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)

During the period 1960 to 1978, 98 patients underwent intracardiac repair of Fallot's tetralogy after palliative operations. Preoperative symptoms were cyanosis, dyspnea, increased fatigue with squatting and hypoxic spells. The hemoglobin concentration varied from 19 to 22 g/100 ml. At correction only 65 of 95 shunts were patent and needed surgical closure. Seventeen early deaths occurred (19%), the main causes being cardiac failure and arrhythmia. One patient died 3 years after correction from pneumonia. The subjective clinical result was excellent or good in all surviving patients. At repeat heart catheterization in 26 patients a high percentage of residual ventricular septal defects and pulmonary stenosis/insufficiency was found. However, the majority of defects were of minimal haemodynamic significance, and so far did not seem to do harm to the patients' subjective function.
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PMID:Correction of Fallot's tetralogy after palliative operations. 8 99

Patterns of breathing at night were recorded in 4 patients with heart-failure. 2 had periodic breathing while awake and in 2 it developed after they fell asleep. In all 4 the phase of hyperventilation disturbed sleep. These cases also illustrate other problems caused by periodic respiration in heart-failure, which range from tiredness during the day to an inability to sleep for more than a few minutes. Nocturnal waking in the hyperventilation phase of Cheyne-Stokes breathing should be differentiated from paroxysmal nocturnal dyspnoea caused by episodes of pulmonary oedema at night.
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PMID:Paroxysmal nocturnal dyspnoea and periodic respiration. 9 69

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

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

Revascularization of the heart is a means of relieving symptoms of coronary artery disease--such as angina, fatigue, and dyspnea. The question of whether revascularization prolongs the life of the patient has been debated. My colleagues and I have reviewed our years of experience with patients treated by implantation of internal mammary arteries into the ventricles. We have compared our series with other groups of patients treated medically. Our conclusion is that revascularization via internal mammary artery implants does increase longevity.
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PMID:Evidence that revascularization by ventricular-internal mammary artery implants increases longevity. Twenty-four year, nine month follow-up. 24 Sep 82

The Asthma Symptom Checklist (ASC), describing the subjective symptoms reported to occur during asthmatic attacks, has been developed previously. In the present study, the ASC key cluster solution was replicated and refined within a sample of 374 asthmatic inpatients. All of the original symptom categories were reporduced, including two mood categories, Panic-Fear and Irritability, a Fatigue category, and two somatic categories. Hyperventilation-Hypocapnia and Airway Obstruction. Two refinements were notable: (1) The Airway Obstruction category was empirically divided into two conceptually clear components, Dyspnea anc Congestion, and (2) three secondary mood categories, Worry, Loneliness, and Anger, were identified, which describe a continuum of mood between the polar extremes of panic and irritability. Of the symptom categories, only Panic-Fear was related to the intensity of the discharge drug regimens recommended 2 to 6 mouths after ASC administration. Panic-Fear scores were independent of pulmonary function measurements. A combined index based on pulmonary functions and panic-fear yielded the best prediction of discharge steroid regiments. Finally, those physicians rated highest in "sensitivity" to their patients by their supervisors prescribed less steroids overall, but most frequently prescribed discharge steriod regimens in relation to their patients' Panic-Fear scores. In contrast, physicians rated lower on sensitivity prescribed higher steroid regimens overall, but based these drug recommendations more cleary on objective pulmonary functioning, and not in relation to their patients' Panic-Fear scores. The results strongly suggest that the ASC Panic-Fear scale is associated with coping behaviors that importantly affect the patient's overall clinical picture by increasing the apparent severity of the asthma, thereby leading to intensified treatment. The findings stress the need to evaluate independently the objective medical condition and subjective symptomatology with its related coping behavior, in order to direct appropriate modes of therapy to each.
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PMID:Obervations on subjective symptomatology, coping behavior, and medical decisions is asthma. 40 66

Nitroglycerin reduces elevated left ventricular filling and pulmonary arterial pressures in resting patients with rheumatic valve disease and reduces symptoms when given over long periods to patients with primary myocardial disease. To determine whether nitroglycerin may prove effective therapeutically in ambulatory patients with heart valve disease, its effects on hemodynamics and exercise capacity were studied in 11 severely symptomatic adults who were already receiving optimal treatment with digitalis and diuretic agents. Seven had predominant mitral valve disease, one had predominant aortic insufficiency and three had equally severe mitral and aortic valve disease. Maximal exercise capacity was assessed with graded treadmill exercise after placebo and after nitroglycerin (0.5 mg sublingually) administered in random sequence to each patient. Exercise capacity (exercise time to limiting fatigue or dyspnea) increased from a mean of 8.3 minutes after placebo to 9.8 minutes after nitroglycerin (P less than 0.005). Eight patients were studied hemodynamically during further intense treadmill exercise. Pulmonary arterial pressure was significantly lower (P less than 0.05) after nitroglycerin than after placebo (mean 44 versus 56 mm Hg), but cardiac output was greater after nitroglycerin (5.0 versus 4.6 liters/min, P less than 0.005). Thus, nitroglycerin appears to increase exericse tolerance and improve the hemodynamic response to exercise in patients with heart valve disease and may be valuable in the long-term pharmacologic therapy of such patients.
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PMID:Nitroglycerin-induced improvement in exercise tolerance and hemodynamics in patients with chronic rheumatic heart valve disease. 41 13

In the period 1957--1976 481 patients under 40 years of age were operated on. Dyspnoea and increased fatigue were dominating symptoms in more than half of the series. In 202 cases the anomaly was discovered at routine examination in the absence of relevant symptoms. Almost half of the patients were operated under hypothermia, in the others extracorporeal perfusion was used. Four hospital deaths occurred, two of which were related to cardiopulmonary bypass.
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PMID:Atrial septal defect of secundum type in patients under 40 years of age. A review of 481 operated cases. Symptoms, signs, treatment and early results. 47 71

Pulmonary emboli seldom recur, and when recurrence does occur it is not associated with permanent sequelae unless there is progressive pulmonary arterial hypertension. Five patients with clinical and perfusion lung scan evidence of recurrent pulmonary embolism presented with abnormal cardiac rhythms without evidence of progressive pulmonary hypertension. Twenty-four-hour ambulatory electrocardiographic monitoring was valuable in diagnosis and in assessing the effectiveness of treatment. Although palpitation was the main complaint, other symptoms included tiredness, mild exertional dyspnoea, and chest discomfort unrelated to effort. Symptomatic improvement coincided with objective evidence of improvement from repeat lung scans and 24-hour ECG records. Antiarrhythmic agents controlled the arrhythmias but were subsequently withdrawn without the return of symptoms. Four of the five patients continued to take anticoagulants for two years. We believe that these five patients represent a group of patients with recurrent pulmonary emboli and a recognisable clinical picture dominated by arrhythmias unrelated to progressive pulmonary arterial hypertension. Long-term anticoagulant treatment was associated with clinical improvement.
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PMID:Recurrent pulmonary thromboembolism presenting with cardiac arrhythmias. 48 14

Dyspnea is the medical term for the patient's or subject's complaint of shortness of breath. It encompasses the respiratory discomfort experienced in many different diease states as well as the shortness of breath felt by a normal subject during or after strenuous exercise. Several parameters which have been shown to correlate with the onset or severity of dyspnea are described, including reduced vital capacity, the ratio of minute ventilation to vital capacity, reduced breathing reserve, the work of breathing, and the oxygen cost of breathing. Attempts at quantitation of dyspnea have usually consisted of measuring physiological parameters associated with the sensation, such as the "dyspneic index". The direct measurement of respiratory sensations using modern psycho-physical methods is at an early stage of development. Since the observation that the existence of dyspnea is often unrelated to any disturbance of arterial blood gas composition, it has been generally held that the mechanism of dyspnea is primarily neurophysiological. The neural pathways may conceptually be divided into those which transmit the "dyspnea message" from the respiratory apparatus to integrating centers in the brain, and those concerned with subsequently bringing the sensation to the level of consciousness. It seems likely that there is no single sensing mechanism and neural pathway which will be able to explain dyspnea in the diverse populations of patients and subjects who experience unpleasant respiratory sensations. Three theories concerning mechanisms of dyspnea are briefly described: "length-tension inappropriateness", vagal afferent activity especially from the J-receptors, and the recent concept of diaphragmatic fatigue. Some specific characteristics of the shortness of breath experienced in certain disease states are described, including chronic bronchitis and emphysema, bronchial asthma, pulmonary fibrosis and congestive heart disease.
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PMID:Dyspnea. 50 81


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