Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A large-scale, prospective, 8-week, office-based study was conducted to evaluate the effects of adding captopril to a therapeutic regimen of diuretic and digoxin or diuretic alone in the management of patients with mild to moderate congestive heart failure (CHF). A total of 2218 primary care physicians evaluated 6669 patients over the study period for efficacy parameters, which included changes in a modified New York Heart Association (NYHA) functional classification, symptomatology, and daily activity levels. Overall, 63.8% of evaluated patients improved with regard to functional ability, with 19% improving two or more modified NYHA classes. Symptoms of CHF, including dyspnea on exertion, fatigue, and orthopnea and signs, including rales and peripheral edema, were reduced in 86% of these patients: 41.5% demonstrated mild improvement; 30.0%, moderate improvement; and 14.5%, marked improvement. Three parameters, with which patients reported having difficulty at study entry, were assessed serially to evaluate changes in functional capacity; 78.5% of patients reported an increased walking distance, 72.3% had increased capacity for climbing stairs, and 60.2% had improved capacity for individual recreational activities. Adverse experiences were reported in 18.1% of all patients; 4.9% of patients withdrew from the study because of an adverse effect. Combination therapy with captopril and diuretic for CHF was shown to be safe and effective regardless of patient age (less than 70 years vs. greater than or equal to 70 years), duration of heart failure (less than 1 year vs. greater than 1 year), presence of digoxin treatment, or the dosing schedule employed.(ABSTRACT TRUNCATED AT 250 WORDS)
Clin Cardiol 1991 Aug
PMID:A large-scale trial of captopril for mild to moderate heart failure in the primary care setting. 191 72

Patients with New York Heart Association functional class II or III heart failure stabilized on furosemide therapy were entered into a randomized controlled trial comparing enalapril (n = 72) and digoxin (n = 73). End points were clinical outcome, treadmill exercise capacity and echocardiographic left ventricular dimensions. Improvement in clinical outcome was defined as a reduction of at least one functional class or withdrawal because of an adverse clinical event. After 4 weeks, 13 patients receiving enalapril showed improvement, 55 had no change and 9 manifested deterioration compared with 7, 49 and 17, respectively, in the digoxin group (p less than 0.01). After 14 weeks, 13 patients receiving enalapril showed improvement, 50 had no change and 9 manifested deterioration, compared with 14, 37 and 22, respectively, in the digoxin group (p less than 0.025). More patients in the digoxin group were withdrawn because of an adverse clinical event (p less than 0.05). Exercise time and percent fractional shortening improved in both groups (p less than 0.001 and less than 0.05, respectively), with no significant difference between groups (p greater than 0.50). Both rate-pressure product and subjectively evaluated exertion during submaximal exercise were reduced only in the enalapril group. Although the majority of patients in both groups did well, those receiving enalapril experienced fewer adverse clinical events and had less fatigue during submaximal exercise.
J Am Coll Cardiol 1991 Dec
PMID:Enalapril versus digoxin in patients with congestive heart failure: a multicenter study. Canadian Enalapril Versus Digoxin Study Group. 196 Mar 3

To determine the clinical, laboratory and hemodynamic profile in patients with primary pulmonary hypertension and associated portal hypertension, 7 new cases and 71 previously reported cases were analyzed. There was no gender predilection and the average age at diagnosis was 41 years. Liver cirrhosis was the most frequent cause of hypertension (82%) and a surgical portosystemic shunt was present in 29%. Almost invariably, portal hypertension either preceded or was diagnosed concurrently with pulmonary hypertension, favoring the hypothesis that in portal hypertension, the pulmonary vasculature may be exposed to vasoactive substances normally metabolized or produced by the diseased liver, possibly inducing vasoconstriction or direct toxic damage to the pulmonary arteries. Clinically, exertional dyspnea was the most frequent presenting symptom (81%); other symptoms, such as syncope, chest pain and fatigue, were present in less than 33%. An accentuated pulmonary component of the second heart sound (82%) and a systolic murmur (69%) were the most common physical findings. At least 75% of these patients had evidence of pulmonary hypertension on electrocardiography (right ventricular hypertrophy) or roentgenography (cardiomegaly or dilated main pulmonary arteries, or both). Hemodynamic findings included severe pulmonary hypertension (mean pulmonary artery pressure 59 +/- 19 mm Hg) with normal pulmonary capillary wedge pressure and cardiac output. Treatment was basically palliative and the mean and median survival times were 15 and 6 months, respectively. In brief, on the basis of clinical presentation and laboratory features, patients with combined primary pulmonary hypertension and portal hypertension seldom represent a diagnostic challenge. Further research is needed on treatment, which remains palliative. The survival rate is poor and worse than that seen in isolated primary pulmonary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1991 Feb
PMID:Association between primary pulmonary hypertension and portal hypertension: analysis of its pathophysiology and clinical, laboratory and hemodynamic manifestations. 199 8

In a controlled, double-blind, crossover study, the effects of guanadrel sulfate and propranolol on blood pressure (BP) and selected cardiopulmonary and metabolic variables were compared in 15 physically active and moderately hypertensive subjects. Guanadrel sulfate reduced systolic and diastolic BP at rest by -16 and -15 mm Hg, and at maximal exercise by -33 and -13 mm Hg, respectively (p less than 0.005), without affecting submaximal oxygen consumption (VO2), maximal VO2, ventilatory threshold, forced vital capacity, forced expiratory volume in 1 second, or fatigue, as assessed by perceived exertion. In contrast, propranolol significantly decreased diastolic BP at rest (-16 mm Hg) and systolic BP at maximal exercise (-44 mm Hg); however, it significantly decreased submaximal VO2 (-3.9 ml.kg-1.min-1), maximal VO2 (-3.9 ml.kg-1.min-1), ventilatory threshold (-0.3 liters.min-1), minute ventilation at submaximal exercise (-7.3 liters.min-1), forced expiratory volume in 1 second (-0.27 liters), and concomitantly increased the rating of perceived exertion at maximal exercise (1.9 U). Guanadrel sulfate was also associated with significant decreases in mean fasting plasma glucose and total serum cholesterol, whereas propranolol resulted in an increase in serum triglycerides (p less than 0.05). In contrast to propranolol, guanadrel sulfate appears to decrease BP without evoking negative metabolic consequences or impairing exercise tolerance.
Am J Cardiol 1991 Mar 15
PMID:Comparison of the effects of guanadrel sulfate and propranolol on blood pressure, functional capacity, serum lipoproteins and glucose in systemic hypertension. 200 Jul 92

The effects of a 12-week aerobic exercise training protocol on 32 symptomatic women with mitral valve prolapse were studied. Subjects were randomly assigned to control or exercise groups. Exercise subjects completed a 12-week (3 times per week) exercise training program based on guidelines established by the American Heart Association for phase II cardiac rehabilitation programs; control group subjects maintained normal activities. Before and after training, subjects underwent maximal multistage treadmill testing, and measurements were obtained for plasma catecholamine levels at rest and during peak exercise; they completed the State Trait Anxiety Inventory and General Well-Being Schedule. Weekly symptom frequency of chest pain, arm pain, palpitations, shortness of breath, fatigue, headache, mood swings, dizziness and syncope were monitored for the 12-week period. Data were analyzed using multivariate analysis of variance, multivariate analysis of covariance, and analysis of covariance with repeated measures. Compared with control subjects, the exercise group showed a significant (p less than 0.05) decrease in State Trait Anxiety Inventory scores, an increase in General Well-Being scores, an increase in functional capacity and a decline in the frequency of chest pain, fatigue, dizziness and mood swings. No statistically significant differences were noted in catecholamine levels at rest or during peak exercise. These findings support the use of aerobic exercise in the management of symptomatic women with mitral valve prolapse.
Am J Cardiol 1991 Apr 15
PMID:Effects of aerobic exercise training on symptomatic women with mitral valve prolapse. 201 86

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)
Am J Cardiol 1991 May 15
PMID:Left and right ventricular systolic function and exercise capacity with coronary artery disease. 202 97

The pattern of oxygen (O2) consumption (VO2), carbon dioxide (CO2) production (VCO2), ventilatory and metabolic responses during and in recovery from supine bicycle exercise was examined in 18 patients with recent myocardial infarction. An increase in VO2 with increasing work load was accomplished by proportional increases in both cardiac output and the arteriovenous O2 difference. During recovery, however, the arteriovenous O2 difference rapidly decreased below levels at rest, whereas VO2 and cardiac output remained elevated, indicating that VO2 during recovery further depended on relatively high cardiac output. The ratio of VCO2 to VO2 further increased after exercise, suggesting that such cardiac output contributed to the remaining high CO2 flow to the lung and therefore enhanced ventilation. Increased arterial catecholamines during exercise remained elevated for the first 5 minutes of recovery. Arterial lactate during this period continued to increase and resulted in profound metabolic acidosis, causing alveolar hyperventilation after exercise. These results suggest that during recovery from exercise, cardiopulmonary responses remain enhanced because of continuing high cardiac output, resulting in subsequent high CO2 flow to the lung and metabolic acidosis, and that this may be associated with profound fatigue or dyspnea after exercise.
Am J Cardiol 1991 Jun 01
PMID:Oxygen utilization, carbon dioxide elimination and ventilation during recovery from supine bicycle exercise 6 to 8 weeks after acute myocardial infarction. 203 36

This is a review of the effects of E on the symptoms of CHF which affect patients' (pts) quality of life and the signs associated with pts' prognosis. The review is based on clinical studies which were included in the New Drug Application for Vasotec (enalapril maleate, MSD) in the United States. There were 3 open-label (242 pts) and 4 double-blind, placebo (P)-controlled (661 pts) studies of at least 1 month and up to about 2 years duration. One of these, the CONSENSUS Trial evaluated mortality in 253 pts with class IV CHF. Dyspnea and fatigue are considered the most disabling symptoms causing pts' functional impairment and thus reducing the quality of life. Left ventricular gallop, pulmonary rales, cardiomegaly, and ejection fractions are known to adversely effect pts' prognosis. Evaluations of these signs, symptoms, and scores related to these symptoms were included in most, but not all, studies. The pts' NYHA cardiac status was evaluated in all studies. E alleviated the signs and symptoms of CHF and improved various scores in significant number of pts. Pts' quality of life improved as indicated by the number of pts "feeling better" after Rx with E (p less than 0.01 vs P) in a multinational study of 256 pts; reductions of cardiomegaly and increases in ejection fraction were significantly greater in E than in P treated pts; and in severe CHF (CONSENSUS Trial) the mortality was significantly reduced (p less than 0.003 vs P).
Acta Cardiol 1991
PMID:Enalapril in the treatment of congestive heart failure: effects on signs, symptoms and mortality. 204 70

The study was performed on 122 patients proved by catheterization to have dominant mitral stenosis so as to define proper endpoints of exercise testing for functional evaluation. This represents the 14-year experience with mitral stenosis in our exercise laboratory. Of them, we investigated 126 who completed clinically event-free Naughton treadmill exercise tests. Excess peak exercise heart rates (over 150 beats per minute, 63%) and exertional hypotensive responses (59%, probably including factitious responses due to unreliable indirect pressure readings) did not correlate with the severity of mitral stenosis. Without limiting symptoms and major ventricular arrhythmias, either of the above as endpoints may cause the test to be halted prematurely in half the cases. Ventricular arrhythmias (60%; in complex forms, 20%; possibly contaminated by aberrancy in atrial fibrillation and aggravated by digitalis/diuretics) did not correlate with severity of stenosis either, but the only one major complication we met was secondary to ventricular tachyarrhythmia. Limiting symptoms (83%; of them 94% being dyspnea/fatigue correlating with severity at P less than 0.01) and complex ventricular arrhythmias as endpoints terminated 85% of the tests safely in this series. Atrial thrombuses (34%, all non-floating) did not cause any related complications. Thus, we concluded that limiting symptoms and complex ventricular arrhythmias are the proper endpoints in evaluating the exercise capacity of patients with mitral stenosis after prior echocardiographic exclusion of those with potentially risky floating thrombus.
Int J Cardiol 1991 Apr
PMID:Endpoints of treadmill exercise testing for functional evaluation of patients with mitral stenosis. 207 Dec 53

To assess whether an inotropic agent may affect quality of life in severe heart failure, a double-blind, placebo-controlled crossover study was performed in 10 patients over three periods of 3 weeks, including an initial control period of 3 weeks and periods on placebo or enoximone, 150 mg t.d.s. Quality of life was assessed by a questionnaire following initial training of patients to evaluate their symptoms after certain stresses, by visual analogue scales of symptoms, and by objective assessments during graded exercise. Daily dyspnoea score decreased from 33.2 +/- 2 (placebo) to 27.7 +/- 4 (enoximone) (P less than 0.01) and daily fatigue score decreased from 14.8 +/- 2.5 (placebo) to 12.6 +/- 2 (enoximone) (P less than 0.05). There were also significant beneficial responses in the mean daily NYHA class and in the duration of a walking test. Self-assessed global quality of life score increased from 2.7 +/- 0.6 (placebo) to 3.6 +/- 0.8 (enoximone) (P less than 0.05). It was concluded that over periods of 3 weeks, enoximone significantly improved self-assessed quality of life.
Int J Cardiol 1990 Jul
PMID:Effects of enoximone on quality of life. 214 35


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>