Here’s the deal. We need to first understand what causes heart disease - or what clogs arteries - in order to begin to think about how to prevent it. If you aren’t totally clear on this, don’t worry, you aren’t alone! I’ve spent more time in the office walking patients through the process of coronary artery disease (blockages of arteries in the heart), than practically anything else (followed closely by the best dietary pattern to prevent heart disease, understanding palpitations, and causes of high blood pressure). Yes, we’ll get to those too.

Why does this matter? Because

1. It’s the number one killer of Americans (yes, even in women! Surprise, it’s not breast cancer) and

2. It starts much earlier than you think. Like in childhood. So let’s get to it.

Atherosclerosis - aka clogged arteries

Atherosclerosis is the build up of cholesterol within the arteries of the body.

When this occurs in the arteries of the heart, it’s called coronary artery disease - it’s what people are typically referring to when they say “heart disease."

It is an inflammatory process.

Cholesterol begins to build up in the arteries to form pre-blockages, called fatty streaks and then over time, plaques. Eventually these can get big enough to actually impair the flow of blood to the heart and cause symptoms, like chest pain or shortness of breath. Other times, these plaques can also rupture  (one of my favorite mentors in fellowship always explained it to patients as “like a pimple popping” - gross, but remains my favorite analogy to this day), causing a heart attack.

Ok, so now that we have the bird’s eye view out of the way, let’s dive in to the nitty gritty. If you’ve got the picture and aren’t interested in a more technical explanation, head down to the take away section.

What clogs arteries?

First, you start with a healthy artery. It has a single layer of cells (called the endothelium) that lines the vessel wall. Cholesterol is transported through our blood in lipoproteins (essentially little vehicles for cholesterol). The most common type of lipoprotein that can get stuck in our arteries is LDL (known to many of us as “the bad cholesterol”). LDL lipoproteins hang out in the bloodstream delivering things to other cells that need it (proteins, cholesterol, etc), but they are also small enough to get between the endothelium and into the cell wall.

The primary driver of this is the LDL particle concentration in the bloodstream - the higher your LDL particle number, the more will move into the vessel wall and get stuck. An improperly functioning endothelium (called endothelial dysfunction) - classically from smoking, diabetes, and high blood pressure - may also contribute to this process.

Heart disease and inflammation

After the cholesterol carrying lipoprotein gets into the vessel, it can get stuck there and modified (oxidized) which is toxic, leading to a massive amount of inflammation.

The oxidized LDL sets off a huge cascade of badness - the release of inflammatory markers and cytokines rallies the immune system, which tries to come in and take care of the problem. Cells from the immune system ingest the oxidized LDL particles. The accumulation of lots of these lead to an early plaque (called a fatty steak) and then eventually a true plaque. Lots of enzymes and molecules get released leading to more inflammation, dysfunction of the endothelium, and recruitment of other cells which leads to further damage of the artery. Et voila, atherosclerosis.

What happens to clogged heart arteries

Over time, plaques can grow bigger and bigger and eventually become obstructive - meaning, they are large enough to impair the flow of blood to the heart muscle. It is not until then that people develop symptoms like chest pain (angina) or shortness of breath when they walk and is when people “fail” stress tests. This is called obstructive coronary artery disease. This type of blockage is treated with a stent or medications, as well as lifestyle.

Other plaques, typically ones that are very full of cholesterol and have only a thin protective cap, can rupture. A blood clot will then form at the rupture site (the body attempting to fix the popped pimple if you will), which then abruptly blocks the artery and causes a heart attack (myocardial infarction), and sometimes tragically sudden death.

Importantly, the plaques that tend to rupture are not always the large, obstructive vessels. Studies have found that the plaques that often lead to heart attacks can just as likely be small and non-obstructive (which are the kind that are not picked up on a typical stress test since they aren’t large enough to impair blood flow). This is an emergency and a stent, to open up the completely blocked artery, is lifesaving.

Risk factors for coronary artery disease

So now that we understand how coronary artery disease develops, we can have a better understanding of the causes. Unfortunately, the most important risk factor is one that we can’t control: age. Since all of these things take time to develop, we are at much higher risk the older we get. Importantly though, the duration of time we have uncontrolled risk factors matters a whole lot too. These risk factors you probably can now guess after the above deep dive and include high blood pressure (hypertension), high cholesterol (hyperlipidemia), tobacco abuse like smoking or vaping, and diabetes/insulin resistance. Other risk factors include above ideal body weight, family history of heart disease, inflammatory disorders (like lupus, psoriasis, HIV), early menopause, pregnancy complications (particularly gestational hypertension, preeclampsia, preterm delivery), and kidney disease.

Symptoms of clogged arteries

Some people have no symptoms at all! For many, it’s a gradual progression of chest pain (angina), shortness of breath, or new fatigue with walking. For others, the first sign is symptoms consistent with a heart attack - typically crushing, left sided chest pain associated with sweating, nausea, and shortness of breath. However, in many, it can be more much more subtle or atypical.

How is coronary artery disease diagnosed

Early heart disease can be detected with a Coronary Artery Calcium score or angiogram (either CT or a more typical invasive angiogram). These modalities are able to detect blockages that are both obstructive (causing impairment of blood flow) and non-obstructive. Once blockages become obstructive, they can be detected on a typical stress test. Only after someone has had a heart attack are they apparent on a regular electrocardiogram (EKG) or echocardiogram.

Coronary artery disease - key take aways

1. We all (yes, both you and I) have fatty streaks. The beginning stages of atherosclerosis begins young.

2. LDL cholesterol (technically the particles) accumulates in the artery and results in plaque formation (blockages). The more LDL particles you have, the better chance more will accumulate in the artery wall and build up

3. This is an inflammatory process. How our body responds is important too.

4. Obstructive coronary artery disease is a process by which the plaque slowly becomes larger until it gradually impairs the flow of blood. This causes the heart to not get enough blood, causing chest pain (angina) or shortness of breath in many.

5. Heart attacks happen when the plaque, often a small plaque that would not have been detected on a stress test, acutely ruptures, causing clot formation and complete, abrupt impairment of blood flow.

6. We have many ways to detect coronary artery disease, some at earlier stages than others

My Final Thoughts

Atherosclerosis is a systemic disease and an inflammatory process. We know that cholesterol (predominantly from LDL particles, but also from Lp(a)) can get trapped in the artery wall and this causes atherosclerosis. While cholesterol is necessary for plaque to build up in the artery, it may not be sufficient. We are increasingly realizing that plaque formation is also dependent upon the body’s inflammatory response to the invasion of cholesterol. Over the last several years, a major paradigm shift has occurred in our understanding of atherosclerosis such that patients may have residual risk, either from a cholesterol standpoint or from an inflammatory standpoint. Ergo, we must target lowering both cholesterol and inflammation - certainly with our lifestyle - and possibly also with medications. It’s also critical to understand this process is a systemic disease - given that sometimes it’s the small plaques that cause the biggest problems, it’s not enough to target just the big, scary looking plaques.

This is why lifestyle therapy (and medications when indicated) can be so powerful.

While all of us have at least the early stages of atherosclerosis, it’s imperative that we optimize our lifestyle and minimize risk factors to curtail it’s progression.