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)

The current techniques of respiratory gas-exchange monitoring during stress testing in patients with congestive heart failure have provided new physiopathologic and clinical data. The "breath-by-breath" measurement of oxygen consumption and carbon dioxide production and the evaluation of the relationship between these parameters and respiratory volumes, allow to determine both ventilatory and metabolic responses during exercise, thus giving a precise estimate of the effective cardiopulmonary functional capacity. The demonstration of peripheral vascular and metabolic abnormalities by these techniques have provided new insights into the mechanism of dyspnea and fatigue in patients with heart failure. Although the relationship between respiratory and metabolic parameters and hemodynamics has been extensively studied, its mechanisms are still unclear. Moreover, controversy still exists as to the link between functional capacity and prognosis. Finally, recent studies on the cardiopulmonary adaptations to exercise training in patients with left ventricular dysfunction, have clearly demonstrated clinical and hemodynamic improvement after conditioning. These data, if confirmed, may provide a new approach in the management of patients with this disorder.
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PMID:[Monitoring of respiratory exchange during ergometric test in patients with heart failure: current aspects and prospects]. 219 41

Quinapril hydrochloride is a nonsulfhydryl angiotensin converting enzyme (ACE) inhibitor that has been extensively tested and found effective when administered once-a-day to hypertensive patients of both sexes and all degrees of hypertension and cardiac compromise, including those with left ventricular hypertrophy, with and without congestive heart failure. Observations with earlier ACE inhibitors led to reports that this class of drugs was relatively ineffective in older hypertensive patients. To ascertain the role of quinapril (greater than or equal to 10 mg/day) in older patients, its blood pressure-lowering effects in 1,175 hypertensive patients less than or equal to 65 years of age were compared with those in 304 patients greater than 65 years of age. An excellent response was observed in patients greater than 65 years of age with mild to moderate hypertension (diastolic BP, 95 to 105 mm Hg) and moderate to severe hypertension (diastolic BP, 106 to 115 mm Hg). The reductions in blood pressure achieved with quinapril were at least comparable to those obtained in the younger hypertensives, and were numerically (but not statistically) greater in the mild to moderate group (-14 mm Hg v-12 mm Hg). In addition, the percentage of patients who experienced adverse experiences was lower in the greater than 65 group than in the less than or equal to 65 group (15% v 19%). The main adverse experiences reported included dizziness, headache, cough, fatigue, and hypotension. These findings indicate that quinapril is at least as safe and effective in older hypertensives as in younger patients.
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PMID:Use of quinapril in the elderly patient. 226 Nov 46

This case report describes a patient with an uncommon type of mitral incompetence caused by a perivalvular communication between the left ventricle (LV) and the left atrium (LA) masked by a considerable fibrotic subvalvular aortic stenosis, endocarditis and congestive heart failure (CHF). A 64 year old farmer with a history of a systolic murmur since childhood complaining of increasing fatigue and dyspnoea, temperature over 39 degrees C, and signs of CHF was admitted and transferred to a cardiological unit. Invasive examination and continuing clinical deterioration caused urgent transfer for surgery under suspicion of a decompensated hypertrophic obstructive cardiomyopathy. Clinical investigation revealed a decompensated subvalvular aortic stenosis and a mild mitral insufficiency. At surgery the advanced fibrotic subvalvular stenosis was resected. After coming off bypass severe mitral insufficiency was detected by intraoperative analysis of the simultaneous intracavitary-pressure tracings. A midsystolic maximum of a high V-wave of the LA-pressure tracing was suggestive of an unusual reason of the mitral insufficiency. Reexploration indicated a perivalvular broad communication from the LA groove to the LV with an otherwise normal mitral valve. The communication was closed using buttressed mattress-sutures. This uncommon type of mitral incompetence via a perivalvular LA-LV communication was probably caused by endocarditis and an intramyocardial abscess in the LA-wall which subendocardially led to LV-LA communication.
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PMID:Uncommon type of mitral insufficiency caused by perivalvular communication between left ventricle and left atrium. 230 25

1. The effects of graded treadmill exercise on renal blood flow (RBF) were examined in seven rabbits, in which congestive heart failure (CHF) was produced by the administration of doxorubicin, 1 mg/kg, twice weekly for 8 weeks, and in seven controls. A third group of five rabbits underwent doxorubicin treatment with the addition of surgical section of the left renal sympathetic nerve. 2. During submaximal exercise, there was a small reduction in RBF in controls, which was greatly exaggerated in CHF. 3. In both control and heart failure rabbits, there was a precipitous fall in RBF as exercise fatigue developed. 4. Renal sympathectomy ablated these changes in RBF during exercise. 5. It is concluded that in heart failure there is an exaggerated, sympathetically mediated, diversion of blood flow away from the kidney. The onset of exercise fatigue in both normal and heart failure rabbits is accompanied by a marked intensification of this process.
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PMID:Vasoconstriction in the renal vascular bed during exercise: studies in control and heart failure rabbits. 234 Jun 45

Two patients with similar symptoms referred for diagnosis and treatment of hepatic failure subsequently proved to have cardiomyopathy as the cause of their hepatic decompensation. Except for fatigue and edema, symptoms of congestive heart failure were absent and no history of dyspnea, orthopnea, or paroxysmal nocturnal dyspnea could be elicited. Hepatomegaly was present in both patients, but neck venous distension and hypotension were not apparent, and both patients were able to lie flat. The diagnosis of cardiomyopathy was made by echocardiogram showing global hypokinesis and low ejection fractions; right atrial pressures were markedly increased. Liver biopsies demonstrated centrilobular necrosis and congestion. Treatment for heart failure led to a prompt response in both patients with rapid return of all hepatic parameters toward normal. Paradoxically, our patients had striking evidence of hepatic failure and a notable absence of symptoms and signs of congestive heart failure. An awareness of this unique presentation may avoid prolonged evaluations in such critically ill patients.
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PMID:Cardiomyopathy unrecognized as a cause of hepatic failure. 236

Key safety parameters of sotalol were examined in 1,288 patients entered into recent controlled trials of ventricular (85% of patients) or supraventricular arrhythmias (15%). Most patients were middle-aged male Caucasians with significant heart disease. The most serious adverse event was proarrhythmia, occurring in 56 patients (4.3%). Of these, 27 had hemodynamic compromise due to malignant ventricular arrhythmias. Most had a history of sustained ventricular tachycardia, myocardial infarction, congestive heart failure (CHF) or cardiomyopathy, or a combination of these. The other 29 had nonsevere events; 38% continued taking sotalol. Proarrhythmia was manifested by torsades de pointes in 24 of the 56 patients. No universal causal relation was found with commonly associated factors such as bradycardia, hypokalemia and long QT interval. The mean QT and QTc at baseline within 1 week of a severe proarrhythmic event were greater than those of patients not having proarrhythmia. Nineteen patients (1%) discontinued therapy with sotalol because of drug-related CHF. Predisposing conditions included low initial baseline ejection fraction, history of CHF, cardiomyopathy or cardiomegaly, or both, male gender and age greater than 65 years. Heart failure usually occurred within 7 to 30 days of initiating therapy. The most common reason for premature discontinuation of the drug in patients treated for sustained ventricular tachycardia was ineffectiveness (39%), whereas adverse effects were the most common reasons among patients treated for complex ventricular ectopy (21%). Dyspnea and bradycardia were the most common cardiovascular effects, and fatigue, dizziness and asthenia the most common noncardiac, adverse effects. Although frequently reported, these adverse effects resulted in discontinuation of only 1 to 4% of the patients at risk.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical safety profile of sotalol in patients with arrhythmias. 240 37

The safety and tolerability of lisinopril were assessed in 1,476 patients [1,165 hypertensives and 311 patients with congestive heart failure (CHF)] and 211 normal volunteers. The duration of lisinopril therapy ranged from 1 day to 16 months, with a mean duration of 105 days. In the hypertensive population, the most frequent clinical adverse experiences on lisinopril alone were headache, dizziness, cough, and diarrhea. Not all of these adverse experiences were thought to be drug related. Five percent of patients were discontinued because of adverse clinical experiences; cough and dizziness were the most common reasons for discontinuation. Two of 1,165 (0.17%) hypertensive patients treated with lisinopril died, compared to 0.41% of hypertensive patients on other therapies. Neither case was considered to be drug related. In patients with CHF, the most frequent clinical adverse experiences were dizziness, diarrhea, hypotension, fatigue, headache, and rash. Not all of these adverse experiences were thought to be drug related. The percent of CHF patients discontinuing because of an adverse clinical experience was 7.4%; the most frequent causes for discontinuation were hypotension, dizziness, or renal impairment. Twelve deaths occurred in 311 CHF patients treated with lisinopril (3.9%) compared to 4/104 (3.8%) of CHF patients treated with placebo and 2/65 (3.1%) treated with captopril. Hypotension, orthostatic effects, or dizziness following the initial lisinopril dose occurred infrequently in patients treated with lisinopril. In hypertensive patients with normal renal function, including those treated previously or concomitantly with diuretic therapy, a first-dose hypotensive episode was reported in six of 955, or 0.6%. The incidence was higher (6.7%) in hypertensive patients with impaired renal function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The safety and tolerability of lisinopril in clinical trials. 244 61

The Cardiac Arrhythmia Pilot Study tested the feasibility of performing a large-scale study to evaluate the effect of therapy of ventricular arrhythmias after acute myocardial infarction (AMI). Ten clinical sites identified patients with greater than or equal to 10 ventricular premature complexes (VPCs)/hour, recorded 6 to 60 days after AMI in patients with an ejection fraction greater than 0.20. Patients were randomized to receive 1 of 5 agents: encainide, flecainide, imipramine, moricizine or placebo. Successful therapy was defined as greater than or equal to 70% suppression of VPCs and greater than 90% suppression of runs of ventricular tachycardia. Randomization to a second agent occurred if a patient did not achieve adequate suppression with the initial agent. Patients initially randomized to placebo continued to receive placebo. Patients were evaluated at 3-month intervals for the next year. Of 30,763 patients screened, 10,734 (35%) were younger than 70 years old and had a qualifying AMI. A Holter recording was obtained in 3,957 patients, of whom 871 (22%) had qualifying arrhythmias and 687 were eligible. Of the 687 eligible patients, 502 (73%) were randomized. Mean age of enrolled patients was 59 years. One-half of patients were randomized within 1 month after AMI. Mean ejection fraction was 0.45, with 175 (35%) patients having an ejection fraction less than 0.40. On baseline drug-free recording, 173 (35%) patients had less than 30 VPCs/hour; 149 (30%) between 30 and 100/hour and 180 (36%) greater than or equal to 100/hour. At least 1 run of ventricular tachycardia was seen in 172 (34%) patients. Drugs taken at baseline were similar in all groups with 116 (23%) patients taking digitalis, 161 (32%) taking diuretics, 203 (41%) taking beta blockers and 200 (40%) taking calcium antagonists. Slightly more patients, 53 (51%), randomized to flecainide were taking calcium antagonists. No significant relation was noted between baseline VPC frequency and ejection fraction, but baseline VPC frequency was correlated with heart rate, arrhythmia noted before AMI and right bundle branch block. As expected, a high ejection fraction correlated with lower peak creatine kinase values, an inferior location of the infarct and fewer signs of congestive heart failure. At baseline, at least 1 adverse symptom was volunteered by 192 (39%) patients. The most common symptoms were unusual tiredness or fatigue, heart beating fast or skipping beats or headache. In this study, over 20 age- and AMI-eligible patients were identified to obtain each randomized patient. The randomization process successfully distributed baseline variables across drug groups.
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PMID:Recruitment and baseline description of patients in the Cardiac Arrhythmia Pilot Study. The Cardiac Arrhythmia Pilot Study (CAPS) investigators. 245 14

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.
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PMID:Compensatory and adaptive mechanisms in congestive heart failure. 248 Apr 83

A randomized, parallel, double-blind study was performed with lisinopril, a long-acting angiotensin-converting enzyme inhibitor, versus captopril, a shorter-acting angiotensin-converting enzyme inhibitor, in the treatment of congestive heart failure. All patients were in New York Heart Association class II, III or IV and had remained symptomatic despite therapy with digoxin and diuretics. After a 4 to 14 day placebo baseline period, patients were randomized to receive either lisinopril, 5 mg orally once per day (n = 94), or captopril, 12.5 mg orally three times per day (n = 95), in addition to continuation of digoxin and diuretics. The dose of study drug could be doubled at 4 week intervals for a total of 12 weeks of double-blind therapy. The maximal dose was 20 mg once per day of lisinopril or 50 mg three times per day of captopril. The addition of either lisinopril or captopril to a regimen of diuretics or digoxin, or both, caused an increase in exercise duration as assessed on a motorized treadmill. When protocol violators were excluded, patients receiving lisinopril had a statistically greater increase in exercise duration than that of patients receiving captopril. In patients with renal impairment (serum creatinine greater than 1.6 mg/dl at baseline), lisinopril was superior to captopril in improving exercise duration. Lisinopril, but not captopril, increased left ventricular ejection fraction in patients with moderately to severely (less than 35%) decreased function (p less than 0.05). Improvement in functional capacity and quality of life, as assessed by the Yale Scale dyspnea/fatigue index, was significantly greater for the lisinopril group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Short- and long-acting angiotensin-converting enzyme inhibitors: a randomized trial of lisinopril versus captopril in the treatment of congestive heart failure. The Multicenter Lisinopril-Captopril Congestive Heart Failure Study Group. 215 58


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