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Query: UMLS:C0015672 (fatigue)
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Of 21 sudden deaths in sportsmen, 18 were thought to be caused by heart attacks either during or after sport. There was firm evidence of ischaemic heart-disease in 9, strongly suggestive evidence in 7, but in 2 there was only suggestive clinical evidence. As a group, these subjects were characterised by (1) a mean age above thirty (above twenty-five for rugby players); (2) a family history of early heart-attacks; and (3) antecedent symptoms of chest pain or pressure in 9, fatigue or blackout in 4, and minor complaints in 2. Most were known to their medical practitioners. Psychological factors were thought to be important in 8. Doctors, players and referees should be aware that severe sporting exertion as in rugby football involves a risk which for most players is relatively minor, but in the minority predisposed to heart-attacks by family history, smoking, or age (as in referees) the risk is more serious. To reduce hazard of sudden death in exercise, players and referees should be warned against smoking and informed of the serious implications of the development of chest pain, pressure, or undue tiredness before, during, or after sport.
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PMID:Sudden death and sport. 4

A case is presented of a 60-year-old woman with fatigue, dyspnea, and chest pain. A chest x-ray film revealed an abnormal cardiac silhouette. Echocardiography revealed a large, echo-free area with well-demarcated, discrete borders adjacent to the right heart border. This structure decreased in size with inspiration and did not show pulsatile cardiac motion. Cardiac catheterization confirmed the extracardiac nature of the lesion and also showed a "constrictive" pattern with equalization of diastolic pressures. Surgical exploration revealed a large cystic thymoma. With removal of the tumor, intracardiac pressures returned to normal.
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PMID:Cystic thymoma simulating contrictive pericarditis. The role of echocardiography in the differential diagnosis. 12 66

Workups by physicians in response to five common complaints in a sample of 104 men and women--52 married couples--were evaluated by chart audit. For the total group of complaints, back pain, headache, dizziness, chest pain, and fatigue, the physicians' workups were significantly more extensive for men than they were for women. These data tend to support the argument that male physicians take medical illness more seriously in men than in women.
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PMID:Response of physicians to medical complaints in men and women. 15 67

The effect of a single oral dose of a plasma FFA-lowering drug (5-(3-pyridyl) tetrazole), which does not act by conversion into nicotinic acid, on exercise tolerance and ECG reaction was studied on a double-blind basis in 15 men with stable angina pectoris. Exercise was performed on a bicycle ergometer in the sitting position with a load increase of 10 W/min. In addition to ECG, time to onset of chest pains and to termination of exercise because of strong chest pains was recorded. 5-(3-pyridyl) tetrazole decreased plasma FFA during exercise from 523 to 299 mumol/l. It reduced significantly the ST depression at corresponding work loads and permitted the patients to exercise 0.6 min longer, corresponding to a 7% higher work load, before the onset of chest pain. However, absolute exercise time was not significantly increased. The most probable explanation of the improved performance is a decreased lipid and increased carbohydrate oxidation by the ischemic heart, although a contribution may have come from hemodynamic effects of the drug, unrelated to effects on myocardial metabolism but perhaps involving heart rate and BP. The lack of a significant effect on performance time may have been due to general fatigue.
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PMID:Effect of plasma free fatty acid lowering on exercise tolerance and ST segment depression in patients with angina pectoris. 39 81

In an effort to determine the usefulness of prodromata for predicting a myocardial infarction, a prospective analysis was made of 211 consecutive patients with chest pain who were admitted to the Stanford University Medical Center Coronary Care Unit. In their subsequent course, 91 patients had a myocardial infarction, 102 had a myocardial infarction ruled-out, and 18 had a noncardiac etiology for their chest pain. Prodromal chest pain in the previous six months had occurred in 65% of patients and unstable angina in 61%. Infarction versus noninfarction patient groups could not be identified on the basis of prodromal ill health, chest pain, unstable angina, typical versus atypical nature of the chest pain, or activity at the onset of pain. Complaints of preceding fatigue and increased perceived stress were common in both groups. Activity at the onset of the admission chest pain was strenuous in 15% of the infarction patients and 12% of the noninfarction patients. We conclude that prodromal symptoms are common in both infarction and noninfarction patients. Although chest pain probably remains the single most frequent identifier of a new cardiac event, it is common in noninfarction patients and cannot be used alone to predict infarction or death.
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PMID:Prodromal characteristics as indicators of cardiac events in patients hospitalized for chest pain. 49 4

When exercise testing 159 patients with prior myocardial infarction, we identified 39 who were limited by fatigue. This group was all in sinus rhythm; none were taking drugs likely to impair the chronotropic response of the heart; none experienced chest pain or developed ischemic ECG changes. In 18 of this group, maximal heart rate achieved with exercise was 2SD or more below the age predicted value, and their heart rate response to exercise was reduced compared to that of the other 21 whose maximal exercise heart rates were within 2SD of age predicted values. A subgroup of 8 subjects with reduced exercise heart rates was studied before and after vagal blockade. In the 4 subjects whose infarction was inferior, the reduction in heart rate response was more profound and persisted after vagal blockade, suggesting either reduced pacemaker responsivness, due to ischemia or infarction, or autonomic imbalance as possible mechanisms. All 8 showed alinear increases in ventilation at higher power outputs and mean blood lactate postexercise was 7.5 mM/I without vagal blockade. Our findings suggest that a reduced heart rate response to exercise, already shown to imply added coronary risk, may be subdivided aetiologically and possibly prognostically. The use of a "Target Heart Rate" in such patients offers no safety margin, and maximal exercise capacity will be grossly over-estimated if extrapolated from the submaximal heart rate response. A cardiovascular limitation to exercise may be detected by an alinear increase in ventilation.
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PMID:Reduced heart rate response to exercise in ischemic heart disease: the fallacy of the target heart rate in exercise testing. 52 31

In order to determine their exercise tolerance, 20 patients with artificial ventricular demand pacemakers below the age of seventy were studied by bicycle ergometry. Only 30% of the patients showed a normal exercise tolerance according to the criteria by Kaltenbach, while 70% stopped the test prematurely because of leg fatigue, dyspnoe or chest pain. In terms of their exercise tolerance, there was no difference between patients who developed normal sinus rhythm or rapid atrial fibrillation during the exercise and those who remained at the fixed pacemaker rate throughout the test. It is concluded, therefore, that the exercise tolerance of pacemaker-patients is not only limited by the fixed heart rate but mainly by the underlying heart disease (coronary heart disease, cardiomyopathy, hypertensive heart disease etc.) and the general physical condition of the patients. In an age-matched control group of 20 patients 50% showed a normal exercise tolerance and the duration of exercise in this group was only slightly longer (21%) than in the pacemaker-group.
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PMID:[Exercise tolerance of patients with artificial cardiac pacemakers (author's transl)]. 54 95

A 27 year old woman was hospitalized for progressive dyspnea, fatigue and retrosternal chest pain. She had progressive cardiac enlargement with clinical and laboratory confirmation of a dilated cardiomyopathy. Transvenous percutaneous right ventricular endomyocardial biopsy yielded a specimen showing a noncaseating granuloma. The patient's dyspnea responded dramatically to steroid therapy with corresponding improvement in radiographic and echographic measures of ventricular performance. This case illustrates the problem of diagnosing cardiac sarcoidosis when there is no apparent evidence of other organ involvement.
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PMID:Cardiac sarcoidosis. Diagnosis with endomyocardial biopsy and treatment with corticosteroids. 67 30

The response to electrocardiographically monitored submaximal exercise stress testing has been studied in 44 patients with mitral leaflet prolapse (MLP). With exercise, ventricular premature contractions occurred in 7, ventricular tachycardia in 1, and atrial fibrillation in 1. Exercise was terminated short of target heart rate in 18 patients, because of chest pain (5), fatigue (7), ventricular arrhythmia (4), dizziness (1) or ST segment depression (1). 23 patients developed postexercise ST segment abnormalities, of whom 5 had 'ischemic' patterns and arteriographically proven coronary artery disease (CAD); among the 18 others, the ST segments were depressed and minimally downsloping in 2, slowly ascending from depressed J point in 3, horizontal for greater than or equal to 80 msec with J depression of less than 1 mm in 12, and cupped in 1. The incidence of arrhythmias provoked by submaximal exercise stress testing in patients with MLP was lower than suggested in previous reports. In all 5 cases where MLP and CAD coexisted, the classical 'ischemic' electrocardiographic response to exercise was not obscured. Even in the absence of CAD, postexercise ST segment abnormalities were common with MLP (18/39 = 46%) and differed from the progressively resolving ST segment deviation characteristic of CAD with angina. Exercise testing can safely be recommended, subject to standard contraindications, in patients with MLP and yields useful information.
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PMID:The electrocardiographic response to exercise in 44 patients with leaflet prolapse. 71 Apr 93

Mitral valve prolapse is a condition that is being recognized with increased frequency. It is not known whether its incidence is increasing, or whether we are better able to diagnose it today. In the idiopathic or familial variety, the mitral valve pathology is almost always that of myxomatous degeneration. Some authors have suggested the presence of a cardiomyopathy because of significant left ventricular dysfunction in many cases. Idiopathic prolapse occurs predominantly in females, often at a young age, and may be associated with chest pain, dyspnea, fatigue, presyncope, syncope, and/or sudden death. The clinical findings are variable and typically consist of a nonejection click and/or late systolic murmur, heard best at the cardiac apex. Diagnosis can be confirmed by echocardiography and/or ventricular cineangiography, the latter permitting accurate recognition of the anatomy of the prolapsed leaflets. The complications of infective endocarditis, severe mitral insufficiency, and life-threatening ventricular arrhythmias represent the major problems of management. It is important to distinguish the idiopathic form of mitral valve prolapse from that due to coronary artery disease and to realize that mitral valve prolapse may occur in Marfan's syndrome, Turner's syndrome, or in association with secundum atrial septal defect or ruptured chordae tendineae. Typical clicks and/or murmurs have also been described in patients with a history of rheumatic fever and in hypertrophic cardiomyopathy. Although much descriptive knowledge has accumulated over the past 15 years, many unanswered questions remain regarding the idiopathic type of prolapse. What is the nature and cause(s) of myxomatous degeneration? What is the relation of the valve pathology to the left ventricular dysfunction? What is the relation of both of these factors to disabling chest pain, electrocardiographic changes, and life-threatening arrhythmias? Hopefully, answers to these and other important questions regarding mitral valve prolapse will be forthcoming.
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PMID:Mitral valve prolapse. 77 95


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