Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 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.
 ...
PMID:Angina pectoris. Diagnosis and treatment. 0 83

Over the past decade, research in blood platelet physiology has led to the suggestion that platelets play an important part in the pathogenesis and complications of coronary artery disease. Occlusive intravascular platelet aggregates have been shown to cause ischemic myocardial damage in the experimental animal and to be present in some patients who die suddenly. The interplay between endothelial damage and platelet aggregation has been implicated in the etiology of atherosclerosis. Products released from platelets during aggregation may cause arterial spasm. Patients with overt ischemic heart disease and with the risk factors associated with coronary artery disease have been found to have abnormally reactive platelets. Clinical studies of drugs that inhibit platelet aggregation have been reported to show a beneficial effect in preventing cardiac deaths or myocardial infarction; other studies have been negative or shown only a trend toward benefit. This report reviews the theoretical and experimental basis for the platelet hypothesis and the current data on the use of antiplatelet drugs in patients with coronary disease.
 ...
PMID:Role of blood platelets in coronary artery disease. 3 67

The association of idiopathic hypertrophic subaortic stenosis (IHSS) with significant coronary atherosclerosis is little known, only 43 cases being available in the literature, 2 of which are personal ones. But the incidence of this association has certainly been underestimated. It is especially found from the sixth decade onwards, and at least 20% of patients with IHSS in and above the age group have stenosing lesions of the coronary artery. It is almost impossible to establish the presence of associated coronary abnormalities from the clinical features of from electrocardiogram. It does however seem worthwhile looking for this condition in IHSS when there is refractory chest pain, especially to beta-blockers, particularly if the patient is aged over 50 and has risk factors for ischaemic heart disease. It is also good to find IHSS associated with known coronary artery disease by using simple non-invasive techniques such as phonomechanocardiography and especially echo-cardiography; it is important not to miss the myocardial lesion and to treat concurrently if there is likely to be an indication for dealing with the coronary arteries surgically. The beta-blockers are the treatment of choice for both conditions, together with anticoagulents. If they fail, myectomy or myotomy together with aorto-coronary bypass graft should be considered.
 ...
PMID:[Obstructive cardiomyopathy and associated coronary atherosclerosis. Review of the literature and report of 2 personal cases]. 10 92

There has, up to now, not been general acceptance in the German literature of a definite relationship between radiologically visible coronary calcification and coronary heart disease. Anglo-American authors in general agree with our coronographic findings, which show a significantly increased incidence of such coronary changes in stenosing coronary artery disease. In a random sample of patients over 40 years of age, coronary calcification was found radiographically in 25%. Two-thirds of these patients were more than 60 years, but one quarter of the 50 to 60 year age group, and 15% of the 40 to 5-year age group showed these findings. In one group of 150 patients with coronary calcification, 68.9% suffered from coronary heart disease, 7.9% were suspicious and 23.2% had no symptoms. Conversely, in 100 patients with coronary heart disease, coronary calcification was present in 42. Calcification in several vessels was confined almost entirely to patients with advanced coronary disease. Coronary angiography in patients with normal E.C.G.'s, both at rest and after exercise, usually showed some reduction in the lumen corresponding to the area of calcification. In these patients the prognostic significance of the calcification in terms of further development of atherosclerosis must be considered. The localisation of the calcification in these cases is of significance. The clinical features, histology, localisation and investigation of the calcification by radiography is discussed. In our view this has considerable significance in the screening of coronary heart disease.
 ...
PMID:[The radiological diagnosis of calcifying coronary sclerosis (author's transl)]. 13 34

Between January, 1965, and December, 1975, 204 patients (138 men and 66 women) underwent aortoiliac reconstruction for atherosclerotic occlusive disease. Eighteen patients (9%) had a hypoplastic aortoiliac segment and an analysis of these 18 patients constitutes the basis of this report. There were 17 women and one man, and their ages ranged from 28 to 60 years, with an average of 43 years. Hyperlipidema was present in nine of 13 patients tested. All patients were heavy cigarrete smokers and had lower extremity claudication with weak or absent pulses. Carotid or subclavian artery disease was found in 50%. Angiography demonstrated hypoplasia of the aorta distal to the renal arteries with either occlusion, diffuse narrowing, or, most often, an "hourglass" stenosis. The iliac and femoral arteries also were narrowed. Reconstruction was achieved primarily by aortobilateral-iliac or femoral bypass. There were no operative deaths and all patients were improved initially. It appears that normally occurring atherosclerosis in this portion of the aorta, along with congenital narrowing, accounts for symptoms at an early age. The predominence in women is a puzzle. The prognosis does not appear to be too grim. This may be due to absence of diabetes mellitus and the infrequency of coronary artery disease. All patients are still alive; there has been one major amputation following graft infection 1 1/2 years after operation. When progression of atherosclerosis occurs, it seems to involve the superficial femoral, carotid, and subclavian arteries.
 ...
PMID:Atherosclerosis and the hypoplastic aortoiliac system. 14 60

Atherosclerosis is the leading cause of death in the United States, and its prevention is now a primary goal of health care personnel. Knowledge of the early history of the disease, which would be particularly helpful in determing its pathogenesis, is still lacking. Studies are only now beginning to be directed at younger individuals without clinical evidence of disease. Hyperlipoproteinemia has been considered a definite risk factor for atherosclerosis for some years, but because of the difficulty involved in relating specific lipid abnormalities to the extent of atherosclerosis in a given patient, unequivocal proof of its role is lacking. Serum lipid and lipoprotein levels used to define hyperlipoproteinemia in the United States are derived from a system in which 95% of the population are regarded as having normal levels. The cut points are set far too high. Mild hyperlipoproteinemia is rampant in this country, as is coronary artery disease, and from the evidence now available, it seems reasonable to try to lower the incidence of the latter by reducing blood lipid levels of the entire population through dietary modification.
 ...
PMID:Not-so-hyper hyperlipo-proteinemia and coronary artery disease. 17 63

Electrocardiographic and cardiovascular responses during maximal exercise were evaluated in 103 normal children and in 82 children with familial hyperlipoproteinemia. The normal and hyperlipidemic children were comparable in regards to age, weight--height index, resting and exercise blood pressures, and maximal working capacity indices. The cohort of 82 hyperlipidemic children included 61 children (29 boys and 32 girls) with well defined "monogenic" familial hyperlipoproteinemia. Segmental ST depression on the exercise electrocardiogram occurred in 8 of these 29 boys (27.6%) as compared to 4 of 55 normal boys (7.3%), P less than 0.025 and in 6 of the 32 girls (19%) as compared to 7 of 48 normal girls (14.6%), P greater than 0.1. Segmental ST depression was present in 14 of 61 (23%) children with "monogenic" hyperlipoproteinemia, as compared to 11 of 103 (10.75%) normal (x2 = 4.47, P less than 0.05). An assessment of the clinical significance of an abnormal exercise electrocardiogram in male children with "monogenic" hyperlipoproteinemia must await the following: (1) two to four decades of observation and study of the development of morbid or mortal coronary disease, or (2) the future development of improved invasive or noninvasive techniques for the early detection of covert coronary occlusive disease. Currently, maximal exercise electrocardiography cannot be contemplated as a useful indicator of eventual premature coronary artery disease in asymptomatic hyperlipidemic children.
Atherosclerosis 1976 Oct
PMID:Maximal exercise stress testing in normal and hyperlipidemic children. 18 80

It is proposed that in vivo immunoadsorption may be utilized in the treatment of coronary artery disease. The proposed method is based on binding of low density lipoproteins and cholesterol to antibodies directed against low density lipoproteins which are bound to a matrix in an extracorporeal hemoperfusion column. The various observations that suggest the hypothesis are presented. The feasibility of the proposed method and some of the problems that may be encountered in its utilization are discussed. The method should be evaluated in animal studies prior to consideration of clinical trials in patients.
Atherosclerosis 1977 Mar
PMID:Possible utilization of extracorporeal hemoperfusion in the treatment of coronary artery disease. A hypothesis and proposal for animal studies. 19 51

Cholesterol, triglycerides, and Lp(a)/pre-beta1 lipoprotein were analyzed in 153 patients typed for liproprotien patterns. Coronary atherosclerosis was determined by selective coronary angiography and graded by a system taking into account proximal, middle and distal segments. Smoking habits, family history and hypertension were also recorded. Normal coronary arteries were encountered in 45, moderate coronary atherosclerosis (less than median score) in 50, and severe changes (greater than median score) in 58 patients. Cholesterol (P less than 0.05), positivity of Lp (a)/pre-beta1 lipoprotein (P less than 0.01), a family history of coronary heart disease (P less than 0.05), and smoking (P less than 0.01) differed between the group of normal arteries and the whole group of luminal obstructions. Serum triglycerides were not associated with coronary atherosclerosis. Cholesterol, positivity of the Lp(a)/pre-beta1 lipoprotein and a family history of coronary heart disease were also associated with the severity of the disease. Smoking was less prevalent in the group with severe changes.
 ...
PMID:Serum lipids in angiographically assessed coronary atherosclerosis. 20 36

This report describes the effects of pharmacologic doses (3 g/d) of nicotinic acid on the plasma distribution and chemical composition of the high density lipoprotein (HDL) subfractions HDL(2) and HDL(3) and examines the influence of the drug on the metabolism of the major HDL apoproteins, apolipoproteins A-I (ApoA-I) and A-II (Apo-II). The drug lowered plasma cholesterol (15%, P < 0.05) and triglyceride (27%, P < 0.01); the former effect a result of a fall in the amount of cholesterol associated with very low density lipoproteins (31%, P < 0.02) and low density lipoproteins (36%, P < 0.02). Conversely, it raised plasma HDL cholesterol (23%, P < 0.05) and increased (by 345%) the plasma HDL(2):HDL(3) ratio. The latter derived from an absolute increment (646%) in circulating HDL(2), coupled with a fall (47%) in HDL(3). This change was not associated with major alterations in the overall cholesterol (free and esterified), triglyceride, phospholipid, or protein content of the subfractions; however, it was accompanied by substantial changes in their protein composition. In particular, the molar ratio of ApoA-I:ApoA-II in HDL(3) declined from 2.7:1 to 2.1:1 during nicotinic acid treatment.Significant perturbations of ApoA-I and ApoA-II metabolism accompanied the drug-induced HDL subfraction redistribution. Specifically, the plasma concentration of ApoA-I rose by 7% (P < 0.05) because of a decrease in its fractional catabolic rate. Moreover, whereas before treatment 6 and 94% of the plasma ApoA-I circulated with HDL(2) and HDL(3), after commencement of nicotinic acid therapy this distribution became 49 and 51% in HDL(2) and HDL(3), respectively. ApoA-II was found mainly in HDL(3), both before and during nicotinic acid treatment. Administration of the drug caused a 14% reduction in its plasma concentration (P < 0.05), which derived principally from a fall (22%, P < 0.01) in its synthetic rate. These data suggest that the effects of nicotinic acid on the HDL subfraction distribution may be mediated via (a) net transfer of ApoA-I from HDL(3) to HDL(2) and (b) a reduction in ApoA-II synthesis. Our present understanding of the association between HDL and atherosclerosis indicates that such changes may have prophylactic value in the prevention of coronary artery disease.
 ...
PMID:Effects of nicotinic acid therapy on plasma high density lipoprotein subfraction distribution and composition and on apolipoprotein A metabolism. 22 31


1 2 3 4 5 6 7 8 9 10 Next >>