Cardiovascular Risk — What You Don't Know Can Kill You. Here Is the Honest Conversation.

YOUR HEALTH — Issue No. 15

The most important health topic for anyone over 50. Plain Medicine covers it plainly.

Every wellness exam I do, I ask the same question.

"Physically — do you have any concerns?"

If you are over 50, I already know what the answer should be. Whether it is or not is a different story.

The answer should be: "Am I doing everything I can to avoid heart disease?"

Not because it is the trendy thing to worry about. Because it is the most likely thing that will kill you. Cardiovascular disease kills more Americans than all cancers combined — more than one in four deaths every year. It does not discriminate by zip code, income, or how healthy you think you look. It builds quietly, over decades, inside arteries too small to see and too narrow to imagine, until the day it announces itself in the worst possible way.

The honest truth is that prevention in your 30s and 40s is ideal. But that is not the reality sitting across from me in the exam room. Most of the people I see are already in their 50s, 60s, and 70s — asking the right questions later than anyone would prefer. And that is okay. Because the data is clear: meaningful risk reduction is possible at any age. You are not out of options because you did not start sooner.

So what can you actually do? How do you know where you stand? How do you know if cardiovascular disease is already happening inside your body — silently, without symptoms — right now?

That is what this issue is about. Not fear. Not guilt about the past. Just the most important health conversation you should be having — and the information you need to have it honestly.

Your cholesterol number is not your risk number

Most people who have had lab work done know their cholesterol number. What most people don't know is what it actually means for their cardiovascular risk — because a cholesterol number alone tells an incomplete story.

A 65-year-old with an LDL of 130 who also has diabetes, hypertension, and a 30-year smoking history carries a fundamentally different cardiovascular risk than a 45-year-old with an LDL of 160 and no other risk factors. Their cholesterol numbers are similar. Their risk profiles are not.

The number that matters is your 10-year ASCVD risk — the estimated probability that you will have a heart attack or stroke in the next 10 years, based on the full picture of who you are and what your body is dealing with. That number is calculated using a validated clinical equation, and most patients have never seen it.

The risk factors — what goes into the equation

Traditional risk factors — the ones we've known for decades:

Age and biological sex are the two most powerful predictors of cardiovascular risk. Risk increases with age, and men generally carry higher risk earlier in life than women — though women's risk rises significantly after menopause.

LDL cholesterol contributes to plaque formation inside artery walls. HDL cholesterol helps remove cholesterol from circulation — though it is worth noting that HDL function and quality matter as much as the number itself. A high HDL does not automatically confer protection if that cholesterol is not functioning effectively.

Blood pressure is one of the most modifiable risk factors in cardiovascular disease. Every 10 mmHg reduction in systolic blood pressure is associated with meaningful reductions in cardiovascular events. One of the most common things I hear from patients is that their blood pressure "just runs high." The honest clinical reframe: it is not well controlled. Chronically elevated blood pressure causes ongoing vascular injury regardless of how long it has been present — and that injury accumulates.

Diabetes doubles cardiovascular risk. The combination of insulin resistance, elevated blood sugar, and the downstream effects on blood vessel walls accelerates atherosclerosis in ways that multiply risk beyond any single factor.

Smoking is one of the most powerful cardiovascular risk factors known. If you currently smoke — this is the conversation your provider most needs to have with you.

Emerging risk factors — the ones your provider may not have mentioned:

Family history is not just biographical detail. A first-degree relative — parent or sibling — who had a heart attack or stroke before age 55 in men or 65 in women meaningfully elevates your risk beyond what the traditional equation captures. This information should be part of every cardiovascular risk conversation.

Lipoprotein(a) — sometimes written as Lp(a) — is a genetic variant of LDL cholesterol that standard lipid panels don't measure. Elevated Lp(a) is present in approximately 20% of the population and is an independent cardiovascular risk factor. Most patients have never had it tested. If you have a strong family history of premature cardiovascular disease despite otherwise normal cholesterol, Lp(a) is worth asking about.

High-sensitivity CRP — hsCRP — is a blood marker of systemic inflammation. It is distinct from the standard CRP test that is often ordered in general clinical settings. The high-sensitivity version detects lower levels of inflammation relevant to cardiovascular risk assessment — and elevated hsCRP can identify patients at higher risk than their standard risk factors would suggest. It is a simple, inexpensive blood test worth discussing with your provider if you are in the intermediate risk category.

The coronary artery calcium score — CAC — is a low-radiation CT scan that detects and quantifies calcium deposits in the coronary arteries. An important clinical nuance: the CAC score measures calcified — or hardened — plaque only. It does not detect soft, non-calcified plaque, which is actually the more vulnerable type and more likely to rupture. Calcified plaque reflects the cumulative burden of long-term atherosclerosis. A meaningful calcium score reasonably suggests that where there is hard plaque, soft plaque has likely been part of that process as well. A score of zero is highly reassuring, though it does not completely rule out soft plaque. A non-zero score confirms atherosclerosis is present and changes the clinical conversation significantly.

The arteries your life depends on

Most people have a general sense that heart attacks involve blocked arteries. What most people don't appreciate is how small those arteries actually are.

The coronary arteries — the vessels that supply the heart muscle itself with blood — range from approximately 4mm in diameter at their widest point to less than 2mm in their distal segments. To put that in perspective: the width of a standard pencil eraser. Some branches are narrower than a grain of rice.

These are the arteries that plaque spends decades quietly building inside. They are the arteries that, when a plaque ruptures and a clot forms, can close off in minutes — cutting off blood supply to the heart muscle and triggering a heart attack.

The margin for error is extraordinarily small. That is why the conversation about cardiovascular risk is not optional, and why waiting for symptoms is not a strategy.

Inflammation — the driver nobody talks about

Cholesterol gets most of the attention in cardiovascular disease. Inflammation deserves more of it.

The inner lining of every blood vessel in the body is a single layer of cells called the endothelium. When the endothelium is healthy, it produces nitric oxide — a molecule that keeps vessel walls relaxed, prevents clotting, and blocks inflammatory cells from taking hold. When it is damaged — by high LDL, high blood pressure, high blood sugar, smoking, or chronic inflammation — that protective function breaks down. LDL particles begin to infiltrate beneath the vessel lining. Inflammatory cells follow. Plaque begins to form.

This process — endothelial dysfunction — is now recognized as the earliest detectable step in atherosclerosis, often preceding visible plaque by years or decades.

What damages the endothelium goes beyond the traditional risk factors. Systemic inflammation from any source — chronic stress, poor sleep, autoimmune conditions, metabolic dysfunction — accelerates the process. And one source of inflammation that consistently surprises patients: oral health.

Periodontal disease — chronic gum inflammation — is associated with increased cardiovascular risk through multiple mechanisms. Oral bacteria can enter the bloodstream and trigger systemic inflammatory responses. The connection between dental health and heart health is not coincidental. It is biological. It is worth mentioning to your provider — and worth taking seriously at your next dental visit.

Ancient civilizations had cardiovascular disease

There are readers right now thinking: "If people would just eat better and stay active, we wouldn't have this problem."

That is not entirely wrong. But it is not the whole story either.

I remember reading years ago about CT scans performed on ancient mummies — and finding atherosclerosis. That finding has stayed with me ever since, because it changes the conversation fundamentally.

In 2013, a landmark study published in The Lancet used CT scanning to examine 137 mummies spanning more than 4,000 years of human history — ancient Egyptians, ancient Peruvians, the Ancestral Puebloans of the American Southwest, and the Unangan people of the Aleutian Islands. These were populations separated by thousands of miles and thousands of years, with dramatically different diets and lifestyles.

Probable or definite atherosclerosis was present in 34% of mummies across all four populations.

The researchers concluded that atherosclerosis appears to be an inherent component of human aging — not a disease created by modern diet and lifestyle alone. These were hunter-gatherers, subsistence farmers, and ancient urban populations who had never seen a drive-through.

This does not mean that diet doesn't matter. It does — significantly. But it means that cardiovascular disease is not purely a lifestyle problem with a simple lifestyle solution. It is a complex biological process shaped by genetics, aging, inflammation, and the choices we make — but not by any one of those factors alone.

The honest clinical message: you cannot eat your way out of cardiovascular risk entirely. But you can move the needle meaningfully — and knowing your risk number is the first step.

Screening — who should get what and when

If you have established risk factors — elevated LDL, high blood pressure, diabetes, smoking history, or family history of premature cardiovascular disease:

A standard lipid panel and complete metabolic panel (which gives your provider an overview of blood sugar levels and kidney function, both of which factor into cardiovascular risk) are the baseline. If you don't already know your ASCVD risk — ask about it at your next visit. Your provider can calculate it in minutes, and it is a conversation worth having.

Depending on your risk profile, additional testing may be appropriate — hsCRP, Lp(a), or a coronary artery calcium score to refine the picture beyond what the standard equation captures.

If you don't have obvious risk factors but want to know where you stand:

This is one of the most important conversations in preventive medicine — and one of the least common. The absence of obvious risk factors does not guarantee low risk. Age alone is a significant risk factor, and family history can elevate risk well beyond what traditional markers suggest.

A baseline lipid panel is a reasonable starting point at any age over 40. For patients in the 40-75 range with no obvious risk factors who want a more complete picture — a coronary artery calcium score is the single most useful test available. A score of zero in a patient with intermediate risk factors substantially reduces the likelihood of a near-term cardiovascular event. A non-zero score, even in a seemingly low-risk patient, changes the clinical conversation.

Know your number

Plain Medicine built a free 10-year cardiovascular risk calculator using the 2023 AHA PREVENT equations — the current clinical standard, replacing the older Pooled Cohort Equations that have been in use since 2013.

It takes approximately two minutes. It requires your most recent cholesterol numbers, blood pressure, and a few clinical details. It produces your 10-year ASCVD risk with a Plain Medicine explanation of what your result means and what to do with it.

No login required. Free.

Calculate your risk at tools.plainmedicine.health

If you don't have your numbers — request a lipid panel and a complete metabolic panel at your next visit. Then come back.

Something worth saying plainly:

In my practice I go through a simple checklist with patients. Blood pressure at goal — check. Cholesterol at goal — check. Non-smoker — check. No diabetes — check. No significant family history — check.

When all of those boxes are checked, the conversation shifts to maintenance. When one or more are not — that box is where we start.

Cardiovascular disease does not announce itself. It does not send warning signs for most of the decades it spends building inside your arteries. The first symptom for a meaningful percentage of people with undetected cardiovascular disease is a heart attack.

You cannot feel your LDL. You cannot feel your blood pressure unless it is very high. You cannot feel plaque forming in a 3mm artery.

What you can do is know your number. Have the conversation. Control what you can control.

That is all this is — and it is enough to make a difference.

The Member deep-dive this week goes further — endothelial dysfunction and the cellular mechanism behind atherosclerosis, the inflammation connection in depth including the colchicine data, and a full breakdown of every medication class with proven cardiovascular outcomes benefit beyond statins.

Next week: Sleep — the cardiovascular risk factor hiding in plain sight.

Plain Medicine is published for educational purposes only and does not constitute medical advice or establish a patient-provider relationship. Always consult your healthcare provider before making medical decisions.

— Kyle