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

In this double-blind study in general practice, 444 patients were randomized to ketanserin (K, 40 mg b.i.d.) and 229 patients were randomized to propranolol (P, 80 mg b.i.d.). After 3 months, more patients on K (15%) than on P (9%) had been withdrawn (p less than 0.02). Although at 3 months the falls in systolic blood pressure (SBP) and diastolic blood pressure (DBP) were similar in both groups, the reduction in SBP was slower on K, and up to 2 months SBP was higher on K than on P (p less than 0.04 or less). At randomization and after 3 months, average weights were similar in both groups. However, during the first month of the study, patients on K gained weight, and this change in weight differed (p less than 0.02) from the unchanged weight on P. On K, BP lowering was greater when weight gain was less. Multiple regression analysis showed that after adjusting for BP at randomization and subsequent weight changes, DBP at 1 month on K was lower with advancing age, whereas SBP and DBP at 1 and 3 months on P were higher with age. Severe adverse effects were absent. However, dry mouth, edema, fatigue, and dizziness occurred more frequently with K (p less than 0.04 or less).
J Cardiovasc Pharmacol 1988 Dec
PMID:Double-blind comparison of ketanserin and propranolol in hypertensive patients. 246 91

Knowledge of the basic alterations of central hemodynamics in congestive heart failure (CHF) has failed to explain many aspects of this important syndrome. Increasing attention has recently been paid to compensatory and adaptive mechanisms occurring after the initiating insult. Thus, new insights have been gained into the pathophysiology of contraction of hypertrophied myocardium and changes of adrenergic receptors in the myocardium due to chronically increased cardiac sympathetic tone. The role of the renin-angiotensin-aldosterone system in early and advanced CHF has been further elucidated and the role of the vasodilating and natriuretic atrial natriuretic peptide is undergoing further definition. New results further clarify the mechanisms leading to breathlessness and muscular fatigue in chronic CHF with emphasis shifting from the traditional concept of the importance of increased filling pressures to changes to the peripheral circulation and the exercising muscles. Although progress has been made in the understanding of the pathophysiology of CHF, many aspects are still poorly understood and await clarification.
J Cardiovasc Pharmacol 1989
PMID:Compensatory and adaptive mechanisms in congestive heart failure. 248 Apr 83

Various opioids were used to investigate the role they might play in the cardiovascular responses to fatiguing isometric contractions. Changes in blood pressure were measured in cats anaesthetised with alpha-chloralose. Fatiguing isometric contractions of the hind limb muscles (ergoreceptor activation) were generated using a microprocessor controlled stimulator (50 Hz, 0.2 ms, 200-800 mV). Baroreceptor inactivation was elicited by carotid artery occlusion. Muscle contraction caused an increase in mean arterial pressure of 51 (SEM 12) mm Hg and carotid occlusion an increase of 56(9) mm Hg above resting levels in control conditions. Injection of dynorphin (0.5-5.0 micrograms.5 microliters-1) into the cerebral aqueduct just rostral to the 4th ventricle eliminated the pressor response to muscular contraction (mean arterial pressure at rest, 80-118 mm Hg: on fatigue, 72-129 mm Hg) but did not affect the pressor response to carotid occlusion in the same cats. Similarly, injections of met-enkephalin (1-100 micrograms.5 microliters-1) or beta-endorphin (10-100 micrograms.5 microliters-1) eliminated the ergoreceptor induced changes in mean arterial pressure during isometric contractions but had no effect on the changes caused by carotid occlusion. Pressor responses to nerve crush were not eliminated. These results support the suggestion that a catecholaminergic-opioidergic pathway in part mediates the cardiovascular responses to ergoreceptor afferent but probably not baroreceptor afferent input.
Cardiovasc Res 1989 Mar
PMID:Effects of opiates during baroreceptor and ergoreceptor induced changes in blood pressure. 257 74

Two cases of leaflet fracture in the Edwards-Duromedics valve at 36 and 38 months after implantation are reported. Both patients were immediately reoperated on and recovered well. In one valve an older housing fracture with partial tissue ingrowth was noted beside a recent transverse leaflet fracture. In the other valve the leaflet was fractured near the pivot mechanism. All larger embolized parts were detected in the iliac artery region by computed tomographic scan and were subsequently removed. Problems in diagnosis and the importance of immediate reoperation, even without exact diagnosis, are discussed. Technical evaluation of the valve revealed crack growth and arrest, giving evidence of fatigue fracture. Scanning electron microscopic examination revealed several areas of pitting and erosion. Although the exact cause of mechanical disruption remains speculative, pyrolytic carbon seems to have the characteristic of fatigue fracture as well as erosion damage. A connection between the two might exist.
J Thorac Cardiovasc Surg 1989 Jan
PMID:Leaflet fracture in Edwards-Duromedics bileaflet valves. 291 Dec

Although heart valve bioprostheses provide a normal quality of life, their durability is still of great concern. Their durability failure is defined as "degeneration," which is considered to be a consequence of metabolic factors. In this study, we demonstrate that mechanical and design factors can also be responsible for bioprosthesis failure. Large numbers of porcine and pericardial bioprostheses were tested in a fatigue-testing system in which the test conditions were proved to be reproducible and accurate by a laser Doppler anemometer. The results have allowed us to define causes of failure, previously insufficiently stressed, in each type of valve tested. There is a clear difference in factors influencing tissue disruption between porcine and pericardial valves. We have compared these in vitro results with in vivo clinical findings. The main inferences are as follows: (1) Bioprostheses rupture and fail in the same fashion in both in vitro and in vivo studies. (2) Mechanical and design factors are involved in tissue failure. (3) The in vitro/in vivo durability ratio is not 1:1. This ratio depends on the test conditions. (4) Pericardial valves fail because of damage during closure, whereas porcine valves are damaged during both opening and closing (mostly opening) because of design features. (5) Once one cusp fails and prolapses, the other cusps will fail in an accelerated fashion. (6) In vitro durability of 100 X 10(6) cycles can be considered excellent and is an achievable goal. (7) Variability is the key impediment to predicting the durability of bioprostheses. Valves can fail within 2 to 3 million cycles or can last more than 100 million cycles. Similarly, bioprostheses may require explantation within a few months or can last 10 to 13 years in patients. (8) Fatigue testing is an excellent and valuable tool to elucidate the mechanical factors responsible for this variability.
J Thorac Cardiovasc Surg 1988 Feb
PMID:Do heart valve bioprostheses degenerate for metabolic or mechanical reasons? 296 76

Between January 1975 and December 1985 214 patients underwent prosthetic aortic valve replacement for isolated aortic regurgitation. Patient follow-up averaged 5.4 years after the operation (range 0.7-10.7 years). Preoperative staging showed 9 patients to be in NYHA stage II, 111 patients in stage III, and 94 patients in stage IV. At follow-up 3 patients complained of increased fatigue, 9 patients remained stable and 167 patients had improved. 103 of these patients were free of symptoms under stress, i.e. NYHA stage I. The hospital mortality was 3.7% (8/214 patients). An additional 26 patients died within an average of 2.8 years. The cumulative 5-year survival rate was 85%; the 10-year survival rate was 81.5%. 10 patients underwent a second operation within an average of 3.4 years. The correlation between the end-diastolic volume and the regurgitated blood volume has prognostic significance. 25 patients with appropriate enlargement of the left ventricle showed a significant decrease of the end-diastolic volume and the roentgenographic heart volume combined with an increase of ejection fraction. None of these 25 patients died from cardiac complications. A control group of 9 patients with myocardial damage showed no significant change in the above parameters. 4 patients in the control group died. We conclude that the relationship of regurgitated blood volume and the left ventricular end-diastolic volume is of prognostic significance for patients with chronic aortic regurgitation presenting with minimal symptoms.
Thorac Cardiovasc Surg 1988 Dec
PMID:Late results of prosthetic valve replacement for aortic regurgitation and the prognostic significance of the end-diastolic and regurgitated blood volumes. 297 38

Dilated cardiomyopathy, owing to any cause, usually culminates in the clinical syndrome of congestive heart failure. Heart failure is characterized by exertional dyspnea and fatigue, but the precise mechanisms that produce these symptoms are still not clear. Sodium retention occurs early in heart failure, but this disturbance is dynamic in nature and is not always present in the patient. The mechanism of early salt and water retention in heart failure is not defined. Gross edema and ascites occur much later, undoubtedly owing to the convergence of a number of factors. The peripheral adaptations to heart failure include activation of the renin-angiotensin system and the sympathetic nervous system, and the release of AVP. The result is an increase in preload with a resultant increase in stroke volume for some patients, but the price is paid in the form of heightened impedance to ejection and circulatory congestion. The sympathetic nervous system disturbances in heart failure are striking, as disturbances in both circulating and myocardial NE levels are consistently found. Vasorelaxant and natriuretic hormones, as well as certain prostaglandins, may be released in an attempt to offset excessive "compensatory" pressor-sodium retentive mechanisms, but the net result seems to be excessive peripheral vasoconstriction and a downward spiral of deterioration in many patients. One would hope that an unraveling of the complex pathophysiology of heart failure would lead to therapy that would change the natural history of the disease. The results of the first V-HeFT trial give room for cautious optimism in this regard.
Cardiovasc Clin 1988
PMID:Pathophysiology of congestive heart failure secondary to congestive and ischemic cardiomyopathy. 304 87

Experimental models of heart failure can be used to address specific questions not easily answered in patients, but no single model can reproduce exactly any of the clinical syndromes of heart failure since these are dominated by fatigue and breathlessness. Heart failure may be induced experimentally by pressure loading, volume loading, myocardial infarction, or by the creation of other disease states within the myocardium. Pressure loading may be especially useful in the study of ventricular hypertrophy, cellular derangements and vascular changes. Volume loading may be useful when examining the pathogenesis of hormone and electrolyte disturbances. Models of myocardial infarction or destruction are likely to be the most suitable for assessing novel therapy provided that peripheral reflexes are maintained. Experimental cardiomyopathy can provide an important means of identifying pathological subcellular mechanisms. They may be of use in the evaluation of vasodilator drugs but caution should be exercised in the study of inotropic agents. Any one model may be useful if it permits study of a single factor or variable in isolation or at a time when information is not obtainable from patients. For greatest clinical relevance, studies should be made in conscious animals with intact reflexes.
Cardiovasc Res 1985 Apr
PMID:Experimental models of heart failure. 315 77

Actinomycosis is an uncommon infection. The regions mostly involved are the cervico fascial area, the thorax and the abdomen. The thoracic variety accounts for approximately 15% of the cases. Clinical pictures of pulmonary neoplasm, abscess, and empyema have been described. Misleading symptoms often delay the right diagnosis. The present study describes a case of actinomycosis with pleuro-pulmonary involvement. A 48-year woman had been well until two and a half years previously, when she developed symptoms suggestive of pneumonia. When referred to a medical clinic with thoracic pain and tiredness, pulmonary embolism was suspected. Inhalation and perfusion scintigraphy showed several perfusion defects. There were several relapses, with clinical pictures suggestive of pulmonary embolism, before an abscess in the left axilla appeared. Drained pus showed no growth of Actinomycetes. Correct diagnosis of the true cause was only possible by direct microscopy. Possible symptoms and the diagnostic difficulties when Actinomycetes is involved are discussed.
Thorac Cardiovasc Surg 1988 Oct
PMID:Thoraco-pleural actinomycosis presenting like diffuse pulmonary embolism. 323 66

Static or dynamic work in patients with chronic cardiac failure elicits a variety of pathophysiologic responses that impair the ability of the cardiopulmonary unit to sustain O2 delivery at a rate that is commensurate with the O2 requirements of working skeletal muscle. Regional abnormalities in the circulation of skeletal muscle may further compromise nutritive blood flow to muscle. As a result, the patient experiences a sense of fatigue during physical activity. Dyspnea, or an abnormal awareness of breathing, may also accompany exercise in these patients. This sense of breathlessness may be due to an abnormally elevated work of breathing secondary to decreased pulmonary compliance, a heightened chemical drive to ventilation, and a possible imbalance in the O2 supply and demand of the respiratory muscles. The ambulatory monitoring of physical activity in patients with chronic cardiac failure has not been systematically examined. Potential monitoring techniques that may provide accurate and reproducible results regarding the exercise response in these patients include the thoracic impedance principle to measure minute ventilation and portable O2 uptake sensors.
Cardiovasc Clin 1988
PMID:Monitoring physical activity in ambulatory patients with chronic cardiac failure. 328 62


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