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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute arterial hypertension causes 3 types of fundus anomalies: hypertensive retinopathy, hypertensive choroidopathy and hypertensive optic neuropathy. Hypertensive retinopathy and optic neuropathy are characterised by retinal and optic disc capillary and precapillary occlusions, and a rupture of the inner hemato-retinal barrier resulting in retinal edema. Hypertensive choroidopathy is characterized by areas of choriocapillaris occlusion resulting in necrosis of the pigment epithelium which causes a rupture of the outer hemato-retinal barrier and retinal edema.
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PMID:[Macular edema in arterial hypertension]. 181 16

The retinal and choroidal vasculatures are supplied by different systems of blood vessels, each having distinct anatomic and physiologic properties. In response to systemic hypertension, tissues supplied by each of these vascular systems of the eye are affected differently and reveal different manifestations. Siegrist's streaks are sequelae of hypertensive choroidopathy, associated with acute systemic hypertension, generally indicative of a poor prognosis for patients presenting with them. A case report of this uncommon clinical condition is described along with a discussion of the associated hisopathology to allow for a better understanding of how the eyes may change secondary to systemic vascular disease.
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PMID:Siegrist's streaks in hypertensive choroidopathy. 339 88

Experimental renovascular malignant arterial hypertension was produced, by modified Goldblatt's procedures, in 60 rhesus monkeys, and hypertensive fundus changes were studied in detail (by serial ophthalmoscopy and fluorescein fundus angiography in all monkeys on a long-term follow-up, and pathologically in 29 eyes). In hypertensive choroidopathy, retinal pigment epithelial (RPE) lesions and serous retinal detachment (RD) were the classic ophthalmoscopic lesions, whereas fluorescein fundus angiography and histopathologic studies revealed marked abnormalities in the choroidal vascular bed, in addition to the changes in the RPE. The RPE lesions could be subdivided into initial acute focal lesions (due to focal RPE infarction), and degenerative lesions, which developed later and were progressive in nature, maximally involving the macular and peripheral regions of the fundus. The RD developed most commonly in the posterior pole and infrequently involved the peripheral retina. The choroidal vascular bed showed impaired circulation and extensive occlusive and ischemic changes. These studies revealed that hypertensive choroidopathy is as important a fundus change as hypertensive retinopathy. The pathogenesis of hypertensive choroidopathy is discussed in detail; the evidence indicates that it is due to choroidal ischemia, and that hypertensive choroidopathy and retinopathy are two independent and unrelated manifestations of renovascular malignant hypertension.
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PMID:Fundus lesions in malignant hypertension. VI. Hypertensive choroidopathy. 380 99

Malignant (accelerated) renovascular arterial hypertension was produced in 57 adult rhesus monkeys by clamping the renal artery (one-kidney model in 25 animals and two-kidney model in 32). The animals were investigated before renal artery clamping and serially thereafter by recording systolic arterial blood pressure (BP), biochemical changes, and changes in the fundus of the eye; the latter was evaluated by ophthalmoscopy, stereoscopic color fundus photography, and fluorescein fundus angiography. All of the animals developed arterial hypertension. The data on BP, biochemical, and fundus findings were analyzed and correlated. The findings of this study clearly showed that the various fundus lesions seen in these hypertensive animals fall into three distinct categories: (1) hypertensive retinopathy, (2) hypertensive choroidopathy, and (3) hypertensive optic neuropathy. The appearance of the retinopathy was significantly earlier than that of the choroidopathy or optic neuropathy (P less than 0.01), but the difference between the times of appearance of the choroidopathy and neuropathy was not significant. There was no significance in the order in which the three types of fundus changes reached their maximum severity. There was no significant difference between the mean BPs when the retinopathy, choroidopathy, or optic neuropathy first appeared, nor between the BPs at the time of their appearance and at the time when they were most marked. In monkeys of the one-kidney model, the rise in BP developed significantly (P = 0.01) faster and the fundus lesions appeared significantly (P = 0.00001) earlier than in those with the two-kidney model.
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PMID:Fundus lesions in malignant hypertension. III. Arterial blood pressure, biochemical, and fundus changes. 395 16

Experimental hypertensive choroidopathy was studied in 29 eyes from 15 monkeys in which accelerated renovascular systemic hypertension developed after a modified Goldblatt procedure. We followed up the animals from five days to 21 months to examine clinically and histopathologically the spectrum of the pathologic process. The pathologic features of hypertensive choroidopathy in our animals may be categorized into three phases: (1) Acute ischemic phase: The initial change in the choroidal vasculature was constriction of arterioles, which leads to focal necrosis of the choriocapillaris and the retinal pigment epithelium and focal subretinal exudate. (2) Chronic occlusive phase: Occlusive changes involving arteries, arterioles, and choriocapillaris occurred later. (3) Chronic reparative phase: With time, recanalization took place at all levels of the choroidal vasculature. The subretinal fluid was reabsorbed, leaving diffuse patchy depigmentation of the retinal pigment epithelium, which followed lobular arrangement of the choriocapillaris. Arteriolization of the choriocapillaris developed; this seems to be a defense mechanism to withstand the elevated systemic blood pressure.
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PMID:Fundus lesions in malignant hypertension. I. A pathologic study of experimental hypertensive choroidopathy. 402 50

Ocular manifestations of hypertension involve both retinal and choroidal circulation. Clinical and pathological studies suggest that choroidal changes are present in benign and malignant hypertension, though significantly greater in the later. Lesions classically described as Siegrist and Elschnig spots are described. Clinical evidence of choroidopathy from hypertension and arteriosclerosis has a significant prognostic value for life.
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PMID:Hypertensive choroidopathy. 713 Jun 11

The effects of systemic hypertension on the posterior segment of the eye are discussed under the headings of hypertensive choroidopathy, hypertensive retinopathy, and hypertensive optic disc edema. The sympathetic nervous control and autoregulatory mechanisms of the retinal and choroidal vasculatures are briefly reviewed. In hypertensive choroidopathy focal occlusion of choriocapillaris leads to necrosis of retinal pigment epithelium (Elschnig spots). Hypertensive retinopathy is described in vasoconstrictive, exudative, and sclerotic phases, followed by complications of the sclerotic phase. Hypertensive optic disc edema is influenced by the blood supply and extracellular tissue fluid pressure of the optic nervehead. In baboons with hypertensive disc edema, accumulation of axoplasmic components is observed in the optic nervehead.
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PMID:Pathophysiology of hypertensive retinopathy. 715 24

We report a case of a rare entity, choroidopathy in association with systemic lupus erythematosus (SLE), previously described in only twelve patients to our knowledge. It manifested by multiple focal serous elevations of the sensory retina and/or serous detachments of the retinal pigment epithelium bilaterally. No retinal vascular changes were observed. The probable pathogenesis is related to choroidal vascular disease due to systemic hypertension secondary to lupus nephritis, vasculitis, or a combination of these.
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PMID:Persistent choroidopathy in systemic lupus erythematosus. 778 85

After having highlighted the main possible ocular abnormalities in patients affected by chronic renal failure treated with hemodialysis, we describe our observations in 12 hemodialyzed patients. Evaluation of the examined fluoroangiographic patterns was interesting because, in seven patients (58.4%), focal choroidal perfusion defects were found, mainly localized in the posterior pole and nasal portion. Similar fluoroangiographic findings have been observed in patients with hypertension and diabetes mellitus and anatomic and histologic studies have proved the existence of diabetic choroidopathy; therefore, we suggest that the onset of choroidopathy in hemodialyzed patients depends on an early arteriolar atherosclerosis of the choroidal membrane, probably secondary to chronic renal failure rather than to extracorporeal dialysis.
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PMID:Fluoroangiographic findings in hemodialyzed patients. 830 89

Numerous theories have been proposed to explain the origin of central serous choroidopathy (CSC). However, it has been shown recently that there is a close relationship between CSC and type A-behaviour pattern (TABP) which is characterized by high adrenergic activity in the body. It is interesting to note that one of our patients who had chronic central serous choroidopathy, and metoprolol treatment for hypertension during one year, developed a recurrence of CSC three weeks after cessation of metoprolol treatment. This was one of the reasons to start this treatment modality for CSC. In this study, we present 6 cases of CSC in which the diagnosis was established by ophthalmoscopy and fluorescein angiography. In these patients, we proposed to analyse the relationship between CSC and a high adrenergic activity by the use of a selective beta-blocker (metoprolol; 50 mg tablets, twice daily). In two of the six cases, laser photocoagulation was also performed prior to commencement of the metoprolol treatment. Visual acuity improved in two patients, stayed at 1.0 in three patients and stabilized on the pretreatment level (0.8) in one patient (case-5). However, the symptoms (metamorphopsia and micropsia) and the signs (serous retinal detachment and angiographic hyperfluorescence) decreased or disappeared in all patients after treatment. Also visual complaints in all patients improved subjectively. No recurrences were noted during the metoprolol treatment in any of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of central serous choroidopathy with the beta receptor blocker metoprolol (preliminary results)]. 851 Apr 13


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