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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

If the failing left ventricle could be given an effective push, other approaches to the treatment of heart failure would not be needed. We have inotropes only for short-term parenteral use. We have no safe inotrope for chronic oral use. The effect of digitalis is only feeble and the phosphodiesterase inhibitors seem to increase mortality from sudden death. Diuretics are dramatic for acute pulmonary oedema and the mainstay for chronic fluid retention but do not improve the pump and by reducing blood volume stimulate the renin angiotensin system to vasoconstriction, further fluid retention and hypokalaemia. Nitrates drop pre-load without reducing blood volume but tolerance is a problem and stroke volume does not increase. Reduction of afterload helps the failing ventricle to empty, the pull and output increases. The angiotensin converting enzyme inhibitors (ACEI) are now the cornerstone of heart failure treatment, reducing mortality in severe heart failure (CONSENSUS) and superior to standard vasodilator therapy (V-HeFT-2) at improving the survival of patients with mild to moderate heart failure. ACEI can reduce the incidence of ventricular ectopy and probably do this through improving left ventricular function, from decreasing sympathetic tone, reducing myocardial oxygen demand or increasing serum potassium but ACEI did not diminish the incidence of sudden death in the SOLVD trial despite reducing mortality. Disappointingly little improvement in exercise tolerance and persistence of chronic fatigue in heart failure concentrated attention on the periphery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The push, the pull and the periphery. 144 45

A 60-year-old man was admitted with general fatigue and jaundice of one year's duration in February, 1981. The hemoglobin (Hb) was 11.4 g/dl and reticulocytes were 1.7%. A diagnosis of chronic cold agglutinin disease (CCAD) was made from the presence of cold agglutinin (CA) 1:2,048, increased serum IgM 267 mg/dl and indirect bilirubin 1.4 mg/dl. His Hb was approximately 11 g/dl in summer and 9 g/dl in winter for the subsequent ten years without therapy. In July, 1990, he was readmitted because of exacerbation of anemia and hepatosplenomegaly. The Hb was 4.6 g/dl, indirect bilirubin 3. 1 mg/dl, CA titer 1:232,144 and reticulocytes were 20%. Serum IgM was 1,065 mg/dl, and immunoelectrophoresis showed IgM-kappa M-protein. Peripheral blood lymphoid cells expressed surface membrane immunoglobulin (SmIg) M and kappa. The bone marrow showed an increased number of lymphoid cells which also expressed SmIg M and kappa. These findings were compatible with those of the features of primary macroglobulinemia (PMG). The M-2 protocol resulted in decrease in serum IgM and CA, but he died of heart failure in February, 1991. The relationship between CCAD and PMG in relation to the pathogenesis was discussed.
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PMID:[Chronic cold agglutinin disease terminating in primary macroglobulinemia after a 10 year history]. 146 90

Clentiazem, 8-chloro diltiazem, is a calcium channel blocker currently undergoing evaluation for the treatment of stable angina and hypertension. As patients with ischaemic disorders often present some degree of heart failure, the aim of this study was to investigate the effect of congestive heart failure on clentiazem (200 micrograms kg-1, i.v. bolus) pharmacokinetics in a canine model. Congestive heart failure was induced in six dogs by rapid ventricular pacing (240 beats min-1) for 3-5 weeks. Clentiazem pharmacokinetics was studied in each dog under the control condition and after the development of clinical signs of heart failure (ascites, dyspnea, fatigue). Blood samples were collected up to 480 min post-dose. Clentiazem plasma concentrations were determined by high performance liquid chromatography. The area under the plasma concentration versus time curves (AUC0-infinity) was significantly increased in congestive heart failure dogs (8.8 +/- 1.6 vs 21.8 +/- 1.4 micrograms min ml-1) (mean +/- SEM). These changes were related to a reduction of the volume of distribution of the central compartment (0.9 +/- 0.1 vs 0.2 +/- 0.11 kg-1) and total body clearance (1.9 +/- 0.4 vs 0.7 +/- 0.21 h-1 kg-1). It is concluded that, in our model, congestive heart failure significantly modifies clentiazem disposition. These results suggest that caution should be exercised when clentiazem is given to patients with a low ejection fraction and a compromised cardiac function. Reduced loading and maintenance doses might be recommended in patients with severe congestive heart failure.
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PMID:Effect of congestive heart failure on clentiazem pharmacokinetics in a dog model. 148 42

To evaluate electrically stimulated muscle grafts for augmenting ventricular function in cardiac insufficiency, dynamic cardiomyoplasty was performed in nine sheep, using latissimus dorsi (LD) muscle wrapped as a pedicle around the left ventricle. Beginning 2 weeks postoperatively, LD was stimulated synchronously with the heart. After 6 and 12 weeks of stimulation, hemodynamic evaluation was done and biopsies were taken for histochemical and biochemical analysis. With intact heart function, stimulation of the muscle was not hemodynamically beneficial. During induced heart failure, cardiomyoplasty increased cardiac output by 25% in two sheep. Eight LD muscles contracted vigorously in synchrony with the heart, one was fibrosed and all were fixed to the thoracotomy incision by scar tissue. ATPase stain showed gradual transformation of muscle fibers into fatigue-resistant Type I. At 12 weeks only Type I were seen. Quantitative enzymatic analyses revealed increase in oxidative and decrease in glycolytic enzymes. Chronic electrical stimulation is concluded to change the muscle characteristics towards those of mainly oxidative and fatigue-resistant muscle, thereby improving opportunities for assisting the depressed heart. Dynamic cardiomyoplasty involves risks of adhesions to adjacent tissues and muscle trauma from chronic stimulation.
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PMID:Experimental dynamic cardiomyoplasty in sheep. 152 92

To determine the reliability and validity of a patient outcome questionnaire for chronic heart failure, a randomized, double-blind, placebo-controlled, 3-month trial of pimobendan, an investigational medication with inotropic and vasodilator activities, was performed. Evaluated were 198 ambulatory patients with primarily New York Heart Association (NYHA) class III heart failure from 20 referral centers. Baseline therapy included digoxin, diuretics and, in 80%, a converting enzyme inhibitor. Oral pimobendan at 2.5 (n = 49), 5.0 (n = 51), or 10 (n = 49) mg daily or matching placebo (n = 49) was administered. The Minnesota Living with Heart Failure (LIhFE) questionnaire was a primary outcome measure, along with an exercise test. Interitem correlations identified subgroups of questions representing physical and emotional dimensions. Repeated baseline scores were highly correlated (r = 0.93), as were the physical (r = 0.89) and emotional (r = 0.88) dimension scores. Placebo did not have a significant effect with median (25th, 75th percentile) changes from baseline scores of 1 (-3, 5), 1 (-2, 3), and 0 (-1, 2), respectively (all p values greater than 0.10). The 5 mg dose significantly improved the total score, 7.5 (0, 18; p = 0.01) and the physical dimension, 4 (0, 8; p = 0.01), compared with placebo. Changes in the total (r = 0.33; p less than 0.01) and physical (r = 0.35; p less than 0.01) scores were weakly related to changes in exercise times, but corresponded well with changes in patients' ratings of dyspnea and fatigue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of patient outcome with the Minnesota Living with Heart Failure questionnaire: reliability and validity during a randomized, double-blind, placebo-controlled trial of pimobendan. Pimobendan Multicenter Research Group. 152 75

Skeletal muscle powered assist ventricles (SMV) are being investigated in animal studies as a treatment for heart failure. Muscle fatigue is almost always dependent upon muscle capillary blood flow. This study examined the relationship between SMV intrapouch pressure and blood flow to the circumferential muscle in a working SMV with a mock circulation. The unconditioned rectus abdominis muscle was used to create an in situ SMV in five dogs. Muscle blood flow was measured by both the radioactive microsphere and the electromagnetic flow probe method as the pouch pressure was varied between 10 and 70 mmHg and as the SMV was stimulated to contract at a rate of 20 min-1. The correlation coefficient for the two methods was 0.908. At pouch pressures of 10, 40, and 70 mmHg, the respective blood flow values were 22.60 +/- 2.50 (1 SEM), 12.20 +/- 2.10, and 4.40 +/- 0.74 ml min-1 (p less than 0.05). When they were corrected for muscle weight, the mean blood flow values at these same pouch pressures were 0.28 +/- 0.03, 0.15 +/- 0.03, and 0.05 +/- 0.01 ml min-1 g-1, respectively (p less than 0.05). SMV output was measured for each pouch pressure that was tested. Pouch output, expressed as ml min-1, was 458 +/- 20 (1 SEM) at an SMV diastolic pouch pressure of 10 mmHg, 309 +/- 22 at a pouch pressure of 40 mmHg, and 103 +/- 6 at a pouch pressure of 70 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of skeletal muscle ventricle pouch pressure on muscle blood flow. 153 16

The use of beta-adrenergic antagonists for primary prevention of gastrointestinal hemorrhage in patients with cirrhosis and esophageal varices is discussed. In five controlled trials, patients with cirrhosis and endoscopically proven esophageal varices were treated with either propranolol or nadolol in doses to reduce heart rate by 20-25% or in doses to decrease hepatic vein pressure by 25% of basal levels or to a level of less than 12 mm Hg. In two of three studies, investigators found that propranolol significantly reduced frequency of initial bleeding in patients with esophageal varices. In one of two studies, nadolol significantly decreased the risk of variceal bleeding in patients with cirrhosis; in the other study, a significant difference in the frequency of initial bleeding was found only among patients who were compliant with therapy. Only one of the five studies showed a significant difference in survival between the treatment group and the placebo group. Adverse effects of therapy included dizziness, fatigue, cardiac insufficiency, Raynaud's phenomenon, and risk of bleeding associated with propranolol withdrawal. Therapy with a nonselective beta-adrenergic antagonist should be considered for primary prevention of gastrointestinal hemorrhage in patients with cirrhosis and suspected or documented large varices; however, abrupt discontinuation of the medication is associated with risk of bleeding.
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PMID:Beta-adrenergic antagonists for primary prevention of gastrointestinal hemorrhage in patients with cirrhosis and esophageal varices. 156 29

The factors that contribute to the symptoms of breathlessness and fatigue, and that limit exercise capacity in patients with chronic heart failure are poorly understood. Recent evidence suggests that the major mechanism is not related to central hemodynamics but to a reduction of skeletal muscle mass and diminished blood flow to skeletal muscle on exercise.
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PMID:Blood flow and skeletal muscle in patients with heart failure. 157 60

Although the pathophysiology of exercise intolerance in patients with chronic heart failure (CHF) is not fully understood, it appears that the cardiac output response plays an important role in limiting exercise in this disorder. Although previous studies have demonstrated that peak VO2 is not related to left ventricular (LV) ejection fraction, studies have consistently identified peak exercise cardiac output as an important predictor of peak VO2. It is likely that a reduced cardiac output to work rate relationship in CHF causes hypoperfusion of both working skeletal muscle and visceral organs, which leads to early anaerobic metabolism and fatigue. Several factors may influence the cardiac output response in patients with severe systolic LV dysfunction, including heart rate, diastolic LV function, and the mitral regurgitation fraction. Although stroke volume increases through use of the Frank-Starling mechanism in many patients with severe systolic LV dysfunction, some patients with this disorder may not increase stroke volume during exercise due to diastolic LV dysfunction or pericardial constraint. The finding that this latter group has more severe exercise intolerance suggests that diastolic dysfunction may further decrease peak VO2 in this disorder. Variations in the mitral regurgitation fraction also have been found to have an important effect on exercise stroke volume in some patients with CHF. Therefore, the finding that LV ejection fraction at rest or during exercise is not related to peak VO2 in patients with systolic LV dysfunction does not necessarily indicate that central hemodynamics do not play a role in exercise intolerance. Rather, it is likely that variability in the LV ejection fraction with exercise, which does not take variable increases in LV end-diastolic volume or mitral regurgitation into account, plays only a modest role in determining the stroke volume and cardiac output response to exercise in patients with severe systolic dysfunction.
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PMID:Central hemodynamic response to exercise in patients with chronic heart failure. 157 62

Multiple compensatory mechanisms operate to preserve exercise tolerance in patients with left ventricular failure. Exercise capacity of most patients with chronic heart failure is limited by dyspnea or fatigue, or both. Maximal stress testing with direct assessment of peak O2 uptake is an essential measurement in planning exercise conditioning programs, which are now attracting patients with chronic heart failure. The biochemical and histologic patterns of skeletal muscle changes seen in chronic heart failure patients are consistent with the effects of long-term exercise deconditioning in normal subjects. Recent studies have suggested beneficial effects of training in subjects with moderate or even severe left ventricular dysfunction by showing increased exercise tolerance or peak O2 consumption, anaerobic threshold, peak leg blood flow, peak central arteriovenous oxygen difference and decreased lactate accumulation. However, a number of questions remain unanswered. Exercise training for the treatment of chronic heart failure should be determined on an individual basis and used with caution.
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PMID:Physical training in patients with congestive heart failure. 157 63


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