Atherosclerosis: The Inflammatory Process We're Treating as Plumbing

Why it's time to move beyond the clogged drain metaphor 🚧

Jul 01, 2025

ICYMI 👉

💊 No live podcast for the next two weeks, but join me again on Tues 7/15 at 5 pm ET for our regularly scheduled live conversation!

Tom walked into my office shortly, worry etched onto his face. He’d recently been told he was at a high risk for a cardiac event and likely needed a stent for an 80% blockage in his LAD artery. As we talked, he shared how his cardiologist had described this blockage: as a "clogged drain" that needed to be cleared before it caused a heart attack.

This “Roto-Rooter” analogy made perfect sense to Tom. As an engineer, he understood pipes and blockages. The images his cardiologist had shared with him even looked like narrowed pipes with buildup along the walls. The plumbing metaphor dominates how we talk about heart disease because it feels logical and actionable. Pipes get clogged with buildup over time. You clear the blockage with tools like angioplasty and stents, or you bypass the problem with surgery. You prevent future clogs by reducing what goes into the system—less cholesterol, less fat.

By this logic, you could think that most heart attacks happen when blockages reach a critical threshold—maybe 80% or 90%—and when blood flow becomes insufficient. But here's what doesn't make sense: most heart attacks actually occur in arteries with less than 50% narrowing. Meanwhile, some people live for years with severe blockages and never experience cardiac events. These contradictions start to make sense when you realize the metaphor is missing something crucial.

It turns out that the plumbing model, while convenient for explanation, doesn't capture the whole story. At its core, atherosclerosis isn’t just a plumbing problem, but an inflammatory disease process. This distinction can help reframe how we approach cardiovascular health.

human organ toy — Photo by Robina Weermeijer on Unsplash

What Atherosclerosis Actually Is

Atherosclerosis begins not with gradual accumulation but with injury—microscopic damage to the inner lining of arteries caused by factors like high blood pressure, cigarette toxins, elevated blood sugar, or oxidative stress. This injury triggers the same inflammatory response your body uses to heal a cut on your finger, except it occurs inside your blood vessels.

Your immune system rushes to the scene, sending white blood cells to clean up and repair the damage. But in the complex environment of the arterial wall, this well-intentioned immune response can go awry. White blood cells meant to clear away oxidized cholesterol particles become overwhelmed and transform into foam cells—essentially immune cells that have gorged themselves on cholesterol and can no longer escape the arterial wall.

As foam cells accumulate and die, they release inflammatory chemicals that attract more immune cells, creating a vicious cycle. The "plaque" that forms isn't simply cholesterol that has settled out of the bloodstream—it's the product of an ongoing inflammatory battle between your immune system and perceived threats within the arterial wall.

This inflammatory process creates two types of plaques with vastly different behaviors. Stable plaques have thick, fibrous caps that can grow large and cause significant narrowing but rarely rupture. Unstable plaques may cause minimal narrowing but have thin, inflamed caps that can suddenly tear open, exposing the inflammatory contents to flowing blood and triggering massive clots.

Why the Distinction Matters

So what does this inflammatory view of atherosclerosis actually mean for you and your heart health?

The vulnerability paradox: A person with a 90% blockage in their coronary artery may be at lower immediate risk than someone with a 30% blockage—if the severe narrowing is from a stable, heavily calcified plaque while the mild narrowing represents an inflamed, unstable lesion ready to rupture.1234

This explains why coronary artery calcium (CAC) scoring has become such a valuable tool. Unlike stress tests that focus on detecting severe narrowing, CAC scans detect the actual plaque burden in your arteries—the end result of years of inflammatory activity. A person with pristine cholesterol numbers but a high calcium score has evidence of significant atherosclerotic disease, while someone with elevated cholesterol but a zero calcium score may have much lower near-term risk.

Thinking beyond basic cholesterol levels: Traditional thinking suggests that lowering cholesterol will prevent "buildup" and reduce heart attack risk. While cholesterol management remains vitally important, it is not sufficient. Focusing on cholesterol levels alone misses the crucial role of inflammation in determining which plaques become dangerous.

Some people have genetically elevated lipoprotein(a), or Lp(a)—a cholesterol-carrying protein that promotes arterial inflammation through pathways that standard cholesterol tests don't measure. Unlike LDL cholesterol, Lp(a) levels can't be modified through diet, exercise, or most medications. For these patients, the inflammatory model becomes essential because traditional "lower your cholesterol" advice simply doesn't address their primary risk factor.

Statin medications, for example, work not just by lowering cholesterol but by powerfully reducing arterial inflammation. This anti-inflammatory effect explains why statins prevent heart attacks even in people with normal cholesterol levels but elevated inflammatory markers.

Reading the Inflammatory Signals

If atherosclerosis is fundamentally inflammatory, then inflammatory markers should provide valuable information about cardiovascular risk—and they do.

High-sensitivity C-reactive protein (hs-CRP) measures systemic inflammation and can help predict heart attack risk independently of cholesterol levels. Elevated CRP levels can identify people at high cardiovascular risk even when their cholesterol numbers look reassuring.

But inflammatory markers require careful interpretation. My patient Jennifer came to me panicked after an urgent care visit for bronchitis revealed her CRP was elevated at 12 mg/L. She'd read online that elevated CRP indicated high heart attack risk and was convinced she needed immediate cardiac evaluation.

What Jennifer didn't realize—and what the urgent care provider failed to explain—is that any acute illness elevates CRP dramatically. Her bronchitis alone would cause significant inflammation. For cardiovascular risk assessment, we need CRP measured when patients are healthy, not during active infections.

This nuance illustrates a broader point: inflammatory markers provide valuable information, but they require medical context and expertise to interpret meaningfully. The same inflammatory process that drives atherosclerosis also responds to infections, injuries, autoimmune conditions, and even psychological stress.

Treating the Process, Not Just the Plumbing

An inflammatory understanding of atherosclerosis opens entirely new avenues for prevention and treatment that go far beyond managing cholesterol and opening blocked arteries.

Anti-inflammatory nutrition: Rather than focusing solely on restricting dietary cholesterol and saturated fat, we can emphasize foods that modulate immune function and reduce systemic inflammation. Mediterranean-style eating patterns rich in omega-3 fatty acids, polyphenols from colorful vegetables, and anti-inflammatory compounds from olive oil and nuts can significantly reduce cardiovascular events.

Stress as a cardiovascular risk factor: Chronic psychological stress promotes inflammatory pathways that accelerate atherosclerosis. This connection explains why meditation and stress reduction techniques can reduce heart attack risk.

Sleep and immune function: Poor sleep quality disrupts immune regulation and promotes inflammation throughout the body, including within arterial walls. Addressing sleep disorders becomes a cardiovascular intervention, not just a quality-of-life issue.

Exercise as anti-inflammatory medicine: Regular physical activity doesn't just improve circulation—it powerfully modulates immune function and reduces inflammatory markers. The cardiovascular benefits of exercise extend far beyond its effects on blood pressure and cholesterol.

Treatments in the Pipeline

Understanding atherosclerosis as an inflammatory disease is driving exciting developments in cardiovascular medicine. Researchers are studying medications that specifically target inflammatory pathways involved in plaque formation and rupture. Some of these anti-inflammatory drugs show promise for preventing heart attacks even without lowering cholesterol.

Imaging techniques are being developed to detect "hot" inflammatory plaques before they rupture, potentially allowing us to identify and treat the most dangerous lesions regardless of their size. This represents a fundamental shift from measuring blockages to assessing inflammatory activity.

The GLP-1 medications (Ozempic, Mounjaro and its cousins) continue to show great promise, not only for their effectiveness with weight loss and cholesterol but also for their anti-inflammatory effects and overall cardiovascular risk reduction.

A More Complete Picture

None of this means that traditional cardiovascular risk factors don't matter—they do. Smoking cessation and managing issues such as high blood pressure, diabetes, and metabolic disease are still crucial to reduce the risk for atherosclerosis and the downstream consequences of it (e.g., heart attack and stroke). And procedures like stents and bypass surgery are still valuable and potentially life saving for people like Tom who needed a stent to restore blood flow to his heart muscle. But understanding atherosclerosis as an inflammatory disease can help arm patients—and perhaps you, too—with a sense of agency over the development or progression of atherosclerosis. It’s a process, one that you can be an active participant in mitigating or managing.

What are your questions about cholesterol, heart disease, stroke, and arterial plaque? I’m all ears!