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)

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 More patients in the digoxin group were withdrawn because of an adverse clinical event (p less than 0.05).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.
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PMID:Enalapril versus digoxin in patients with congestive heart failure: a multicenter study. Canadian Enalapril Versus Digoxin Study Group. 196 Mar 3

Most research in the field of chronic heart failure during the last 20 years has been directed toward defining and understanding the abnormalities of systolic function seen in this disorder, but systolic performance is not a determinant of effort tolerance. Several lines of evidence, however, suggest a strong relation between exercise capacity and abnormalities of diastolic function in chronic heart failure. Of all the commonly measured hemodynamic variables, effort tolerance (whether limited by dyspnea or fatigue) varies more closely with the level of left ventricular filling pressure than the left ventricular ejection fraction. Consequently, drugs that lower ventricular filling pressures are more likely to enhance exercise capacity than drugs that primarily increase cardiac output and left ventricular ejection phase indexes. Vasodilator drugs do not reduce left ventricular filling pressure, however, by simply redistributing central blood volume to the peripheral capacitance circuits because these agents do not predictably decrease left ventricular volumes. Instead, clinically effective drugs seem to reduce left ventricular filling pressure primarily by producing a favorable shift in the left ventricular diastolic pressure-volume relation. Conversely, agents that adversely affect the diastolic pressure-volume relation frequently cause clinical deterioration. These findings suggest that abnormalities of diastolic rather than systolic performance may be the most important determinants of the clinical status and exercise intolerance of patients with chronic heart failure.
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PMID:Abnormalities of diastolic function as a potential cause of exercise intolerance in chronic heart failure. 196 59

The sympathetic nervous system becomes activated in heart failure, and while this is initially beneficial, the consequences of prolonged raised levels of catecholamines can be counterproductive. Xamoterol, a partial agonist that acts on the cardiac beta 1-adrenergic receptor, modifies the response of the heart to variations in sympathetic activity. At rest, it produces modest improvements in cardiac contractility, relaxation, and filling without increase in myocardial oxygen demand. The improvements are maintained during exercise although the attendant tachycardia is attenuated. The beneficial effects of xamoterol on both systolic and diastolic function suggested that it would be effective in patients with mild-to-moderate heart failure, and this was demonstrated in small placebo-controlled studies where effort tolerance and symptoms were improved. A large multicenter study program comprised of four studies demonstrated that patients with mild-to-moderate heart failure randomized to xamoterol (n = 617) 200 mg b.i.d. for 3 months significantly (p less than 0.0001) improved exercise capacity by 37% as compared with the placebo group (n = 300) with an increase of 18%. The xamoterol group also showed significant improvements in symptoms of breathlessness, fatigue, and life values as compared with the placebo group. In one of the multicenter studies in which 433 patients were randomized to xamoterol (n = 220), placebo (n = 109), and a positive control, digoxin 0.125 mg b.i.d. (n = 104), the percentages of improvement in exercise work were 33%, 5%, and 17%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Review of clinical experience with xamoterol. Effects on exercise capacity and symptoms in heart failure. 196 61

Five patients were studied 5-13 months after dynamic cardiomyoplasty for refractory heart failure. In two, muscle flap stimulation caused a pronounced increase in cardiac index (mean 55%) and ejection fraction (mean 75%); no patient showed improvement in cardiac filling pressure. 2 years after surgery, one of the patients with haemodynamic improvement died from ventricular fibrillation, and histochemistry of the stimulated muscle flap revealed predominantly fatigue-resistant type I fibres, without evidence of fibrosis. In selected cases, dynamic cardiomyopathy could be of long-term benefit.
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PMID:Preliminary report: follow-up after dynamic cardiomyoplasty. 197 65

The long term effects of treatment with xamoterol in 14 patients aged 44-73 with mild to moderate heart failure as a result of ischaemic heart disease are reported. After 18 months' treatment with xamoterol, patients were assessed in a randomised double blind crossover comparison of xamoterol (200 mg twice a day) and placebo, each given for one month. Compared with placebo, xamoterol significantly increased exercise duration and work done on a bicycle ergometer and reduced the maximum exercise heart rate. Assessment of symptoms and activities at 12 months by visual analogue and Likert scales showed a trend towards the relief of symptoms of breathlessness and tiredness and an improvement in activity. There was an improvement in the clinical signs of heart failure and no haemodynamic deterioration over a 12 month period as assessed by ejection fraction. The improvement in exercise tolerance, symptoms, and activities was sustained for 18 months without side effects or development of tolerance.
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PMID:Ischaemic left ventricular failure: evidence of sustained benefit after 18 months' treatment with xamoterol. 197 39

Skeletal muscle function was measured as force production and fatigue in both the quadriceps (a large locomotive muscle) and adductor pollicis (a small intrinsic hand muscle) in five healthy volunteers, five patients with mild chronic heart failure, and five patients with severe chronic heart failure. The quadriceps of patients with chronic heart failure had a reduced muscle cross sectional area, a reduced maximum isometric force production, and an increased tendency to fatigue. Isometric force production and fatigue of the adductor pollicis, however, were not significantly different between the three groups under control conditions. But during circulatory occlusion fatigue in the adductor pollicis increased more in the patients with severe chronic heart failure. These differing findings in quadriceps and adductor pollicis suggest that skeletal muscle atrophy and reduced isometric force production are not a necessary consequence of chronic heart failure per se, because they were only present in the large locomotive muscle. The normal values for muscle fatigue observed in adductor pollicis in patients with chronic heart failure imply that skeletal muscle blood flow must increase normally during muscle activation when only a small muscle mass is used. These results are not compatible with the concept of a generalised impairment of normal vasodilatation within active skeletal muscle. In contrast, activation of a large muscle, such as quadriceps, results in the rapid onset of fatigue in patients with severe chronic heart failure. This fatigue may be related to the inability of the cardiovascular system to provide the required blood flow for the activation of a large muscle mass. The finding of a relatively greater increase in fatigue of adductor pollicis during circulatory occlusion in patients with severe chronic heart failure supports the hypnosis of an intrinsic abnormality of skeletal muscle in these patients.
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PMID:Direct measurement of skeletal muscle fatigue in patients with chronic heart failure. 199 26

1. Fifty patients with symptoms due to chronic heart failure despite diuretic therapy were randomised to receive additional treatment with either hydralazine or captopril. The dose was titrated; 24 received hydralazine and 26 captopril up to a maximum daily dosage of 225 mg and 75 mg respectively. Forty-three patients had coronary heart disease and seven dilated cardiomyopathy. 2. Dyspnoea and tiredness were assessed using a visual analogue scale (0-100) before and during 12 weeks' treatment. Captopril produced a significantly greater reduction in breathlessness (F = 31.6, P less than 0.001) and tiredness (F = 65.8, P less than 0.001) compared with hydralazine. 3. There was an increase in treadmill exercise time during treatment with both hydralazine (from 5.5 (3.47-7.53) min to 6.9 (4.87-8.93) min), and captopril (from 5.0 (3.05-6.95) min to 7.8 (5.85-9.75) min), but the degree of improvement was significantly greater in the patients treated with captopril (F = 7.4, P less than 0.001). 4. There was no significant change in right ventricular ejection fraction (from 27.9 (19.3-36.5)% to 28.7 (20.1-37.3)%) or left ventricular ejection fraction (from 22.2 (14.2-30.2)% to 23.9 (15.9-31.9)%) during treatment with hydralazine. However, both right and left ventricular ejection fraction increased significantly during treatment with captopril (from 27.1 (18.9-35.3)% to 32.0 (23.8-40.2)%, P less than 0.05; and from 25.0 (17.2-32.8)% to 29.6 (21.8-37.4)%, P less than 0.05 respectively). 5. These results suggest that in patients with symptoms due to chronic heart failure despite diuretic therapy, treatment with captopril produces a greater symptomatic and haemodynamic improvement than treatment with hydralazine.
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PMID:Which vasodilator drug in patients with chronic heart failure? A randomised comparison of captopril and hydralazine. 201 67

The patient responded to treatment at the first onset of heart failure but gradually became irresponsive to treatment, experiencing fatigue and malaise as the chief complaints and suffering from gradually progressive decrease in exercise capacity and body weight. Dose of DOA gradually increased to maintain well clinical state of the patient. Unusual for heart failure, he had bradycardia as the basal rhythm without showing a tendency for tachycardia. Cardiac catheterization revealed pulmonary hypertension and low cardiac output, however, left ventricular ejection fraction was 37%. There were no notable changes in ultrasonic cardiogram or CTR through the clinical course. Tl-201 myocardial images and pulmonary perfusion images showed gradual worsening corresponding to progressive worsening of clinical state. From these findings, the patient was determined as a candidate for heart transplantation.
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PMID:[Tl-201 myocardial images in a patient with dialated cardiomyopathy, who finally received heart transplantation]. 202 Jan 39

Many studies on cardiac assist devices using skeletal muscle ventricle (SMV) require preconditioning for 6-9 weeks as a countermeasure to prevent skeletal muscle fatigue. Therefore this method does not seem to be indicated in cases of acute heart failure. However we performed experiments to develop Alternate-Drive Twin SMVs as a cardiac assist device without preconditioning. Adult mongrel dogs were used. In order to obtain adequate alternating SMV during pattern, fundamental experiments were performed. The function of SMVs prepared by rolled pedunculated sartial muscle was studied hydrodynamically in three groups; continuous driving for one hour in group a (n = 3): intermittent driving for 3 hours in group b (n = 15): intermittent driving for 12 hours in group c (n = 3). Group b was divided into three subgroups with interval for 10 minutes in subgroup I (n = 5), for 20 minutes in subgroup II (n = 5), for 30 minutes in subgroup III (n = 5). In group b and c, the recess interval between driving was set the same as the driving interval in each subgroup. All SMVs were stimulated by electrical bursts. In every experiment pump pressure, pump max dp/dt and pump stroke work index/10 kg body weight were measured for 3 hours. In subgroups I and II, pump function decreased gradually, however, the parameters did not show any change for up to 3 hours in subgroup III. We defined the reduction ratio as the difference of parameters before and after driving divided by the value at the start of driving.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiac assist device with skeletal muscle ventricle--alternate-drive twin pump system as a countermeasure to prevent skeletal muscle fatigue]. 202 16

The response of patients with chronic severe heart failure to extended infusions (greater than or equal to 48 hours) of milrinone was evaluated in a multicenter, baseline-controlled, phase III efficacy and safety trial in 189 patients in the United States. Milrinone was given as loading and maintenance infusions according to one of four dose regimens. An effective response was defined as greater than or equal to 20% increases in cardiac index or decreases in pulmonary wedge pressure. All loading doses (range, 37.5 to 75 micrograms/kg/10 min) were effective short term, and maximum response occurred at 15 minutes. For the three effective regimens, cardiac index increased initially (at 15 minutes) by 24% to 42%, and pulmonary wedge pressure decreased by 24% to 33%. Systemic vascular resistance was reduced by 15% to 31%. The maximal acute response was effective in 99% of individual patients. During maintenance therapy, effective responses were seen at infusion doses of 0.375, 0.50, and 0.75 micrograms/kg/min, whereas an infusion of 0.25 micrograms/kg/min was ineffective. During 2 days of maintenance therapy, cardiac index remained augmented by 34% to 39% for the low and intermediate doses and by 44% to 73% for the high-dose infusion regimen. Pulmonary wedge pressure decreased an average of 18% on day 1 and 30% on day 2. Systemic vascular resistance was reduced by 20% to 25%, and stroke work index was augmented by 21% to 58%. Symptomatic improvement was common during intravenous milrinone therapy for symptoms of dyspnea (61% response), orthopnea (63%), edema (62%), and fatigue (40%). Improvement occurred more frequently in those with worse baseline functional indexes and in those with greater hemodynamic responses to therapy. Safety and tolerance were exceptionally good for these patients with advanced heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic and clinical benefits with intravenous milrinone in severe chronic heart failure: results of a multicenter study in the United States. 203 27


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