For at least 20 years the skeptical cardiologist has been trying to communicate the current paradigm of coronary heart disease to his patients.
My job has been to translate the physician/scientific description of atherosclerosis : what happens to the arteries in the heart over time, how this results in heart attack and angina, and what we can do to prevent symptoms, heart attacks, and death.
This description, written in a Circulation editorial entitled ” Coronary Artery Disease as Clogged Pipes: A Misconceptual Model” and published 8 years ago, is still a good scientific summary of the process of atherosclerosis:
we know that the interactions between dietary fat, serum cholesterol, and arterial endothelium are complex and dynamic. Although high-grade stenoses can cause chronic angina, most cardiac events occur at lesions that appeared mild on previous angiography. These plaques contain a lipid-rich core covered by a thin fibromatous cap. Inflammatory cells (eg, macrophages and mast cells) within the plaque may become activated by microbes, autoantigens, or inflammatory molecules (activated plaque model). The activated cells secrete cytokines and proteases that weaken the fibrous cap, causing it to erode or rupture. The newly exposed subendothelium and procoagulant factors precipitate platelet aggregation and local thrombus formation, sometimes leading to infarction. Before rupture, these plaques often do not limit flow and may be invisible to angiography and stress tests. They are therefore not amenable to percutaneous coronary intervention (PCI).
But most of my patients, despite my valiant attempts at translating the above into layspeak are still focused on the plumbing problem. They want to know what percentage blockage they have and they want to see that percentage go down. The clogged pipe analogy for coronary artery disease is so simple and resonant to most patients that it remains fixed in their minds despite my best efforts to explain the problem.
The Pimple Analogy of Coronary Heart Disease
Recently, I heard a different analogy to explain coronary artery disease, – the pimple analogy which may have a greater chance to resonate with patients.
The New York Times reported on this in a 2007 article entitled “How it happens: It’s not the plumbing:”
When Dr. Peter Libby, chief of cardiovascular medicine at Brigham and Women’s Hospital in Boston, talks to his patients about heart disease, he often has to start by disabusing them of a popular misconception.
Most think cholesterol silts into arteries, blocking them like a clogged pipe. When, one day, an artery gets completely blocked, a heart attack occurs — no blood is getting through to the heart.
But the plumbing image is not only mistaken, cardiologists say. It can also lead patients to make disastrous errors in trying to protect themselves from a heart attack.
Heart attacks are caused by plaques inside the lining of the coronary arteries which are vulnerable to rupture:
Plaque is actually a pimple-like growth inside an artery wall. The pimples, stuffed with what Dr. Libby describes as a “kind of chronic pus,” usually grow outward so they do not obstruct the blood vessel for many years. But once plaque gets started, Dr. Libby says, it covers the walls of the arteries. “It’s likely that no part of the artery is normal,” he adds.
When pathologists look at the coronary arteries of autopsied hearts they see different kinds of plaque created by the process of subclinical atherosclerosis typically scattered throughout the artery.
There is the large, ugly yellow plaque that led to the heart attack. It popped open one day, attracting red blood cells that formed a clot on its surface, blocking the artery. There also are grayish-white plaques, old ulcerated plaques that became calcified. There is so-called vulnerable plaque, the pustules that are ready to burst. And there are yellowish streaks, thought to be plaques starting to develop.
Patients typically have dozens of vulnerable plaques, and it is impossible to know which will burst and which of those will result in a blood clot that blocks an artery.
In the the setting of an acute heart attack when the pus has already burst from the zit and set up a clot blocking blood flow to the heart muscle we know that balloon angioplasty and stenting to acutely open the artery saves heart muscle and lives.
Otherwise, the best treatment to save heart muscles and lives involves calming down all of those pus-filled pimples (whether they are narrowing the artery 25% or 90%) with a combination of medications and lifestyle changes.
Coronary Calcium and Acne Scars
The pimple analogy also works to explain a tricky aspect of coronary calcium scans (CAC). A high CAC score alerts your doctor to premature or excessive build-up of those dangerous plaques or pimples in the coronary arteries. Once this high-risk state is identified we utilize drugs and lifestyle changes to minimize the risk over time.
Patients naturally want a way to monitor this reduction in risk and it seems logical that if a high CAC score predicted risk initially with treatment that score will come down. Unfortunately, coronary calcium persists and almost always increases over time even with very effective risk reduction.
The pimple analogy compares the coronary calcium to the scarring one sees as an inflamed pimple is healed and the skin attempts a repair. The American Society of Dermatologic Surgery describes the scarring process with acne as follows:
Acne scars are usually the result of inflamed blemishes caused by skin pores engorged with excess oil, dead skin cells and bacteria. The pore swells, causing a break in the follicle wall. Shallow lesions are usually minor and heal quickly. But if there is a deep break in the wall of the pore, infected material can spill out into surrounding tissue, creating deeper lesions. The skin attempts to repair these lesions by forming new collagen fibers. These repairs usually aren’t as smooth and flawless as the original skin.
An acne scar is a marker for an acute inflammatory process that happened months or years ago and it can persist for a lifetime. Similarly, the plaques that start as fatty streaks in your coronary artery lining progress ultimately to scar represented by coronary calcium and that calcium is just a marker of an inflammatory and dangerous process that happened months or years earlier.
This figure from a JACC state of the art review emphasizes that we can identify coronary pimples long before they become inflamed, rupture, and wreak havoc. Once significant premature pimples are identified (by CAC or vascular imaging) we should consider patients as needing secondary prevention and treat aggressively to prevent progression. Progression results in ruptured plaques (coronary events) and progressive narrowing of the arteries.
Does the pimple analogy help you gain a deeper understanding of coronary artery disease? Will it reduce the obsession with the percent narrowing of arteries? Can it reduce unnecessary stenting procedures and bypass operations?
Let’s spread it far and wide. Let me know how it resonates with you.
17 thoughts on “Is Coronary Heart Disease a Plumbing Problem or a Pimple Problem?”
As a layman with no medical training, finding your pages is both interesting and confusing(trying to follow the science). A 74 year old with average HDL in the 90s, LDL around 100(prior to Atorvastatin) and Triglycerides averaging <50 BUT with a Cardiac Screening score of 644 I struggle for the right path. My PCP started the statin(I’m at 10mg/day) and my LDL is down in the 70s and Triglycerides to about 40. My reading of late is due to my concerns about Type 2 diabetes risk and I have been trying to justify statins considering my low risk numbers, excluding the screening. The cardiac screening was done in 2015 and has prompted the statin course. After reading your posts and some associated paper sysnopses the fact that my cardiac score is so high makes me think that my PCP did the right thing. Risk seems to be larger than what shows in my lipid test scores. Would you agree?
I think you and your PCP are making the right decisions. The risk of diabetes with low dose statin is extremely low but they will help substantially lower your risk of heart attack and stroke.
Just as an aside, I also had a very high CAC score. 700 on a CAC scan. As a 47M with a family history of heart attacks, my cardiologist said I could get an angiogram. We did the angio, and interestingly, they redid my CAC score during the angio and it came in around 622. But, they said there was no luminal interference or blockages in both the arteries, so I dunno. Hope the calcified plaque or whatever is stable and in the arterial walls.
I’m thinking you had a coronary CT angiogram, a noninvasive test? An invasive angiogram would be a very bad idea in that situation as it carries significant risk and you might end up with a stent you really didn’t need. Also, the invasive angiogram is a very poor way of looking at early CAD. The calcium score is only obtained by CT based testing.
This difference between a lot of early plaque build up in the lining of the artery but nothing protruding into the lumen or causing blockage is precisely what I was trying to describe in the article.
With good lifestyle and medical treatment the plaque will stabilize and you can do very well.
Hi Dr p,
No, not CT Angio, but invasive angio. They didn’t stent since they found no blockages. But, yes, I do know about the risks of the invasive angio, including radiation exposure. Also, I’m very much well aware that my CAD could still lead to a heart attack down the road given the pimple analogy. Right now, I’m on a low fat diet and 10 mg statin. My LDL went from 130’s down to 30’s. HDL still in the 70’s. Inflammation markers like hs-CRP cut in half.
Hopefully I can stabilize my CAD and it doesn’t progress much further. But, we’ll see.
Dr. P, outstanding and enlightening even more than usual! Thank you for the continuing education.
Very informative, thank you! Perhaps a silly question: are there any links between the inflammatory processes that lead to actual pimples and those that lead to plaques in arteries? As someone in his mid 40s with a family history of heart problems and life-long acne I wonder if that acne could be a suggestion that I might be more likely to have plaques as well.
Nothing to suggest that acne is associated with higher risk of arterial plaques.
This study showed lower risk of coronary disease in those with acne (but higher risk of prostate cancer)
Good topic! I remember when I first started researching CVD, I thought it was stenosis and occlusion that caused heart attacks. I was half right as you pointed out, but to my surprise it wasn’t the luminal constriction from plaque (although that is also a contributor and can be a source if extremely stenotic) it was the instability of those endothelial lesions that usually are the troublemakers resulting in thrombii and then emboli when they break free. The pathology behind it is so fascinating but also reminded me of something else that happens in nature. These phenomenon are underwater volcanoes that occasionally erupt due to plate tectonic movement. The analogy goes like this, the crater of the volcano being the calcified endothelial lesion, the ocean floor’s surface being the endothelium of the lumen, the magma chamber being the sub endothelial space and the lava being the foam cells, a combination of oxidized lipid laden macrophages and cytokines and the ocean water being the blood. When the plates shift, (endothelial dysfunction) allow the most superficial portion of the rock to fissure (endothelial rupture). This fissure releases molten magma (endothelial lesion) into the water (blood). This magma cools incredibly fast (the clotting factors that coagulate and form thrombii). My analogy however does not explain the most crucial part, the occlusion and potential ischemia that comes from the thrombii ( a fixed clot) that breaks away in the artery and then becomes a moving clot (embolii).Maybe if I used a cave or tunnel? Oh well it works for me.
Nice analogy! The thing that is unique about the coronary arteries compared to the ocean bottom or the facial skin is that they occur in a small tunnel. The coronary arteries are really small and when the inflamed pus in the pimple bursts out and a clot forms in this little tunnel a total obstruction can occur resulting in an MI/heart attack.
Hello Dr. ACP
So if someone wants to put a stent in you or do a coronary bypass how do you tell them “no, there is no about to burst pimple”?
Assuming you are not in the throes of an acute heart attack you should ask how the stent will or CABG will help lower your risk of heart attack better than optimal med therapy and lifestyle.
Do you feel COURAGE and ISCHEMIA apply to stenting occlusions that resolve with TPA or other anti-thrombotics (AT) but still have significant calcified lesions imaged by CTA? Do the specific artery (RCA vs LAD) and location in artery (distal vs proximal) play apart in the decision making process or do the previous trials indicate those variables are inconsequential? Do you think this could apply to cerebrovascular emboli that resolve with AT but significant calcified lesions are present.
Has someone compiled a list of CAD risk by country?
So, a high CAC score but normal angiography doesn’t necessarily rule out coronary events in the future, correct? Is this because the CAC scan doesn’t rule out stable calcified plaques vs the unstable soft plaques? Using the pimple analogy, old pimples that are now scarred skin tissue vs. new pimples that are filling up with pus and ready to burst?