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

The physician who understands the pathophysiology of angina pectoris can apply rational therapeutic measures based on an appreciation of the determinants of myocardial oxygen supply and demand. Most patients with angina secondary to coronary atherosclerosis can be treated conservatively using a systematic approach that includes correction or removal of underlying causes or precipitating factors and the judicious use of sublingual nitroglycerin. In patients with more resistant angina, use of oral or topical nitroglycerin or sublingual isosorbide dinitrite as well as propranolol can be advised. Aortocoronary bypass surgery can offer significant improvement in carefully selected patients with frequent angina poorly controlled by medical therapy. The most important consideration in the treatment of angina is protection of coronary blood flow reserve by primary prevention of the atherosclerotic process itself. All individuals from families prone to coronary artery disease should be evaluated for alterable risk factors, the most important being cigarette smoking, hypertension, and hypercholesterolemia. Considering the high risk of unheralded sudden death in previously asymptomatic patients with coronary atherosclerosis, angina can, in a sense, be considered a fortunate harbinger of coronary stenosis, identifying candidates for secondary preventive measures aimed at retarding the progression of vascular disease. More importantly, angina serves as an index for detecting families at high risk of coronary artery disease, in whom early application of primary prevention may afford a more promising outlook.
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PMID:Angina pectoris. Diagnosis and treatment. 0 83

Intraparenchymal renal aneurysms have been reported with increasing frequency; yet, to our knowledge, this subject has not been reviewed in radiologic literature. The spectrum of such aneurysms includes congenital aneurysms, those secondary to disease usually affecting the main renal arteries, those associated with renal masses, microaneurysms, and false or pseudo aneurysms. Seemingly unrelated conditions, such as atherosclerosis, bacterial endocarditis, and trauma, can all produce similar radiographic appearance of aneurysmal dilatation within the kidney, albeit through differing mechanisms. In addition, there are several etiologies for renal microaneurysms, even though this finding has been considered specific for polyarteritis in the past. Although there were a few guidelines for recognizing certain specific etiologies based solely on the angiographic appearance, it must be appreciated that many of these conditions may be indistinguishable. The possibility of hemorrhage from such intrarenal aneurysms, and the question of whether such lesions are responsible for renovascular hypertension are also discussed.
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PMID:Intrarenal arterial aneurysms. 1 Jan 34

Plasma cholesterol was lower in spontaneously hypertensive rats (SHR), while plasma triglyceride and free fatty acid were increased in comparison with control normotensive Wistar-Kyoto (WK) rats. Correspondingly, [1-14C]-acetate incorporation into liver cholesterol was clearly decreased in SHR as compared with WK. As for lipogenic enzyme activities, glucose-6-phosphate dehydrogenase, malic enzyme and acetyl-CoA carboxylase in SHR were respectively decreased, increased and not significantly different, in comparison with WK rats. Liver cholesterol was rather low and cardiac triglyceride was slightly increased in SHR. Aortic cholesterol and triglyceride levels were not significantly different between SHR AND WK rats. Thus, SHR have an abnormality in lipid metabolism, especially in cholesterol synthesis, but the pathological implication of this in hypertension and related vascular lesions is not yet clear.
Atherosclerosis 1977 Nov
PMID:Lipid metabolism in spontaneously hypertensive rats (SHR). 2 30

The opinion is emerging that beta-blocking drugs have an important role in management of patients following acute myocardial infarction. Already beta-blocking drugs are accepted as the treatment of choice in hypertension and in angina pectoris--in the major risk factor and consequence respectively of coronary atherosclerosis, and both commonly recognized in patients who survive acute myocardial infarction. But beta-blocking drugs also may be of benefit in reducing the incidence and risk of subsequent infarction, and so may be of value for long term treatment of patients who have no symptoms whatever following acute infarction.
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PMID:The role of long term beta-blockade after myocardial infarction: Paper 1. 3 Apr 41

Arteriosclerosis is caused by many factors. These pathogenic factors especially over-nutrition, nicotinabusus, deficiency of muscular exercise, muscular overstrain, emotional stress and concomitant basic diseases, especially arterial hypertension, diabetes mellitus and dyslipidemia are the most important points for preventive and therapeutical action. When possible the risk factors has to be eliminated, arterial hypertension, diabetes mellitus and dyslipidemia have to be treated orderly. In the pathogenesis of arteriosclerosis and atherosclerosis are known disturbances of the lipid metabolism, the blood coagulation and the metabolism of the arterial wall cells most important. Application of anticoagulants and lipid lowering medicaments did not come up to our expectations. Experiences with animal models and a double blind study (secondary prevention of myocardial infarction) have given good reason for recommending antirheumatic or as we like to say, mesenchyme suppressive drugs.
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PMID:[Prevention and therapy of arteriosclerosis (author's transl)]. 3 60

Cardiovascular disease is a major cause of morbidity and mortality in the U.K. and other developed countries. In the U.K., mortality from coronary heart disease has increased progressively over the past 25 years, particularly in males. This paper examines the possible role of trace metals in the development of cardiovascular disease, with particular reference to the effects of cobalt, cadmium and lead in myocardial disease, atherosclerosis and hypertension. It is concluded that cobalt is an unimportant factor in community levels of cardiovascular disease, that cadmium has striking effects on blood pressure in animals and that there is some evidence for an association between environmental lead and high blood pressure.
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PMID:Cardiovascular disease and trace metals. 4 Feb 34

The media of arteries is virtually avascular. Thus, oxygen and nutrients must reach the cells of the media by diffusion from the lumen of the vessel and from adventitial vessels. The thickness of the thoracic aorta of man and dog exceeds the effective diffusion distance of oxygen, but nutrition is supplemented by vasa vasorum which enter into the outer layers of the media. Occlusion of vasa vasorum in dogs produces medial necrosis, which indicates that these vessels are essential for the nourishment of the aorta. Recently the microsphere method has been used to provide the first measurements of blood flow through vasa vasorum. There is substantial flow to the outer layers of media of the thoracic aorta in dogs, with virtually no blood flow in the inner layers. The vessels are very responsive to physiological stimuli: they dilate during infusion of adenosine and constrict during stimulation of sympathetic nerves. During acute increases in arterial pressure, blood flow to the media decreases probably from distortion of vasa vasorum. Vasa vasorum may play role in disease states. Insufficient blood flow through vasa vasorum may contribute to medial necrosis of the aorta and to aortic atherosclerosis. A role of vasa vasorum in aortic changes in hypertension and other vascular diseases merits further study.
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PMID:Role of vasa vasorum in nourishment of the aorta. 4 7

This study was carried out to determine the evolution of atherosclerotic lesions during a therapeutic period during which regression might be appreciated. We produced aortic and coronary atherosclerosis in 27 young adult stumptail macaques (Macaca arctoides) by feeding a diet supplemented with 2% cholesterol and 25% fat. Hypertension was produced by bilateral or unilateral narrowing of the renal artery. After six months of this regimen, four monkeys were killed (group 1) and 23 monkeys were divided into three groups: group 2 received unsupplemented diet; group 3 received the same diet as group 2 and drug treatment for hypertension; group 4 was continued on the atherogenic diet and received antihypertensive drug treatment. The results indicate that deleting the atherogenic diet leads to a decrease in the lipid content of the lesions and a transformation of the lipid laden atherosclerotic plaques into lipid-poor, fibro-collagenous lesions, with a decrease in the amount of coronary luminal narrowing. Partial control of systolic hypertension by antihypertensive drugs did not accelerate the involution of the atherosclerotic lesions over the relatively short period of this study. No statistically significant correlation by regression analysis was observed between the level of blood pressure elevation, the plasma renin activity, or the degree of the drug response, and the severity and extent of the atherosclerotic lesions. Furthermore, severe arterial hypertension without an atherogenic diet (group 5) produced arteriosclerosis of the aorta, and intensified branch cushions in the coronary arteries, without inducing lipid deposition in either vascular bed.
Atherosclerosis 1978 Apr
PMID:Diet-induced atherosclerosis and experimental hypertension in stumptail macaques (Macaca arctoides). Effects of antihypertensive drugs and a non-atherogenic diet in the evolution of lesions. 9 44

Not every case of angina pectoris occurring in a hypertensive patient is indicative of coronary atherosclerosis. Nine patients with essential hypertension of moderate degree had attacks of angina of sufficient severity to require investigation by arteriography. In these patients, the coronary arteriogram was normal but ventriculography showed hypertrophy of the walls of the left ventricle of restrictive or obstructive type. These appearances were confirmed by echocardiography which also showed hypertrophy of the septum and, in certain cases, confirmed the involvement of the ventricle, while by contrast the electrocardiogram and radiological appearances of the heart were essentially normal. The beta-blockers may have an important part to play in such conditions, and echocardiography is suggested as part of the routine investigation in cases of hypertension.
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PMID:[Angina pectoris in a hypertensive patient with left ventricle hypertrophy: echo-angiographic comparisons]. 10 Nov 81

Prostaglandins (PG) are highly unsaturated, cyclic fatty acids with 20 carbon atoms which are biosynthesized from dihomo-gamma-linolenic, arachidonic and eicosapentaenoic acids. These fatty acids are either ingested or are biosynthesized from linoleic and linolenic acids, respectively. The PG-precursor fatty acids are liberated from membrane phospholipids by phospholipase A and are converted to prostaglandins by the multienzyme complex PG-synthetase. The activity of the PG-system is influenced by extracellular hormonal, neural and mechanical stimuli and by intracellular factors such as ion-concentration and activity of the enzymes adenyl- and guanylcyclase. Prostaglandins are tissue hormones or autacoids which act on their receptors near their site of synthesis and degradation. The prostaglandin family constitutes a group of more than 10 natural occurring compounds showing a variety of biological actions. In arteries and veins the different PG:s have vasodilating as well as vasoconstricting effects. In addition, they are involved in the regulation of vascular smooth muscle proliferation. Within the kidney PG:s have vascular and tubular actions. They antagonize the effect of ADH, mediate renin secretion and are involved in the control of electrolyte balance. In the regulation of platelet aggregation and platelet adhesion PG:s have opposite functions: Prostacyclin which is synthesized in the vascular wall antagonizes the aggregating action of Thromboxane A2 which is formed in the platelets. A defect or an imbalance in the production of PG:s in the vascular wall, in platelets or in the kidney is assumed to play a pathogenetic role in a variety of cardiovascular and renal diseases such as in hypertension, atherosclerosis, persistent ductus arteriosus and Bartter's syndrome.
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PMID:[Prostaglandins in cardiovascular and renal function. Biochemical, physiological and clinical findings (author's transl)]. 10 97


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