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

Chronic congestive heart failure not controlled by conventional therapy was treated with intravenous amrinone, a new non-glycosidic, non-catecholamine cardiotonic agent. Eight patients with New York Heart Association functional class III-IV symptoms were hemodynamically monitored. At peak effect, cardiac index (CI) increased from 1.84 +/- 0.32 to 2.74 +/- 0.44 l/min/m2 (mean +/- SD) (p less than 0.001) and left ventricular filling pressure (LVFP) decreased from 25.8 +/- 6.2 to 19.5 +/- 6.8 mm Hg (p less than 0.05), while heart rate and mean aortic blood pressure did not change significantly. Mean endocardial circumferential fiber shortening (mean Vcf), determined by echocardiography, increased from 0.61 +/- 0.27 to 0.89 +/- 0.34 cir/sec (p less than 0.05). The duration of action after bolus infusion varied from 60--90 minutes. During continuous infusion of amrinone, sustained increases in CI and reductions in LVFP, similar to those at the time of peak effect after bolus administration, were maintained for 180 minutes. These marked cardiotonic effects of amrinone in patients already taking digitalis for severe heart failure occurred without side effects of arrhythmias or altered arterial pressures. The fact that the drug is orally active makes amrinone a v:ry promising inotropic agent for the treatment of chronic heart failure in man.
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PMID:Amrinone: a new non-glycosidic, non-adrenergic cardiotonic agent effective in the treatment of intractable myocardial failure in man. 43 2

Chronic congestive heart failure is typically accompanied by an abnormal production of vasoconstrictor antinatriuretic hormones and vasodilator natriuretic hormones. Decompensation occurs when the former prevail over the latter. These neuroendocrine abnormalities are increasingly taken into account to determine the prognosis and to decide on the best therapeutic approach in individual patients with chronic heart failure.
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PMID:[Neuroendocrine adaptations in chronic congestive heart failure]. 182 95

Chronic congestive heart failure is a frequently occurring disease associated with an impaired quality of life and significant mortality rate. Progress has been made in dissecting the pathophysiologic changes of congestive failure and in using vasodilators, newer positive inotropic agents, and other treatment modalities. Despite these advances, the overall mortality rate from congestive heart failure has not decreased. Further, many unanswered questions remain: How and why does a myocardial cell die? How should quality of life be measured? When should vasodilators and positive inotropic agents be given? What role do receptors play in pathogenesis and therapy? Can sudden death in heart failure be prevented? These and other questions will provide the stimulus for further studies in congestive heart failure.
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PMID:Chronic congestive heart failure. Where have we been? Where are we heading? 394 65

Renal digoxin clearance was compared in patients suffering from atrial fibrillation with well preserved cardiac function (n = 9; salt intake +/- 170 mmol daily) and patients with chronic congestive heart failure (n = 10; salt intake 50 mmol daily and maintenance treatment with diuretics). There was no difference between the groups concerning digoxin dosage, creatinine clearance, diuresis or sodium excretion in the urine. Digoxin clearance in chronic heart failure proved to be significantly lower than in atrial fibrillation (48 +/- 21 vs 71 +/- 36 ml X min-1, p less than 0.05), and Cdig/Ccreat was similarly reduced at 0.73 +/- 0.15 compared to 1.09 +/- 0.27 (p less than 0.005). Steady state serum digoxin concentration was significantly higher in patients with congestive heart failure (1.44 +/- 0.47 vs 0.87 +/- 0.33 micrograms X 1(-1), p less than 0.01). Chronic congestive heart failure is a state with reduced digoxin clearance by the kidney, which could lead to digoxin intoxication not explicable by overdose, reduced renal function or the effect of interacting drugs.
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PMID:Decreased renal clearance of digoxin in chronic congestive heart failure. 400 28

Chronic congestive heart failure is one of the risk groups of acquired hypercoagulant and hyperviscous state. In a group of patients with medium and severe cardiac failure the administration of sulodexide led to an increased activation of the fibrinolytic potential--a drop of PAI-1 and fibrinogen, to an increased activation of anticoagulatory potential--an increase of AT III and reduced plasma viscosity. Global coagulation and biochemical screening parameters were not affected by treatment. Administration of the preparation did not exert important undesirable effects and was well tolerated.
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PMID:[Hemocoagulation and hemorheology in heart failure and the possible effects of glycosaminoglycans]. 771 90

Chronic congestive heart failure is a common yet devastating syndrome and is a leading cause of morbidity and mortality in the industrialised countries. The incidence and prevalence of chronic congestive heart failure is increasing, placing a growing burden on the health care system. Despite many advances in treatment for heart disease, chronic heart failure is a terminal condition with a death rate as high as that for many malignant tumours. Patients suffering from chronic congestive heart failure report a poor quality of life because of physical symptoms, functional disability, emotional and economic burdens, frequent hospitalisations, and poor prognosis. In the context of heart failure, mortality risk (prognosis quoad vitam) can be measured using a variety of physiological variables; left ventricular (LV) dysfunction plays a primary role in the pathogenesis of congestive heart failure and correlates with prognosis, but a strong quantitative relation between exercise performance and indexes of LV function has not been demonstrated. This finding underscores the importance of psychosocial interventions in improving the quality of life and care outcomes for patients with heart failure. For this reason, questionnaires of quality of life, assessed by direct patient self-reports, have recently been imposed in cardiology, they have been used specially for evaluating most treatment of cardiac failure. The refinement of a definition of quality of life improved methods to study quality of life will contribute to a better understanding of this complex concept in heart failure patients.
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PMID:[The concept of quality of life in cardiac failure]. 918 58

Chronic congestive heart failure of various etiologies is characterized by progressive chamber dilation. Although myocyte lengthening is involved, it is not known if this cellular change can account for all of the chamber dilation. The controversy is due largely to technical limitations in collecting data on chamber circumference, myocyte length, and sarcomere length simultaneously. To address this issue, the contributions of myocyte and sarcomere lengthening to progressive chamber dilation in spontaneously hypertensive heart failure (SHHF) rats was examined using a new approach. Female SHHF rats (n=31) were examined at various time points between 2 months of age and the onset of end-stage heart failure (18 months or older). A new method enabled simultaneous collection of data on myocyte length, sarcomere length, and chamber circumference using formalin-fixed tissue. Reliability of cellular measurements was confirmed with an alternate method. LV myocyte length increased linearly between 2 and 24 months of age due to series addition of sarcomeres. Myocyte length increased in direct proportion to chamber circumference during this period (r=0.93, P<0.001). Results suggest that myocyte lengthening alone can account for chamber dilation in the progression to heart failure. Excessive myocyte lengthening is a slow, progressive change that begins long before clinical signs and symptoms of heart failure appear in this model of hypertension and failure. Since myocyte remodeling in hypertensive humans with and without failure is known to resemble that in SHHF rats, these data should provide important insight into chamber dilation and the progression of heart failure in humans.
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PMID:Correlation of myocyte lengthening to chamber dilation in the spontaneously hypertensive heart failure (SHHF) rat. 992 55

Chronic congestive heart failure is a syndrome with a poor prognosis. Currently, the only therapy providing the possibility of long term survival is heart transplantation. Therefore, new therapeutic strategies continue to be investigated. One such new approach may be the application of recombinant human insulin-like growth factor (IGF)-1. IGF-1 has both acute and long term cardiovascular effects. Acute administration of IGF-1 resulted in a reduction in afterload and positive inotropic effects in patients with heart failure. In vitro and animal studies have demonstrated that IGF-1 can stimulate myofibril formation. In addition, IGF-1 administration has beneficial metabolic effects. The benefits of prolonged IGF-1 therapy have yet to be investigated.
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PMID:Insulin-like growth factor I: an attractive option for chronic heart failure? 1058 72

Chronic congestive heart failure is associated with high morbidity and mortality, frequent hospital admissions, and high treatment costs. As the prevalence and incidence of the disease are increasing, there is a clear need to improve the management of heart failure patients. Continuous hemodynamic monitoring with an implanted device is technically feasible and safe. It provides reliable information on central hemodynamic parameters and allows for analysis of long-term hemodynamic trends. It has been suggested that continuous hemodynamic monitoring might improve the management of patients with chronic heart failure. This article describes the technical details of the monitoring system and presents possible clinical applications, with a focus on beta-blocker therapy, diuretics, and volume management. A case is reported, illustrating how hemodynamic long-term trends might add valuable information during up-titration of beta-blockers. Future implications of hemodynamic monitoring are discussed.
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PMID:Continuous hemodynamic monitoring in heart failure. 1184 71

Chronic congestive heart failure is not uncommonly associated with ventricular arrhythmias. In a small percentage of these cases, the arrhythmias may become refractory to medical therapy and exacerbate the patient's underlying heart failure. The authors report such a case, in which ventricular failure necessitated insertion of a Jarvik 2000 FlowMaker left ventricular assist device (Jarvik Heart Inc., New York, NY). In addition to normalizing the cardiac output, this axial-flow device controlled the previously unremitting ventricular arrhythmia.
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PMID:Jarvik 2000 FlowMaker axial-flow left ventricular assist device support for management of refractory ventricular arrhythmias. 1531 79


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