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)

According to recent prospective studies, hypofibrinolysis due to elevated plasma plasminogen activator inhibitor 1 levels appears to be an independent risk factor for myocardial reinfarction in men, and hyperinsulinaemia, a major indicator of insulin resistance is considered as a risk factor for coronary disease. It has recently been shown that insulin resistance is accompanied by an increased plasma plasminogen activator inhibitor 1 concentration: A significant correlation coefficient was demonstrated between plasminogen activator inhibitor 1 and fasting plasma insulin in the normal population, in obese subjects, in Type 2 (non-insulin-dependent) diabetic patients and in angina pectoris. Attempts to decrease insulin resistance such as fasting, diet, or administration of an oral anti-diabetic drug such as Metformin induced a parallel decrease in plasma insulin and plasminogen activator inhibitor 1 levels. This inhibitor is produced by endothelial cells and by hepatocytes in culture. Plasminogen activator inhibitor 1 synthesis by hepatocytes in culture was stimulated by an increasing insulin concentration, or low density lipoproteins, whereas the endothelial cell synthesis was stimulated by very low density lipoproteins especially when they were obtained from hypertriglyceridaemic patients. Therefore, a direct effect of insulin or lipoprotein changes on the cells which synthesize plasminogen activator inhibitor 1 could be responsible for its increased plasma concentration in insulin resistance states. The increase in plasma plasminogen activator inhibitor 1 levels linked to hyperinsulinaemia is a tempting partial explanation for the association between insulin resistance and coronary disease.
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PMID:Increased plasma plasminogen activator inhibitor 1 levels. A possible link between insulin resistance and atherothrombosis. 191 49

This intervention program investigated the applicability and the effects of intensive physical exercise and low-fat diet on the progression of coronary atherosclerotic lesions and stress induced myocardial ischemia in patients with stable angina pectoris. Patients participating in this study were recruited following routine coronary angiography for angina pectoris. Inclusion criteria were male sex, stable symptoms, a willingness to participate in the study for at least twelve months, and coronary artery stenoses well documented by angiography. Exclusion criteria were unstable angina pectoris, left main coronary artery stenosis greater than 25% luminal diameter reduction, severely depressed left ventricular ejection fraction (less than 35%), significant valvular heart disease, insulin-dependent diabetes mellitus, primary hypercholesterolemia (type II hyperlipoproteinemia, low-density lipoprotein greater than 210 mg/dl), and conditions precluding regular physical exercise. 18 patients participated in this program for one year; they consumed a low-fat, low-cholesterol diet (less than 20 energy % fat, cholesterol less than 200 mg/day) and exercised for more than 3 h/week. Myocardial oxygen consumption was estimated from maximum rate-pressure product at peak exercise; it was correlated to stress induced myocardial ischemia, as measured by 201Tl-scintigraphy. Results were compared with those of 18 matched patients on "usual care". In the intervention group, physical work capacity (161 +/- 34 W vs. 194 +/- 42 W) and maximum rate pressure product (25.0 +/- 6.3 x 10(3) vs. 27.2 +/- 5.3 x 10(3)) increased significantly (p less than 0.01). Patients willing to devote time and effort to intensive physical exercise and to comply with a low-fat diet may benefit from this form of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Modification of risk factors through physical training and low-fat diet]. 191 19

Overweight and obesity may develop in individuals with genetically determined low resting energy expenditure. Drugs are among the recognised precipitating factors. The obesity promoting impact of beta-blockers is, however, less well known. Resting energy expenditure, and thermogenesis induced by stimuli such as meals, cold and heat exposure, stress and anxiety, have a facultative component mediated by the sympathoadrenal system through catecholamines working on beta-adrenoceptors. Treatment with beta-blockers reduces the facultative thermogenesis by 50-100 kcal/d, which corresponds to the weight gain of 2-5 kg/year reported in clinical trials. Treatment with beta-blockers also results in insulin resistance, which may aggravate existing diabetes and elicit diabetes in predisposed patients. Overweight and obesity are frequently complicated with hypertension and angina pectoris, which are often treated with beta-blockers. Obesity is associated with a defective sympathetic activity, and treatment with beta-blockers may further reduce facultative thermogenesis and promote weight gain. The consequence may be aggravation of hypertension, insulin resistance and other atherogenic factors. The causal therapy of android overweight and obesity complicated with diabetes or hypertension is a sufficient weight loss. If pharmacological treatment is inevitable, combined treatment with diuretics and ACE-inhibitors are most appropriate.
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PMID:[Obesity and diabetes as side-effects of beta-blockers]. 197 28

Cardiovascular disease is a frequent complication of insulin-dependent diabetes mellitus (IDDM), but the prevalence, interrelations, and risk factors of its principal components (coronary, cerebrovascular, and lower-extremity arterial disease) and of medial arterial wall calcification are not well understood. To address these issues, data from the Epidemiology of Diabetes Complications Study (n = 657) baseline examination were examined. The term coronary heart disease (CHD) was applied to those with myocardial infarction or angina, whereas lower-extremity arterial disease (LEAD) was applied to those who had undergone amputation of a lower limb or who had an ankle to arm blood pressure ratio less than 0.8 at rest or after exercise. Calcification of the lower-extremity arteries was considered to be present if ankle pressure was more than 100 mm Hg higher than brachial pressure. Although the prevalence of CHD was low, LEAD was significantly more common in women than in men (p less than 0.01), whereas calcification was more frequent in men than in women (p less than 0.01). Ten percent of those with LEAD also had CHD, and 8% with LEAD had calcification. Modeling of potential risk factors (e.g., diabetes duration and glycosylated hemoglobin) revealed that duration, female gender, fibrinogen, low density lipoprotein cholesterol, high density lipoprotein cholesterol, and high density lipoprotein cholesterol to apolipoprotein A-I ratio were independent predictors of LEAD, whereas for CHD only, diabetes duration and hypertension contributed to CHD. Calcification revealed a mixed pattern, with duration, hypertension, and triglyceride to apolipoprotein A-I ratio being the statistically significant associated factors. The results suggest that although LEAD, CHD, and calcification often coexist, their risk factor profiles differ.
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PMID:Cardiovascular disease and arterial calcification in insulin-dependent diabetes mellitus: interrelations and risk factor profiles. Pittsburgh Epidemiology of Diabetes Complications Study-V. 206 46

Abdominal fat distribution estimated by the waist/hip ratio (WHR) was studied in 85 subjects (55 men, 30 women) with treated noninsulin-dependent diabetes mellitus (NIDDM), and its association with cardiovascular disease and cardiovascular risk factors was analyzed. In men, WHR was highly correlated with the body mass index (BMI; r = 0.697), but this was not true in women (r = 0.091). In men, WHR was significantly and positively correlated with mean diastolic blood pressure (DBP) level. In women, this correlation was also positive, but of lesser degree. Fasting plasma insulin was highly correlated with BMI and WHR in men, but not in women. In both sexes, WHR was positively correlated with fasting serum triglyceride and negatively correlated with serum high-density lipoprotein cholesterol. In addition, mean WHR, but not BMI, was significantly greater in subjects with cardiovascular disease (positive electrocardiographic signs and/or history of angina, myocardial infarction, stroke, intermittent claudication).
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PMID:Male-type fat distribution is associated with cardiovascular risk factors and the prevalence of cardiovascular disease in noninsulin-treated diabetics. 215 Dec 25

Calcium entry blockers have been used for cardiovascular disturbances such as angina pectoris and hypertension. Calcium is, however, involved in the release of several hormones. The process of insulin secretion by the pancreatic beta-cells is dependent on calcium. Thus, calcium-entry blockers may interfere with insulin secretion. This effect has been confirmed in vitro in isolated islets as well as in animal studies. A few case reports describe the deterioration of glycaemic control or development of frank diabetes mellitus during treatment with nifedipine or diltiazem. In general, however, there are no important negative effects of calcium-entry blockers on glucose tolerance, either in non-diabetic persons with hypertension, or in patients with diabetes mellitus. Hence, these drugs appear to be a good choice for use in diabetic patients with cardiovascular diseases.
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PMID:Calcium entry blockers and their effects on glucose metabolism. 217 50

The prevalence of ischemic heart disease (IHD) in older adults by glucose tolerance status was evaluated in 2,223 white men and women, aged 50-89 years, in the Rancho Bernardo cohort who were studied between 1984 and 1987. Impaired glucose tolerance (IGT) and non-insulin-dependent diabetes mellitus (NIDDM) were classified according to World Health Organization criteria. End points of ischemic heart disease were defined by Rose Questionnaire and resting electrocardiogram (ECG) according to the Minnesota Code. IHD by electrocardiographic changes was classified as asymptomatic (without history of chest pain or overt IHD) or symptomatic (with history). IHD by all criteria combined was significantly more common in men and women with NIDDM, and in women with IGT, than in those with normal glucose tolerance. The prevalence of myocardial infarction, defined by major Q wave, Rose Questionnaire chest pain criteria, or personal history, was higher in persons with NIDDM than in persons without; the difference was highly significant in women (odds ratio, 2.08 [1.22, 3.56]; p = 0.009). Angina pectoris was not significantly related to NIDDM or IGT in either sex. Electrocardiographic evidence of asymptomatic IHD was significantly more prevalent in both men and women with NIDDM as compared with those with normal glucose tolerance (odds ratios, 1.75 [1.10, 2.81] for men and 1.80 [1.07, 3.01] for women; p less than 0.05). This significant association persisted after excluding persons on digitlis or diuretic therapy and, in women, was also independent of the effect of major known IHD risk factors. These population-based data are consistent with clinical reports suggesting an association of diabetes with silent myocardial infarction or ischemia. The presence of ischemic resting electrocardiographic abnormalities in the asymptomatic diabetic patient is likely to have prognostic and therapeutic implications.
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PMID:Resting electrocardiographic abnormalities suggestive of asymptomatic ischemic heart disease associated with non-insulin-dependent diabetes mellitus in a defined population. 230 39

Cohorts of diabetic (n = 121) and non-diabetic (n = 584) patients were prospectively followed for up to ten years after having suffered from a stroke. All but six of the diabetic patients had Type 2 (non-insulin-dependent) diabetes mellitus. The diabetic patients had more risk factors associated with stroke: heart failure (p less than 0.001) and angina pectoris (p less than 0.001), than the non-diabetic patients. Neither body mass index nor blood pressure levels differed between the groups at admission. Haematocrit levels were higher in the diabetic group (p less than 0.01). The diabetic patients were more commonly afflicted by cerebral embolism and to a lesser extent by transient ischaemic attacks than the non-diabetic patients. When calculated by log-rank tests, the diabetic group had an increased risk of death (p less than 0.001), recurrent stroke (p = 0.001), and of myocardial infarction (p = 0.001) after the initial stroke. Autopsy-verified causes of death between the groups did not differ significantly, although half of all deaths during the period one to six months after stroke were caused by pulmonary embolism in the diabetic group. Thus, diabetes increases the risk of death after a stroke, and it also increases among stroke survivors the risk of recurrent stroke and myocardial infarction.
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PMID:Prognosis after stroke in diabetic patients. A controlled prospective study. 234 37

In a retrospective study of 962 diabetic (male: 441, female: 521) patients in the Diabetic Outpatient Clinic of the National Institute of Cardiology between 1st November 1967 and 31st October 1988 the survival time of diabetics treated with first generation sulphonylureas was considerably less after the first attack of angina pectoris or acute myocardial infarction compared with that of individuals controlled with regime alone or being on glibenclamide or insulin treatments. The systolic blood pressure proved to be higher in diabetics treated with first generation sulphonylureas. During the observation, among the 183 patients on insulin- as well as in the 262 individuals on first and 230 on second generation sulphonylurea treatments, and in the 287 diabetics controlled with regime alone, 547 (male: 241, female: 306) patients died, 403 of them due to cardiovascular and renal failures. Between the diabetics suffering from ischaemic heart diseases no difference could be detected relating the risk factors except the higher systolic blood pressure. The alterations in the cardiovascular states during the survey, the improvement of therapeutical interventions, the alterations in the carbohydrate and lipid metabolism are not supposed to be involved in the shorter survival time of diabetics treated with first generation sulphonylureas. The shorter survival time might be explained by the arrhythmogenic activity of first generation sulphonylureas described in earlier studies. On this basis we are tempted to draw the conclusion that second generation sulphonylureas must be selected in the diabetes care, if the metabolic state could not be normalized by diet and regime only.
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PMID:[Effect of antidiabetic treatment in ischemic heart diseases]. 240 34

Since beta-adrenoceptor blocking drugs were originally discovered and shown to be important therapeutic agents in the management of both angina pectoris and hypertension, many other similar drugs have become available. These share the common property of beta-adrenoceptor antagonism, though they may vary in terms of potency. However, they differ from one another in terms of their additional pharmacological properties--cardioselectivity, partial agonist activity, and membrane stabilizing activity. Cardioselectivity refers to the ability of some drugs, notably atenolol and metoprolol, to block beta 1 receptors without blocking beta 2 receptors. This has been considered to be of potential importance in patients with obstructive airways disease, patients with peripheral vascular disease, and patients with insulin-dependent diabetes during hypoglycemic crisis. Partial agonist activity is the intrinsic activity that some drugs have to stimulate the beta adrenoceptor while they are competitively antagonizing catecholamines. In consequence, they may have less effect on resting heart rate, cardiac output, peripheral vascular blood flow, and resting respiratory function. However, there is no good evidence that major adverse effects of beta-adrenoceptor blocking drugs such as congestive heart failure, bronchospasm, or symptoms of peripheral vascular disease are prevented by drugs with partial agonist activity: bradycardia may be improved, but its importance has probably been overemphasized. Membrane-stabilizing activity appears to be unimportant. As far as pharmacokinetic differences between drugs are concerned, lipid solubility is seen to be of increasing importance. The more water-soluble drugs have longer elimination half-lives, produce less interindividual variation in steady-state plasma concentrations, and penetrate the central nervous system less readily.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacological characteristics of beta blockers and their role in clinical practice. 243 20


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