Israel Medical Association Journal

Background: The causative role of diffuse macular edema in various etiologies is often undetermined.

Objectives: To describe an association between extrafoveal vitreous traction and non-diabetic diffuse macular edema secondary to various ocular entities.

Methods: In a retrospective study of eyes with non-diabetic diffuse macular edema, charts and optical coherence tomography scans demonstrating extrafoveal vitreous traction were analyzed. Excluded were diabetic patients and eyes that had vitreofoveal traction. A control group (n=12) allowed for mapping of normal macular thickness.

Results: Five eyes with macular edema were associated with extrafoveal traction, each secondary to and representing a different etiology. The causes were penetrating injury, cataract extraction, branch retinal vein occlusion, central retinal vein occlusion, and idiopathic. Vitreous traction was detected either at the papillomacular bundle (n=3), superonasally to the fovea (n=1), and at the optic nerve head (n=1). The associated retinal edema (all eyes) and serous retinal detachment (four eyes) at the traction sites were in continuum with the foveal edema in each eye, manifesting as diffuse macular edema. Of the two modalities, the OCT[1]-Line group program and the OCT-Automatic central program, only the former enabled detection of extrafoveal traction in each.

Conclusions: Diffuse macular edema secondary to various ocular diseases may be associated with extrafoveal vitreous traction. The OCT-Automatic central program may omit some of these extrafoveal traction sites. Further studies are required to validate these findings and to assess whether early vitrectomy may improve visual prognosis in these eyes.

Background: In recent years there has been an increase in endovascular repair of thoracic aortic aneurysms. In cases of insufficient neck length, occlusion of left subclavian artery achieves proper sealing and is usually well tolerated. Selected cases require revascularization of the left subclavian artery, including patients after coronary bypass surgery (left internal mammary to left anterior descending) and those with arm claudication or subclavian steal syndrome.

Objectives: To evaluate the tolerability of left subclavian artery occlusion by stent graft without revascularization.

Methods: Thirty patients with thoracic aortic aneurysms underwent endovascular repair between July 2000 and November 2004. Eleven of them had occlusion of the left subclavian artery that required revascularization in two. Follow-up (average 3 years) included a) blood pressure measurements of both arms at rest, after effort and pulse palpation, and b) vertebral blood flow by duplex scan.

Results: Of nine patients with no revascularization, 8 (89%) tolerated left subclavian artery occlusion with no claudication or steal syndrome; one (11%) suffered mild claudication only after effort and required no intervention. No left radial pulses were palpated in the nine patients. Blood pressure measurements in the left arm showed an average decrease of 40%, which remained constant after induced effort in all patients and was clinically insignificant. Duplex scan demonstrated reverse flow in the left vertebral artery in 8 of 9 patients (89%) and occlusion in 1 (originating in the arch and covered by the stent graft) with no clinical symptoms.

Conclusions: Left subclavian artery occlusion by stent graft is a tolerable procedure in the long term. In most cases, the constant decrease in blood pressure remained unchanged during follow-up and had no significant adverse affects. Most patients do not require revascularization prior to the endovascular procedure.
 

Renal vein occlusion in adults is usually a result of vein thrombosis, which is frequently associated with the nephrotic syndrome. The anatomy of renal vascularization is of primary importance for understanding its pathophysiological responses and the clinical and diagnostic presentation of patients with this condition. The reaction of the kidney to its vein occlusion is determined by the balance between the acuteness of the disease, extent of the development of collateral circulation, involvement of one or both kidneys and the origin of the underlying disease. Renal vein occlusion is generally a complication of some other condition, but may also occur as a primary event. The main goals of therapy should be to conserve renal parenchyma in order to maintain renal function and prevent thromboembolic phenomena.

Background: Previous studies have demonstrated myocardial salvage by basic fibroblast growth factor administration following chronic myocardial ischemia or acute myocardial infarction.

Objectives: To study the effect of bFGF[1] on left ventricular morphometry following coronary occlusion and reperfusion episode in rats.

Methods: bFGF (0.5 mg) or placebo was continuously administered for a period of one week using an implanted osmotic pump. Animals were sacrificed 6 weeks after surgery and myocardial cross-sections were stained with Masson-trichrome and with anti-proliferating cell nuclear antigen antibody.

Results: LV[2] area, LV cavity diameter, LV cavity/wall thickness ratio, and injury size were unchanged compared with control animals. Proliferating endothelial cells were significantly more abundant in injured compared with normal myocardium, but with no differences between animals treated or not treated with bFGF.

Conclusions: One week of systemic bFGF administration following coronary occlusion and reperfusion had no additional effect on LV geometry or cellular proliferation in rats.

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[1] bFGF = basic fibroblast growth factor

[2] LV = left ventricular