Atheroma

Based on Wikipedia: Atheroma

Here's a troubling statistic: for about sixty-five percent of men and forty-seven percent of women, the first symptom of cardiovascular disease is either a heart attack or sudden death. Not chest pain. Not shortness of breath. Not a warning sign that sends them to a doctor. The first indication that something is wrong is a catastrophic event—or the end of their life.

How can this be? How can something so deadly give so little warning?

The answer lies in a quiet accumulation happening inside your arteries right now. It's called atheroma, and understanding it might be one of the most important things you can do for your health.

The Silent Buildup

An atheroma is essentially a pimple inside your artery wall. It starts when certain white blood cells—specifically a type called macrophages—begin accumulating in the innermost layer of an artery. These cells are doing what they're supposed to do: cleaning up debris, in this case oxidized cholesterol that has seeped into the artery wall. But like a cleanup crew that gets overwhelmed by the mess, these macrophages gorge themselves on so much fatty material that they transform into something pathologists poetically call "foam cells."

When foam cells die, they spill their contents. This attracts more macrophages, which eat more cholesterol, become more foam cells, and die in turn. Over years and decades, this cycle builds a growing mass of cellular debris, fats, calcium, and fibrous tissue inside the artery wall.

Notice something important here: the buildup is happening inside the wall, not blocking the opening where blood flows. This distinction matters enormously.

The Artery's Clever Disguise

Your arteries are not passive tubes. They're living, dynamic structures that respond to what's happening inside them. When an atheroma begins growing within an artery wall, the muscular middle layer of the artery—called the media—stretches outward to accommodate it. It's like a garden hose that expands slightly to make room for a bulge in its wall.

This process, called remodeling, is both a blessing and a curse.

The blessing: the artery maintains its internal diameter. Blood keeps flowing normally. You feel fine.

The curse: because you feel fine, you have no idea anything is wrong. The atheroma can grow until it occupies half the artery wall's cross-section before the opening where blood flows starts to narrow at all.

This is why traditional diagnostic methods fail so spectacularly. Stress tests detect problems with blood flow. Angiograms—those images where dye is injected to visualize arteries—only show the channel where blood flows, not the walls containing it. An artery could have massive atheroma buildup, but as long as remodeling keeps pace, these tests show nothing wrong.

It's like inspecting a house by only looking through the windows. You might think everything is fine, completely unaware that termites have hollowed out the walls.

When Things Go Wrong

So if atheroma can grow quietly for decades without blocking blood flow, what actually causes heart attacks?

The answer is rupture.

Each atheroma is separated from the bloodstream by a thin fibrous cap, like the skin over a blister. In some plaques—doctors call them "vulnerable plaques"—this cap becomes dangerously thin. When it tears, the contents of the atheroma spill into the bloodstream.

What happens next occurs in fractions of a second. Your blood encounters what it perceives as a wound and foreign material. Platelets rush to the site. Clotting factors activate. A blood clot forms—not to harm you, but to heal what the body interprets as an injury.

But this clot, combined with the debris showering downstream, can suddenly block blood flow. If this happens in a coronary artery feeding your heart muscle, you have a heart attack. In an artery feeding your brain, a stroke. The debris particles larger than five micrometers—five thousandths of a millimeter—are too big to pass through capillaries, so they lodge wherever they end up, blocking the tiny vessels that deliver oxygen to tissue.

Here's the truly frightening part: a significant proportion of these catastrophic events occur at locations where the artery wasn't even that narrowed. The blockage doesn't need to be large. It just needs to rupture.

Why Arteries, Not Veins?

If you've ever wondered why we worry about clogged arteries but not clogged veins, there's a simple answer: pressure.

Arteries carry blood away from your heart under high pressure—that's why when you cut an artery, blood spurts rather than oozes. This constant pulsing pressure creates mechanical stress on artery walls. Veins, carrying blood back to the heart under low pressure, don't experience this same stress and don't develop atheroma.

There's elegant proof of this in bypass surgery. When surgeons take a vein from your leg and graft it in to bypass a blocked coronary artery, that vein is now subject to arterial pressure for the first time. And guess what? It develops atheroma faster than a native artery would. The same tissue that remained healthy as a low-pressure vein begins accumulating plaque once it experiences arterial forces.

The reverse is also true. In laboratory experiments with rabbits, when arteries are grafted to function as veins—experiencing low pressure instead of high—they don't develop atheroma at all.

The Aneurysm Alternative

Sometimes remodeling goes too far. Instead of just expanding enough to accommodate the atheroma, the artery keeps stretching until it forms an aneurysm—a dangerous bulge in the vessel wall.

Aneurysms are most common in the abdominal aorta, the large artery running through your midsection. The aorta is about the diameter of a garden hose in a healthy person. When an aneurysm develops, it can balloon to two or three times normal size.

The problem is that bigger isn't stronger. As the wall stretches, it thins. The main structural proteins—collagen and elastin—that give artery walls their strength become spread thin, like pizza dough stretched too far. Eventually, the wall may become so weak that the normal pressure of your pulse is enough to cause it to fail.

When an aortic aneurysm ruptures, the result is catastrophic bleeding. Many people don't survive long enough to reach a hospital.

A Disease That Begins in Youth

Autopsy studies have revealed something that might surprise you: fatty streaks—the earliest precursors to atheroma—can be found in children and teenagers. Soldiers killed in the Korean and Vietnam wars, often in their late teens and twenties, frequently showed early atherosclerosis upon autopsy.

This isn't a disease of old age. It's a disease that begins in youth and progresses silently for decades. By the time people reach their thirties and forties, the process of narrowing—if remodeling fails to keep up—becomes increasingly common.

The medical implications are profound. By the time someone has symptoms, they may have had atheroma building for thirty or forty years. Prevention and early detection aren't just nice ideas—they're essential if we want to catch this process before it becomes deadly.

The Detection Problem

This is where medicine has struggled for over a century.

The coronary arteries feeding your heart are particularly difficult to monitor. They're small—starting at about five millimeters in diameter and tapering down to microscopic branches. They're buried deep in your chest. And they never stop moving, contracting with every heartbeat.

Angiography, developed in the 1960s, became the standard way to look for arterial problems. But remember: angiograms only show the channel where blood flows. They reveal severe narrowings that have already occurred, not the vulnerable plaques quietly building in the walls. Some experienced cardiologists have learned to spot a halo of calcification around arteries in older patients, but this represents very advanced disease.

Stress tests have similar limitations. They're designed to detect reduced blood flow, which means they typically only catch narrowings greater than about seventy-five percent—by which point the disease is far advanced. Some nuclear stress tests can detect narrowings of fifty percent, but that still means missing all the dangerous plaques that haven't yet restricted flow.

Newer technologies are changing this picture. Intravascular ultrasound can image the artery wall directly, showing atheroma that angiography misses entirely. Carotid intima-media thickness scans—measuring the thickness of artery walls in the neck using standard ultrasound—have been endorsed by the American Heart Association as perhaps the most useful method for identifying atherosclerosis. CT scans can detect calcification within plaques, though the plaques need to be fairly advanced for the calcium deposits to show up clearly.

Paradoxically, research suggests that smaller, spotty plaques may actually be more dangerous than large, heavily calcified ones. The calcified plaques are older, more stable, less likely to rupture. It's the younger, softer plaques—the ones harder to detect—that pose the greatest risk.

The Classification System

Pathologists have developed a classification system for atheroma that traces the progression from earliest beginnings to dangerous late stages. It runs from Type I through Type VIII, telling the story of a disease in slow motion.

Type I is the beginning: isolated foam cells scattered in the artery wall. Type II shows multiple layers of these cells accumulating. Type III represents the intermediate stage, a "preatheroma" where a true lesion is beginning to form.

Type IV is the true atheroma—a developed plaque with a lipid core. Type V adds a fibrous cap over this core, creating what's called a fibroatheroma. Type VI is where things get dangerous: a plaque that has fissured, ulcerated, bled into itself, or developed clots.

Types VII and VIII represent different endpoints. Type VII plaques are heavily calcified—stable but indicative of advanced disease. Type VIII plaques are predominantly fibrous, with less of the dangerous lipid core that characterizes vulnerable plaques.

What Can Be Done?

The good news is that atheroma progression can be slowed, stopped, and in some cases even reversed. The approaches fall into two broad categories: lifestyle changes and medical interventions.

Diet matters significantly. Plant-based foods—fruits, vegetables, nuts, beans, and whole grains—have consistently shown benefits. Omega-3 fatty acids, found in fish and certain plant oils like flaxseed, appear to help. Reducing abdominal fat, which is metabolically active tissue that promotes inflammation, makes a difference.

Exercise helps, particularly aerobic activity. Maintaining normal blood pressure and blood sugar levels reduces the stress on artery walls. Even low-dose aspirin has shown benefits, likely by reducing the clotting response that makes plaque ruptures so dangerous.

Statins—drugs that inhibit cholesterol synthesis—have become a cornerstone of medical prevention. By reducing the amount of cholesterol available to oxidize and accumulate in artery walls, they slow or stop atheroma progression.

Some research has explored more novel approaches. Scientists found that a compound called 2-hydroxypropyl-β-cyclodextrin could actually dissolve cholesterol out of plaques in mice. Unfortunately, later studies concluded this approach didn't effectively cause atherosclerosis regression in more realistic conditions—a reminder that the journey from laboratory promise to clinical reality is long and uncertain.

When atheroma becomes severe enough to threaten blood flow or life, physical intervention becomes necessary. Coronary artery bypass grafting—taking a vessel from elsewhere in the body and using it to route blood around a blockage—has been performed since the 1960s. Angioplasty, often with stents to hold arteries open, offers a less invasive alternative. Carotid endarterectomy involves actually cutting open a blocked artery in the neck and scraping out the plaque.

These interventions can be lifesaving. But they come with important caveats. Bypass surgery carries a one to four percent mortality rate; angioplasty, one to one and a half percent. More sobering: clinical trials have shown these procedures have at best minimal effect on overall survival. They treat the consequences of atheroma without addressing the underlying disease process.

Perhaps most importantly, both bypass and angioplasty are typically performed after someone has already become symptomatic—often already partially disabled. And neither procedure prevents future heart attacks. The disease process continues in other arteries, in other plaques.

A Shifting Paradigm

For decades, cardiology focused on finding and fixing blockages—the plumbing model of heart disease. Find the clogged pipe, open it up or route around it, problem solved.

But this model doesn't match what we now understand about how heart attacks actually happen. Most don't result from gradually worsening blockages finally closing off completely. They result from sudden ruptures of plaques that might not have even been causing significant flow restriction.

This realization is driving a fundamental shift in how cardiologists think about cardiovascular disease. The focus is moving from "blockages" to "atheroma"—from the dramatic narrowings visible on angiograms to the silent accumulations throughout the arterial system. From fixing acute problems to preventing them from developing.

The implications extend to inflammation, which plays a crucial role in atheroma formation and plaque instability. Immune cells drive the process from the very beginning. Inflammatory signals determine whether a plaque remains stable or becomes vulnerable to rupture. Understanding and addressing this inflammatory component may prove as important as managing cholesterol.

Living with Silent Disease

The most unsettling aspect of atheroma is its invisibility. You almost certainly have some degree of atherosclerotic change in your arteries right now. If you're over thirty, the process has likely been underway for at least a decade, possibly two or three. Yet you probably feel fine. Your stress test would probably be normal. Your doctor has probably never mentioned it.

This isn't medical failure—it's the nature of the disease. Atheroma is silent by design, hidden by the artery's own compensatory mechanisms. The challenge for modern medicine is detecting and managing a condition that reveals itself only through catastrophe.

The good news is that the factors driving atheroma progression are largely modifiable. Diet, exercise, blood pressure, blood sugar, cholesterol—these aren't just numbers on a lab report. They're the daily inputs that determine whether the plaques in your arteries grow slowly or quickly, remain stable or become dangerous.

Every meal, every walk, every night's sleep is a vote for one trajectory or another. The atheroma are there. What happens next is partly up to you.