Why The Clogged Pipe Analogy For Arteries Should Be Abandoned


“Although the image of coronary arteries as kitchen pipes clogged with fat is simple, familiar, and evocative, it is also wrong.” – Dr. Rothberg

Imagining coronary arteries as pipes that become clogged leads to performing heart bypass operations, angioplasty surgeries, and stenting which have been found not to prevent heart attacks:

Indeed, at least 12 randomized trials conducted between 1987 and 2007 and involving >5000 patients have found no reduction in myocardial infarction attributable to angioplasty in any of its forms.


Evaluation of 61 trials of PCI* conducted over several decades shows that despite improvements in PCI technology and pharmacotherapy, PCI has not been demonstrated to reduce the risk of death or [myocardial infarction] in patients without recent [acute coronary syndrome].

* PCI is percutaneous coronary intervention, another way of saying angioplasty-plus-stent.

Those quotations are from:

Coronary Artery Disease as Clogged Pipes, A Misconceptual Model, Circulation, a Journal of the American Heart Association, 2013

Here’s Dr. Rothberg’s description of the intractable and erroneous “clogged pipe” model:

According to this model, cholesterol plaques in the arterial walls slowly encroach on the lumen, causing silent ischemia first, then angina, and eventually infarction. Diagnosis begins with physiologic stress testing, looking for supply–demand mismatch, and progresses to angiography to find blockages. Treatments based on this theory include both coronary bypass and angioplasty, the latter often explained to patients as a Roto-Rooter or in the case of the magazine ad, as a Rotablator. Results of such revascularization procedures are visually striking and, in stable disease, may lead to the erroneous conclusion that the plumbing problem has been fixed and the risk of myocardial infarction ameliorated.

That’s the model I learned in school years ago. It’s outdated. Here’s what actually happens to cause a heart attack:

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).

I tried to find a visual representation of an artery with plaque that does not limit blood flow, that may be hard to detect on an angiography, but that is ripe for causing a heart attack. This is the best I could find. Note that blood flow is barely restricted until after the rupture and thrombus forms, after the heart attack:


So, there is plaque involved, but the reason angioplasty, stents, and even bypass surgeries (that aren’t meant to fix an acute problem) don’t work is because the plaques most likely to rupture can’t be seen, and so, can’t be stented or bypassed.


As many as half of all elective PCIs may be inappropriate.

Imagine! All that money wasted, all that sense of false security perpetuated.

Heart attacks are more about inflammation than about plaque narrowing arteries. In terms of diet, the fat we eat, says Rothberg, is not directly deposited into arterial plaques. It can, however, increase the production of LDL cholesterol in the liver, LDL that may then “infiltrate vascular endothelium, where it can initiate a complex inflammatory response.” So dietary fat, especially saturated fat (“saturated fat increases LDL”) is still a problem. Rothberg says that HDL cholesterol can help “neutralize” the risks associated with high LDL. But as we now know, HDL can also be pro-inflammatory. HDL is a chameleon.

Here’s Rothberg explaining what actually happens to cause a heart attack, in simple terms:

Coronary artery disease … is an inflammatory disease in which cholesterol from the blood is deposited in artery walls, causing an inflammatory reaction, like a pimple. When those pimples pop, they cause the blood in the arteries to clot at the site. If the clot closes off the entire artery, that causes a heart attack, and emergent medical attention is required to remove the clot. Thus, for patients who have coronary disease, it is crucial to take steps to reduce the inflammation, including both evidence-based lifestyle changes (smoking cessation, exercise, stress reduction, and a Mediterranean diet) and taking medications that reduce inflammation and prevent thrombosis (aspirin and statins).

I love his pimple analogy. I’m not on the statin boat, but here, in his mention of the antiinflammatory aspirin, does he reinforce his heart-disease-is-an-inflammatory-disease argument, does’t he.

Why, in the face of this overwhelming evidence, does the plumbing model persist? Listen to Rothberg tell the truth:

[Evidence-based lifestyle changes] are likely to encounter opposition, partly because it is difficult to admit that in the past we got it wrong and performed what now appear to have been unnecessary procedures, but also because our current payment system continues to reward interventions based on the old model and cardiac procedures are an important source of hospital revenue. It is unlikely that hospitals will begin to advertise the power of generic medications and lifestyle changes to combat heart disease. Nor will physicians quickly abandon a practice that both supports their income and seems to make sense.

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