Heart disease probably isn’t the first thing that comes to mind when you think about the menopausal transition, but it may be one of the most important things to consider during this time. I’ve been taking a 6-week course on heart disease with a naturopath in order to get a different perspective, and, funny enough, everything I’ve been learning has been reinforced at The Menopause Society Conference I’ve just attended in San Diego.
Heart disease remains the leading cause of death in the United States, including among women, and cardiovascular disease accounts for roughly one in five female deaths. We spend a great deal of time discussing breast cancer prevention, which is important, but we rarely give heart disease the same attention during routine menopause care.
This topic is close to my heart (pun intended). My healthy, fit father had a triple bypass at age 72 and ended up dying from a stroke. I’ve had high cholesterol and been on treatment for years. We are living proof that you can feel healthy, exercise regularly, eat nutritious food, and maintain a comfortable weight, yet still have significant cardiovascular risk.
Lately I’ve been seeing new patients whose cholesterol levels appeared reassuring to their previous provider, only to discover that with additional testing, their lipids were in fact concerning. I’ve been checking and finding more people had elevated lipoprotein(a), a genetic risk factor that isn’t included in routine cholesterol testing, which puts a person at significantly higher risk for a cardiovascular event.
Your cholesterol can look perfectly reasonable while cardiovascular disease is quietly developing.
This becomes even more critical during midlife because menopause can accelerate changes in your blood vessels, cholesterol, and metabolism that have been developing for decades.
I want you to understand these changes so you can recognize your risks early and make informed decisions about protecting your health.
Your Heart Notices Menopause, Too
Estrogen influences much more than reproduction. It helps regulate blood vessel function, cholesterol metabolism, inflammation, and the way your body manages glucose and fat. During your reproductive years, estrogen generally supports healthy vascular function, partly by influencing nitric oxide, a molecule that helps your blood vessels relax and respond to changes in blood flow.
As estrogen levels decline during menopause, several cardiovascular changes can occur. Your LDL cholesterol and the number of cholesterol-carrying particles measured by ApoB may increase, your arteries may become less flexible, and you may be more likely to accumulate visceral fat around your abdominal organs. Insulin resistance can also become more common, and blood pressure often rises as you age. Aging, genetics, lifestyle, and hormonal shifts influence these changes, so we can’t attribute everything to the loss of estrogen.
One important theme in menopause research that I learned at the Menopause Society conference is that cardiovascular risk doesn’t suddenly appear when your ovarian reproductive function ends (aka “menopause”). Atherosclerosis, the accumulation of cholesterol-rich plaque within your artery walls, develops over many years. The menopause transition can accelerate some of the risk factors involved in this process, making midlife an especially important opportunity to evaluate what’s happening beneath the surface.
We need to approach menopause as a time to reassess your overall health, rather than focusing exclusively on whether you need hormone therapy. You may have had excellent cholesterol levels and blood pressure at 40, but that doesn’t mean those numbers will stay the same at 55 or 60. We can’t change our genetics or eliminate every cardiovascular risk, but we can often influence how quickly vascular disease develops and progresses. This may be why your family physician or internist may be better prepared to do this whole-person assessment than your gynecologist.
Cholesterol: Why the Standard Numbers Don’t Tell the Whole Story
Most of us are familiar with a standard cholesterol panel, which measures total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides. These measurements are useful, but they don’t always tell us everything we need to know about cardiovascular risk.
LDL is commonly called “bad cholesterol” because LDL particles transport cholesterol through your bloodstream and can contribute to plaque formation when they enter and become trapped within artery walls. HDL is often called “good cholesterol” because it helps transport cholesterol away from tissues. However, HDL is more complicated than we once believed. Although higher HDL levels are generally associated with lower cardiovascular risk, simply raising HDL cholesterol with medication hasn’t consistently reduced heart attacks or strokes.
Triglycerides provide additional information about your metabolic health. When triglycerides are elevated, particularly alongside low HDL, I start thinking about insulin resistance and the possibility that you have more cholesterol-carrying particles circulating in your blood.
The amount of cholesterol in your blood isn’t necessarily the same as the number of particles carrying it. You can have an LDL cholesterol level that appears acceptable while still having an elevated number of particles that can enter your artery walls and contribute to plaque formation. Many medical providers still haven’t recognized this.
This distinction becomes particularly important during and after menopause, when changes in insulin sensitivity, abdominal fat, and cholesterol metabolism can alter your cardiovascular risk. I now recommend additional testing rather than relying entirely on a standard cholesterol panel. The two additional tests I am now always ordering are ApoB and Lipoprotein(a).
ApoB: A Better Look at the Particles That Cause Plaque
Apolipoprotein B, usually called ApoB, is a protein found on the surface of the lipoprotein particles that can contribute to atherosclerosis, including LDL, certain triglyceride-rich remnants, and lipoprotein(a). It measures ALL of the harmful particles circulating in your bloodstream, not just one type.
Think of your LDL cholesterol as measuring how much cholesterol is being transported, while ApoB tells us approximately how many vehicles are carrying it. Sometimes those vehicles carry less cholesterol than expected, so you can have a relatively normal LDL cholesterol level but more particles traveling through your arteries.
This is particularly relevant if you have insulin resistance, elevated triglycerides, diabetes, or increased visceral fat. In these situations, LDL cholesterol and ApoB can be discordant, meaning they suggest different levels of cardiovascular risk.
ApoB can provide valuable information about atherosclerotic risk, particularly when LDL cholesterol is “borderline” (130-159) or even when it is told to be normal (100-129).
It becomes very important to know your arteries’ lifetime exposure to the particles that contribute to plaque formation, because that cumulative exposure helps determine your long-term cardiovascular health. Measuring this during perimenopause is critical since the number can increase as estrogen starts to decrease.
Lipoprotein(a): The Risk Factor You May Never Have Heard Of
Another test I believe deserves much more attention is lipoprotein(a), pronounced L-P-little-a and abbreviated Lp(a). Lp(a) is a cholesterol-carrying particle that resembles LDL but contains an additional protein called apolipoprotein(a). Elevated levels increase the risk of atherosclerotic cardiovascular disease and calcific aortic valve stenosis, a condition in which the valve controlling blood flow out of your heart becomes narrowed.
Lp(a) levels are determined primarily by genetics. Unlike LDL cholesterol, which can be influenced by nutrition, physical activity, and medications, Lp(a) generally remains relatively stable throughout adulthood, but may worsen after the menopausal transition.
Approximately one in five people has elevated Lp(a), depending on the population and threshold used, and most have no idea. It isn’t included in a standard cholesterol panel, so an elevated level may not show up on the standard panel. For this reason, this inherited risk can go undetected for decades.
Major cardiovascular guidelines increasingly support measuring Lp(a) at least once in adulthood. If initially tested before menopause, I recommend retesting after menopause. A level of 50 mg/dL (125 nmol/L) or higher is commonly considered a risk-enhancing threshold.
We don’t yet have an approved medication specifically indicated to lower Lp(a) for the purpose of preventing cardiovascular events, although several promising therapies are being studied. Some existing medications can modestly lower Lp(a), but our main strategy is to manage the other risks we can influence, particularly LDL cholesterol, blood pressure, diabetes, and smoking.
If your Lp(a) is elevated, your cardiovascular future has not already been determined. You might need to be more proactive about protecting your arteries and do the healthy things like quit nicotine and alcohol, eat more plants, and move your body every day.
Blood Pressure: The Risk Factor You May Not Feel
High blood pressure is one of the most important modifiable risk factors for heart disease, stroke, kidney disease, and cognitive decline. It’s also remarkably easy to overlook because most people with hypertension feel perfectly normal.
As your arteries become stiffer with age, your heart must pump against greater resistance. Over time, elevated blood pressure can damage blood vessel walls and contribute to cardiovascular disease. The prevalence of hypertension rises substantially during and after menopause, although this reflects a combination of aging, hormonal changes, genetics, and metabolic health.
I encourage you to know your actual blood pressure rather than relying on someone telling you it was fine. For most adults, a blood pressure consistently below 120/80 mmHg is considered optimal. Readings of 130/80 or higher may meet criteria for hypertension under U.S. guidelines, although treatment decisions depend on your overall cardiovascular risk and medical history.
Home blood pressure monitoring can be especially helpful because measurements taken in a medical office don’t always reflect what happens in daily life. If your blood pressure is elevated, addressing it is one of the most effective ways to reduce your risk of cardiovascular complications. And when we treat hypertension, we protect more than your heart. We’re also protecting your kidneys, eyes, and brain.
Coronary Calcium Scoring: Looking Inside Your Arteries
One of the most useful tools we have for clarifying cardiovascular risk in selected patients is a coronary artery calcium scan, commonly called a CAC scan.
This low-radiation CT scan measures calcified plaque in the coronary arteries, the blood vessels that supply oxygen-rich blood to your heart muscle. Unlike a cholesterol test, which helps estimate the likelihood of developing atherosclerosis, a CAC scan can show whether calcified coronary plaque is already present.
The result is reported as an Agatston score. A score of zero means no calcified coronary plaque was detected, which is generally reassuring, although it doesn’t exclude noncalcified plaque or guarantee that you won’t have a cardiovascular event. Scores between 1 and 99 indicate detectable calcium, while scores of 100 or greater suggest a more substantial plaque burden and often strengthen the case for cholesterol-lowering treatment. Scores of 300 or higher are generally associated with greater cardiovascular risk.
Your age and sex also influence how we interpret these results. A relatively small amount of coronary calcium at 45 may be more concerning than the same score at 75 because it suggests that atherosclerosis developed earlier in life. Women also tend to have more soft plaque, which does not show up on the CAC, so a score of 0 while having other concerning risk factors does not mean that there are no underlying changes happening
I find CAC scoring particularly useful when your estimated cardiovascular risk is uncertain or when we’re deciding whether medication would be beneficial. Sometimes the results reveal that someone with apparently acceptable cholesterol has already developed coronary atherosclerosis, which can substantially change our approach to prevention.
However, I don’t recommend CAC scans for everyone. They’re most useful when the results could change a treatment decision, and a score of zero shouldn’t automatically override important risk factors such as diabetes, smoking, a strong family history, elevated ApoB, or Lp(a).
One thing to note, particularly if you’re already taking cholesterol-lowering medication, is that even if coronary plaque is present, repeating calcium scans simply to see whether treatment is working is usually not helpful. Statins can stabilize plaque and may increase its calcification even while reducing the risk of heart attack and stroke.
That means your calcium score could increase during treatment without necessarily indicating that your cardiovascular health is getting worse. I interpret these results alongside your cholesterol, ApoB, blood pressure, metabolic health, family history, and other risk factors rather than relying on the scan alone.
Your Arteries Have a History
We often think of cardiovascular risk as something that becomes important in our 60s or 70s, but our arteries carry the cumulative effects of decades of exposure to cholesterol, blood pressure, glucose, smoking, inflammation, and other influences.
Atherosclerosis can begin early in adulthood and progress slowly without causing symptoms. The longer your arteries are exposed to elevated ApoB-containing particles and other risk factors, the more opportunity plaque has to develop. This is why prevention earlier in life can have such a powerful effect on long-term cardiovascular health.
If your LDL cholesterol has been elevated since your 30s, you may have accumulated decades of exposure that matter more than a cholesterol level that first becomes elevated at 65. Menopause is an important turning point, but it doesn’t erase your previous vascular history.
Know your family history! If a parent or sibling experienced a heart attack or stroke at a relatively young age, that may suggest inherited cardiovascular risk. My father ate a strict Mediterranean diet and exercised every day of his life, then had a stroke that ended up taking his life while exercising!
There are aspects of your reproductive history that can provide important clues, including preeclampsia, gestational hypertension, gestational diabetes, and premature menopause.
These experiences may have occurred decades ago, but they remain relevant to your cardiovascular health today. Unfortunately, routine cardiovascular risk assessments don’t always include them, even though they can help identify people who would benefit from closer monitoring and earlier prevention.
What About Menopausal Hormone Therapy?
Because estrogen influences blood vessel function and cholesterol metabolism, it’s understandable that you might wonder whether replacing estrogen can prevent heart disease.
The answer is more complicated than we once hoped, and this was hotly debated at the Menopause conference.
Menopausal hormone therapy can improve certain cardiovascular risk markers, and its effects may differ depending on when treatment begins, which hormones are used, and how they’re delivered. Observational studies and some analyses of clinical trials suggest that starting hormone therapy closer to menopause may have a more favorable cardiovascular profile than beginning treatment many years later.
However, improving cholesterol or other risk markers doesn’t necessarily mean that a treatment prevents heart attacks or strokes. Menopausal hormone therapy has not been established as a treatment for preventing cardiovascular disease, and I don’t prescribe estrogen specifically for that purpose.
If you’re experiencing bothersome menopausal symptoms and are an appropriate candidate for hormone therapy, treatment can be enormously helpful for improving your quality of life. But your provider should still assess your cardiovascular risk before making that decision. Your age, time since menopause, blood pressure, cholesterol, metabolic health, history of blood clots, and any evidence of established cardiovascular disease all influence the discussion.
The route of estrogen administration can also influence certain risks. For example, transdermal estrogen avoids first-pass metabolism through the liver and appears to carry a lower risk of venous blood clots than oral estrogen in observational studies. However, we shouldn’t assume that an estrogen patch prevents heart attacks or that all hormone formulations have the same cardiovascular effects.
If you already have coronary artery disease, a history of stroke, or certain other cardiovascular conditions, hormone therapy may carry additional risks and requires particularly careful evaluation.
I don’t want you to be frightened away from hormone therapy when it could significantly improve your symptoms, but I also don’t want you to believe that taking estrogen is necessary to protect your arteries. We need to understand what hormone therapy can do, what it cannot do, and where the research is still evolving.
What Can You Do to Protect Your Heart?
I don’t want this conversation to leave you feeling that your cardiovascular future is determined entirely by genetics or menopause. There is a great deal we can influence, and many of the things that protect your heart also support your metabolic health, brain health, and physical independence. And yes, I am going to repeat this over and over because our lifestyle plays a critical role in our longevity and vitality.
Regular physical activity improves blood pressure, insulin sensitivity, vascular function, and cardiovascular fitness. I encourage a combination of aerobic exercise and resistance training because each provides different benefits. Walking, cycling, swimming, dancing, and other activities that increase your heart rate help strengthen your cardiovascular system, while resistance training preserves the muscle that supports glucose regulation and healthy aging.
Nutrition also plays an important role. A Mediterranean-style eating pattern rich in vegetables, legumes, whole grains, nuts, olive oil, and fish has substantial evidence supporting cardiovascular health. Replacing some saturated fats with unsaturated fats and increasing soluble fiber can help lower LDL cholesterol. I don’t believe you need to follow a perfect diet, but I do want you to understand how your daily food choices influence your long-term health.
Sleep is important too, especially when menopause symptoms interfere with restorative rest. Untreated sleep apnea can contribute to hypertension and cardiovascular risk, even if you don’t fit the stereotypical image of someone with sleep apnea. Avoiding tobacco, limiting alcohol, managing diabetes, and treating high blood pressure are also important parts of prevention.
And sometimes lifestyle changes aren’t enough.
I prescribe cholesterol-lowering medications when appropriate because we have substantial evidence that reducing LDL cholesterol and ApoB-containing particles lowers the risk of cardiovascular events. Statins remain a cornerstone of treatment, and medications such as ezetimibe and PCSK9 inhibitors can provide additional LDL lowering when needed.
Taking medication doesn’t mean you’ve failed to live a healthy lifestyle. You can do everything you’re supposed to do and still have elevated cardiovascular risk because of your genetics, lifetime cholesterol exposure, or plaque that developed years ago. I openly admit that I take a high-dose statin and ezetimibe and have been for years. And I still think well and have no side effects from it. And contrary to social media, there is absolutely no proof that it causes breast cancer or dementia. But plaque in the small vessels in the brain does.
I want you to have access to effective prevention, which should always involve lifestyle changes, and you are not a failure if it also includes medication.
Your Heart Is Part of Your Future
Earlier in this series, we talked about bone health and preserving the strength that helps you stay active and independent. Last week, we explored metabolic health and why your weight tells us so little about what’s happening inside your body. Cardiovascular health connects these conversations because your blood vessels deliver oxygen and nutrients to every organ, including your brain, kidneys, muscles, and sexual organs.
When I think about healthy aging, I’m thinking about much more than preventing disease or extending life expectancy. I want you to have the body that takes you through your 60s, 70s, 80s, and 90s with grace. Your cardiovascular health supports all of those possibilities, and protecting it deserves the same attention we give to managing menopausal symptoms.
This week, I encourage you to look beyond being told that your cholesterol is normal. Ask for your actual LDL cholesterol and triglyceride levels, and get your ApoB or Lp(a) tested. Know your blood pressure and whether your family or reproductive history suggests that you need a more thorough cardiovascular assessment. If you’re in midlife, talk with your clinician about whether coronary calcium scoring or other testing would help guide your prevention decisions.
You deserve a thoughtful assessment of your cardiovascular health that goes beyond your weight, age, and a single cholesterol number.
I want you to have the opportunity to live a long life, but even more than that, I want you to have the health, strength, and freedom to enjoy the years ahead.