RISK FACTORS FOR DEVELOPMENT OF
NON-ARTERITIC AION

All the available evidence indicates that non-arteritic AION is multifactorial  in nature and the risk factors fall into two main categories:

Our studies⁴⁴ in non-arteritic AION revealed that, compared with the prevalence reported in the general population, young (<45 years), middle-aged (45 to 64 years) and elderly (>65 years) patients with AION showed a significantly higher prevalence of arterial hypertension (p<0.02), diabetes mellitus (p<0.01), and gastro-intestinal ulcer (p<0.02). Also, middle-aged and elderly patients showed a significantly higher prevalence of ischemic heart disease (p<0.01) and thyroid disease (p<0.01). Middle-aged patients exhibited significantly higher rates of chronic obstructive pulmonary disease and cerebrovascular disease (p<0.01). On follow-up, AION patients with both arterial hypertension and diabetes mellitus showed a significantly higher incidence of cerebrovascular disease (p<0.01). In addition, AION patients may also have a number of other systemic diseases which may directly or indirectly act as risk factors in the development of AION,^11,44 and these include systemic collagen vascular diseases, herpes zoster, systemic arterial hypotension, malignant arterial hypertension,⁵³ renal hemodialysis, massive or recurrent systemic hemorrhages,^22,44 atherosclerosis,³² arteriosclerosis, migraine and other vasospastic disorders, hematologic disorders, internal carotid artery disease,⁶² cardiac valvular disease, defective cardiovascular autoregulation, and possibly type A behavior pattern and sleep apnea.³⁰ Our studies have suggested that among the systemic risk factors, nocturnal arterial hypotension (i.e. fall of blood pressure during sleep) seems to play a very important role in the development of non-artertitic AION.^{28,30,47,50,51,52,58}

Fig. 2: Three examples of 24-hour ambulatory blood pressuring records, starting from about 10 A.M.: For a larger view of a picture, click on image

A. Diagrammatic representation of mean hourly systolic and diastolic blood pressures over a 24-hour period in persons with normal blood pressure (normotensive) and those with high blood pressure (hypertensive). (Reproduced from Hayreh et al.58) B. Actual ambulatory blood pressure and heart rate monitoring records (based on individual readings) over a 24-hour period in a patient with non-arteritic AION in the right eye. The blood pressure is perfectly normal during the waking hours but shows a marked fall during sleep at night. (Reproduced from Hayreh et al.50) C. Ambulatory BP and heart rate monitoring records over a 24-hour period in a patient on two regimens of verapamil (a calcium channel blocker) regimens, as indicated on the chart. The upper record shows that when she was using verapomil at bedtime, there was marked degree of fall of blood pressure during sleep which improved markedly on stopping the bedtime dose, as seen in the lower chart. (Reproduced from Hayreh et al.28)

Role of fall of blood pressure during the night  (nocturnal arterial hypotension) in development of AION:

We have discussed this at length elsewhere.^{28,30,33,36,47,50,51,58} Typically patients with non-arteritic and often those with arteritic AION discover visual loss on waking in the morning.^8,47 In our series of non-arteritic AION cases, about 75% gave a definite history of discovering the visual loss on waking up in the morning or from a nap, or early in the morning at first opportunity to use vision critically; the remaining 25 % were not sure of the time of onset.⁴⁷ Our 24-hour ambulatory BP monitoring studies showed a steep drop in BP on falling asleep at night and recovery to normal on waking in the morning (Fig. 2-A,B). These studies also showed that arterial hypertensives on oral hypotensive therapy have a significant (p = 0.004) association between progressive visual field deterioration in AION and nocturnal arterial hypotension.^50,58 The fall of BP during sleep is a physiological phenomenon but it is much aggravated by many factors, including drugs such as beta-blockers (both oral and eyedrops⁵¹), calcium-channel blockers, angiotensin converting enzyme inhibitors, terazosin hydrochloride (used in enlarged prostate to reduce frequency of urination during the night), amitriptyline and other similar compounds - particularly the number and amount of drugs taken and the time of day they are taken.^28,33,50,58 For example, when these drugs were taken at bedtime, they produced a far more marked degree of nocturnal hypotension (Fig. 2-C) than when taken in the morning, because they aggravate the naturally occurring fall of BP during sleep.

Our studies suggest that in an optic nerve head already susceptible to ischemic disorder, nocturnal arterial hypotension may act as "the straw that breaks the camel's back".^28,30,50,58 It seems that the very potent arterial hypotensive drugs currently available to treat hypertension may be emerging as an important risk factor for arterial hypotension (particularly nocturnal hypotension), especially when used aggressively and/or given at bedtime. In view of all this evidence, it seems that in some persons non-arteritic AION may possibly be occurring as an iatrogenic disease. A combination of arterial hypertension during the day and hypotension at night can play an important role in either the development or the progression of non-arteritic AION.³³

This brief discussion, then, gives some idea of the great complexity of mechanisms of development of non-arteritic AION and the role of nocturnal arterial hypotension in it. A whole host of systemic and local factors acting in different combinations and to different extents may derange the optic nerve head circulation,³⁸ with some making the optic nerve head susceptible to ischemia and others acting as the final insult. Nocturnal hypotension seems to be an important precipitating factor in the susceptible patient.

There is a significant association between non-arteritic AION and a number of eye and optic nerve head conditions. These conditions include absent or small cup in the optic disc,³ raised eye pressure (e.g., during the immediate post-operative period after cataract extraction¹⁶, in acute angle closure glaucoma, or prolonged pressure on the eyeball from any cause), marked optic disc edema due to any cause,¹³ location of the watershed zone of the posterior ciliary arteries in relation to the optic disc,²⁵ vascular disorders in the blood vessels of the optic nerve head, and defective blood flow autoregulation,³⁸ vasospasm, arteriosclerosis, atherosclerosis,³² disorders of ophthalmic artery and/or posterior ciliary arteries, and other conditions which may make the optic nerve head susceptible to ischemic disorders.^27,38

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