What is Coronary Steal Phenomenon?

Coronary Steal (or Coronary Steal Phenomenon) is a vascular diversion where an alteration in coronary circulation redistributes blood flow away from an already ischemic area of the myocardium toward a non-ischemic area. Physiologically and clinically, it manifests in two distinct ways: Pharmacological (Microvascular) Steal and Anatomical (Macrovascular) Steal.

1. Pharmacological Collateral Steal

This is the classic physiological model exploited during vasodilator stress testing.

• The Baseline State: A severely stenosed or completely occluded epicardial artery (the recipient) relies entirely on collateral blood flow from a neighboring patent artery (the donor). To maintain baseline tissue perfusion, the auto-regulatory microvascular resistance arterioles downstream of the stenosis are already maximally dilated at rest. Their Coronary Flow Reserve (CFR) is essentially zero.
• The Trigger: A potent microvascular arteriolar vasodilator—most classically Adenosine, or Dipyridamole is administered.
• The “Steal”: Because the ischemic arterioles are already maxed out, the drug acts exclusively on the arterioles in the healthy donor territory. Vascular resistance in the healthy zone plummets, turning it into the path of least resistance. The driving pressure across the collateral network drops, and blood is actively diverted away from the ischemic zone into the normal myocardium.

The Pharmacological Nuance: Why Nitrates Don’t Steal

This mechanism explains why Nitroglycerin (NTG) relieves ischemia while dipyridamole can provoke it. NTG preferentially dilates large epicardial conductance vessels and the collateral channels themselves, while leaving the tiny microvascular resistance arterioles largely unchanged. By widening the supply conduit without opening a parallel low-resistance sink, NTG increases net forward flow to the ischemic bed.

2. Anatomical Macrovascular Steal

The most clinically famous structural variant is Coronary-Subclavian Steal Syndrome (CSSS).

• The Setup: A patient has undergone a CABG utilizing a Left Internal Mammary Artery (LIMA) to Left Anterior Descending (LAD) graft.
• The Pathology: The patient develops a hemodynamically significant stenosis in the proximal left subclavian artery (upstream of the LIMA take-off).
• The “Steal”: At rest, perfusion to both beds may be adequate. However, when the patient exercises their left arm, the muscular resistance vessels in the upper extremity dilate. The pressure in the distal subclavian drops below the pressure in the coronary tree, causing blood to flow retrograde up the LIMA—stealing blood from the LAD to perfuse the arm. The patient experiences angina triggered specifically by upper-extremity exertion.

Other structural shunts: A true macrovascular steal also occurs in large, high-flow Coronary Artery Fistulas. Arterial blood takes the path of least resistance, bypassing the high-impedance myocardial capillary bed entirely to dump directly into a low-pressure cardiac chamber (like the right atrium or pulmonary artery).