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

A 50-year-old man complained of lumbar pains, lack of energy, dysarthria and ataxic gait. Investigation revealed progressive anaemia (haemoglobin initially 10.5 g/dl, later 6.8 g/dl) and thrombocytopenia (initially 67,000/microliters, later 25,000/microliters). In addition he had unexplained pyrexia of up to 39.8 degrees C. Lactate dehydrogenase was 780 U/l and fragmented red cells were noted in the blood film. Because of suspicion of thrombotic thrombocytopenic purpura, treatment with fresh plasma by infusion was immediately initiated. On the third day of treatment he developed left ventricular failure; auscultation revealed a blowing early diastolic murmur over Erb's point together with a spindle-shaped early diastolic murmur over the right second intercostal space. Computed tomography of the skull showed recent haemorrhage into the left half of the cerebellum and an older right posterior infarct. The abdominal ultrasound scan suggested a haemorrhagic spleen infarct. In view of these findings the diagnosis was revised to embolizing aortic endocarditis with aortic reflux (confirmed by colour Doppler echo-cardiography). Aortic valve replacement was performed immediately, and the patient was treated with gentamycin 80 mg/d and teicoplanin 400 mg/d for four weeks. Postoperatively he was given 12 units of platelet concentrate and the platelet count remained stable thereafter (greater than 100,000/microliters). Splenectomy became necessary because the splenic haematoma increased in size during oral anticoagulant therapy. After a 6 week hospital stay the patient was discharged in good condition.
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PMID:[Embolizing aortic valve endocarditis in the differential diagnosis of thrombotic thrombocytopenic purpura]. 153 83

Multiple compensatory mechanisms operate to preserve exercise tolerance in patients with left ventricular failure. Exercise capacity of most patients with chronic heart failure is limited by dyspnea or fatigue, or both. Maximal stress testing with direct assessment of peak O2 uptake is an essential measurement in planning exercise conditioning programs, which are now attracting patients with chronic heart failure. The biochemical and histologic patterns of skeletal muscle changes seen in chronic heart failure patients are consistent with the effects of long-term exercise deconditioning in normal subjects. Recent studies have suggested beneficial effects of training in subjects with moderate or even severe left ventricular dysfunction by showing increased exercise tolerance or peak O2 consumption, anaerobic threshold, peak leg blood flow, peak central arteriovenous oxygen difference and decreased lactate accumulation. However, a number of questions remain unanswered. Exercise training for the treatment of chronic heart failure should be determined on an individual basis and used with caution.
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PMID:Physical training in patients with congestive heart failure. 157 63

Eleven cases with 13, incidentally found coronary-pulmonary fistulous communications were discovered out of about 11,000 diagnostic coronary angiograms performed in different patients, over the period 1968 to 1989. These patients were followed-up for an average period of 4.4 years (range 2-11 years). The majority had a fistulous malformation originating from the proximal part of the left anterior descending artery and terminating in the pulmonary trunk. In three subjects, the right coronary artery participated in formation of the shunt. The fistulas consisted either of a convoluted mass of serpentive vessels, sometimes with aneurysmal formation, or of a solitary single vessel. Angina pectoris, atypical chest pain and fatigue were the most common symptoms. All patients were treated conservatively except one, who underwent ligation of the fistula and coronary arterial bypass grafting. Two subjects are still free of symptoms. No death occurred. None of the patients developed subacute bacterial endocarditis, acute myocardial infarction or left ventricular failure during the period of follow-up of more than four years. Three individuals, prior to the follow-up period, had suffered myocardial infarction contralateral to the shunt. They had no recurrence.
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PMID:Coronary-pulmonary fistula: long-term follow-up in operated and non-operated patients. 236 8

The relation between exercise left ventricular ejection fraction and blood pressure (BP) responses after an acute myocardial infarction (AMI) was investigated. Twenty-eight to 37 days after an uncomplicated AMI, 224 consecutive patients underwent exercise radionuclide angiography in the 40 degrees semisupine position. In 180 patients (group A, 80%), BP increased more than 5 mm Hg every stage; in 44 patients, BP responses were abnormal; in 33 (group B, 15%), BP did not increase during 2 stages; in 11 (group C, 5%), it decreased more than 5 mm Hg after an initial increase. Ejection fraction did not differ significantly among the 3 groups at rest (51 +/- 13 in group A, 50 +/- 18 in group B, 47 +/- 13 in group C [difference not significant]) or at peak exercise (51 +/- 16% in group A, 46 +/- 19% in group B, and 43 +/- 16% in group C, [difference not significant]). Exercise-induced left ventricular failure or hemodynamic decompensation occurred in 22 patients. In these patients, ejection fraction at rest was 44 +/- 19% and decreased to 35 +/- 16% (p less than 0.05) with exercise. Only 9 of these patients (41%) had abnormal BP responses, with the other 13 (59%) showing a normal BP responses. The The 35 patients with abnormal BP responses in the absence of hemodynamic decompensation were asymptomatic, terminating exercise because of fatigue. The ejection fraction at rest and during exercise in these patients was similar to that in patients with normal BP responses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Significance of abnormal blood pressure response during exercise-induced myocardial dysfunction after recent acute myocardial infarction. 359 78

The cause of exercise intolerance in congestive heart failure is unclear. Hemodynamic and ventilatory responses were measured during symptomatic maximal upright bicycle exercise in 28 patients with chronic severe left ventricular failure who achieved a maximal oxygen uptake of only 12 +/- 4 ml/min/kg (+/- standard deviation). All patients reached anaerobic metabolism as the respiratory exchange ratio rose and arterial pH fell significantly. Pulmonary capillary wedge pressure increased from 20 +/- 10 mm Hg at rest to 38 +/- 9 mm Hg at peak exercise and cardiac index increased from 2.51 +/- 0.73 to 4.54 +/- 1.65 liters/min/m2 (both p less than 0.001). Systemic vascular resistance decreased, but pulmonary vascular resistance did not change during exercise. Despite the marked pulmonary venous hypertension at peak exercise, blood gases were unchanged (PaO2, 96 +/- 15 mm Hg; PaCO2, 35 +/- 7 mm Hg). Systemic arterial oxygen content increased from 16 +/- 2 to 17 +/- 2 vol% (p less than 0.01). Changes in pulmonary capillary wedge pressure did not correlate with changes in arterial oxygen content. Results were similar whether patients were limited by dyspnea or fatigue. Thus, exercise intolerance in patients with severe left ventricular failure is associated with marked elevation of pulmonary capillary wedge pressure and anaerobic metabolism without hypoxemia or altered carbon dioxide tension. These findings suggest that exercise ability in congestive heart failure is more dependent on cardiac output than on ventilatory consequences of pulmonary congestion.
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PMID:Relation between hemodynamic and ventilatory responses in determining exercise capacity in severe congestive heart failure. 641 73

The demographics and natural clinical history of canine congenital subaortic stenosis (SAS) were evaluated by retrospective analysis of 195 confirmed cases (1967 to 1991), 96 of which were untreated and available for follow-up evaluation. Of these, 58 dogs had left ventricular outflow systolic pressure gradients available for assessment of severity. All 195 dogs were used for demographic analysis. Breeds found to be at increased relative risk included the Newfoundland (odds ratio, 88.1; P < .001), Rottweiler (odds ratio, 19.3; P < .001), Boxer (odds ratio, 8.6; P < .001), and Golden Retriever (odds ratio, 5.5; P < .001). Dogs with mild gradients (16 to 35 mm Hg) and those that developed infective endocarditis or left heart failure were diagnosed at older ages than those with moderate (36 to 80 mm Hg) and severe (> 80 mm Hg) gradients. Of 96 untreated dogs, 32 (33.3%) had signs of illness varying from fatigue to syncope; 11 dogs (11.3%) developed infective endocarditis or left heart failure. Exercise intolerance or fatigue was reported in 22 dogs, syncope in 11 dogs, and respiratory signs (cough, dyspnea, tachypnea) in 9 dogs. In addition, 21 dogs (21.9%) died suddenly. Sudden death occurred mainly in the first 3 years of life, primarily but not exclusively, in dogs with severe obstructions (gradient, > 80 mm Hg; odds ratio, 16.0; P < .001). Infective endocarditis (6.3%) and left heart failure (7.3%) tended to occur later in life and in dogs with mild to moderate obstructions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The natural clinical history of canine congenital subaortic stenosis. 788 29

Symptoms tend to develop late in the course of both chronic mitral and chronic aortic regurgitation, and when the regurgitation is stable patients may enjoy many years of full activity free from disability. In the absence of complicating atrial fibrillation or coronary artery disease the onset of dyspnoe and fatigue usually indicate myocardial failure and possibly a lost opportunity for a low risk operation and long term benefit. Valve replacement for aortic regurgitation is a good operation which reduces left ventricular work. However, mitral valve replacement is unphysiologic and not surprisingly, the operative mortality and long term results are worse with an excess of deaths caused by left ventricular failure. While the need for operation is obvious when patients already have symptoms or when valvar regurgitation is increasing, timing is far more difficult for patients with severe, chronic, stable regurgitation who still enjoy a high quality of life. It is even more difficult in mitral regurgitation because the stakes are higher with a higher operative risk, but suitability for mitral valve reconstruction justifies earlier operation and therefore makes it mandatory for cardiologists to identify such patients.
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PMID:Optimal timing of surgery for chronic mitral or aortic regurgitation. 826 Nov 61

Propranolol, a nonselective beta-adrenergic blocking agent, although prescribed frequently, has not been monitored for its adverse reactions in Indian population. A collaborative ADR monitoring study was planned in 2661 hypertensive patients. Exclusion criteria were associated circulatory insufficiency, heart block, left ventricular failure, diabetic mellitus and airway obstruction. The incidence of ADR was 2.1%, which is lower than reported incidence of 8.7 to 43.7 percent in other studies. This could be attributed to improper selection of patients, differences in methodology of monitoring, or to racial variation. In the present study ADR of fatigue (1.1%), dizziness (0.4%) and headache (0.2%) constituted the bulk. Additional reaction of pain in chest (0.2%), heart block (0.1%), hypoglycemia (0.1%), loss of libido (0.1%) and shock (0.03%), were also observed.
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PMID:Adverse reactions to propranolol, a non-selective beta-adrenergic blocking agent in hypertensive patients--a collaborative study. 844 49

We successfully treated a case of active infective endocarditis in the remission phase of virus-associated hemophagocytic syndrome (VAHS). A 21-year-old man was admitted to our hospital for fever, arthralgia, and general fatigue. His blood cultures revealed staphylococcus epidermidis. He underwent urgent aortic valve replacement and closure of the abscess cavity because of an ineffective antibiotic therapy and a progressive left heart failure. Operative findings showed about 100 ml bloody pericardial effusion, fresh vegetation on the aortic left coronary and non-coronary leaflets, and aortic root abscess just below the left coronary ostium. The aortic root abscess extended to the left ventricular wall between the base of left atrial appendage and the base of main pulmonary artery and was in the state of impending rupture. The left main coronary artery was fully exposed after debridement in the abscess cavity. It was thought that left atrial appendage as a pedicle was useful for filling up the abscess cavity to protect infection.
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PMID:[A case of active infective endocarditis in the remission phase of virus-associated hemophagocytic syndrome]. 972 Mar 81

The suggested role of oxidative stress in the pathogenesis of heart failure is largely based on utilizing left heart failure models. The present study on rats evaluated changes in antioxidants as well as oxidative stress in relation to hemodynamic function subsequent to the right heart failure induced by monocrotaline (50 mg/kg, i.p.). During the post-injection period, monocrotaline (MCT)-treated rats demonstrated a persistent growth depression. Two to three weeks after the injection, MCT-treated rats showed signs of fatigue, peripheral cyanosis and dyspnea. In these rats, right heart hypertrophy was confirmed by a significant increase in right ventricular weight as well as right ventricle to body weight ratio. In MCT-treated rats, there was also a significant increase in right ventricular systolic as well as end diastolic pressures. No change in lung and liver wet/dry weight ratios between MCT-treated and control animals was observed. Based on the hemodynamic data as well as other clinical observations, the functional stage achieved was compensated heart failure. Myocardial antioxidant enzymes, catalase, glutathione peroxidase and superoxide dismutase, in the MCT-treated rats were not different compared to control rats. Vitamin E levels were significantly depressed in the RV and there was no change in retinol levels. There was a significant increase in lipid hydroperoxide concentrations in MCT-treated rats as compared to the control group. These data provide evidence that right heart failure is associated with an increase in oxidative stress.
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PMID:Myocardial oxidative stress changes during compensated right heart failure in rats. 1044 2


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