Dear Editor

Digoxin remains a frequently prescribed cardiac glycoside used in the treatment of supraventricular dysrhythmias and congestive cardiac failure. Cardiac glycosides have a narrow therapeutic index, and there is considerable overlap in serum concentration of the drug between patients with and without digoxin toxicity. Features of digoxin are usually not specific and consist of cardiac and not cardiac effects. Disturbances of vision, for example, blurring, central scotomas, glare effects, and altered color perception, are a less common but more specific presenting complaint. Symptomatic color vision disturbances, for example, xanthopsia (blue-yellow axis), are found in up to 15% of intoxicated patients. Although formal testing reveals a much higher incidence of color deficiency. Impairment in both the tritan (blue-yellow axis) and red-green axis have been found. Digoxin inhibits membrane-bound alpha subunits of sodium-potassium ATPase, thereby promoting sodium-calcium exchange, leading to an intracellular calcium concentration that is available to contractile proteins. Digoxin can also inhibit sodium-potassium ATPase in retinal Muller cells, photoreceptors, and pigment epithelium, and result in alteration of retinal electrical properties. Although the precise mechanism is not fully understood, xanthopsia due to digoxin toxicity is likely associated with a selective effect on receptors of the retina. We investigated 16 cardiac male patients hospitalized in Istituto Nazionale per il Ricovero e Cura degli Anziani (INRCA) from Cosenza province (Calabria, Southern Italy). Obviously, this choosing allowed us to avoid Lyon genetic phenomenon showed in the females where the compensation X chromosome phenomenon is present. In our work, 8 out 16 patients showed normal color vision; 7 out 16 patients showed color vision deficiency; 1 out 16 patients showed red-green inherited colorblindness. The age onset of the cardiac disease is 30 months (range 0,2-72 months); New York Association Class mean was II (range I-III); digoxin treatment mean time was 53 months (range 2-144 months). Color vision deficiency in 7 out 16 patients were subdivided as follows: left eye, 2 patients showed light protan/deutan color vision deficiency on red/green axis; 1 patient showed great protan/deutan color vision deficiency on red/green axis; 3 patients showed light tritan color vision deficiency on blue/yellow axis. Regarding the right eye, we showed 4 patients with normal color vision; 2 patients showed light tritan color vision deficiency on blue/yellow axis; 1 patient showed great protan/deutan color vision deficiency on red/green axis. We excluded inherited colorblind patient from the analysis of the results. 8 patients showing normal color vision were treated with digoxin with a mean time of 4 years than the group of patients showing color vision deficiency.

In conclusion, in this present manuscript regarding a pilot study in Cosenza province on the effects of digoxin on color vision brain pathway, we can confirm the Literature to-day previously shown. In any way, we can think that we can extend in the next time the investigation from a strictly epidemiological point of view not only in the hospitalized patients

Acknowledgement

Authors thank Fondazione Cassa di Risparmio di Calabria e Lucania for its contribution