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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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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

With advancing age of the population and with echocardiographic means of diagnosis, amyloid disease of the heart is of increasing clinical interest. Advanced age, restrictive myocardiopathy, arrhythmias, and conduction disorders are familiar features of this disease. A 92 year old man with past history of hemiblock followed by complete heart block and transvenous pacemaker was admitted to the hospital because of increasing fatigue and the abrupt development of dyspnea. Examination revealed paradoxic pulse, markedly elevated central venous pressure, and echocardiographically demonstrated large pericardial effusion. Shortly after admission signs of tamponade developed; 1,000 ml of pericardial fluid was removed with prompt relief of dyspnea dna disappearance of paradoxic pulse and return of central venous pressure to normal. However, dyspnea soon recurred and subsequent hemodynamic measurements indicated increased right ventricular and left ventricular filling pressures. Echocardiography revealed no recurrent effusion or ventricular hypokinesis. Left ventricular ejection fraction by radionuclide ventriculogram was 64 percent. Echocardiography revealed ventricular wall thickening, normal chamber size, and glittering, sparkling myocardial echoes. On postmortem examination, there was extensive myocardial amyloidosis. There was no evidence of constrictive pericarditis or recurrent effusion. The unique aspect of this case was the combined presence of restrictive myocardiopathy and pericardial tamponade. To our knowledge, no previous case of tamponade due to amyloid heart disease had been reported.
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PMID:Pericardial tamponade, a new complication of amyloid heart disease. 709 Nov 68

Optical light microscopy and electron microscopy were used to examine 22 or eleven hearts of pigs which had been killed in a state of extreme fatigue due to transport. Samples were taken and fixed within five minutes from stunning. The following histological findings were obtained: Glycogen depletion of the myocardiac fibres was conspicuous in most cases, usually with high glycogen levels in Purkinje's fibres. Discrete, easily overseeable changes of scattered fibres or groups of fibres in the form of granular or hyaline degeneration were recorded from 73 per cent of the cases, with degeneration having been granular in 59 per cent and hyaline in 54 per cent. Fibre oedema was rare and recordable from only two cases. Changing prestatic hyperaemia was established from terminal vessels, while no visible alterations were found in capillary endothelia by optical light microscopy. The following results were gained by means of electron microscopy: Glycogen depletion was accompanied by differently pronounced expansion of parts of both the sarcoplasmic reticulum and T-system. Unchanged mitochondria were detected together with incipient mitochondrial swelling to different degrees, accompanied by cristolysis, in certain rare instances, as well as by partial or total homogenisation of interior mitochondrial structures, in more frequent cases. Z-strips were widened in eight cases. Limited decomposition of fibrils in some myocardiac cells was observed in samples of three animals. There were signs of usually moderate interfibrillar and perinuclear oedema and of predominantly inconspicuous capillary endothelia. Most of the changes were reversible and less strongly pronounced, and they were likely to suggest the presence of disorders in energy metabolism and impairment of stimulus conduction. They are interpreted as secondary myocardiopathy, caused by haemodynamic-hypoxic factors, following primary insufficiency of peripheral circulation.
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PMID:[Light and electron microscopic studies of cardiac pathomorphology in swine due to transport fatigue (porcine stress syndrome)]. 721 34

In a dog with advanced dilatative cardiomyopathy, dynamic cardiomyoplasty resulted in improvement in clinical status and systolic function. Dynamic cardiomyoplasty involved surgical isolation of the right latissimus dorsi muscle on its neurovascular pedicle, transposition of the muscle into the thoracic cavity, wrapping the ventricles with the muscle, and implantation of a myostimulator for cardiosynchronous stimulation of the muscle. After a 2-week period, the latissimus muscle underwent a 50-day period of progressive burst stimulation to transform the muscle to a fatigue resistant phenotype. Thereafter, the muscle received cardiosynchronous stimulation at a 3:1 R-wave-to-burst ratio. This procedure may offer hope for long-term treatment of dilatative cardiomyopathy in dogs.
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PMID:Dynamic cardiomyoplasty for treatment of idiopathic dilatative cardiomyopathy in a dog. 769 21

Interferon alpha is a biologic agent with demonstrated anti-tumor activity in a variety of hematologic and solid malignancies. Many patients treated with interferon experience acute toxicity manifested as a flu-like syndrome of fever, chills, myalgias, and malaise. However, fatigue, anorexia, bone marrow suppression, nausea, vomiting, dizziness, and confusion may also occur. Cardiotoxicity is a rare complication of interferon therapy that most frequently presents as transient episodes of hypotension and tachycardia, with few significant life-threatening cardiovascular effects reported. A small number of cases of suspected interferon-induced cardiomyopathy, all of which improved after discontinuing interferon, have recently been documented. We report a patient with multiple myeloma who developed severe congestive cardiomyopathy while receiving interferon alpha that did not reverse subsequent to discontinuation of interferon therapy. Although the patient had previously received doxorubicin, the presence on endomyocardial biopsy of a prominent intracellular lipid accumulation within myocytes and only grade 2 anthracycline cardiotoxicity suggested that other or additional factor(s) contributed to the severity of this patient's cardiomyopathy. Etiologies of cardiac dysfunction other than interferon and doxorubicin were excluded. While a direct cause-effect relationship between interferon alpha and irreversible congestive cardiomyopathy cannot be firmly established in this case report, patients who either concurrently or sequentially receive interferon and anthracyclines should be carefully monitored for evidence of cardiac toxicity.
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PMID:Irreversible, severe congestive cardiomyopathy occurring in association with interferon alpha therapy. 771 76

Mitochondrial cytopathies are due to genetic anomalies in the oxidative phosphorylation enzymes (excepting Krebs cycle, pyruvate and certain other mitochondrial enzymes). Recently discovered, these diseases have a characteristic heterogeneous clinical expression because of the ubiquitous nature of this intracellular organelle. We observed a case in a 16-year-old girl who had cytochrome C oxidase deficiency. The child was born to non-consanguinous parents and had a healthy brother. The first manifestation of the disease was a systolic murmur heard at the age of 4 years. Progressively, exertion dyspnoea, lipothymia with cyanose led to the first echocardiography at 8 years revealing non-obstructive cardiomyopathy. Functional inadaptation of cardiac performance worsened requiring various symptomatic treatments. At the age of 16, the symptomatology included lower limb fatigue and the diagnosis of a metabolic disease was entertained. Phosphorylase A and B activity and phosphokinase activity were normal. High lactic acid levels after exertion suggested a mitochondrial enzyme deficiency. The diagnosis of cytochrome C oxidase deficiency was confirmed by spectrophotometric and polarographic assay of mitochondria from a peripheral muscle biopsy. Treatment with riboflavin, ascorbic acid, factor P, menadione, carnitine and iron sulfate has currently provided some symptomatic improvement. In patients with unexplained cardiomyopathy, the diagnosis of mitochondrial cytopathy should be entertained if oxidoreduction potentials (lactate/pyruvate ratio) are perturbed. The diagnosis is confirmed by enzyme studies of fresh muscle mitochondria. Currently therapeutic prospects are at best very poor. Genetic counselling may be advisable.
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PMID:[Hypertrophic cardiomyopathy caused by cytochrome-oxidase deficiency]. 782 67

Postpartum fatigue may be a symptom of significant medical or psychiatric illness and must be distinguished from tiredness, which is a common adaptive response after delivery. Anemia, infections, thyroid disorders, mood disorders and cardiomyopathy are important causes of fatigue in the postpartum period. Recognition and treatment of these conditions improves the medical care of women following delivery.
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PMID:Postpartum fatigue. 801 47

Manganese superoxide dismutase (SOD2) converts superoxide to oxygen plus hydrogen peroxide and serves as the primary defense against mitochondrial superoxide. Impaired SOD2 activity in humans has been associated with several chronic diseases, including ovarian cancer and type I diabetes, and SOD2 overexpression appears to suppress malignancy in cultured cells. We have produced a line of SOD2 knockout mice (SOD2m1BCM/SOD2m1BCM) that survive up to 3 weeks of age and exhibit several novel pathologic phenotypes including severe anemia, degeneration of neurons in the basal ganglia and brainstem, and progressive motor disturbances characterized by weakness, rapid fatigue, and circling behavior. In addition, SOD2m1BCM/SOD2m1BCM mice older than 7 days exhibit extensive mitochondrial injury within degenerating neurons and cardiac myocytes. Approximately 10% of SOD2m1BCM/SOD2m1BCM mice exhibit markedly enlarged and dilated hearts. These observations indicate that SOD2 deficiency causes increased susceptibility to oxidative mitochondrial injury in central nervous system neurons, cardiac myocytes, and other metabolically active tissues after postnatal exposure to ambient oxygen concentrations. Our SOD2-deficient mice differ from a recently described model in which homozygotes die within the first 5 days of life with severe cardiomyopathy and do not exhibit motor disturbances, central nervous system injury, or ultrastructural evidence of mitochondrial injury.
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PMID:Neurodegeneration, myocardial injury, and perinatal death in mitochondrial superoxide dismutase-deficient mice. 879 Apr 8

The rationale for the development of new drug combinations is to combine optimal doses of drugs with single agent activity which are not cross-resistant and have non-overlapping toxicities. Anthracyclines are widely accepted as the agents of choice for first-line treatment of metastatic breast cancer and have been tested in combination with the taxoids, docetaxel (Taxotere) and paclitaxel (Taxol). Toxicity problems have emerged using anthracyclines and paclitaxel, with sequence- and schedule-dependent toxic effects including dose-limiting typhlitis and mucositis, as well as febrile neutropenia and, in one study, cardiomyopathy. The dose-limiting toxicities of the combination of docetaxel and doxorubicin are neutropenia and infection, and preliminary results indicate a response rate of 89%. There is a need to develop a combination treatment regimen which is non-cross-resistant with anthracyclines. Vinorelbine (Navelbine) has single agent activity against metastatic breast cancer and has been used in combination with taxoids. The dose-limiting toxicities of the vinorelbine-paclitaxel combination are febrile neutropenia, pelvic pain, fatigue and paraesthesias. The dose-limiting toxicities of the combination of docetaxel and vinorelbine are febrile neutropenia and mucositis. The overall response rate for this combination was 67% and studies are ongoing.
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PMID:Taxoids in combination chemotherapy for metastatic breast cancer. 886 12

Cardiomyoplasty is a method for managing patients with dilated cardiomyopathy. We evaluated the means of carbon fiber electrode stimulation of the nerve to the latissimus dorsi muscle (LDM) in dogs to increase skeletal muscle contractility. Histochemical examination of biopsies of muscle electrically conditioned by a single pulse stimulator via the thoracodorsal nerve demonstrated transformation of muscle into fatigue resistant slow fibers without damage to muscle or nerve tissue. Canine experiments confirmed that carbon fibers are one of the best electrodes for chronic LDM stimulation. Between 1988 and 1992, we operated on ten patients, New York Heart Association (NYHA) Class III (4 patients) and Class IV (6 patients), with a mean left ventricular ejection fraction (LVEF) of 23%. The indications for cardiomyoplasty were idiopathic (7 patients) and ischemic (3 patients) cardiomyopathy refractory to maximum medical therapy. The operative procedure was performed via median sternotomy (5 patients) and left thoracotomy (5 patients). There was one operative mortality and two additional deaths during the late follow-up period. The mean postoperative LVEF increased to 27%. Functional class, quality-of-life, and ventricular performance were improved after cardiomyoplasty. Two of the surviving patients are in NYHA Class I, four in Class II, and one in Class III.
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PMID:Electrostimulated cardiomyoplasty: from experimental to clinical studies. 917 Jan 44


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