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)

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

This prospective study of symptom-limited supine ergometry was conducted to determine the contributions of right ventricular (RV) and left ventricular (LV) systolic function to the exercise capacity of a cohort of patients with coronary artery disease (CAD). Patients with unstable angina, angiographically proven CAD (n = 53) and stable symptoms after medical therapy or angioplasty were included. Documented myocardial infarction (greater than or equal to 2 weeks before exercise) was present in 43 of 53 patients. Angina was the limiting symptom in 11 of 53; the other 42 stopped exercise with dyspnea or fatigue, or both. Oxygen consumption was measured on-line during exercise with a metabolic cart. RV ejection fraction and LV ejection fraction were measured by validated methods from gated blood pool radionuclide ventriculography. There were weak but statistically significant correlations between exercise oxygen consumption and exercise RV ejection fraction (r = 0.30, p less than 0.05) and between exercise oxygen consumption and exercise LV ejection fraction (r = 0.38, p less than 0.01). Multivariate regression analysis, including exercise RV ejection fraction, exercise LV ejection fraction and exercise heart rate versus exercise oxygen consumption revealed a better relation (r = 0.48, p less than 0.005) than any variable in univariate regression. The values of RV and LV ejection fraction at rest did not correlate significantly (r = 0.2, difference not significant), but the exercise values did correlate weakly (r = 0.41, p less than 0.01). The reserve of LV ejection fraction, defined as exercise minus rest value, correlated weakly with exercise oxygen consumption (r = 0.32, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left and right ventricular systolic function and exercise capacity with coronary artery disease. 202 97

We conducted a study on the clinical and angiographic characteristics of 140 patients with unstable angina. Average age of 57, male/female ratio 4 to 1. The most frequent risk factors: tobacco smoking (73%) and arterial hypertension (42%). They had old infarct (57%), and unstable angina at rest (37%). We did early submaximal stress test to 31% of them; in 38.6% test was stopped due to angina, 25% for fatigue. 91% had ischemic changes, there weren't any severe complications. Regarding significant coronary obstruction: 20% had one vessel, 26% two, 50% three and left trunk 4%. Normal ventriculogram 43%. Eight patients died; the causes were: disease of the trunk (37.5%) and "active" angina (87.5%), 25% during catheterization . All survivors responded to medical treatment. 54 patients were not candidates for surgical treatment, among them 70.3% were released in class I (NYHA). At follow up 90% were in class I-II, 12% had unstable angina recurrence, 3% had acute infarct. In the pathogenesis of unstable angina intervene fixed atherosclerosis, obstructive lesions, repetitive spasms and non-occlusive thrombosis, this physiopathologic behavior is responsible for the stages of ischemic activity. Treatment should be directed to maintain the balance between the distribution and the demand of O2, and also treating spasm and thrombosis.
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PMID:[Unstable angina: clinical and angiographic characteristics of 140 cases]. 224 1

In order to study the association between vital exhaustion and different manifestations of coronary heart disease, a prospective study was conducted among 3877 males, aged 39-65. This group was studied during a mean period of 4.2 years. Vital exhaustion, a mental state characterized by unusual fatigue, a feeling of being dejected or defeated, and increased irritability, were assessed by means of the Maastricht Questionnaire. Subjects who scored in the upper third were labelled as exhausted and were compared with those who scored in the lower or middle third. The age-adjusted relative risk of angina pectoris at screening that was associated with vital exhaustion was 4.17 (p less than 0.01); that of unstable angina pectoris at screening was 17.21 (p less than 0.001). No association was observed between vital exhaustion and past myocardial infarction, except in the youngest age group (OR = 3.76; p = 0.05). Among the subjects free from coronary heart disease at screening, 54 cases of angina pectoris, 38 cases of non-fatal myocardial infarction, and 21 cases of fatal myocardial infarction were observed during follow-up. The age-adjusted relative risk of angina pectoris at follow-up was found to be 1.86 (p less than 0.03) and that of non-fatal myocardial infarction was found to be 2.28 (p less than 0.001). No association was found between vital exhaustion and fatal events.
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PMID:Fatigue and heart disease. The association between 'vital exhaustion' and past, present and future coronary heart disease. 262 76

Pathologic evidence indicates that thrombosis in coronary arteries is most frequently initiated by fissures in atheromatous plaques and that the associated hemorrhage induces platelet aggregation. Less frequently, thrombosis may be initiated by arterial spasm or by pathologic abnormalities affecting the platelets or the mechanisms of plasma coagulation. For the rational development of antithrombotic drugs on the basis of aggregation inhibitors, the cause (or causes) of plaque fissure and of the ensuing platelet aggregation need therefore to be elucidated. Our current research is based on the working hypothesis that fissuring occurs when plaques have acquired a particular composition that can be disrupted by the cumulative effect of continuously varying hemodynamic forces (reminiscent of fatigue failure in artificial materials), and that fissure-associated hemorrhage, like hemorrhage anywhere else, initiates platelet aggregation via a concurrence of hemodynamic and biochemical mechanisms. Detailed studies are currently being directed toward establishing the sequence of events that determine the contributions of adenosine diphosphate, thromboxane A2, and other endogenous agents in promoting hemostatic platelet aggregation in real life and, by implication, arterial thrombosis. Important recent evidence has demonstrated repeated thrombosis in unstable angina patients. In such patients, aspirin diminishes by about half the incidence of myocardial infarction and death. Presumably, it prevents the formation of platelet thrombi, which would tend to be produced in the turbulent blood flowing through arterial segments severely narrowed by hemorrhage plaques or in spasm. Several other platelet-active drugs are also under investigation.
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PMID:Polypharmacologic interactions in the management of thrombosis. 266 84

Although beta blockers are effective for the treatment of angina pectoris, chronic adverse effects produced by these agents--including lethargy, fatigue, and male impotence--can adversely affect patient acceptance and treatment compliance. To assess the clinical effects of switching from anti-anginal treatment with beta blocker only (phase I) to half-dose beta blocker plus the calcium blocker nifedipine (phase II) or nifedipine alone (phase III), 18 patients with chronic stable angina pectoris and side effects to beta blockers were evaluated in a 12-week, open-label trial. Three patients did not complete the study, one secondary to new unstable angina and two secondary to nifedipine side effects. Of the 15 patients completing the trial (13 men and two women; mean age, 54 +/- 5 [SEM] years), all sequentially participated in the one-month phases. Weekly angina frequency assessed from patient diaries was significantly less for treatment with nifedipine only (phase III) as compared with beta blocker (phase I) (1.7 +/- 1 versus 3.9 +/- 1 episodes per week), while phase II was not significantly different. Exercise test time was maintained throughout all phases (phase I, 457 +/- 39; phase II, 458 +/- 40; and phase III, 498 +/- 48 seconds, p not significant). All 15 patients in phase I (100 percent) had side effects to beta blockers, but these side effects were lessened in 12 patients (80 percent) in phase II and 13 patients (86 percent) in phase III, with total alleviation of symptoms in two patients (13 percent) in phase II, and eight patients (53 percent) in phase III. Thus, in patients with side effects to beta blockers, switching to nifedipine is associated with a significant reduction in beta blocker adverse symptoms and equal anti-anginal efficacy.
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PMID:Alternative medical treatment for patients with angina pectoris and adverse reactions to beta blockers. Usefulness of nifedipine. 287 34

We investigated exercise capabilities of the elderly patients with significant coronary artery lesions and angina pectoris. The heart rate increased according to workload, but there were few cases in which maximal heart rate was obtained. There was a marked increase in VO2 at endpoint before sufficient work load was achieved. It suggested an increase in O2 demand of the myocardium and entire body. Left ventricular dysfunction from skeletal muscle fatigue and work load-induced myocardial anoxia were also suggested. The conditions of coronary arteries of aged patients and the method of treatment were studied on the basis of coronary angioplastic findings and exercise tolerance. We reviewed percutaneous transluminal coronary angioplasty (PTCA) performed in 49 aged patients (older than 70 years) with angina and investigated long-term results. In this group including 18 patients (43%) with multivessel disease, there was a high success rate (90%), and significant improvements in workload responses were achieved in early stages after PTCA. The rate of recurrence was higher in this group than non aged patients, however, angioplasty was repeated successfully in all of the patients. Dilated sites were recognized as patent in a majority of patients. Late cardiac events occurring six months after PTCA were acute myocardial infarction in only one case (2.2%) and unstable angina in three cases (6.8%). There was no cardiac death. The five-year cumulative survival rate was high (97%). During a follow-up interval of averaged 32 months, chest pain disappeared in 70% of patients and 48% enjoyed daily life without restriction. Since the quality of life appears to be improved and long term results are sufficiently acceptable, we concluded that PTCA is highly recommended for the elderly patients.
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PMID:[Clinical characteristics of ischemic heart disease in the aged: significance of coronary revascularization and role of PTCA]. 327 11

Visual monitoring at the central station of coronary care units (CCUs) may not adequately assess the presence and frequency of transient asymptomatic ST segment changes in patients with unstable angina. We have performed continuous 24-h electrocardiographic recordings over a total period of 50 days in 10 patients admitted to our CCU with frequent attacks of angina at rest. Over the corresponding period, at the central monitoring station (6 beds), the nursing-staff detected only 31 transient ischaemic episodes (27 with ST elevation, 4 with depression, 9 of which were asymptomatic). By contrast the retrospective analogue analysis of tapes identified 213 ischaemic episodes: 143 with ST elevation (greater than or equal to 0.2 mV) and 70 with ST depression (greater than or equal to 0.2 mV); usual CCU monitoring failed to report changes during 13 episodes (8 with ST elevation, 5 with depression) accompanied by anginal pain. When the tapes were played back in real time on a CCU monitoring scope, a cardiologist (who had the option of interrupting the play-back whenever tired) recognized 48% of the episodes when presented in groups of 4 and randomly positioned on the screen together with 2 other electrocardiographic tracings not related to the study; he recognized 92% of the episodes when only one ECG was presented on the screen. Thus conventional visual monitoring in a CCU considerably underestimates the incidence of transient ischaemic ST segment changes, some of which were accompanied by pain. This low rate of detection is the result of the presentation on the central monitoring station of several ECGs and of fatigue.
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PMID:Unreliability of conventional visual electrocardiographic monitoring for detection of transient ST segment changes in a coronary care unit. 649 51

Unstable angina pectoris and feelings of fatigue and general malaise are often mentioned as premonitory symptoms of myocardial infarction. From a psychological point of view these feelings of fatigue and malaise reflect a syndrome of vital exhaustion and depression (VED). A questionnaire which measures this syndrome was given to 3,571 males who participated in a voluntary health check up. It was found that the prevalence of "imminent myocardial infarction," defined as unstable angina pectoris plus electrocardiographic signs of ischaemia, was more than four times higher among exhausted and depressive persons, than among persons not so affected.
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PMID:Imminent myocardial infarction: a psychological study. 652 Mar 93

Eight patients who improved their exercise duration to angina or marked fatigue (greater than or equal to 25%) on timolol 10 to 30 mg twice daily over that on placebo 8 to 14 mo previously were subjects in a double-blind, randomized, crossover 4-wk study of the effect of timolol on exercise duration 2 and 12 hr after medication. One patient was discontinued from the study because unstable angina developed on placebo. Mean exercise duration on timolol over control was increased at 12 hr (p less than 0.02) and at 2 hr ( p less than 0.001) after drug. There was an increase in exercise duration greater than or equal to 25% on timolol over control compared with placebo in three of seven patients (43%) 12 hr after drug and in seven of seven (100%) 2 hr after drug. Timolol 10 to 30 mg twice daily prolongs exercise duration to angina or marked fatigue at 2 hr after drug and in some responders at 12 hr after drug.
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PMID:Exercise duration to angina at two and twelve hours after timolol. 700 83


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