Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A six year old girl complained of sudden severe headache, became hemiplegic and unconscious. A right carotid arteriogram revealed an obstruction of the right anterior cerebral artery and many sulvian branches. Death occurred four days later. At autopsy, a recent softening of nearly all the right middle cerebral arterial territory was found. Thrombus filled the sylvian artery and its main branches. Histologic examination of the vessel walls showed a dissecting infiltration of blood between the internal elastic lamina and the media. This particular form of dissecting aneurysm, occurring in young subjects, in the absence of atherosclerosis, high blood pressure and idiopathic medial necrosis, represents a distinct medial necrosis, represents a distinct nosologic entity that has been called "Obstructive parietal hemodissection of intracranial vessels." The pathogenesis of the disease is unknown: trauma has been mentioned, also congenital defects in the elastic lamina or other morphologic abnormalities of that lamina.
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PMID:[Obstructive parietal hemodissection of the intracranial vessels, a particular form of dissecting aneurysm]. 83 66

Side effects, especially cardiovascular, of oral contraception in healthy women are discussed. A causal relationship between ovulation inhibitors and thromboembolic disease has been demon demonstrated epidemiologically and experimentally. Thrombus formation may be due to disturbances of blood coagulation, lesions, of the vascular wall, or blood flow disorders; the "pill" influences all 3 components. The role of the "pill" in the etiology of hypertension has not been explained, but there is no doubt of its existence. Although the risk to a healthy woman with no predisposing factors is small, it is real, and must be considered by the patient and her physician.
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PMID:[Oral contraceptives: pharmacotherapy of normal women (author's transl)]. 125 Aug 21

Thrombus formation in the left atrium and left ventricle is primarily due to stasis of blood which causes activation of the coagulation system. Migration of thrombotic material into the circulation depends on the dynamic forces of the circulation. Atrial fibrillation is the commonest underlying cardiac disorder predisposing to thromboembolism. Rheumatic mitral stenosis, left atrial enlargement, prior myocardial infarction, hypertension, and echocardiographic left ventricular hypertrophy are risk factors for thromboembolic stroke in elderly patients with chronic atrial fibrillation. Non-valvular atrial fibrillation accounts for 45% of cardiac sources of thromboembolic stroke and includes patients with ischemic heart disease, hypertension, thyrotoxic heart disease, hypertrophic cardiomyopathy, chronic sinoatrial disorder, and idiopathic atrial fibrillation. 15% of cardiac sources of thromboembolic stroke are associated with acute myocardial infarction, 10% with left ventricular aneurysm and mural thrombi remote from an acute myocardial infarction, 10% with rheumatic valvular heart disease, and 10% with prosthetic cardiac valves. Mitral valve prolapse, mitral annular calcium, nonischemic cardiomyopathies, infective endocarditis, nonbacterial thrombotic endocarditis, left atrial myxoma, paradoxical embolism associated with congenital heart disease, calcific aortic stenosis, and complex atherosclerotic plaque within the proximal aorta also contribute to thromboembolism.
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PMID:Etiology and pathogenesis of thromboembolism. 176 43

Epidemiological surveys show the clear association of hypertension with an increased risk of developing ischaemic heart disease. One method of quantifying atherosclerosis is to measure, at necropsy, the percentage of the intimal surface of the coronary arteries or aorta which is occupied by raised plaques. When this is done in a large number of subjects the amount of intimal involvement in any particular geographical population correlates directly with the frequency of ischaemic heart disease. In all these populations, whether at a high risk or low risk of developing ischaemic heart disease, hypertensive subjects have a greater intimal involvement by plaques than normotensive subjects. Thus, the increased risk in hypertension is, in part, mediated by possession of more plaques. Plaque growth is due to the accumulation of lipid from the plasma, the ingress of monocytes with their conversion to lipid filled foam cells and the formation of collagen by smooth muscle cells. Hypertension may act by altering endothelial function to potentiate all these processes. Mechanical stress on endothelial cells will evoke the formation of growth factors for smooth muscle cells. Plaque growth in man is also episodic due to the formation of thrombi; a proportion of these episodes are symptomatic producing acute myocardial ischaemia but the majority are silent leading to sudden plaque expansion. Thrombi over plaques are either due to endothelial denudation injury or more commonly due to the tearing of the cap of a plaque leading to deep intimal injury. Necropsy surveys of control populations show that subjects with hypertension have a greater frequency of recent plaque tears compared with normotensive subjects.
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PMID:Hypertension and atherosclerotic (ischaemic) heart disease. 194 81

Treatment of anemia with human recombinant erythropoietin (EPO-R) and its effect on bone marrow was studied in 10 anemic patients on periodic hemodialysis (HD). Blood transfusion was not required once treatment started. Hemoglobin (Hb) levels normalized at six months in all patients (7.2 +/- 0.2 vs 12.4 +/- 3 g/dl, p less than 0.01). Serum ferritin levels decreased progressively as Hb increased (r = -0.5609), and six patients needed iron supplement since the third month. Bone marrow iron deposits decreased significantly (p less than 0.001), together with an increase of cellularity and improvement of erythrodysplasia. EPO-R was associated with worsening hypertension in previously hypertensive patients, although it could be controlled with more aggressive treatment. Thrombotic events either systemic or at the vascular access, were not observed. EPO-R corrects the anemia in uremic patients undergoing HD. Iron stores and blood pressure in hypertensive patients on treatment with EPO-R must be monitored regularly.
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PMID:[Treatment of anemia with recombinant human erythropoietin and the bone marrow response in uremic patients undergoing periodic hemodialysis]. 224 77

Long-term performance of Starr-Edwards silastic ball (SESB, n = 168) and St Jude Medical bi-leaflet (SJMB, n = 93) valves in patients who were alive 30 days after implantation (1980-86) for aortic stenosis was compared. Mean follow-up was 3.0 years (0.1-7.9 years). The SESB and SJMB groups differed as regards female gender (18% vs 47%, P less than 0.0001), NYHA classes III-IV (59% vs 72%, P less than 0.05), coronary artery disease (CAD, 32% vs 62%, P less than 0.01) in patients with coronary arteriography (n = 82 and n = 55, respectively), and prosthetic annulus diameter (26 +/- 1 vs 23 +/- 2 mm, P less than 0.0001). Five-year survival +/- SE in SESB vs SJMB patients was: total population, 89 +/- 3% vs 80 +/- 6% (NS); coronary arteriography population, no CAD, 90 +/- 4% vs 100% (NS), and with CAD, 71 +/- 11% vs 60 +/- 13% (NS; P = 0.01 for CAD). Five-year event-free survival +/- SE in SESB vs SJMB patients was 95 +/- 2% vs 97 +/- 2% (NS) for thromboembolism, 95 +/- 2% vs 89 +/- 4% (NS) for coumadin-related haemorrhage, 98 +/- 1% vs 99 +/- 1% (NS) for endocarditis, 98 +/- 1% vs 94 +/- 5% (NS) for paravalvular leak, 88 +/- 3% vs 79 +/- 6% (NS) for all valve-related complications, and 98 +/- 1% vs 95 +/- 4% (NS) for prosthesis replacement. Thrombotic occlusion or structural failure were not observed. No patients without CAD experienced thromboembolic events. Cox regression analyses (in both total population and coronary arteriography population) of survival as well as the various complications revealed that the type of prosthesis did not have predictive influence. CAD was an independent risk factor for thromboembolism, haemorrhage, and all valve-related complications. Previous systemic hypertension was independently predictive of haemorrhage. The SESB and SJMB prostheses showed comparable and acceptable long-term performance. Only patient-related variables, notably CAD, influenced late results. The proven durability and relatively low price of the SESB valves together with the excellent haemodynamic performance of even small-sized SJMB valves should be considered in the light of the present results.
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PMID:Long-term performance of Starr-Edwards silastic ball valves and St Jude Medical bi-leaflet valves. A comparative analysis of implantations during 1980-86 for aortic stenosis. 231 12

Changes in the choroidal artery were examined at autopsy in 16 Japanese patients with hypertension and insulin-dependent diabetes mellitus. These changes could be divided into 1) arteriosclerotic ones consisting of intimal thickening due to migration of smooth muscle cells, 2) hyaline deposits in the subendothelium, 3) extensive degeneration (moth-eaten atrophy and necrosis) of medial smooth muscle cells, and 4) changes resulting from fibrinoplatelet thrombi and their organization (recanalization and obstruction). The intimal thickening and medial damage correlated with aging, were accelerated by hypertension, and were remarkable in arterioles less than 60 micron in diameter. Diabetes mellitus apparently did not enhance these vascular changes. Thrombotic occlusion or narrowing of the choroidal artery was frequently observed in the arterioles of patients with hypertension and diabetes mellitus who had chronic azotemia or renal insufficiency. Subendothelial hyaline deposits were increased in patients with diabetes. The narrowing or obstructive changes in the choroidal artery were extensive in the intraocular blood vessels. These changes may be secondary and induce damage to other intraocular blood vessels and tissues, including the retina.
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PMID:Clinical choroidal thrombosis, hypertension, and diabetes mellitus: an electron microscopic study. 333 93

Two cases of complete sagittal sinus occlusion with multiple brain hemorrhages, elevated intracranial pressure, and disseminated intravascular coagulation are described. These patients were successfully managed using pentobarbital-induced coma to ameliorate intracranial pressure elevation. This therapy was combined with monitoring of intracranial pressure and intermittent drainage of cerebrospinal fluid to further control intracranial pressure elevations. Thrombus and coagulopathy resolved with pentobarbital alone in one patient and after pentobarbital plus heparin therapy in the second patient. It is suggested that cases of severe distal sagittal sinus thrombosis with brain hemorrhage and intracranial hypertension may benefit from combined pentobarbital coma and intraventricular drainage. This allows for stabilization of bleeding tendencies before instituting heparin therapy when necessary. Management of sagittal sinus thrombosis with barbiturates or ventricular drainage is best performed in an intensive care unit environment with continuous monitoring of intracranial pressure and substantial electrophysiologic and neuroradiologic support.
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PMID:Treatment of sagittal sinus thrombosis associated with cerebral hemorrhage and intracranial hypertension. 338 62

Although lipids have received most attention in relation to atherosclerosis, vessel injury also has a role in the development of atherosclerotic lesions. Thrombi that form at sites of injury can be incorporated into the wall, causing thickening, and platelets that adhere to damaged vessel walls release a growth factor (PDGF) that stimulates smooth muscle cell proliferation. The early lesions of atherosclerosis are focal and develop around vessel orifices and branches in relation to the patterns of blood flow and areas of increased permeability and endothelial cell damage. Platelets also contribute to the complications of advanced atherosclerosis caused by occlusive thrombi, thromboembolism, and spasm. The causes of vessel wall injury are not established, although there is evidence pointing to disturbed blood flow, hypertension, antigen--antibody complexes, complement, materials originating from platelets and white blood cells, bacteria, endotoxin, viruses, smoking, dietary lipids, homocystinemia, diabetes, other metabolic disorders, and stress. Platelets do not adhere to intact endothelium, but they adhere to the constituents of the subendothelium, release the contents of their granules (including PDGF), and form thromboxanes. If blood flow is disturbed, platelet--fibrin thrombi can form at sites of injury. Platelet adherence to a damaged wall does not require von Willebrand factor except under conditions of high wall shear. Repeated injury of a vessel wall leads to the development of lipid-rich atherosclerotic lesions, even in normocholesterolemic animals, but these lesions do not form if the experimental animals are made thrombocytopenic before injury is induced. Measurable changes in platelets that are associated with the clinical complications of atherosclerosis include shortened survival, release of granule contents (platelet factor 4, beta-thromboglobulin, thrombospondin), formation of thromboxanes, and decreased buoyant density. "Antiplatelet drugs" such as aspirin are proving to be beneficial in selected groups of patients, such as those with unstable angina. Thromboxane synthetase inhibitors and agents that block the thromboxane receptor on platelets are under investigation. Long term administration of "antiplatelet drugs" to affect the rate of development of atherosclerosis seems neither feasible nor desirable. Modification of dietary and smoking habits and control of hypertension are more likely to be beneficial for most individuals.
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PMID:The role of platelets in the development and complications of atherosclerosis. 351 36

We have analyzed the safety of doing pulmonary angiography in 67 consecutive patients with moderate-to-severe primary pulmonary hypertension or hypertension secondary to chronic thromboembolic occlusions of the pulmonary arteries. The average (+/- SD) pulmonary arterial systolic and diastolic pressures were 74 +/- 19 and 34 +/- 10 mm Hg, respectively. Fourteen patients had a right ventricular end-diastolic pressure of 20 mm Hg or more. Selective left and right main pulmonary artery injections were done using ionic contrast agents in 56 patients and nonionic contrast agents in 11. No major rhythm disturbances or systemic hypotension requiring therapy occurred, and there were no deaths. Thrombotic occlusions of the pulmonary arteries were identified in 52 patients and confirmed in all 42 of those who had a thromboendarterectomy. At autopsy, 3 of the 15 patients who had normal angiograms were found not to have had thrombotic occlusions. We conclude that pulmonary angiography can be done safely despite the presence of severe pulmonary hypertension and right ventricular failure, and that the procedure leads to the identification of chronic, major-vessel thromboembolic pulmonary hypertension that may be alleviated by thromboendarterectomy.
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PMID:Pulmonary angiography in severe chronic pulmonary hypertension. 363 91


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