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

Digitalis and diuretics constitute conventional therapy of congestive heart failure, but systemic vasodilators offer an innovative approach in acute and chronic heart failure of decreasing increased left ventricular systolic wall tension (ventricular afterload) by reducing aortic impedance and/or by reducing cardiac venous return. Thus, vasodilators increase cardiac output (CO) by diminishing peripheral vascular resistance (PVR) and/or decrease increased left ventricular end-diastolic pressure (LVEDP) (ventricular preload) by diminishing venous tone. Concomitantly, there is reduction of myocardial oxygen demand, thereby reliably reducing angina pectoris in coronary disease, and potentially limiting infarct size and ischemia provided systemic arterial pressure remains normal. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload versus impedance: nitrates principally cause venodilation (decrease LVEDP); nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation (decrease LVEDP and increase CO) provided left ventricular filling pressure is maintained at the upper limit of normal; whereas hydralazine predominantly effects arteriolar dilation (increases CO). With depressed CO plus highly increased LVEDP and increased PVR, nitrates also induce some increase of CO by reducing PVR. Combined nitroprusside and dopamine synergistically enhance CO and decrease LVEDP. Mechanical counterpulsation aids nitroprusside in acute myocardial infarction. The 30-minute venodilator action of sublingual nitroglycerin is extended for 4 to 6 hours by cutaneous nitroglycerin ointment, by sublingual and oral isosorbide dintrate, and by oral pentaerythritol tetranitrate and sustained-release nitroglycerin capsules. Ambulatory oral vasodilator therapy is provided by long-acting nitrates (relieve pulmonary congestion); hydralazine (improves fatigue); prazosin alone, combined nitrate-hydralazine combined prazosin-hydralazine (improve both dyspnea and fatigue).
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PMID:Afterload reduction and cardiac performance. Physiologic basis of systemic vasodilators as a new approach in treatment of congestive heart failure. 9 30

The effects of the beta-adernergic blocking drug acebutolol were studied in 23 patients with angina pectoris and angiographically documented coronary artery disease. Patients were evaluated clinically, by graded treadmill testing and by 24-hour Holter monitoring in the control state, after 2 weeks treatment with placebo, and after 2 weeks treatment with 600 mg. and then 1,200 mg. of acebutolol. Acebutolol (in a daily dose of 600 mg.) was an effective antianginal drug: the number of clinical attacks of angina pectoris (p less than 0.001) and the consumption of sublingual nitrate decreased (p less than 0.01), there was a significant increase in the treadmill effort tolerance as measured by the time to appearance of ischemic ECG changes (p less than 0.001) and the total work performed (p less than 0.001), and there was also a significant decrease in ischemic ST segment depression on 24-hour Holter monitoring. Treatment with 1,200 mg. acebutolol was associated with a further decrease in heart rate and a further improvement in effort tolerance on treadmill testing (p less than 0.05). On the large dose of the drug, however, there was no further clinical improvement, and no further improvement on 24-hour ECG monitoring; several patients complained of weakness and fatigue. Graded treadmill testing was an excellent objective method for assessing physical effort tolerance and its improvement after treatment with the beta-blocking drug. Twenty-four-hour Holter monitoring was a useful and complementary test, especially in patients who stopped exercising on the treadmill because of fatigue or weakness, and especially for assessing the efficacy of beta-blockade in controlling emotionally induced tachycardia and ischemia in the patient's own daily environment.
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PMID:Evaluation of the beta-blocking drug acebutolol in angina pectoris. 49 6

Exercise tolerance has been studied by two different methods, heart-rate-controlled exercise and stepwise increased load, in 12 patients with angina pectoris. The response to a beta-adrenergic blocking agent, alprenolol, and an alkyl nitrate derivative, pentaerythritol trinitrate (PETRIN) was studied by the two methods after double-blind administration of the drugs. Rating scales were used to quantitate the degree of dyspnoea, angina pectoris and tiredness in the legs. After PETRIN both methods showed significant increases in exercise tolerance (19 and 21 per cent). The heart-rate-controlled test showed a significant increase (33%) after alprenolol, but the change was not significant by the other method. In the patients studied, heart-rate-controlled exercise discriminated between active drug and placebo better than the stepwise increased load test, what might have been due to more optimal matching of the loads obtained in the heart-rate-controlled test. Indications are given about how to design an exercise study in patients with angina pectoris.
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PMID:Exercise tolerance in patients with angina pectoris after pentaerythritol trinitrate and alprenolol studied by two different methods. 78 82

The clinical efficacy of xamoterol, alpha beta 1-adrenoceptor partial agonist, was determined in a multicentre double-blind, randomized, parallel group study of 240 patients with mild to moderate heart failure. At entry, 62% of patients were receiving diuretics (thiazides, or loop diuretics at a dose no greater than the equivalent of 80 mg of frusemide); 32% were taking nitrate formulations and 14% digoxin for control of atrial fibrillation. Assessments were carried out after a 1-week placebo run-in and after 3 months of treatment with either xamoterol or placebo. 198 patients completed the study of whom 186 had valid exercise tests. Mean exercise duration increased by 7% after placebo and by 19% after xamoterol during a progressive treadmill exercise protocol. Xamoterol significantly reduced peak exercise heart rate compared with placebo. Subjectively, there was improvement in breathlessness on the visual analogue scale after treatment with xamoterol compared with placebo, but no change in fatigue. We conclude that xamoterol produces sustained improvement in symptoms and exercise duration in mild to moderate heart failure.
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PMID:Clinical efficacy of xamoterol, a beta 1-adrenoceptor partial agonist, in mild to moderate heart failure. U.K. Xamoterol Study Group. 257 8

Stripping and ligation of the renal lymphatics has been a standard operation for patients with chyluria in Japan. However, recently, inguinal lymph node-saphenous vein anastomosis and lymphangiovenous anastomosis in the spermatic cord or the lower limb are introduced as a microsurgical treatment of chyluria with good result from China. We present a case of 50-year-old female with chyluria, which was cured by the lymphatic-venous anastomosis at the groin. The patient had lived in Okinawa, an area of endemic filariasis, till 23 years of age. She noted chyluria for the first time at 28 years of age, when it was treated by irrigation of the renal pelvis with silver nitrate solution. The symptom recurred at 48 years of age, and fatigue developed two months before admission. The conservative treatments including rest, low fat diet and repeated irrigation of the renal pelvis were carried out, but these were ineffective. Therefore, bilateral inguinal lymph node-saphenous vein anastomosis and lymphangiovenous anastomosis in the same wound on the right were performed. The chyluria disappeared five months after the operation. The lymphatic-venous anastomosis at the superficial part of the body may be the surgical procedure of choice, because they are effective, simple, less invasive and less traumatic.
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PMID:[Chyluria treated with inguinal lymphangiovenous and lymph node-venous anastomosis: a case report]. 799 Mar 8

The influence of graded leg muscle ischaemia on the adaptation to training and on the acute response to exercise was studied in healthy subjects. Graded ischaemia during supine exercise was induced by application of 50 mmHg external pressure on the legs. This procedure reduced leg blood flow by 16%, venous oxygen saturation by 12 percentage units, and markedly increased lactate release (p < 0.05 for all). One-legged training was performed during four weeks, 4 sessions per week. Each session started with one leg training for 45 min with reduced blood flow (ischaemic training). The contralateral leg, serving as a control, was then trained with an identical power-output profile for 45 min but without flow restriction (non-ischaemic training). Ischaemic training enhanced the adaptation to training. Peak oxygen uptake and time to fatigue increased more (p < 0.05) with ischaemic than with non-ischaemic training. Citrate synthase activity, capillaries per fibre, and glycogen content were greater (p < 0.05) in the trained than in the detrained state. In the ischaemically trained leg, the type IIb fibre proportion was lower (p < 0.05) and the I fibre proportion tended to be higher (p = 0.06) in the trained than in the detrained state. Maximum voluntary dynamic strength was decreased by 8% (p < 0.01) in the ischaemically trained leg, but was unaffected in the non-ischaemically trained leg. During acute ischaemic exercise, as compared to non-ischaemic exercise, there was a higher degree of glycogen depletion, a greater depletion of type II, but not of type I fibres, a greater electromyographic activity, higher catecholamine concentrations, lower intramuscular ATP and creatine phosphate content, and an increased nitric oxide formation as estimated by increased plasma nitrate content. In conclusion, the mechanisms underlying the potentiation of the adaptation to training by ischaemia are assumed to depend on the operation of stimuli which were amplified during acute ischaemic exercise.
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PMID:Exercise and training during graded leg ischaemia in healthy man with special reference to effects on skeletal muscle. 814 Sep

The goals of stable angina pectoris treatment are: (i) symptom relief and increase in angina-free walking time; and (ii) reduction of mortality and adverse outcome. Strategies used for plaque stabilisation resulting in a reduction in cardiovascular mortality and morbidity are: smoking cessation; aspirin (acetylsalicylic acid); blood pressure control; lipid lowering agents when low density lipoprotein cholesterol is elevated despite dietary therapy; coronary bypass surgery in patients with left main stem disease or triple vessel coronary disease and diminished left ventricular function; and use of estrogen in postmenopausal women. For symptom relief and to increase angina-free walking time, long acting nitrates, beta-blockers, calcium antagonists and potassium channel openers can be used. Drugs from these 3 classes are all effective when used optimally and choice of initial therapy should consider the presence of concomitant disease and underlying left ventricular function. However, none of the long acting nitrates provide continuous prophylaxis because nitrate tolerance develops during long term therapy. In patients with uncomplicated stable angina, nitrates, beta-blockers and calcium antagonists are all effective. Intermittent nitrate therapy is not associated with tolerance, but headache is a common adverse effect and the patient is unprotected at night and in the early hours of the morning. Concomitant treatment with a beta-blocker may be beneficial if the patient experiences withdrawal or early morning angina. For patients with stable angina and hypertension, therapy with a beta-blocker or a calcium antagonist rather than nitrate is indicated. beta-Blockers are preferred in patients who have had a myocardial infarction, or in those with a history of supraventricular tachyarrhythmias. beta-Blockers may produce excessive slowing of the heart rate, fatigue and bronchospasm in susceptible patients. Calcium antagonists are indicated as initial therapy when beta-blockers are either not tolerated or contraindicated. beta-Blockers and nondihydropyridine calcium antagonists should not be used in patients with sinus bradycardia and those with greater than first degree atrioventricular (AV) block because of the possibility of further slowing of heart rate and/or the development of high grade AV block. When monotherapy with one class is ineffective or associated with adverse effects, the patient should be switched to another class rather than given an additional drug. Optimal monotherapy is often as effective as combination therapy. If maximum monotherapy is only partially effective, a combination therapy which is not additive in terms of adverse effects should be chosen. Triple therapy may be deleterious and no more effective than dual therapy.
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PMID:Choosing the most appropriate treatment for stable angina. Safety considerations. 967 56

The shock syndrome has been classically considered as a consequence of both decreased tissue perfusion and O2 supply; however, in some types of shock like septic or traumatic ones, regional blood flows may be increased. A decade ago, mitochondrial alterations consistent with uncoupling of oxidative phosphorylation were reported in either endotoxemic or hemorrhagic experimental shock or in humans. Recently, the discovery of nitric oxide (NO) and its increase in the shock state, has opened new perspectives in the understanding of this problem. Nitric oxide produces vasodilatation and, at the same time, increases the mitochondrial production of O2 active species like superoxide anion. Both radicals react to form a strong oxidant that is able to nitrate the phenolic rings of proteins: peroxynitrite. This effect leads to the impairment of the activities of different mitochondrial enzymes like succinate dehydrogenase and ATPase and the mitochondrial function and finally, to decreased energy levels and to multiorgan failure. The increase in NO release is due to the effects of circulating peptides and of increased adhesion of neutrophils to the endothelium and to the positive effects of inflammatory mediators like TNF-alpha and cytokines on inducible NOS (iNOS) expression in endothelium and tissues. It is suggested that the shock state is the consequence of an imbalance between NO and O2 and their metabolites.
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PMID:[Shock: concepts for a definition]. 981 94

The present study was designed to evaluate whether nitroglycerin administration preceding the injection of technetium-99m labelled metroxy-isobutyl-isonitryl ((99m)Tc-sestamibi), improves the detection of myocardial perfusion defect reversibility. Moreover, we assessed whether myocardium kinetics improved after the percutaneous transluminar coronary angioplasty (PTCA) study. The study population consisted of 12 patients, 8 males and 4 females, 48-73 years old (mean age: 60.41 years) with chronic stable angina, resting wall dyskinesia, and >/=50% stenosis or occlusion of at least one coronary artery, who were scheduled to undergo PTCA. A gamma-camera gated single photon emission tomography myocardial perfusion scintiscan was performed as a baseline study with (99m)Tc-sestamibi (GSPET-B) and another similar scintiscan after nitrate augmentation (GSPET-N) before PTCA and two to six months after PTCA (GSPET-R), to assess the extent of perfusion defects, contraction abnormalities and myocardial viability. Cedars QGS software was used for semi quantitative assessment and sum perfusion scores were calculated for each study. According to our results from the 174 hypoperfused segments studied by GSPET-B, 137 segments had tracer activity <50%. From the 137 segments with tracer activity of <50% only 51 (37%) remained unaltered after PTCA. Twenty-six of them (51%) were described as nonviable after the GSPET-N study and the remaining 25 were defined as viable. Our study demonstrated significant perfusion improvement after nitrate augmentation (mean sum perfusion score decreased from 34+/-9 in the baseline study (SBS) to 23+/-11 in the GSPECT-N study (SNS), P=0.04. There was no significant difference between SNS and mean sum perfusion score after revascularisation (SRS), 23+/-11 and 24+/-13 respectively (P=0.833). The specificity, sensitivity and accuracy of the perfusion improvement after PTCA, were calculated as: 52%, 85% and 76% respectively. The low specificity in our study could be due to performing GSPET-R in some patients, six months after PTCA; during this time restenoses may occur. Two of our patients whose perfusion and myocardial wall motion kinetics had worsened and also had clinical symptoms of pain and fatigue, were considered to have developed restenosis. In the present study, myocardial wall motion kinetics showed non-significant improvement of global ejection fraction (EF). EF increased from 43.9%+/-3.3% to 48.9% after nitrate augmentation (P=0.262) and to 47.2%+/-6.4% after revascularization (P=0.091). Myocardial wall motion hypokinesia showed significant improvement of severity scores in the GSPET-N study, as well as after PTCA revascularization (P<0.01). It is concluded that GSPET-N (99m)Tc-sestamibi imaging significantly improves the detection of defect reversibility. On the basis of our results, it appears appropriate to recommend GSPET-N (99m)Tc-sestamibi imaging only in patients with perfusion defects and tracer activity of <50%. In such cases it is recommended to perform GSPET not only for perfusion but also for a myocardial wall motion kinetic study. The follow up study to evaluate the result of PTCA is recommended to be performed within 2 months after PTCA, before restenosis may occur and 6 months after PTCA if restenosis is suspected.
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PMID:Assessment of myocardial viability with (99m)Tc-sestamibi -gated SPET images in patients undergoing percutaneous transluminar coronary angioplasty. 1588 54

Transcription profiling of genes encoding components of the respiratory chain and the ATP synthesizing apparatus of Mycobacterium tuberculosis was conducted in vivo in the infected mouse lung, and in vitro in bacterial cultures subjected to gradual oxygen depletion and to nitric oxide treatment. Transcript levels changed dramatically as infection progressed from bacterial exponential multiplication (acute infection) to cessation of bacterial growth (chronic infection) in response to host immunity. The proton-pumping type-I NADH dehydrogenase and the aa3-type cytochrome c oxidase were strongly down-regulated. Concurrently, the less energy-efficient cytochrome bd oxidase was transiently up-regulated. The nitrate transporter NarK2 was also up-regulated, indicative of increased nitrate respiration. The reduced efficiency of the respiratory chain was accompanied by decreased expression of ATP synthesis genes. Thus, adaptation of M. tuberculosis to host immunity involves three successive respiratory states leading to decreased energy production. Decreased bacterial counts in mice infected with a cydC mutant (defective in the cytochrome bd oxidase-associated transporter) at the transition to chronic infection provided initial evidence that the bd oxidase pathway is required for M. tuberculosis adaptation to host immunity. In vitro, NO treatment and hypoxia caused a switch from transcription of type I to type II NADH dehydrogenase. Moreover, cytochrome bd oxidase expression increased, but cytochrome c oxidase expression decreased slightly (nitric oxide) or not at all (hypoxia). These specific differences in respiratory metabolism during M. tuberculosis growth arrest in vitro and in vivo will guide manipulation of in vitro conditions to model bacterial adaptation to host immunity.
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PMID:Changes in energy metabolism of Mycobacterium tuberculosis in mouse lung and under in vitro conditions affecting aerobic respiration. 1622 31


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