Marco Coassin, MD, PhD
Systemic vascular diseases cause marked effects on the structures and function of the eye. Hypertension, diabetes, and vascular embolization may induce pathological changes at the level of the retinal, choroidal, and optic nerve circulations—resulting in a wide range of clinical signs. Moreover,the general state of the cardiovascular system and the condition of the vessels’ wall may have a direct impact on the aforementioned retinopathies, choroidopathies, and optic neuropathies. Finally, systemic macular disease can have a direct impact on the status of the central retina: macular edema is a ﬁnal result of different pathways and severely penalizes patients’ vision and quality of life.’
Sixty-seven percent of US adults older than 60 years have elevated blood pressure (systolic Z140 mm Hg or diastolic Z90 mm Hg), and in 90% of these patients the cause of hypertension is unknown.1 Hypertension is characterized by persistent pathologic elevation of arterial pressure associated with increased total peripheral resistance, inducing generalized retinalarteriolar constriction. In the eye, the vasospasm of the retinal vessels is associated with the vascular thickening induced by the arteriolosclerosis.2,3 The current classiﬁcations of hypertensive retinopathy reﬂect this relationship, although it is impossible to keep these 2 factors separated because hypertension has a deﬁnite effect on the evolution of arteriosclerotic changes. It is not clearwhether other factors, such as hyperlipidemia, play a distinct role as risk factors in the development of retinal arteriolar changes.4 The most distinctive sign of hypertensive retinopathy is arteriolar narrowing from essential vasospasm that induces a reduction of the
INTERNATIONAL OPHTHALMOLOGY CLINICS Volume 52, Number 1, 11–23 r 2012 by Lippincott Williams & Wilkinswww.internat-ophthalmology.com | 11
normal arteriole-to-venule ratio of 2 to 3. Generalized and diffuse arteriolar vasospasm usually results from chronic hypertension, whereas localized narrowing is often reversible. These ﬁndings are seen in about 10% of the adult nondiabetic population.1 Arteriolosclerosis induces progressive thickening of the small arteries wall and narrowing of their lumen, bymeans of increasing of the elastic and muscular components and hyalinization. These changes are caused by aging and can be accentuated by hypertension and diabetes. At ophthalmoscopic examination, the arteriolosclerotic changes of the arterioles modify the characteristics of the light reﬂex coming from the vessels. In normal vessels, only the column of blood is visible with a thin line ofreﬂected light in the middle of the blood column. In thickened wall, the light reﬂex loses its brightness and becomes broader taking on the appearance of a ‘‘copper wire.’’ When the thickening increases markedly and the column of blood is not visible, the arteriole assumes the appearance of a ‘‘silver wire.’’ Arteriolovenous crossings (where arterioles and venules have a common adventitia) are alsoaffected by arteriolosclerotic thickening of the arteriole. Here, the venule becomes compressed with ‘‘nicking’’ (Gunn sign) or deﬂected (Salus sign).5 Retinal microaneurysms may be present in hypertension but are not speciﬁc. It is interesting to note that retinal arterial macroaneurysms are common in patients with systemic hypertension. Patients with retinal arterial macroaneurysms have high prevalenceof systemic hypertension and are at risk for retinal vein occlusions.6 A severe and sustained episode of high blood pressure can induce a breakdown of the inner blood-retinal barrier and may present with intraretinal edema and hemorrhages, cotton-wool spots (CWS), hard exudates, capillary occlusion, and retinal ischemia. If the acute hypertensive episode evolves into a malignant stage, a...