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Coronary steal syndrome

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Coronary steal syndrome

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Coronary steal syndrome

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Coronary steal syndrome produces (typical/atypical) chest pain in patients with ischemic heart disease.

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Content Reviewers:

Viviana Popa, MD

Coronary steal syndrome is a condition that occurs due to dilation of coronary arteries in the presence of coronary artery disease, which is when there’s a partial or complete blockage in the lumen of another coronary artery.

The result is a redirection of blood flow from heart muscle supplied by the blocked artery, to other regions of the heart.

Coronary steal syndrome is a finding observed during a pharmacological cardiac stress test, which is used to diagnose coronary artery disease.

Now, the heart pumps out blood for all of our organs and tissues to use - but the heart also needs blood.

So it also pumps blood to itself, through the coronary arteries on the outside of the heart.

And coronary arteries are linked to one another through teeny tiny blood vessels called collateral vessels, which are normally in an inactive state, meaning blood doesn’t flow through them.

Now, with coronary artery disease, there’s ischemia, or reduced blood flow to the region of myocardium supplied by that artery.

In this context, collateral circulation may become active. For example, let’s say two coronary arteries,

A and B, are linked by a collateral vessel, and coronary artery B has developed a block.

As a result of ischemia, in the myocardium supplied by coronary artery B, the myocardial cells don’t receive enough oxygen, which is called hypoxia.

In response to hypoxia, myocardial cells release signalling molecules called cytokines, which cause dilation of the segment of coronary artery B beyond the blockage.

This slightly improves the blood flow and ameliorates hypoxia.

But at the end of the day, blood flow within coronary artery B is still decreased, while blood flow in coronary artery A remains the same.

This creates a pressure gradient across the collateral vessel, which pulls blood from the region of higher pressure, of coronary artery A, through the collateral vessel, and into the region of lower pressure, or the dilated segment of coronary artery B.

In other words, the low-pressure region acts like a vacuum!

Now, the sudden gush of blood through the collateral vessel stretches its walls and deforms the endothelial cells, which stimulates the production of growth factors like the vascular endothelial growth factor, or VEGF, from the vessel wall.

These growth factors act on the collateral vessel wall and bring about two changes.

First, they cause vasodilation, which allows more blood to flow through the collateral vessel.

Second, they promote the proliferation of the smooth muscle cells in the vessel wall, which makes the vessel wall thicker and stronger.

Over time, this results in maximal vasodilation beyond the obstruction, and it helps the collateral vessel redivert blood to the ischemic myocardium.