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

We produced experimental renovascular malignant arterial hypertension by modified Goldblatt's procedures, in 60 rhesus monkeys. Hypertensive retinopathy was studied in detail (by ophthalmoscopy, and stereoscopic color fundus photography and fluorescein fundus angiography on long-term follow-up). Cotton-wool spots (CWSs) were found to be an important, early retinal lesion. On ophthalmoscopy, they had a characteristic appearance. Fluorescein fundus angiography of these lesions revealed focal retinal capillary nonperfusion. The CWSs usually lasted for over 3 weeks and resolved within 6 weeks, leaving permanent obliteration of the retinal capillaries in their distribution, secondary intraretinal microvascular abnormalities, and retinal nerve fiber loss. We discuss pathogenesis and other features of CWSs. There is overwhelming evidence that CWSs are due to occlusion of the terminal retinal arterioles, resulting in acute focal inner retinal ischemia; hence the scientifically valid term for them would be 'inner retinal ischemic spots'.
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PMID:Cotton-wool spots (inner retinal ischemic spots) in malignant arterial hypertension. 274 98

In 60 rhesus monkeys with experimental renovascular malignant arterial hypertension (25 one-kidney and 35 two-kidney model animals), we studied the so-called 'hard exudates' or white retinal deposits in detail (by ophthalmoscopy, and stereoscopic color fundus photography and fluorescein fundus angiography, on long-term follow-up). Some manifestation of hypertensive retinopathy developed in 19 one-kidney and 19 two-kidney animals, and white deposits formed in 14 and 5 monkeys, respectively. The onset of white deposits showed no correlation to severity of arterial hypertension or of retinopathy. All eyes with white deposits had antecedent macular or retinal edema. The deposits were everchanging, taking months or even more than a year to resolve. Our study suggests that in hypertensive retinopathy the white retinal deposits are most probably the result of exudative and/or neural degenerative processes. All the available pieces of evidence indicate that it is more appropriate to call the white deposits 'lipid deposits' than 'hard exudates'.
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PMID:Retinal lipid deposits in malignant arterial hypertension. 274 99

We produced experimental renovascular malignant arterial hypertension by a modified Goldblatt's procedure in 60 rhesus monkeys (25 one-kidney model and 35 two-kidney model), and studied various macular lesions by detailed serial ophthalmoscopy, and stereoscopic color fundus photography and fluorescein fundus angiography on a long-term follow-up. The various lesions which developed in the macular region included retinal edema, cystic retinal changes, serous retinal detachment, retinal pigment epithelial changes (initially acute focal and later degenerative lesions), and lipid deposits. In addition to these, the usual retinal lesions associated with hypertensive retinopathy, e.g., focal intraretinal periarteriolar transudates, cotton-wool spots and retinal hemorrhages, were also frequently seen in the macular retina. Findings on the various lesions are described in detail, and the pathogenesis of macular edema in malignant arterial hypertension is discussed.
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PMID:Macular lesions in malignant arterial hypertension. 274

Sixteen patients with CT evidence of a single cerebral lacuna had no clinical findings to indicate stroke syndromes. All patients had systemic arterial hypertension; 12 (75%) had cardiographic evidence of left ventricular hypertrophy, ten (63%) had radiologic evidence of cardiomegaly, and ten (63%) had clinical signs of hypertensive retinopathy. All lacunas were located in the supratentorial region (seven in the anterior capsular limb, three in the caudate, two in the external capsule, two in the putamen, one in the corona radiata, and one in the thalamus). During the three-year follow-up period, seven had clinical lacunar stroke syndrome, three had cortical stroke, two had myocardial infarction, and one died suddenly of unknown cause.
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PMID:Neurologically asymptomatic patients with a single cerebral lacuna. 276 3

Using computerized M-mode echocardiography we have investigated 58 hypertensive subjects in order to assess whether a correlation could be demonstrated between left ventricular changes induced by hypertension and age of the patients, the duration and severity of hypertension, and damage to other target organs. Various morphological changes of the left ventricle were detected: 14 patients (24%) had concentric hypertrophy of the left ventricle, 12 (20%) had asymmetric septal hypertrophy, 5 (8%) had dilated left ventricle without hypertrophy. Left ventricular mass was increased, when compared to normal controls in 24 patients (41%). With respect to functional abnormalities, the peak lengthening rate of left ventricular dimension in diastole was decreased (+dD/dt less than s-1) in 25 patients (43%). Eight of these patients (14%) also had depressed peak shortening rate of left ventricular diameter in systole (-dD/dt less than 1.9 s-1). Hypertensive retinopathy was present in 23 patients (39%) and impairment of renal function in 8 (14%). Left ventricular mass and systolic and diastolic parameters of left ventricular function did not correlate significantly either with the age of the patients, or with the duration and severity of hypertension, or with the damage present in target organs other than the heart. Left ventricular mass was inversely correlated with the index of left ventricular relaxation (r = -0.53; P less than 0.001), whereas neither the latter nor left ventricular mass were correlated with peak systolic stress. Instead, peak systolic stress was inversely correlated with peak shortening rate of left ventricular diameter, an index of systolic function (r = -0.50; P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Functional anatomy of the left ventricle in hypertensive subjects. Correlations with the clinical severity of hypertension]. 297 24

We present two patients with proved chronic glomerulonephritis who had severe refractory hypertension and chronic renal failure. In both patients normal-sized kidneys were demonstrated in addition to vascular bruits and Grade III hypertensive retinopathy. These findings raised the suspicion of an etiological condition other than chronic glomerulonephritis underlying the hypertension and renal failure. Renal angiography revealed bilateral severe renal artery stenosis. In both cases renal revascularization was followed by a drop in blood pressure to normal or near normal levels. In selected cases with severe hypertension and chronic renal failure, renal artery stenosis should be considered, despite the coexistence of chronic glomerulonephritis.
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PMID:Symptomatic renal artery stenosis superimposed on chronic glomerulonephritis. 315 24

We conducted a detailed investigation into retinal hemorrhages in renovascular malignant arterial hypertension experimentally produced in rhesus monkeys. The hypertension was produced by modified Goldblatt's procedures in 60 rhesus monkeys and hypertensive fundus changes were studied by ophthalmoscopy, stereoscopic color fundus photography and fluorescein fundus angiography. Our study revealed that, in hypertensive retinopathy due to malignant hypertension, retinal hemorrhages usually did not constitute either one of the earliest or one of the most conspicuous retinal lesions, but, on the contrary, were a minor feature of the retinopathy. Neither the time of onset of retinal hemorrhages nor their peak severity showed any significant correlation with the level of the arterial hypertension. The hemorrhages were usually situated in the nerve fiber layer, and could be located anywhere in the fundus but were usually found in the distribution of the radial peripapillary retinal capillaries. There was no association between the presence of retinal hemorrhages and retinal venous changes; the latter were seen only in a minority of animals and consisted of retinal venous stasis, venous collaterals and arteriovenous shunts.
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PMID:Retinal hemorrhages in malignant arterial hypertension. 322 3

In order to assess the incidence and the determinants of hypertensive vascular changes in the retina of patients with coarctation of the aorta, fifty (37 male and 13 female) were analyzed. The mean age of the group was 18.7 +/- 10.3 years. No one had evidence of nephropathy. Different degrees of hypertensive retinopathy (Puig-Solanes classification) were observed in 54%. Of the patients, no one had papilledema. Retinal vascular damage was not related to either age or sex. The group of patients with retinal vascular lesions had a mean level of systolic arterial pressure higher than the group with normal retinas. Multivariant statistical analysis of the results permitted the identification of systolic arterial pressure higher than 150 mm Hg, age greater than 15 years and cardiomegaly as the three variables more frequently associated with retinal vascular lesions. Surgical correction of the aortic malformation resulted in normalization of both systolic and diastolic arterial pressures in 98% of the total number of patients as determined one year postoperatively. It is concluded that, in coarctation of the aorta, vascular damage of the retina appears to have an incidence that is similar to that observed in patients with other forms of systemic arterial hypertension. The development of these retinal lesions in patients with coarctation of the aorta would seem to be determined by the severity and duration of the hypertensive process.
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PMID:[Hypertensive retinopathy in patients with aortic coarctation]. 324 26

In 205 patients with histologically evaluated glomerulonephritis, 69 patients with essential hypertension and 12 patients with renovascular hypertension, the retina was examined and evaluated by fundus photography. Changes of the retina were classified according to the recommendations of WHO: mild to severe changes of retinal arteries were termed as mild hypertensive retinopathy, and exaggerated changes, including exudates, hemorrhages and optic disc changes, as severe hypertensive retinopathy. In spite of the short duration of renal disease and the young age of the patients in many cases, retinal changes in patients with renal hypertension were significantly more severe: especially in focal segmental sclerosis and membranoproliferative glomerulonephritis was severe hypertensive retinopathy observed. Mild hypertensive retinopathy was more prevalent in essential hypertension. When renal disease progresses the retinal findings tended to deteriorate as well. Since the 24-hour blood pressure profile was comparable in most of the groups studied, it was supposed that the vulnerability of the retina and probably other vascular beds (e.g. kidneys) was increased. We conclude that the retina of these patients should be examined even in the case of relatively mild hypertension (greater than 180/100 mm Hg) and early antihypertensive treatment is an important requirement.
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PMID:Severe hypertensive retinopathy. Increased incidence in renoparenchymal hypertension. 343 98

We present a case report of a patient suffering of severe hypertension and grade IV hypertensive retinopathy according to the Keith-Wagener classification. Simultaneously hypertensive encephalopathy was present confirming the poor prognosis of discoedema occurring in the course of hypertension when left untreated. Hypertension was related to chronic poisoning with glycyrrhiza, and its hyperaldosteronism like effect. Pathogenesis of discoedema in malignant hypertension is discussed.
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PMID:[Hypertensive retinopathy and papilledema. Apropos of a case of glycyrrhizin poisoning]. 345 Jul 2


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