Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty patients with different cardiac diseases and healthy volunteers were given omega-I-123-heptadecanoic acid (HDA) intravenously. Tracer kinetics were followed for 90 min, and tracer elimination curves were obtained regionally. In addition, circumferential washout profiles were evaluated for 26 patients and interpolative as well as constant background subtraction was performed for comparison in selected patients. Rest and stress radionuclide ventriculography allowed formation of a group with normal ventricular function (control group); the remaining patients had an abnormal ventricular function at rest or under stress. Regions of patients in the control group were significantly different (P less than 0.005) from regions of patients with CHD or CMP with regard to the initial half-life or the component ratio between a fast and a slow component (Ca/Cb). Regions of patients after MI without exercise-induced angina did not differ strikingly from control regions. Circumferential washout analysis showed homogeneous tracer kinetics in healthy subjects, bus some individuals showed increasing regional activity, mainly by late activity uptake of the stomach. Dynamic heart scintigraphy with HDA is an additional nuclear cardiologic tool that makes possible the classification of patients with myocardial disease and abnormal ventricular function already under resting conditions. Initial half-life allows reasonable discrimination between different severely diseased patient groups; expansion of acquisition time to 90 min refines biexponential tracer analysis which, by means of an altered component ratio Ca/Cb, may allow better clinical judgement of the individual patient. Circumferential washout analysis and interpolative background correction lead to a better specificity of examination.
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PMID:Tracer elimination in I-123-heptadecanoic acid: half-life, component ratio and circumferential washout profiles in patients with cardiac disease. 408 8

The article compares the results of the screening of 3820 males aged 40 to 59 years, representative of the open population, and the mortality rate over a 6-year-follow-up. Mortality was the highest in males in whom angina pectoris was combined with "ischemic" codes on the ECG and the lowest in subjects without CHD symptoms and without codes of left ventricular hypertrophy. The study showed a fairly high prognostic value of the epidemiologic method of CHD diagnosis.
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PMID:[Mortality rate among men aged 40-59 based on the data of intravital screening]. 624 May 60

Bicycle ergometry in 40-59 year-old male patients with coronary heart disease, identified during mass prophylactic examination on the basis of epidemiological criteria, has shown that in patients with angina pectoris of effort and no myocardial infarction in history positive exercise tests are observed in 20,8% of cases, while in patients with painless CHD forms positive results are observed in 15.4% of cases. Positive exercise tests are the most often in patients with daily anginal attacks and in those with ST depression and flat negative T waves.
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PMID:[Bicycle ergometry test results in persons with ischemic heart disease detected in mass screening]. 686 Apr 81

From an urban Swedish population, samples of 25 and 55 year old men and women were examined with questionnaires, oesophageal manometry including acid perfusion test. An exercise ECG was performed in 55 year old men with anginalike pain. Oesophageal dysfunction (OD) defined as either a hiatal hernia, severe dysmotility or a positive related acid perfusion test was found in 12% of the younger population and in 29% of the older one. The frequency of angina pectoris according to the Rose questionnaire was 5% in the 25 year olds and 13% in the 55 year olds. OD was found in 44% of the older male group with angina pectoris at history. In the angina group objective signs of ischemic heart disease was found in 32%. At interview by a cardiologist in connection with exercise ECG, the angina pectoris diagnosis as assessed by questionnaire was reduced to 4% in the 55 year old men. In this group objective signs of ischemic heart disease or a history of myocardial infarction (CHD) were found in 94%. The others, classified by a physician as possible or no angina pectoris had a lower rate of CHD of 25% and 13% respectively. The angina pectoris group diagnosed according to Rose questionnaire contains more people with OD than with CHD. The diagnosis angina pectoris as ischemic heart disease should therefore not be set on the history alone.
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PMID:Oesophageal dysfunction and angina pectoris in a Swedish population selected at random. 694 50

Ceruloplasmin- and placebo-treated CHD patients were studied for severity of angina pectoris, changes in central hemodynamics, exercise tolerance. It is shown that ceruloplasmin promoted an increase in exercise tolerance, higher quality of life, arrest of the disease progress. Combined treatment of CHD incorporating ceruloplasmin produced a positive effect on central hemodynamics and contractile, pump capacities of the myocardium.
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PMID:[The clinico-hemodynamic effects of the antioxidant ceruloplasmin in IHD patients]. 778 70

Seventeen patients with a more than 5-month-history of angina pectoris were allocated a diet for 4 weeks. The diet was supplemented with 6.15 g of omega 3-polyunsaturated fatty acids (PUFA) in 125 g canned Far-Eastern sardine. This increased the proportion of eicosapentaenic (EPA) and docosahexaenic acids from 1.28 +/- 0.72 to 9.02 +/- 2.83% and from 2.48 +/- 0.91 to 6.54 +/- 2.01%, respectively; p = 0.0003) in the total serum lipid fraction. The levels of omega 6-PUFA decreased due to linoleic acid (from 24.9 +/- 3.9 to 19.7 +/- 5.2%, p = 0.0014). The EPA/arachidonic acid ratio rose from 0.23 +/- 0.11 to 1.76 +/- 0.58 (p < 0.001). The levels of triglycerides decreased by 36.4% (from 162.3 +/- 55.2 to 103.9 +/- 42.4 mg/dl; p < 0.0005); those of very low density lipoproteins and total cholesterol by 36 and 6.8%, respectively (from 32.5 +/- 11.0 to 20.8 +/- 8.5 mg/dl; p < 0.0005 and from 234.8 +/- 43.2 to 218.4 +/- 39.7 mg/dl; p < 0.05, respectively). The concentrations of high density lipoproteins remained unchanged. Thus, a short-term supplementation of canned Far-Eastern sardine to the diet of patients with CHD caused a substantial changes in blood fatty acid composition and favourable shifts in the levels of lipids and lipoproteins. This allows the Far-Eastern sardine to be regarded as a valuable source of omega 3-PUFA which can be used in the secondary prevention of coronary heart disease.
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PMID:[Dietary effect of omega-3 polyunsaturated fatty acid supplementation on blood fatty acids, lipid and lipoproteins in patients with ischemic heart disease]. 796 23

We examined the relationship between the risk of CVD mortality and morbidity and HCT over a period of 34 years of follow-up in the 5209 men and women in the Framingham cohort. There was an increased risk of all-cause death as well as morbidity and mortality due to CVD in subjects with HCT values in the highest quintile. There was no evidence of a decrease risk of CVD in men with lower than median HCT values, and women actually showed increased risk of CVD events with lower HCT values, indicating a J- or U-shaped relationship between HCT and CVD events. The impact of HCT on CVD events appears to differ for different age groups and by sex. HCT is significantly related to the incidence of CVD, including CHD, MI, angina pectoris, stroke, and IC in younger men. In younger women, HCT is related to the incidence of CVD, CHD, MI and mortality from CVD and CHD. A negative association with CHF incidence and stroke death is noted in elderly women. These results support the hypothesis that HCT is an important risk factor for some CVD events, an association that merits further investigation.
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PMID:Hematocrit and the risk of cardiovascular disease--the Framingham study: a 34-year follow-up. 812 18

The vascular endothelium is the site of formation of several powerful mediators. One of these is NO, a chemically unstable radical formed by enzymatic conversion of L-arginine in the presence of molecular oxygen. NO elicits relaxation of VSMC by activating cytosolic guanylate cyclase. NO also counteracts platelet adhesion and aggregation. The biological actions of NO make it a key substance in the endogenous defense against vascular occlusion and thrombosis. The basal formation of NO maintains a moderate but significant vasodilation in the systemic resistance vessels and counteracts platelet activity. When blood flow in conduit arteries is increased there is an augmented endothelial formation of NO, eliciting flow-dependent vasodilation. Beside this, several vasodilators (acetylcholine, bradykinin, histamine, substance P) operate by stimulating endothelial NO formation. On the other hand, drugs like nitroglycerin and papaverine operate independently of the vascular endothelium. Vasodilator mechanisms, physiological as well as pharmacological, may therefore be characterized as endothelium-dependent (i.e. NO-mediated), or endothelium-independent (i.e. not mediated by NO). Physiologically, mixed mechanisms occur. Failure of the vascular endothelium to elicit NO-mediated vasodilatation may be due to decreased formation, increased degradation, decreased sensitivity to the NO formed, or a mixture of these factors. Irrespective of the mechanism behind, this is referred to as endothelial dysfunction. Endothelial dysfunction occurs in several cardiovascular settings, like atherosclerosis, hypercholesterolaemia, diabetes, and essential hypertension. Endothelial dysfunction leads to an impaired tissue perfusion, increased local vascular resistance, decreased defense against thrombus formation, and possibly also decreased defense against hypertrophy of the VSMC in the vessel wall media. In patients with CHD, endothelial dysfunction leads to an impaired coronary flow response to physical and mental stress, and to promotion of platelet adherence and aggregability. Endothelial dysfunction is thereby a probable aggravating factor in the atherosclerotic process, adding a functional component on top of the structural lesions characterizing this disease. A particular form of endothelial dysfunction, limited to the arterial resistance vessels, may explain the symptoms and clinical characteristics of microvascular angina. In patients with essential hypertension, endothelial dysfunction prevails, adding a functional component to the structural factors also in this disease. Hitherto, the only therapeutic tools available to restore endothelial dysfunction appear to be restriction of the dietary intake of lipids, possibly reinforced with intake of antioxidants like fish oil and vitamin E. However, large clinical trials to confirm the efficacy of such therapy in reversing endothelial dysfunction have not been conducted. In the future, more directly acting therapeutic regimens, aimed at supporting or substituting the endogenous formation of NO, are likely to appear as well.
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PMID:Endothelial nitric oxide and cardiovascular disease. 815 Dec 63

In this presentation an effort has been made to review the impact of resistance to insulin-mediated glucose uptake and/or hyperinsulinaemia on various metabolic end-points and clinical syndromes. Insulin resistance is present in the great majority of patients with states of glucose intolerance, but frank decompensation of glucose homoeostasis does not occur if individuals can maintain a state of compensatory hyperinsulinaemia. Although compensatory hyperinsulinaemia may prevent the development of NIDDM in insulin-resistant individuals, there is substantial evidence that insulin resistance and/or hyperinsulinaemia is associated with higher plasma concentrations of triglyceride, uric acid and plasminogen activator inhibitor 1 and with lower HDL cholesterol concentrations. Obesity, decreased physical activity and possibly cigarette smoking accentuate the degree of insulin resistance and its manifestations, and a genetic basis is also involved. Resistance to insulin-mediated glucose uptake and/or hyperinsulinaemia have been shown to be associated with high blood pressure, microvascular angina and CHD. Thus, resistance to insulin-mediated glucose uptake is a common phenomenon, which makes a major contribution to the aetiology and clinical course of common and serious diseases. Based on the above considerations, it is difficult to over-emphasize the health-related implication of a defect in insulin-mediated glucose uptake.
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PMID:Insulin resistance and risk factors for coronary heart disease. 830 13

Angina pectoris before and after MI was evaluated in a sample of 729 men and women from a general population in whom MI developed during a 36-year period of follow-up. Relations of AP to subsequent CHD events and mortality after initial MI were analyzed by proportional hazards regression models and were adjusted for covariates (age, sex, blood pressure, serum cholesterol, body mass index, glucose intolerance, cigarette smoking, and antihypertensive medications) obtained from routine biennial examinations preceding the initial MI. Comparisons of the influence of angina were made between pre-MI angina, post-MI angina, and absence of AP. The sample had 484 men and 245 women (mean ages, 63 and 69, respectively) who survived greater than / equal to 30 days after MI. The initial MI was clinically unrecognized in 165 (34%) men and 115 (47%) women. Data on covariates were complete for 622 subjects, among whom 30% had pre-Ml angina, 18% had post-MI angina, and 52% did not have AP. Angina was half as common in persons with unrecognized MIs as in those with clinically recognized MIs. During an average of 8.7 years of follow-up, 57% of subjects developed subsequent CHD events, including recognized and unrecognized MI, coronary insufficiency, and CHD death, and 74% died. Both pre-MI angina (hazard ratio, 1.49; 95% CI, 1.17 to 1.91) and post-MI angina (hazard ratio, 1.43; 95% CI, 1.06 to 1.94) adjusted for accompanying risk factors were associated with increased risk for subsequent CHD events compared with those without AP. Neither pre-MI nor post-MI angina was associated with excess overall mortality.
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PMID:Epidemiologic assessment of angina before and after myocardial infarction: The Framingham study. 870 60


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