Author(s): Tamás Fischer*
The endothelial system assures unhindered functioning and stability of the internal milieu maintaining vascular health and protecting against vascular injury, noxa. by producing, synthesising and excreting various substances: vasodilators and vasoconstrictors, growth factors and their inhibitors, pro-inflammatory and antiinflammatory agents, pro-thrombotic and fibrinolytic factors, and by keeping them in a strict equilibrium: endothelial dysfunction is the change of these properties, what is inappropriate with regard to the preservation of organ function. In the genesis and later development of age-related macular degeneration (AMD), endothelial dysfunction (ED) has a crucial key role. AMD-risk factors often are identical wih the risk factors of (cardio)vascular (CV) diseases, so the two conditions have a similar pathogenesis. These risk factors lead to vascular injury through the same mechanism of actions, by inducing oxidative stress (OS → ED!): harm (noxa, i.e. |AMD| risk factors) → oxidative stress [OS] → endothelial activation [EA], endothlial dysfunction [ED], respectively → vacular injury, vascular disease). Disordered function of endothelium in the vessels supplying the affected ocular structures with blood (ED) have a key role in the genesis and development of age-related macular degeneration. Wall of blood vessels including thoose in choroids may be triggered by several repeated and/or prolonged mechanical, physical, chemical, microbiological, immunologic, and genetic influences-impacts-stimuli (noxa), against which protracted response, the so-called host defense response may develop, and in consequence of this, vascular damage pathological consecutive changes ending in AMD, ultimately, may develop. As the human vascular system is uniform and consubstantial, the medicines/non-medicinal methods desribed below [the RAAS-inhibiting (1) angiotensin converting enzyme ihibitors and (2) angiotensinreceptor blockers |AT1 receptor blocker telmisartan included|; (3) direct renin inhibitors;(4) statins;(5) acetylsalicylic acid; (6) trimetazidin; (7) third generation beta blockers; (8) PPARgamma agonist; (9) folate; (10) vitamin D; (11) “causal” AOVs; (12) melatonin; (13) AGE crosslink breakers alagebrium; (14) ET receptor antagonist Bosentan; (15) coenzyme Q10;]; (16) the antioxidant N-acetyl-cysteine], beneficial in ED also exert a favourable effect on the vessels of the eye, in the choroid/retina.- Consequently, based on the preceding discussion, as the human vascular system is uniform and consubstantial, it seems logical to presume that, as a part of our primary and secondary preventive activity: (A) Such medicines - exerting a favourable effect on the vessels of the eye, in the choroid/retina - should be given to: (a) Patients who have no macular degeneration, but have risk factors of AMD [and ones of cardiovascular (CV) disease] inducing ED, and are older than 50 years. (b) Patients who have been diagnosed with unilateral AMD, in order to prevent the damage of the contralateral eye due to macular degeneration. (c) Finally patients who have been diagnosed with bilateral AMD, in order to avert deterioration and in the hope of a potential improvement. (B) In addition lifestyle modifications of AMD patients (modifying lifestyles behavours of diet, smoking and physical activity) is of indispensable importance. (C) We should strive to completely eliminate the risk factors of macular degeneration (and ones of the CV disease) which induce OS and consequential ED, in addition.- Of course, the performance of randomised, prospective, multicentric clinical trials is necessary. Nevertheless, also until then we can begin – while taking the contraindications into consideration – the above outlined medication/methods that bear(s) the burden of few side effects.