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)

A method for measuring blood serum glycogen phosphorylase (GP) activity is described, informative at early stages of myocardial infarction. The method is sensitive and available for clinical biochemistry laboratories. It consists in preliminary purification of GP from serum proteins and metabolites by affinity chromatography in micro-columns and subsequent measurement of the activity in the eluate. The procedure involves selective GP sorption on starch, washing, and subsequent desorption with glycogen solution. GP activity is measured by the kinetic spectrophotometric technique, based on enzymic measurement of glucose-1-phosphate, the product of glycogen consumption reaction, at a wavelength of 340 nm. Conditions of serum GP chromatographic purification are modified in the suggested procedure, this improving the sensitivity of the enzyme measurement. Blood serum GP activities were measured in patients with various cardiac diseases--myocardial infarction (15 cases), angina of rest and effort (53), essential hypertension (30). Different methods of GP activity measurements are considered. Recommendations on the use of the described method, a sensitive test for the diagnosis of myocardial infarction, are given.
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PMID:[The determination of the glycogen phosphorylase activity in blood serum]. 171 85

Felodipine, a dihydropyridine calcium-channel antagonist, significantly reduces systolic and diastolic blood pressure (BP) in patients with hypertension and has been associated with beneficial hemodynamic effects in patients with chronic stable angina pectoris or congestive heart failure (CHF). In hypertensive patients, felodipine does not appear to significantly affect glomerular filtration rate, creatinine clearance, glucose tolerance, or plasma lipoprotein concentrations. Studies comparing felodipine with other agents as monotherapy in mild to moderate hypertension have demonstrated felodipine to be at least as efficacious as hydrochlorothiazide (HCTZ) and HCTZ plus amiloride hydrochloride in combination. Comparisons of felodipine with other agents as adjuncts to beta-blocker or diuretic therapy have shown felodipine to be at least as effective as HCTZ, propranolol hydrochloride, prazosin hydrochloride, and nifedipine. Evaluations of patients with chronic stable angina are limited, and additional studies are needed before felodipine can be recommended for the routine management of angina pectoris. Similarly, additional studies are essential to delineate the role of felodipine, if any, in the management of CHF. In the management of hypertension, felodipine 5-40 mg/d significantly reduces systolic and diastolic BP. Although some patients may be controlled throughout the entire dosing interval when felodipine is administered bid, many patients will require more frequent dosing to obtain adequate BP control. Adverse effects associated with felodipine are similar to those of other dihydropyridine calcium-channel antagonists and include peripheral edema, headache, dizziness, flushing, and fatigue. A potentially clinically important drug interaction was observed when felodipine was administered concomitantly with theophylline aminopropanol; significant decreases in theophylline concentrations were noted. In summary, felodipine appears to be safe and effective for the management of hypertension when used alone or in combination with other antihypertensive agents. The efficacy of felodipine in the management of chronic stable angina pectoris and CHF requires further investigation.
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PMID:Felodipine: a new dihydropyridine calcium-channel antagonist. 176 37

The UK Prospective Diabetes Study (UKPDS) is a multi-centre, prospective, randomised, intervention trial of 5100 newly-diagnosed patients with Type 2 (non-insulin-dependent) diabetes mellitus which aims to determine whether improved blood glucose control will prevent complications and reduce the associated morbidity and mortality. Newly presenting Type 2 diabetic patients aged 25-65 years inclusive, median age 53 years, median body mass index 28 kg/m2 and median fasting plasma glucose 11.3 mmol/l, were recruited and treated initially by diet. Ninety five percent remained hyperglycaemic (fasting plasma glucose greater than 6 mmol/l) and were randomly allocated to different therapies. In the main randomisation, those who were asymptomatic and had fasting plasma glucose under 15 mmol/l were allocated either to diet policy, or to active policy with either insulin or sulphonylurea aiming to reduce the fasting plasma glucose to under 6 mmol/l. Over 3 years, the median fasting plasma glucose in those allocated to diet policy was 8.9 mmol/l compared with 7.0 mmol/l in those allocated to active policy. The Hypertension in Diabetes Study has been included in a factorial design to assess whether improved blood pressure control will be advantageous. Patients with blood pressure greater than or equal to 160/90 mm Hg were randomly allocated to tight control aiming for less than 150/85 mm Hg with either an angiotensin-converting enzyme inhibitor or a Beta-blocker or to less tight control aiming for less than 200/105 mm Hg. The endpoints of the studies are major clinical events which affect the life and well-being of patients, such as heart attacks, angina, strokes, amputations, blindness and renal failure. To date, 728 patients have had at least one clinical endpoint. Surrogate endpoints include indices of macrovascular and microvascular disease detected by ECG with Minnesota Coding, retinal colour photography and microalbuminuria. The studies also aim to evaluate potential risk factors for the development of diabetic complications such as smoking, obesity, central adiposity, plasma LDL- and HDL-cholesterol, triglyceride, insulin, urate and other biochemical variables. The studies are planned to terminate in 1994, with a median follow-up of 9 years (range 3-16 years) for the glucose study and 5 years (range 2-6 years) for the hypertension study.
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PMID:UK Prospective Diabetes Study (UKPDS). VIII. Study design, progress and performance. 177 53

The recent advances in cardiovascular pathophysiology have changed our interpretation of the interplay between myocardial metabolism and contractile function which takes place during acute ischemia. For instance, the use of nuclear magnetic resonance (NMR) spectroscopy has allowed to document that the rapid impairment in contractility seen during acute myocardial ischemia is not directly related to depletion of high energy phosphate levels, nor to decreased availability of intracellular calcium. Rather, acidosis and inorganic phosphate accumulation cooperate to decrease myofilament sensitivity to calcium. Marked alterations of cardiac function and metabolism may also accompany the postischemic period. Positron emission tomography studies have shown that myocardial uptake of glucose remains disproportionately elevated in areas of myocardium which have been rendered transiently ischemic by an episode of stress-induced angina in patients with coronary artery disease. This phenomenon may have important practical applications, as it may be used as a metabolic marker to detect areas of myocardium which is viable, but potentially at risk for ischemic episodes. Reduced ATP levels are another biochemical alteration which can be typically found in postischemic hearts. Again, NMR spectroscopy has allowed to establish that these hearts often display near-normal mitochondrial function, and that the delayed resynthesis of ATP is due to lack of purine nucleotide precursors. A most interesting functional peculiarity of postischemic hearts is represented by the prolonged impairment of contractility, which largely outlasts the duration of the period of flow deprivation. This phenomenon, which eventually subsides over the course of hours or days, has been termed myocardial stunning, to underline its occurrence despite the absence of ultrastructural signs of irreversible damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Metabolic changes and their mechanical consequences in acute myocardial ischemia]. 184 94

The effects of glutamate on anginal threshold, cardiac metabolism and hemodynamics were studied in 11 patients with stable angina pectoris, positive stress test results, and pacing-induced myocardial lactate release due to coronary artery disease (CAD) (n = 9) or syndrome X (n = 2). Data were obtained before, during and after 2 identical periods of coronary sinus pacing, the second being preceded by an intravenous injection of monosodium glutamate 1.2 (n = 7) or 2.5 (n = 4) mg/kg body weight. After glutamate administration, pacing time to onset of angina increased from mean +/- standard deviation 103 +/- 53 to 166 +/- 71 seconds (p less than 0.01) and ST-segment depression after pacing decreased from 2.3 +/- 1.0 to 1.6 +/- 1.1 mm (p less than 0.01). Arterial glutamate concentration increased 60% (p less than 0.01) after the low dose and 150% (p less than 0.01) after the high dose of glutamate. Regardless of dose, myocardial glutamate uptake increased by 25% (p less than 0.01). Pacing-induced cardiac release of lactate diminished 50% (p less than 0.05), whereas the releases of xanthine and hypoxanthine were unchanged by glutamate. Arterial free fatty acids decreased 20% (p less than 0.01). Circulating levels and cardiac exchanges of alanine, glucose and citrate were unchanged. Glutamate did not influence heart rate, arterial blood pressure, coronary blood flow, coronary vascular resistance or myocardial oxygen consumption. One patient complained of short-lasting burning sensations after receiving the high glutamate dose. In conclusion, augmented provision of glutamate enhances pacing tolerance in stable angina, presumably by a metabolic improvement of cardiac energy production during ischemia.
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PMID:Antiischemic and metabolic effects of glutamate during pacing in patients with stable angina pectoris secondary to either coronary artery disease or syndrome X. 185 69

The effects of glutamate on exercise tolerance, ischemic threshold and venous substrate concentrations were studied in 20 patients with stable angina pectoris and positive stress tests. Each patient underwent 4 upright bicycle exercise tests on consecutive days. The first and fourth tests were performed without medication while the second and third tests were preceded by a low and high bolus dose of monosodium glutamate, either 0.8 and 1.5 mg/kg body weight intravenously (10 patients) or 40 and 80 mg/kg orally (10 patients). Comparison of the first and fourth tests revealed good reproducibility of electrocardiographic, hemodynamic and metabolic data. Glutamate increased exercise duration (p less than 0.05) in a dose-related way when given intravenously (59 +/- 14 and 153 +/- 14 seconds) and when given orally (53 +/- 21 and 90 +/- 23 seconds; all data are mean +/- standard error of the mean). It also delayed the onset of ST-segment depression (p less than 0.05) by 73 +/- 19, 120 +/- 23, 62 +/- 27 and 80 +/- 30 seconds, respectively. Hemodynamics were not changed by glutamate at rest or at comparable workloads, but at onset of ST-segment depression the heart rate-blood pressure product was increased (p less than 0.05). Glutamate administration induced dose-related 1.5- to 10-fold elevations in plasma glutamate, 15 to 50% decreases in plasma free fatty acids (p less than 0.05) and 5 to 30% increases in plasma alanine contents. Circulating levels of glucose, lactate, citrate and albumin were not modified by glutamate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of glutamate on exercise tolerance and circulating substrate levels in stable angina pectoris. 196 10

We studied the effects of heparin, given as 12,500 units intravenously, on cardiac metabolism during catheterization of the coronary sinus at rest and during repeated rapid atrial pacing in 8 patients with stable angina pectoris, positive stress tests and coronary arterial disease and in 8 patients with normal coronary arteries without objective signs of ischemic heart disease. Heparin did not influence angina, ST-segment depression or myocardial lactate production induced by pacing in the group with diseased coronary arteries. In both groups, heparin increased the arterial levels (70%) and the myocardial uptake (40-50%) of free fatty acids, the latter only during non-ischemic conditions. Myocardial net uptakes of glucose, lactate and glutamate and the release of alanine were reduced by heparin in the subjects with normal coronary arteries but not in those with ischemic heart disease. Myocardial oxygen consumption was unchanged. In the patients with normal coronary arteries, the levels of free fatty acid in the arteries were positively related to myocardial uptake of fatty acids and the release of citrate but inversely related to cardiac uptake of lactate and glucose. These relations were lacking in the patients with diseased coronary arteries. The metabolic effects of heparin on the heart, therefore, were diminished in patients with ischemic heart disease when compared to controls. This is probably due to an altered regulation of substrate preference in ischemic hearts.
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PMID:Cardiac metabolic effects of heparin differentiate between patients with normal and stenotic coronary arteries. 197 Aug 7

Calcium channel blockers, originally developed for the treatment of angina and supraventricular arrhythmias, have been shown to lower elevated blood pressure effectively in hypertensive patients. Verapamil, nifedipine, and diltiazem represent prototype compounds for unique chemical classes with differing pharmacologic properties. These drugs lower elevated blood pressure with efficacy comparable with other commonly used antihypertensives. Combination therapy with other agents usually results in an additive response. Side effects are usually mild and reversible and usually are an extension of the drug's pharmacologic effects. Moreover, adverse metabolic effects on lipid, glucose, or potassium levels are not common. Because of the excellent antihypertensive effects of calcium channel blockers and their potential importance in a variety of other disease states, these agents should be routinely considered for use as a first-line antihypertensive agent in appropriately selected patients with hypertension of any severity as part of a comprehensive plan to minimize cardiovascular risk.
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PMID:The role of calcium channel blockers in the treatment of essential hypertension. 199 52

Patients in this study were assessed by coronary angiography because of classic effort angina and a positive exercise test. Of these patients, 320 had untreated primary hypertension and 320, similar in age and gender distribution, were normotensive. In all patients coronary angiography documented that at least one major epicardial branch was restricted by 50% or more. Prevalence of single- and double-vessel disease in the fourth and fifth decades of life was similar in the two populations and in both tended to decline with age. Prevalence of triple-vessel disease was also similar in the two populations in the fourth and fifth decades; in either population it rose with age and reached a peak at the seventh decade of life. The percentages of hypertensive patients in the sixth and seventh decades with triple-vessel disease was significantly (p less than 0.01) greater (40% and 50%, respectively) than the corresponding values in normotensive individuals (25% and 31%, respectively). The left main coronary artery was not significantly more involved in the high blood pressure group. Pressure was moderately and similarly raised at any age in hypertension; serum cholesterol and triglyceride levels, blood glucose, and smoking habits were comparable in the two populations. These results suggest that hypertension does not accelerate the appearance of significant coronary narrowing or multiple vessel involvement. Starting from the sixth decade, the natural age-related evolution of coronary disease seems to be aggravated in hypertensive subjects, as reflected by an augmented number of diseased vessels. This process is probably related to high blood pressure in itself; whether the severity of hypertension might also exert an influence is not deducible from this study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coronary angiographic patterns in hypertensive compared with normotensive patients. 200 32

The human heart in the fasting state extracts free fatty acids (FFA), glucose, lactate, pyruvate, and ketones from circulating blood. The utilization of FFA accounts for most of the oxygen consumed and energy produced at rest. Patients with angiographically demonstrable coronary artery disease and stable angina pectoris have a resting myocardial metabolism similar to that of normal individuals. During atrial pacing in normal persons, there is a significant enhancement of glucose uptake but that of FFA is unchanged, and the oxidation of carbohydrates accounts for more than 60% of the energy produced. In patients with stable angina, myocardial perfusion becomes regionally inadequate during stress. Despite the increase of myocardial glucose utilization, carbohydrate oxidation is negligible. Pyruvate will not be oxidized but in the presence of increased amounts of reduced coenzymes will be reduced to lactate. In addition, a greater amount of alanine will be released by the myocardium through the transamination of pyruvate, with a concomitantly greater uptake of glutamate that serves as the NH2 donor. In addition, glutamate may be used as an anaerobic fuel through conversion to succinate coupled with GTP formation. Although coronary hemodynamics, including myocardial perfusion, return to baseline within a few minutes after stress, a longer time course is needed for myocardial metabolism to become normal. In particular, myocardial utilization of exogenous glucose remains higher well after the normalization of hemodynamic parameters. This is more pronounced in postischemic myocardium, but it also occurs in nonischemic muscle, and glucose is presumably used for rebuilding glycogen stores that were depleted during ischemia.
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PMID:Metabolic markers of stress-induced myocardial ischemia. 202 52


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