Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Depression has been reported to be common in patients with coronary artery disease (CAD), using a variety of criteria for the diagnosis of depression. However, many studies have relied solely on the presence of symptoms such as a dysphoric mood and fatigue in making a diagnosis of depression. Both fatigue and dysphoric mood are also associated with medical illnesses, and psychiatric diagnoses based on such nonspecific symptoms may lack the specificity necessary to predict the need for psychiatric treatment. To assess the incidence of depression likely to require and respond to psychiatric treatment, 50 patients documented to have CAD by coronary angiography underwent psychiatric diagnostic interviews. Current research-based criteria (DSM-III) were used to make diagnoses of major depressive disorder. In addition, the applicability of a brief screening inventory the (Beck depression inventory) for detecting the presence of depression in these patients was tested. Nine patients (18%) met criteria (DSM-III) for major depressive episode. Depression was not related to the extent of CAD, age or use of beta blockers. There was a relation between depression and smoking. Only 2 of the 9 depressed patients had been diagnosed previously and were being treated for depression. When a score of greater than or equal to 10 on the Beck depression inventory was used to distinguish patients with depression, it had moderate sensitivity (78%) and specificity (90%) for the identification of depression.
 ...
PMID:Major depressive disorder in coronary artery disease. 368 79

Previous studies show no correlation between resting systolic left ventricular performance assessed as the ejection fraction and exercise tolerance. This study examined the relation between left ventricular diastolic performance and exercise tolerance in 63 patients with left ventricular dysfunction (ejection fraction less than 50%) due to known or suspected coronary artery disease. The 51 men and 12 women, aged 54 +/- 8 years (mean +/- standard deviation), underwent symptom-limited upright exercise testing on a bicycle ergometer. The exercise end-points were angina (n:5), dyspnea (n:16), and fatigue (n:42). The patients were divided into three groups: group 1 (n:28) with normal exercise tolerance (9.5 +/- 2.4 minutes), group 2 (n:18) with mild exercise intolerance (5.8 +/- 0.5 minutes), and group 3 (n:17) had severe exercise intolerance (3.7 +/- 0.9 minutes). The three groups did not differ in age, ejection fraction, end-diastolic volume, exercise end-point, exercise heart rate, and left ventricular peak filling rate at rest. The exercise peak filling rate was, however, significantly higher in group 1 (p = 0.03). Stepwise multivariate discriminant analysis of important variables identified the exercise peak filling rate as the only predictor of exercise tolerance (F = 6.0). Thus, variation in exercise peak filling rate may in part explain the variability of exercise tolerance in patients with left ventricular dysfunction; patients with preserved exercise capacity have higher exercise peak filling rate than those with exercise intolerance.
 ...
PMID:Relation between left ventricular diastolic function and exercise tolerance in patients with left ventricular dysfunction. 379 6

This study was conducted to determine if the limiting symptom in patients with coronary artery disease (CAD) influenced the pattern of oxygen consumption (VO2) over the final 90 seconds of a maximal exercise test. The pattern was classified according to the presence or absence of a plateau. Twenty-six normal persons and 55 patients with CAD were studied. They rated the severity of fatigue, dyspnea and angina at end exercise using the Borg scale and designated which symptom was the limiting factor. A plateau of VO2 over the final 90 seconds of exercise was observed in 77% of normal subjects and patients with CAD. Eighty percent of patients limited by angina achieved a plateau. In normal subjects and patients with CAD, peak VO2 was more reproducible than the pattern of VO2 over the final 90 seconds of exercise. There were no differences in the cardiac responses to exercise at maximal effort between patients who achieved a plateau of VO2 and those who did not. These results indicate that the limiting symptom of exercise, even angina pectoris, does not influence the ability to exercise maximally. Therefore, the peak value of VO2 during symptom-limited treadmill exercise is a valid measure of maximal cardiovascular capacity irrespective of the limiting symptom or the pattern of VO2 in the final 90 seconds of exercise.
 ...
PMID:Effects of the limiting symptom on the achievement of maximal oxygen consumption in patients with coronary artery disease. 395 34

During the past 20 years there have been great developments in the scientific understanding of the role of nutrition in health and physical performance. Epidemiological and physiological studies have provided evidence that certain forms of dietary behaviour may be linked with an increased risk of developing disorders such as high blood pressure, coronary artery disease and some cancers. This has resulted in dietary recommendations that are intended to reduce the incidence of these disorders in the community. The science of nutrition in relation to sports performance has progressed from empirical studies investigating the effects of dietary manipulations, such as restriction and supplementation, to the direct investigation of the physiological basis of the specific nutritional demands of hard physical exercise. This review is based on the premise that it is "what comes out' rather than "what goes in', which provides the clues to ideal nutrition for athletic performance. Various aspects of the physical demands of athletic exercise are viewed as stresses that induce specific biochemical, and hence nutritional, strains in the athlete. Training is the predominant demand in the athletic lifestyle. This is characterised by acute bouts of high power output. During one hour of hard training an athlete may expend 30% of his or her total 24-hour energy output. These high power outputs have important implications for energy substrate and water requirements. Carbohydrate, specifically muscle glycogen, is an obligatory fuel for the high power outputs demanded by athletic sports. Muscle glycogen is a limiting factor in hard exercise because it is held in limited amounts, utilised rapidly by intense exercise, and fatigue occurs when it is depleted to low levels in the active muscles. Liver glycogen may also be exhausted by hard exercise and low blood glucose contributes to fatigue. High sweat rates are demanded during severe exercise and large water deficits commensurate with energy expenditure are incurred during extended periods of hard training and competition. Salt, potassium, and magnesium are lost in nutritionally significant amounts in the sweat, but vitamins and trace elements are not. Adaptive mechanisms protect athletes against electrolyte depletion. Iron loss in sweat may contribute to the iron deficiency seen in some endurance runners. Protein is degraded and amino acids are oxidised during physical exercise. Protein is also retained during muscle building training. Recent investigations indicate that the minimal protein requirements of athletes may be substantially higher than those for sedentary persons.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Nutrition and sports performance. 639 Jun 9

Endorphins and endorphin receptors are believed to modulate pain perception. To investigate whether naloxone, a specific antagonist, could initiate anginal pain during exercise-induced myocardial ischemia in asymptomatic patients with angiographically defined coronary artery disease, a single-blind trial was conducted in 10 men with prior positive exercise electrocardiograms. Multistage treadmill exercise tests were performed twice within a week. On the second test, patients received naloxone, 2 mg intravenously, by a syringe infusion pump. Exercise was terminated because of fatigue in 6 patients and completion of the protocol in 4. No patient reported chest pain during exercise. Naloxone did not significantly alter exercise duration, heart rate, blood pressure and ST-segment changes compared with control testing. It is concluded that endorphins do not play a significant role in the recognition of anginal pain in patients who have asymptomatic exercise-induced ischemia.
 ...
PMID:Naloxone and asymptomatic ischemia: failure to induce angina during exercise testing. 649 61

The purpose of this study was to determine whether an exercise-induced decrease in ejection fraction in patients with coronary artery disease and left ventricular dysfunction at rest represents ischemia or the nonspecific response of a compromised left ventricle to exercise stress. Accordingly, radionuclide ejection fraction responses of 246 patients with coronary artery disease and an ejection fraction at rest of less than 0.50 were compared with those of a "nonischemic" control group of 48 patients with idiopathic dilated cardiomyopathy and a similar degree of ventricular dysfunction. The significance of the ejection fraction response in the group with coronary artery disease was further examined by relating it to the angiographic extent of coronary artery disease, severity of angina, incidence of chest pain and electrocardiographic ST segment depression during exercise and long-term prognosis. The ejection fraction decreased by greater than or equal to 0.01 and greater than or equal to 0.05 during exercise in 48 and 28%, respectively, of the patients with coronary artery disease compared with only 8 and 2%, respectively, of the patients with cardiomyopathy. When exercise was limited by fatigue at a submaximal heart rate, the ejection fraction decreased in 25% of the patients with coronary artery disease but in none of the patients with cardiomyopathy. Patients with coronary artery disease whose ejection fraction decreased during exercise had a significantly higher incidence of three vessel disease, exercise-induced chest pain or ST depression and late mortality than did patients whose ejection fraction did not decrease. These relations were confirmed equally in subgroups of patients with moderate (ejection fraction 0.30 to 0.49) and severe (ejection fraction less than 0.30) left ventricular dysfunction. Thus, in patients with coronary artery disease and left ventricular dysfunction at rest, a decrease in ejection fraction during exercise is more likely to indicate ischemia than a nonspecific left ventricular response to exercise stress. In the individual patient, a decrease of 0.05 or greater, or a decrease during submaximal exercise, appears to be highly specific for ischemia. A decrease in ejection fraction identifies a subgroup of patients with a high prevalence of multivessel coronary artery disease and a high risk of death during long-term follow-up on medical therapy.
 ...
PMID:Mechanism and significance of a decrease in ejection fraction during exercise in patients with coronary artery disease and left ventricular dysfunction at rest. 669 May 59

To address the hypothesis that physical conditioning may improve left ventricular function in patients with coronary artery disease, we performed first-pass radionuclide ventriculography in 53 patients at rest and during upright bicycle exercise before and after 6 to 12 months of exercise training. The peak bicycle workload achieved before the onset of fatigue, dyspnea, or angina increased by an average of 22% (p = .0001) after training, and mean heart rate at a workload equal to the pretraining maximum workload was decreased by 10 beats/min after training (p = .0002). Of 21 subjects with angina or exertional ST segment depression before training, 15 (71%) were able to exercise to the same workload without these manifestations of ischemia after training. Whereas neither mean resting left ventricular ejection fraction (LVEF) nor LVEF at peak exertion was significantly altered, mean LVEF at the pretraining maximum workload was increased from 0.50 to 0.54 (p = .002) after training. There was a significant correlation between the magnitude of training bradycardia and the increment in LVEF at the pretraining maximum workload (p = .009). We conclude that the relative bradycardia at comparable exercise workloads produced by exercise conditioning is associated with improvements in left ventricular performance as assessed by the LVEF. This observation is compatible with the hypothesis that training bradycardia in conditioned subjects with ischemic heart disease is associated with lower myocardial oxygen demand and lesser degrees of ischemia at comparable workloads. However, training effects on ventricular afterload or on ischemia contractile performance of the heart cannot be excluded.
 ...
PMID:Effects of physical conditioning on left ventricular ejection fraction in patients with coronary artery disease. 672 12

The action of nifedipine (N), acebutolol (A), and their association (A+N) was studied in 16 patients suffering from effort angina with documented coronary artery disease. The therapeutic action was valued by bicycle effort stress test after oral administration of medications in comparison with placebo (P), following a double-blind random sequence of treatments. Working capacity significantly increased after A (507 +/- 450 mkp, p less than 0.05), after N (1,140 +/- 767 mkp, p less than 0.001), and after A+N (1,198 +/- 644 mkp, p less than 0.01). The increments of work after P administration were not significant. Moreover, fatigue instead of angina appeared as a stopping criterion in 8 patients after A+N, and in only 1 patient after P, A, and N.
 ...
PMID:Effects of nifedipine, acebutolol, and their association on exercise tolerance in patients with effort angina. 703 97

The beta-Blocker Heart Attack Trial (BHAT) was a National Heart, Lung, and Blood Institute-sponsored, multicenter, randomized, double-blind, and placebo-controlled trial designed to test whether the regular administration of propranolol hydrochloride to men and women who had experienced at least one myocardial infarction would result in a significant reduction in total mortality during a two- to four-year period. During a 27-month interval, 3,837 persons between the ages of 30 and 69 years were randomized to either propranolol (1,916 persons) or placebo (1,912 persons), five to 21 days after the infarction. Depending on serum drug levels, the prescribed maintenance dose of propranolol hydrochloride was either 180 or 240 mg/day. The trial was stopped nine months ahead of schedule. Total mortality during the average 24-month follow-up period was 7.2% in the propranolol group and 9.8% in the placebo group. Arteriosclerotic heart disease (ASHD) mortality was 6.2% in the propranolol group and 8.5% in the placebo group. Sudden cardiac death, a subset of ASHD mortality, was 3.3% among the propranolol patients and 4.6% among the placebo patients. Serious side effects were uncommon. Hypotension, gastrointestinal problems, tiredness, bronchospasm, and cold hands and feet occurred more frequently in the propranolol group. Based on the BHAT results, the use of propranolol in patients with no contraindications to beta-blockade who have had a recent myocardial infarction is recommended for at least three years.
 ...
PMID:A randomized trial of propranolol in patients with acute myocardial infarction. I. Mortality results. 703 57

To determine the prevalence and clinical significance of increased lung thallium-201 uptake during submaximal exercise myocardial scintigraphy performed 2 weeks after acute myocardial infarction, 61 patients underwent submaximal exercise testing (target heart rate, 120 beats/min), multigated blood pool imaging at rest and coronary angiography before hospital discharge. Thallium lung uptake on the initial anterior projection image was graded qualitatively by comparing the intensity of thallium-201 activity in the lungs with that in the mediastinum. In 39 patients (64 percent), it was normal (equal to mediastinal activity) and in 22 (36 percent), it was increased (greater than mediastinal activity). Compared with patients with normal lung uptake, those with increased uptake had a greater prevalence of prior infarction (13 versus 36 percent, probability [p] less than 0.05), less global cardiac reserve as assessed by the four level New York Heart Association classification (p less than 0.05), more advanced Killip class in the coronary care unit (p less than 0.05), a higher Norris coronary prognostic index (2.6 +/- 1.9 versus 4.6 +/- 2.3 [mean +/- standard deviation], p less than 0.01), failure to achieve the target heart rate because of dyspnea, fatigue or angina (36 versus 86 percent, p less than 0.01), a greater prevalence of exercise-induced S-T segment depression (18 versus 45 percent, p less than 0.05), a greater number of anterior thallium-201 myocardial defects (p less than 0.05); a lower radionuclide ejection fraction at rest (50.4 +/- 6.1 versus 39.6 +/- 9.3 percent, p less than 0.01) and a greater number of asynergic left ventricular segments (p less than 0.05). Thus, the occurrence of increased lung thallium-201 uptake during submaximal exercise scintigraphy in the early postinfarction period is frequent and appears to be a marker of severe and functionally more important coronary artery disease associated with left ventricular dysfunction.
 ...
PMID:Clinical implications of increased lung uptake of thallium-201 during exercise scintigraphy 2 weeks after myocardial infarction. 708 Oct 48


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