Glaucoma, recognized as optic neuropathy is the second largest cause of blindness worldwide. The disease is characterized by progressive loss of retinal ganglion cells and visual field defects. The pathophysiological factors involved in the onset and progression of glaucoma are not fully understood. However, it is now well accepted that elevated intraocular pressure is not the only causative factor. The pathophysiology of glaucoma involves multiple factors that interact in a highly complex manner to favor development of glaucomatous optic neuropathy. As the knowledge of molecular mechanisms involved is expanding, more and more therapeutic targets are being recognized for the development of safe and effective pharmacotherapy of glaucoma. Although at present the intraocular pressure lowering drugs are still the first line of treatment, the prospect of introducing neuroprotective therapies that can directly protect and perhaps stimulate regeneration of dying and dead retinal ganglion cells, shows considerable promise. This review presents recent developments in the pathophysiology and pharmacotherapy of glaucoma.
Coarctation of the aorta is a congenital anomaly presented by the combination of upper body hypertension and weak or absent femoral pulses. Increased morbidity and shortened life span of infants born with coarctation suggest that the malformation should be treated early in life. Surgical intervention has been recognized as the gold standard of treatment for children born with this defect. Unfortunately, studies in many institutions have shown that the diagnosis of coarctation of the aorta is often missed. As a consequence, many patients with coarctation of the aorta are not detected until adult life. Long-term follow-up of adult patients following surgical intervention for coarctation of the aorta reveals ongoing risks; hence, less invasive endovascular therapy becomes an alternative approach. Literature’s review was performed to compare the results of endovascular therapy (stenting and angioplasty) with surgical techniques to repair adult with coarctation of the aorta. The immediate improvement in hypertension and the morbidity were similar. Although stenting can be expected to show superiority to balloon angioplasty alone, that was not apparent when comparing these two endovascular approaches. The morbidity, mortality, and repeat intervention rates were just as high for stenting as they were for angioplasty or for a combination of both modalities. The majority of surgical complications were minor (i.e., vasculitis, bleeding), whereas the majority of endovascular complications could be considered more severe (i.e., dissection, traumatic aneurysm, stroke). Surgical therapy was associated with a very low risk of restenosis and recurrence, whereas endovascular therapy had a much higher incidence of restenosis and the need for repeat interventions. In conclusion, surgical therapy is superior compared to other modes of interventional therapy for adult with coarctation of the aorta, and it shall remain as current mode of therapy for adult with coarctation of the aorta.