SOURCE: Catena FC, et al. J Am Soc Hypertens 2015;9:167-175.

The relationship between homocysteine (hCYS) and vascular disease has been recognized for at least two decades. Indeed, the strength of the association between plasma hCYS levels and coronary atherosclerosis surpasses that of cholesterol. Once this relationship was publicized, a flurry of enthusiasm for modulation of hCYS ensued, based largely on the strong observational data and the simplicity with which hCYS can be lowered: supplementation with folate and B vitamins. Since these treatments are not associated with meaningful toxicity at appropriate doses, there appeared to be much to celebrate: an easy, inexpensive fix for an important health problem.

After a bevy of trials in which hCYS lowering failed to show risk reduction for CV events, need for revascularization, etc., one editorialist confidently announced “The homocysteine hypothesis is dead!”. Well, apparently some still feel a faint pulse.

Catena et al published their data looking at the relationship between hCYS and carotid disease among hypertensive patients. They found that carotid intima-media thickness was linearly related to hCYS levels, independent of age, BP, and CRP.

Since no clinical trials have shown a favorable impact of hCYS modulation, why should clinicians care? The authors bring up the interesting proposition that since elevated hCYS is a recognized risk factor for vasculopathy, it might help influence treatment decisions for management of persons at risk for CVD. Perhaps, for instance, elevated hCYS might tip the balance of a treatment decision for persons with a strong family history of vascular disease, but borderline risk factors (e.g., BP, lipids, glucose).