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.