Take a look at this picture of corneal arcus, reproduced with the patient’s permission. This is classic for the arcus of hyperlipidemia (arcus lipoides) in that there is a gap between the limbus and the white arcus deposit. The arcus of old age (arcus senilis) fuses into the limbus blurring the border. We think that arcus lipoides is located slightly in from the limbus because that is where the capillaries to the cornea bend toward the pupil creating flow turbulence. Cholesterol © deposition occurs most frequently at areas of flow turbulence.
I use arcus lipoides as a sign that the patient is depositing C in inappropriate places. It makes me more aggressive with lipid treatment. The literature on the value of corneal arcus as a CAD risk factor is mixed, however. For example, Antonio Fernandez and I found that corneal arcus was a CAD risk factor in the Framingham database, but not after adjustment for age, ( Am J Cardiol. 2009 Jan 1;103(1):64–6), but I am suspicious that the Framingham clinicians did not distinguish arcus lipoides from arcus senilis.
This patient was referred with a total cholesterol of 284 mg/dL, but her HDL-C was a whopping 119, her triglycerides 63 and her LDL only 149. I am concerned that the HDL-C was high because the C was stuck in the HDL particle and not being transported back to the liver for excretion. Recent abstract data suggests that the risk of CAD decreases with increasing HDL-C up to 80 mg/dL, but then the risk increases, possibly because of this postulated failure of HDL reverse cholesterol transport. It may also be why some of the cholesterol ester transferace (CETP) inhibitors, that increase HDL a ton, did not reduce CAD. So, I do not avoid lipid treatment in patients with high HDLs if they also have high LDLs. I consider other factors like coronary calcium scores and…corneal arcus. I think it was a mistake that we labeled HDL-C the “protective risk factor”. It is only one piece of the puzzle.