our hormone and what cardiometabolic implications that has for women. But it is a time-sensitive change that happens. And what does that change show us? That again, that decrease in estrogen, increase in FSH, that can also happen even before the final menstrual period changes that shift for cardiometabolic health. Estrogen is involved in many different regulations for us, and the decline of it can cause more ovarian aging. Increase in FSH, especially decreases your lean muscle mass, it increases your insulin sensitivity, it produces visceral fat all through lipogenesis in the liver. To some women can have fatty liver disease that shows up at this age, insulin resistance at this age, and also can increase that carotid intermedial thickness. All of these risk factors can include, can show up for metabolic disease. And this is and this is the Swan study, the study women's health across the nation. This is the longest longitudinal study that took women from 1996, ages 42 to 52, and kind of followed them over the decades. And so you can see here using that reproductive stage and also applying it to that final menstrual period, everything changes. Waist circumference goes high, HDL is lower, glucose is increased, your triglycerides are higher, and your blood pressure increases. Those are all risk factors for metabolic syndrome. And all of these are happening in that time period. So again, I want you to shift that thinking of menopause is just a reproductive change, it is a cardiometabolic risk factor. And it's showed through longitudinal studies over the decades that it's it's a it's a time-sensitive period, not just to discuss in an OBGYN office, but firmly belongs in conversation with your primary care doctor or your cardiologist. So that's why I want to say use that transition. Use that patient who's coming to you for lack of sleep or palpitations as a teachable moment for primary prevention. And again, challenge what heart disease is. Heart disease is not a disease of older men, gray-haired men, but it can look like all of us. Half population in the room. About 21 million women experience menopausal symptoms per year. So this is a big moment for us to kind of use that information, use that time period to have that primary prevention talk. So shifting to vasomotor symptoms, it's not just a discomfort issue. It's not just a hot flashes that'll go away, but understand why that is and what implication does that have for cornear artery disease. Vasomotor symptoms are described as typically hot flashes, palpitations, lack of sleep that can occur for severe symptoms, can be daily, six or more days over a two-week period. It's considered to be severe. This is the most common symptom that women can experience. But why is that? Why does that happen? It is a estrogen actually plays a role in the hypothalamus to regulate temperature. This is the same system that protects us when we have a fever, the same system that helps us understand what shivering is when we're cold. And that gets dysregulated when there's lack of estrogen, that shift in estrogen. That that pathway is dysregulated. So you're more sensitive to heat, you're more sensitive to cold, and that can increase sudden temperate increases in temperature, can increase inflammation and endothelial stress. And that is the perfect setup, unfortunately, for endothelial dysfunction. You have that inflammation, that heat increases your TNF alpha, increases your oxidative species, more inflammatory factors, and it decreases the ability for your blood vessel to make nitroglycerin and use nitroglycerin. That can eventually change structural changes, increase cardiointimum thickness, you have more deposition of collagens along the blood vessels, and you have increased sympathetic tone, which can also trigger autonomic instability, all leading to large artery stiffness, hypertension, and something that we always pay attention to as cardiologists, increased afterload, and onset of diastolic dysfunction. Almost all of our patients seem to have this, you know, a lot of that co-reports that we would impaired relaxation, diastolic dysfunction. We know it does also disproportionately affect women post-menopausal age. But all of these can be seen how it can just be from that increased heat inflammation triggering a cascade of events can eventually increase your risk of heart disease. And there's no other, I guess, pathology that kind of intersects both the menopause transition symptoms and couples that with coronary vascular disease and microvascular disease. Microvascular disease is described as a disease of the small blood vessels. And you can see here how the vessels are impaired by impaired vasodilation, vasoconstriction, myocardial remodeling, all of the things that we can see that happens in women with postmenopause and high vasomotor symptoms. So how does this patient look like to you in your clinic? Could be a postmenopausal woman coming to you for angrial chest pain. You know, I have chest, you want to exercise, you do a heart cat or a diagnostic angiogram, and they have no coronary artery disease. They say, hey, it looks fine, you're normal, go home. And they're back in your clinic, still having chest pain. How do you approach that? What's the next step to do? So we have coronary PET here at uh HVC, where we can again test the entire microvasculature to see how is their coronary flow. So they might have a normal stress test, completely normal stress test. When we use our PET CT scanner, you can see they have no coronary calcification on the image there. But you can see on the top right, their flow reserves are all low. And you can see LAD, circumflex, RCA global, everything is below two. That is considered to be microbascular disease. So you can more confidently tell your patient this is a disease of the small butt vessels, and they can usually respond better to amylopine or renexa. But we have different tools to help us diagnose and more quantify what that angina really is, what level of degree that vascular disease is using cardiac PET. So again, don't the let's not dismiss basomotor symptoms or just hot flashes, they'll go away. You need time, but really try to understand how often are you having them? You know, how much during the day are you having them? How is your blood pressure doing? So just really try to understand that that's just a tip of the iceberg, and the problem really exists deeper down into endothelial dysfunction, inflammation can lead to vascular remodeling. Briefly on the evolution of hormonal therapy, I think I'll just keep this non-controversial as possible and say that what I think the Women's Health Initiative did wrong probably was take older women who were not having any symptoms and gave synthetic estrogen for to see what the outcomes would be. And of course, we all know that increased their risk of stroke cardiovascular disease. And her study was done in women for secondary prevention. So there are actually women who already had established cornear artery disease and were given oral estrogen, again, showed to have increased risk of stroke and heart disease. More contemporary studies like elite and keeps are actually more appropriate for those women within 10 years of menopause, younger, without onset of atherastrotic disease, were shown to actually have it safe to take menopause therapy. And some studies also show there is reduced CIMT progression, that intomedial thickness progression, and transdermal in the KEEP study was even safer. And why is that? Because when you actually give it to a younger patient within 10 years of metopause symptoms onset, aged less than 60, their endothelium is still reactive. It can still, I mean, hasn't set in, the collagen hasn't set in, the increased intimate micness hasn't set in. So that blood vessel is more responsive to MHG or menopause hormone therapy. Whereas if you're already giving that two estrogen to somebody with a disordered endothelium, you're actually causing inflammation and leading to plaque instability. That's why, again, the timing hypothesis matters. Who you're giving it to matters. Younger patients, symptomatic patients without already established CAD. You know, the KEEP studies showed transdermal is safer than oral. Why? Transdermal or patch or a gel does not go through the liver. It passes the hepatic, the bypass, bypasses the liver, so it does not trigger those prothrombotic proteins in the liver. So that's why I think either our intermediate harvest patients that can safely take estrogen to control their vasomotor symptoms. Again, I want to make that point that hormone replacement therapy or menopause therapy is not given for cardiac benefit. It's really only given for vasomotor symptoms and other symptoms that the patient is having. But progesterone is also considered to be safe. Mycronized progesterone is metabolically neutral. And a brief dose, a brief talk on testosterone, given in low doses with your OGOIN, I think it can positively impact your body composition, insulin sensitivity. And briefly about what about my high-risk patients? You know, that my patient that already has established cardiovartery disease, what are her options? There are still plenty of other non-hormonal options that we can think about. Peroxetine, cetalopram, um, paxol, you can be given, but just you know, be mindful of their cardiovascular implications too. Some of these medicines can increase your QT prolongation, especially if given in higher doses. Uh, venlofaxine, desphenolfaxine, very effective for vasomotor symptoms, but increases your risk of hypertension and tachycardia. The newest one that neurokinin antagonist, phaseolinitant, I practice that one, does not have any cardiac implications, no QT prolongation, and seems to be very beneficial for treatment of vasomotor symptoms. And that is the same receptor that I showed you on the picture for the hypothalamus, where that works, that acts as that estrogen. Um, gabopentin, I think this is Dr. Bott's favorite medicine of all time, um, can uh increase your risk of having peripheral edema, fluid retention, increased risk of MI if used excessively over a long period of time. Uhonidine's been previously used, but we all we all know there's hypotension and dizziness and poorly tolerated in general. And oxybutin can also be used, but it can also cause sometimes tachycardia. So it's very important to understand that even if you choose non-hormonal therapy, really important to understand what their cardiovascular side effects could be as well. And so, how do I risk assess? I again I strongly believe that having that conversation about perimenopause and that shift in the reproduction has to be coupled with your primary prevention talk. And so, again, we use ASCBD prevent calculator to understand who is that low-risk patient that can safely take an oral estrogen and who should I avoid oral estrogen not triggering increased risk of clotting factors. So low-risk patients, um, recent menopause, normal weight, normal blood pressure, an ASCBD, or a prevent score now of less than three or five. Um, intermediate risk, anybody who has risk factors, they might still not have any corneal artery disease, but they certainly have diabetes or smoker, they're high hypertension, they might be safe if we use it for transdormal options. And high risk, again, congenital heart disease, somebody with a history of PE, um, you know, VTE, stroke, or ASCBD risk score of greater than 10%. But again, even the highest risk patient, they can still have topical estrogen, vaginal estrogen if they need to for urogenitary symptoms. So I don't want you to deny patients of what medicine they might need for their symptoms. So, you know, prevent ASCBD risk calculator, which one do I use? I think the menopause society just represents that you just gotta do it. It doesn't matter what calculator you use, whatever you're talking about to them, but you have to do the cardiovascular risk assessment at that time when you're talking about um menopause symptoms. Just do it. So to help um our patients and help our you know clinicians in the community, we've come up with this tool called IRIS. It stands for index of cardiovascular risk during transition. And this is available, will be available on our uh HVC website, but you can use the QR code. And this is just meant to open up that conversation. You know, somebody like Harsh Patel, I don't know where he went, but um, somebody like Dr. Ahmad, who is going to talk to that patient about a ablation and what what route to do, he should feel comfortable if someone's complaining to him about palpitations in that age group and say, hey, when was your last menstrual period? What can we do to identify your symptoms? So the calculator that we looked up has um ASCBD risk score, has some, I think still some places where you can enter lipoprotein A, calcium score if you have it, um, and how you know, and then what are your symptoms? What are your menopause symptoms? Most common ones are reflected on there, and also add to their female specific, like you know, history of pre-eclampsia, history of gestational diabetes, and it gives a nice little printable summary showing your risk as well as showing your your what your options are. So maybe a patient can use that to approach their physician, or you can use that at that moment of having that conversation. Let's look at your overall risk, let's look at this more holistically. So, again, in summary, the key takeaways are I hope I've helped you understand that when you're having a conversation about menopause, please also reframe that conversation to talk about primary prevention. Um, aggressively monitor lipids, screen for hypertension, diabetes, subclinical atherosclerosis where available, like a calcium score, and check again for lipoprotein A. Recognize, understand, those hot flashes, they're not just discomfort, they actually can signal a cardiometabolic risk or cardiovascular risk. And treating matters. The age of the patient matters, the route of treatment matters, and how long you give it for matters. So that's my study. Sorry, one other thing I want to um I forgot to mention that I'll ask everybody to you, but what is one of the best things you can do to decrease that endothelial dysfunction during menopause transition?

unknown 20:44

Dr.

SPEAKER_00 20:45

Ingalls, you can't answer. It's not a drug.

unknown 20:52

Exercise.

SPEAKER_00 20:53

Exercise, correct. I heard it exercise. Exercise, because of the sheer stress on the vessels, it actually increases the stimulus to make nitroglycerin. And oxalate helps increase your glutathione oxidase, which is actually increasing, it neutralizes your inflammatory markers. There's one thing you can also tell your patients you have to exercise to help counteract some of those endothelial dysfunction. That's my talk.