Diurnal variation in the onset of branch retinal vein occlusion: early morning blood pressure surge as a possible risk factor.

Artery-over-vein crossings are at special risk of damage from disordered haemodynamics. Even in normotensive persons, the artery-over-vein complex has characteristics which affect blood flow, such as focal venular constriction and an abrupt deflection of the associated vein [6] . The obstructive effect of these sites in the microvasculature is exaggerated in the hypertensive state, the risk factor par excellence of BRVO. Therefore artery-overvein crossings represent sites in the retinal circulation where there is potential for venular endothelial injury secondary to fluctuations in perfusion. In this regard, Meyer et al. [7] have remarked that ‘venous endothelial damage increases the potential role of haemostatic risk factors in the pathophysiology of retinal vein occlusion’. In essence, the ‘high-flow’ hypothesis professed here (to explain the apparent diurnal variation in onset of BRVO) states that the combination of an EMBPS and weakened retinovascular autoregulation favours venous intimal injury. A damaged endothelial surface at a site of stenosis (arteriovenous crossing) creates an optimal environment for thrombosis. Previously, the literature has considered only venous hypoperfusion in the pathogenesis of retinal vein occlusion (the prothrombotic ‘low-flow’ state presumed to arise from nocturnal hypotension). However, the EMBPS, already characterised as a Oh et al. [1] observed that branch retinal vein occlusion (BRVO) symptoms were often apparent between 6.00 a.m. and noon in their patients, suggesting that these retinovascular events occurred during sleep or in the initial hours after awakening. To explain this finding, the authors referred to the hypothesis that nocturnal arterial hypotension is an instigator of ocular ischaemic events. However, discussions on the diurnal variability of retinal vein occlusion might also acknowledge the ‘early morning blood pressure surge’ (EMBPS) [2] when considering mechanisms. The EMBPS is a normal circadian phenomenon whereby systemic arterial pressure is boosted in most persons from awakening to about 4–6 h thereafter [3] . This ‘supercharging’ of the circulation is believed to explain the well-noted pattern of early morning stroke and myocardial infarction [4] . Notably, with increasing age, the EMBPS becomes more pronounced and furthermore meets a retinal end-arteriolar system that has a decreased reflex response to variations in systemic arterial pressure [2, 5] . Hence, the combination of an enhanced EMBPS and an age-related weakening of retinal autoregulation can conceivably lead to pathogenic rheology in the retina. Received: January 17, 2008 Accepted: January 31, 2008 Published online: October 10, 2008