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

Chronic heart failure is associated with neurohumoral activation and alterations of the peripheral circulation and skeletal muscle. Several mechanisms are involved in the impaired peripheral perfusion, including increased sympathetic tone and increased vascular stiffness. Recently, data have suggested an important role of the endothelium for perfusion of skeletal muscle in heart failure. Endothelium-dependent dilation of resistance vessels is blunted in patients with severe chronic heart failure. Conceivably, this abnormality may be involved in the impaired reactive hyperemia seen in patients with chronic heart failure. In conductance vessels, flow-dependent dilation is attenuated in patients with chronic heart failure as compared with normal subjects, indicating endothelial dysfunction of large conduit vessels. Dysfunctional endothelium may contribute to impaired tissue perfusion in heart failure. Beyond an impairment of perfusion, skeletal muscle itself is altered in chronic heart failure. The metabolic abnormalities of skeletal muscle in patients with heart failure do not result from inadequate O2 delivery, but from inadequate O2 utilization by mitochondria, consistent with previous findings that the oxidative capacity of mitochondria in skeletal muscle is reduced. It appears that the impaired muscular endurance in heart failure is related to an enhanced glycolytic metabolism secondary to the reduced oxidative capacity of skeletal muscle. The observed low muscular strength appears to be due to a smaller muscle cross-sectional area. Despite successful heart transplantation, only partial improvement of bioenergetic abnormalities was noted in patients 15 months after heart transplantation.
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PMID:Changes in the peripheral circulation in heart failure. 761 76

Chronic heart failure (CHF) impairs endothelium-dependent vasodilatation of large conductance arteries. We investigated whether a similar reduction also occurs in small arteries, and whether such a reduction can be prevented by the angiotensin converting enzyme inhibitor perindopril (P) in a rat model of CHF (left coronary artery ligation). After 1 month treatment with placebo or P (2 mg/kg/day), rats were anesthetized and arterial pressure, left ventricular end-diastolic pressure, and central venous pressure were measured with a micromanometer. Segments of aorta and mesenteric artery (mean diameter, 281 +/- 8 microns) were then isolated, cannulated, and perfused at constant pressure using an arteriograph. Responses to increasing concentrations of acetylcholine (Ach), nitroprusside, and to 10(-4) mol/L NG-nitro-L-arginine methyl ester (L-NAME) were studied after preconstriction by phenylephrine. Heart failure resulted in a decrease in systolic and diastolic pressures, an increase in left ventricular end-diastolic and central venous pressures, and a significant depression of Ach-induced dilatation of the mesenteric artery (maximal dilatation, from 90 +/- 4% to 63 +/- 4%, P < .05) but not of the aorta (from 56 +/- 8% to 45 +/- 5%, NS) without any modification in the endothelium-independent vasodilatation induced by nitroprusside. In the group treated by the angiotensin converting enzyme (ACE) inhibitor perindopril, systolic and diastolic pressures were slightly decreased, whereas left ventricular end diastolic, central venous pressures, and the endothelium-dependent vasodilating response to Ach were normalized. Responses to L-NAME were not affected by CHF or perindopril. Perindopril also decreased hypertrophy, as evidenced by a significantly lower heart weight in treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevention of endothelial dysfunction in small and large arteries in a model of chronic heart failure. Effect of angiotensin converting enzyme inhibition. 764 44

Chronic heart failure is a progressive syndrome characterized by diffuse coronary artery disease (CAD) or left ventricular failure not amenable to acute interventions of myocardial revascularization. A spectrum of treatment options is available to such patients. Medical therapies consist largely of pharmacologic alternatives and are used in the early stages of heart failure to slow the processes of ventricular remodeling. Surgical interventions are used as adjunctive therapies in the later stages of heart failure. These procedures include coronary endarterectomy, high-risk surgical revascularization, automatic internal cardioverter-defibrillator insertion (Coronary Artery Bypass Grafting in Conjunction with Implantable Cardioverter Defibrillator Trial), cardiac transplantation, and dynamic cardiomyoplasty. This article provides an overview of each of these surgical therapies. Indications for each procedure and patient selection criteria are outlined. A description of each surgical procedure is included. Guidelines for postoperative nursing care are provided, and postoperative complications are discussed.
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PMID:Surgical alternatives for patients with heart failure. 768 96

Chronic heart failure (CHF) is characterized by increased systemic vascular resistance and diminished blood flow to exercising skeletal muscle. The pathogenesis of the increased resistance is not known, and may be due to muscle atrophy, functional abnormalities of resistance vessels or to structural changes in the microcirculation such as endothelial cell swelling. We have compared the ultrastructure of the microvasculature in needle biopsies of the quadriceps muscle from seven control subjects with normal left ventricular function to 10 patients with moderate or severe heart failure, optimally treated and without evidence of fluid overload. Samples were processed for ultrathin sectioning using ruthenium red as a specific basement membrane (BM) stain. Electron micrographs were taken of 10 transversely cut capillaries from each specimen. The total cross-sectional area of the vessels and the area of the endothelium was determined, and the short axis diameter was measured as an index of vessel diameter. The BM thickness was calculated from the mean of six readings around the periphery of the vessel. The short axis diameter in the two groups was not significantly different (controls 3.37 +/- 0.21 microns, CHF 3.56 +/- 0.37 microns, mean +/- 1SD). No difference in total cross-sectional area (controls 11.64 +/- 1.86 microns 2, CHF 13.56 +/- 2.78 microns 2) or area of the endothelium (controls 4.90 +/- 1.18 microns 2, CHF 6.00 +/- 1.58 microns 2) was observed. The thickness of the BM was marginally increased in subjects with CHF when compared to control subjects (0.31 +/- 0.077 microns vs 0.246 +/- 0.047 microns, P = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ultrastructural analysis of skeletal muscle. Microvascular dimensions and basement membrane thickness in chronic heart failure. 783 61

Chronic heart failure is a complex clinical syndrome characterized by many neuroendocrine manifestations by which the organism responds to the reduced cardiac output--the reduced minute volume. In order to ensure the blood flow to vitally important organs in several regions of the circulation vasoconstriction occurs. The plasma noradrenaline (NA) level rises and this correlates with the stage of chronic heart failure. In chronic heart failure the renin production in the kidney and vascular wall rises and thus also the angiotensin II (AG II) formation is increased. AG II is an affective direct arterial constrictor which facilitates NA release from terminal nerve endings and stimulates aldosterone secretion. AG II conditions also myocardial hypertrophy. Arginine vasopressin (AVP) is usually also elevated in chronic heart failure. In vasoconstriction associated with chronic heart failure participates also endothelin, an effective vasoconstrictor substance which modulates the renin-angiotensin-aldosterone system and has also an antinatriuretic effect. As a compensating response to the increased formation of vasoconstrictor substance during chronic heart failure endogenous vasodilatating and natriuretic substances are formed. Another vasodilatating factor is the atrial natriuretic factor (ANF) which is secreted by atrial myocytes as a result of atrial distension, hypernatremia or tachycardia. ANF inhibits renin, aldosterone and AVP formation. The ANF level correlates closely with the grade of chronic heart failure. With advancing heart failure also down regulation of receptors for ANF occurs. Dopamine, a natural precursor of NA, is also a vasodilatating substance and is secreted during stimulation of the sympathetic nerve. In chronic heart failure the formation of vasoconstrictor substances predominates above vasodilating ones.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Neuroendocrine changes in chronic heart failure]. 809 65

Chronic heart failure is a common clinical syndrome with high associated mortality and morbidity. Recent advances in therapy for the condition with vasodilators and, in particular, angiotensin-converting enzyme inhibitors, have led to hopes for improvement in survival. Several large scale studies examining the role of vasodilators have reported over the last few years, and the role of vasodilators in the treatment and prevention of chronic heart failure is being delineated. There is new hope for patients with symptomatic heart failure; symptoms can be alleviated and prognosis improved. Increasingly, it appears as if there is a role for drug therapy in preventing the onset of chronic heart failure. In this paper, we examine the results of these studies and of some smaller studies in order to discuss the implications for current therapy and future research.
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PMID:New evidence for improved survival in chronic heart failure. 816 26

Chronic heart failure is a growing problem affecting an increasing number of patients. Medical therapies exist, but many patients are not able to fully benefit from these therapies. Few surgical therapies have been effective in managing chronic heart failure. This article provides a comprehensive overview of dynamic cardiomyoplasty. This surgical therapy is a new procedure being utilized to enhance myocardial function in patients with end-stage heart failure. Also discussed are patient selection criteria, skeletal muscle transformation, and pulse train stimulation. The surgical procedure is described and postoperative nursing care guidelines are outlined. Surgical outcomes are presented.
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PMID:Dynamic cardiomyoplasty and its use in patients with chronic heart failure. 829 52

Chronic heart failure represents a significant challenge to caregivers because these patients are fragile, care is complex, and the numbers of patients are increasing dramatically. The anticipated illness trajectory is also rapidly changing due to the advent of pharmacologic interventions that offer greatly improved outcomes and quality of life for these patients. Despite such advances, mortality and morbidity remain high. Therefore, an important goal is to develop and evaluate nonpharmacologic interventions as adjuvant therapy to the traditional pharmacologic approach. Although relatively few studies have examined nonpharmacologic treatment strategies, it appears that many patients with heart failure may benefit significantly from participation in long-term aerobic exercise conditioning programs. Psychological and biobehavioral interventions also have the potential to substantially enhance treatment outcomes and quality of life for patients with chronic heart failure. This article reviews the available literature about nonpharmacologic strategies in the treatment of heart failure along with specific recommendations for practice.
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PMID:Nonpharmacologic interventions in the treatment of heart failure. 865 37

Chronic heart failure is a disabling and lethal disorder with high incidence and prevalence in Western societies. Treatment with angiotensin-converting enzyme (ACE) inhibitors and heart transplantations diminish both mortality and morbidity, although both still remain high. Increased understanding of some of the pathophysiologic mechanisms involved in the development of left ventricular dysfunction and the transition from asymptomatic systolic dysfunction to symptomatic heart failure has opened gates to new dimensions for the treatment of this disorder. The initial event in the pathophysiologic process is damage to the myocardium, most frequently a myocardial infarction. Almost simultaneously, activation of different neurohormonal systems occurs. The renin-angiotensin system and sympathetic nervous system are activated. Increased concentrations of hormones with counteractive activity have also been found, such as ANP and BNP. Interestingly, prolonged neurohormonal activation seems to occur only in patients with large infarcts or in patients with poor systolic function of the left ventricle. Moreover, available data from an echocardiographic study indicates that in patients with high concentrations of neurohormones in plasma a week after their infarction, left ventricular dilatation and systolic dysfunction of the left ventricle are highly likely to develop during long-term follow-up. Several studies have showed that ACE inhibitors are efficacious in chronic heart failure and among patients with reduced ejection fraction after myocardial infarction. What these patients have in common is prolonged neurohormonal activation, which theoretically may be harmful to myocardial cell structure and function. ACE inhibitors reduce the breakdown of angiotensin I to angiotensin II and increase the concentration of circulating bradykinins and prostaglandins. Further modulation of neurohormonal activity might be beneficial. Therefore, future treatment of chronic heart failure or asymptomatic left ventricular dysfunction might include beta-adrenergic blockers, neutral endopeptidase inhibitors, ANP, BNP, angiotensin II receptor antagonists, and modulators of sympathetic activity.
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PMID:The role of neurohormonal activation in chronic heart failure and postmyocardial infarction. 867 61

The relationship between stressed and total blood volume, total vascular capacitance, central blood volume, cardiac output (CO), and pulmonary capillary wedge pressure (Ppcw) was investigated in pacing-induced acute and chronic heart failure. Acute heart failure was induced in anesthetized splenectomized dogs by a volume load (20 mL/kg over 10 min) during rapid right ventricular pacing at 250 beats/min (RRVP) for 60 min. Chronic heart failure was induced by continuous RRVP for 2-6 weeks (average 24 +/- 2 days). Total vascular compliance and capacitance were calculated from the mean circulatory filling pressure (Pmcf) during transient circulatory arrest after acetylcholine at three different circulating volumes. Stressed blood volume was calculated as a product of compliance and Pmcf, with the total blood volume measured by a dye dilution. Central blood volume (CBV) and CO were measured by thermodilution. Central (heart and lung) vascular capacitance was estimated from the plot of Ppcw against CBV. Acute volume loading without RRVP increased capacitance and CO, whereas after volume loading with RRVP, capacitance and CO were unaltered from baseline. Chronic RRVP reduced capacitance and CO. All interventions, volume +/- RRVP or chronic RRVP, increased stressed and central blood volumes and Ppcw. Acute or chronic RRVP reduced central vascular capacitance. Cardiac output was increased when stressed and unstressed blood volumes increased proportionately as during volume loading alone. When CO was reduced and Ppcw increased, as during chronic RRVP or acute RRVP plus a volume load, stressed blood volume was increased and unstressed blood volume was decreased. Thus, interventions that reduced CO and increased Ppcw also increased stressed and reduced unstressed blood volume and total vascular capacitance.
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PMID:Vascular capacitance and cardiac output in pacing-induced canine models of acute and chronic heart failure. 878 19


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