Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Muscle fatigue is a prominent symptom in patients with chronic heart failure (CHF). To determine whether it results from an intrinsic abnormality of vasodilating capacity of the vasculature in exercising muscle, we studied local forearm blood flow (FBF) during exercise in 13 patients with severe CHF and in eight normal untrained subjects of similar age. Intermittent forearm static exercise was performed by squeezing a hand dynamometer for 5 seconds, three times per minute, for 5 minutes at 15%, 30%, and 45% of maximum voluntary contraction. FBF was measured by mercury-in-rubber strain gauge venous plethysmography at baseline before exercise and during the last 3 minutes of each exercise state. Exercise was repeated after 24 hours of intravenous administration of milrinone in the patients with CHF. FBF increased with forearm exercise in a reproducible manner during 24 hours in the normal subjects: rest, 2.54 +/- 0.23 (0 hours), 2.90 +/- 0.23, (24 hours); 15%, 7.25 +/- 0.92, 5.85 +/- 0.56; 30%, 9.20 +/- 1.08, 10.05 +/- 0.85; 45%, 14.62 +/- 1.64, 13.85 +/- 1.09 ml/100 ml/min; p = NS, 0 versus 24 hours. In patients with CHF, FBF was reduced at baseline compared with normal subjects (1.70 +/- 0.15 ml/100 ml/min, p less than 0.05), but no significant differences from normal subjects were observed during exercise (15%, 5.04 +/- 0.65; 30%, 7.64 +/- 0.99; 45%, 12.56 +/- 1.20 ml/100 ml/min). Peak exercise blood flow was correlated negatively with central venous pressure (r = -0.65, p less than 0.05) and positively with right ventricular ejection fraction (r = 0.59, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Muscle blood flow during forearm exercise in patients with severe heart failure. 237 94

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

Heart failure is a syndrome of breathlessness, fatigue and oedema. The effects of ageing on myocardial function and the prevalence of often multiple cardiac pathologies makes heart failure a disease of the elderly, usually characterized by primary or secondary myocardial systolic dysfunction. Appropriate treatment, which requires precise diagnosis, involves correction of precipitating or aggravating factors and the rational use of drug therapy. Diuretics and ACE inhibitors offer a combination of both symptom control and improvement in prognosis. Other agents such as digoxin, xamoterol and nitrates may be particularly useful in the treatment of patients with associated problems such as atrial fibrillation and angina. Because both ageing and heart failure may alter pharmacokinetics and pharmacodynamics, safe and effective treatment of heart failure in the elderly requires understanding of the clinical pharmacology of the drugs used.
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PMID:Treatment of heart failure in the elderly. 240 42

All major types of human interferons (IFNs) have been purified and clinically administered as antitumor agents. We summarize here experience to date with toxicity of IFNs in cancer patients. The acute syndrome consists of fever, chills, myalgias, arthralgias, and headache, with some variation according to type of IFN, route of administration, schedule, and dose. Fatigue, perhaps reflecting CNS toxicity, is the most prevalent nonacute symptom. At high doses, IFNs are neurotoxic; the abnormalities seen by EEG resemble those in diffuse encephalitis. Hematologic toxicity consists mainly of leukopenia, but anemia and thrombocytopenia occur in some patients. Nausea, vomiting, and diarrhea are the main gastrointestinal symptoms. Elevation of serum transaminases seems to reflect liver toxicity. Renal function is well preserved, except for rare instances of acute renal failure. Cardiac toxicity remains questionable, although heart failure and arrhythmias have been associated with the administration of IFNs. Most, if not all, of these effects are reversible or can be ameliorated. With IFN alpha, the type most widely used in clinical studies, doses of 1 million to 9 million units (MU) are generally well tolerated, but doses greater than or equal to 18 MU yield moderate to severe toxicity. Doses greater than or equal to 36 MU can induce severe toxicity and significantly alter the performance status of the patient.
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PMID:Clinical toxicity of interferons in cancer patients: a review. 241 69

Dynamic cardiomyoplasty aims at restoring ventricular contractility by means of a skeletal muscle sutured around the heart. It consists of transferring a latissimus dorsi muscle flap onto the heart through a window created in the thoracic wall by partial resection of the second rib. The skeletal muscle may be used to reinforce the ventricular systole in ischemic or dilated cardiomyopathy, or to replace the myocardium after resection of a large aneurysm or an extensive tumour. The electronic pacing material includes an implantable cardiomyostimulator, muscle stimulating electrodes and R wave detecting electrodes. Muscular pacing begins 2 weeks after the operation, this being the time required for adhesions to be formed between the heart and the muscle. A progressive and sequential electrostimulation procedure results in the transformation of glycolytic muscle fibres that are fatigue-sensitive into fatigue-resistant oxidative fibres. The purpose of this biomechanical cardiac assistance system, where cardiac surgery is combined with plastic surgery and biomedical engineering, is to prolong life and improve its quality in patients with severe heart failure.
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PMID:[Cardiomyoplasty. Experimental bases, operative technic, indications]. 250 64

We encountered two cases of legionella pneumonia which ran a dramatic course and isolated Legionella dumoffii from one patient and Legionella pneumophila serogroup 5 from the other patient. The patient from whom L. dumoffii was isolated was a 59-year-old male with no basic disease. He presented chill, fever, coughing and other symptoms, starting on July 3, 1986, his disease was diagnosed as pneumonia at the clinic of his company. The patient was then introduced and admitted to our hospital. On admission chest radiography disclosed zonal pneumonia with an unclear border in the right superior lobe of the lung; a beta-lactam preparation was administered, but no effect was obtained and the lung lesion showed a rapid advance. From this condition, we suspected legionella pneumonia and changed the therapy to treatment with erythromycin and rifampicillin. Despite this, no improvement occurred and the patient died on the 26th hospital day. Colonies like Legionella colonies were separated from a total of seven specimens of biopsy aspirated matter from the airway and autopsy collected lung abscess and tracheal secretions, and the bacterium was identified L. dumoffii based on the biochemical and serological properties. In addition, the patient's serum was found to have an increased antibody titer against L. dumoffii. Based on these findings, the patient's disease was diagnosed as pneumonia as caused by L. dumoffii, a relatively rare bacterium as a member of the genus Legionella. The patient from whom Legionella pneumophila serogroup 5 was isolated was an 81-year-old man with basic diseases such as heart failure, anemia and hypothyroidism. He presented fever, general fatigue, anorexia and other symptoms, starting around June 2, 1987; pneumonia was suspected and the patient was urgently admitted to our hospital. The patient died of pneumonia of unknown cause on the second hospital day. To clarify the cause, autopsy was conducted; a large number of colonies like Legionella colonies were noted in the lung tissue. Identification test was then conducted and the bacterium was identified as L. pneumophila; we concluded that the patient's pneumonia had been caused by the identified bacterium L. pneumophila. The isolate was further subjected to slide agglutination test and identified as L. pneumophila serogroup 5.
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PMID:[Legionella dumoffii and Legionella pneumophila serogroup 5 isolated from 2 cases of fulminant pneumonia]. 250 80

Fatigue, that cardinal symptom of heart failure, expresses muscle deconditioning and is becoming the main complaint of our patients. Dyspnoea also is, at least partially, a consequence of muscle deconditioning; however, the wide use of diuretics which reduce water and salt retention has improved the "pump" function an therefore dyspnoea. The "muscle deconditioning" syndrome in heart failure has two causes: reduction of the nutritive blood flow in skeletal muscle, and specific alteration of mitochondrial oxidative metabolism. The syndrome appears only after a lasting reduction of physical activities. Its anatomical substrate is a mild muscular fibrosis and, mainly, reduced area of oxidative mitochondrial cristae. It remains for approximately three months, which accounts for the delayed improvement of exercise tolerance under vasodilatator treatment with angiotensin-converting enzyme inhibitors. This syndrome explains the success of retraining techniques which, in ou opinion, should become part of our therapeutic armamentarium.
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PMID:[The syndrome of "muscle deconditioning" in chronic cardiac insufficiency]. 250 99

1. Xamoterol (Corwin, Carwin, Corwil, Xamtol, ICI 118,587), a beta 1-adrenoceptor partial agonist, improves both systolic and diastolic function in heart failure patients. 2. Double-blind, randomised studies comparing xamoterol with placebo showed that the beneficial haemodynamic effects of xamoterol produced significant improvements in exercise capacity and symptoms in patients with mild to moderate heart failure. These studies formed the basis for a large European multicentre study programme which recruited over 1000 patients, randomised to xamoterol (200 mg twice daily, n = 617), digoxin (0.125 mg twice daily, n = 135) or placebo (n = 300) for 3 months. 3. Efficacy was assessed by measuring exercise capacity and symptoms. The xamoterol group improved exercise capacity by 37% compared with an 18% improvement in the placebo group. Differences in the symptom scores measured by visual analogue scales and Likert scores indicated significant improvements by xamoterol in the cardinal symptoms of heart failure, dyspnoea and fatigue. 4. Analyses of data from subsets of patients in the study showed that elderly patients, patients on no other heart failure therapy and patients with cardiomegaly all had similar improvements in exercise and symptoms to those seen in the whole study population. In the subset which included digoxin treatment, xamoterol produced significantly greater improvements in exercise capacity than digoxin (33% vs 17%, P less than 0.05) and was associated with fewer side-effects. 5. Xamoterol is therefore a promising addition to heart failure therapies currently available.
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PMID:Xamoterol, a beta 1-adrenoceptor partial agonist: review of the clinical efficacy in heart failure. 257 51


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