[2][3] Coronary artery ectasia occurs 4 times more frequently in males than in females and in people who have risk factors for heart disease such as smokers.

[2] The permanent dilation of the artery is thought to be mainly caused by inflammation, triggered by disease, chemicals, or physical stress of the vessel.

[8] Inflammation elevated oxidative stress is increased, and antioxidant activity is depressed in coronary artery ectasia.

[9] The activation of the inflammatory response causes a detectable increase in C reactive protein, interleukin-6, tumor necrosis factor alpha and cell adhesion molecules, which can be used as a diagnostic marker,.

Experts in the field urge clinicians to consider anti-platelet therapy, such as Aspirin, to reduce thrombus formation in pocket vortices associated with turbulent blood flow.

Some studies have also suggested the use of angiotensin converting enzyme inhibitors, as ACE gene polymorphisms have been implicated in disease progression.

Risk factor modification is recommended; including tobacco cessation, blood pressure control and avoidance of illicit substance use, specifically cocaine.