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

Growing experience in terms of immunosuppression, recipient and donor selection as well as organ preservation has established thoracic organ transplantation as a therapeutic option for many children with end-stage cardiopulmonary diseases. While dilated cardiomyopathy and isolated myocardial failure represent the main indications for cardiac transplantation, replacement of the lungs or heart and lungs is necessitated in cystic fibrosis, primary and secondary pulmonary hypertension as well as some types of complex congenital heart defects involving the pulmonary arteries. We have performed a total of 20 heart, 4 heart-lung, 2 single lung and 1 double lung transplantation in the paediatric group up to 17 years of age. While with respect to the limited experience worldwide, early mortality after lung and heart-lung transplantation is still high (50%), long-term results in isolated cardiac transplantation using triple drug immunosuppression are excellent (79% survival after 6 years) without major impairment of renal function, arterial blood pressure, growth development and physical rehabilitation as well as social reintegration. Freedom from graft atherosclerosis of the allografted heart is documented over a 5 year follow up, while no data are available on the incidence of obliterative bronchiolitis after lung transplantation in the paediatric group. Despite only limited evidence of long-term dysfunction, diagnosis and prevention of chronic rejection should be given utmost attention to allow for a normal life span in this younger age group.
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PMID:Thoracic organ transplantation in the paediatric age group. The Hannover experience. 134 7

Cardiac involvement in 75 cases (mean age 21.1 +/- 6 years) with non-specific aorto-arteritis was studied. Detailed clinical examination, echocardiography and cardiac catheterization, including angiography, were done in all the cases, as was coronary angiography. Features of cardiac failure like sinus tachycardia, cardiomegaly, left ventricular third heart sound gallop and pulmonary congestion were detected in 27 cases with reduction of left ventricular ejection fraction (25-48%). Systemic hypertension was seen in 60 cases. Central aortic pressure, left ventricular systolic pressure and left ventricular end-diastolic pressure were increased in 66 cases. Pulmonary hypertension and increased pulmonary vascular resistance were detected in 6 cases. Aortic and mitral regurgitation were seen in 15 and 12 cases, respectively. Three patients had features of dilated cardiomyopathy such as generalized cardiomegaly, systemic and pulmonary congestion but without any cardiac murmurs and with normal central aortic pressure. The coronary angiogram revealed obstruction of the left anterior descending artery in 3 cases and right coronary artery obstruction in another 3 cases. Histopathological studies revealed non-specific inflammatory changes with fibrosis in cardiac musculature and the great vessels.
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PMID:Cardiac involvement in non-specific aorto-arteritis. 134 27

Catecholamines acting through beta 1- and beta 2-adrenergic receptors cause positive inotropic and chronotropic effects in the human heart. However, recent evidence suggests that in the human heart other receptor systems can also affect heart rate and contractility. Positive inotropic effects can be mediated by receptor systems acting through accumulation of intracellular cyclic adenosine monophosphate (cAMP; Gs-protein-coupled receptors such as 5-hydroxytryptamine(5-HT)4-like, histamine H2, and vasoactive intestinal peptide) or by receptor systems acting independently of cAMP, possibly through the phospholipase C/diacylglycerol/inositol-1,4,5-trisphophate pathway (such as alpha 1-adrenergic, angiotensin II, and endothelin). In the nonfailing human heart, activation of all these receptor systems induces only submaximal positive inotropic effects compared with those caused by beta-adrenergic receptor stimulation, indicating that in humans the cardiac beta-adrenergic receptor/Gs-protein/adenylate cyclase pathway is the most powerful mechanism to increase heart rate and contractility. However, the human heart contains only a few spare receptors for beta-adrenergic receptor-mediated positive inotropic effects and nearly all beta-adrenergic receptors are needed to cause maximal inotropic effects. Thus any decrease in the number of beta-adrenergic receptors will automatically lead to a reduction in functional responsiveness of beta-adrenergic receptors. In chronic heart failure the number and responsiveness of cardiac beta-adrenergic receptors are reduced, presumably because of the enhanced sympathetic drive to the heart and hence endogenous down-regulation by an elevated release of (cardiac-derived) norepinephrine, and this loss in cardiac beta-adrenergic receptor function is strongly related to the severity of the disease. However, beta 1- and beta 2-adrenergic receptors are differentially changed in different forms of heart failure. In dilated cardiomyopathy and possibly in aortic valve disease the number of cardiac beta 1-adrenergic receptors is selectively reduced without alteration in the number of beta 2-adrenergic receptors (although beta 2-adrenergic receptors become somewhat uncoupled). In ischemic cardiomyopathy, mitral valve disease, and possibly tetralogy of Fallot, the number of both beta 1- and beta 2-adrenergic receptors is concomitantly decreased. Because of the lack of a substantial receptor reserve, such a decrease in the number of beta-adrenergic receptors is accompanied by reduced inotropic and chronotropic responses to beta-adrenergic receptor stimulation in vitro and in vivo.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Receptor systems affecting force of contraction in the human heart and their alterations in chronic heart failure. 135 62

Incessant, rapid, supraventricular tachycardia may be complicated by cardiac failure with ventricular dilatation and hypokinetic wall motion on echocardiography: so-called tachycardia-induced cardiomyopathy. The diagnosis is simple when the cardiac rhythm is not sinus rhythm. The authors report the cases of 4 children aged 7 months to 12 years, referred for diagnosis and treatment of apparently primary cardiomyopathy. The findings of spontaneous or vagally-induced atrioventricular conduction defects, a permanently rapid atrial rhythm though influenced by 24 hour variations, or periodic abnormal rate increases, suggested myocardial dysfunction due to an ectopic atrial tachycardia. This was an essential step in management as the control of the tachycardia by amiodarone or betablocker therapy resulted in regression of symptoms and normalisation of left ventricular function. However, some atrial tachycardias are very resistant to medical treatment and, in such cases, there should be no hesitation in using more radical approaches, surgery or ablation, even and especially in patients with severe cardiac failure. In conclusion, apparently primary dilated cardiomyopathy in children may be due to chronic atrial arrhythmia and it is essential to perform at least Holter monitoring in order not to miss this diagnosis.
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PMID:[Rhythmogenic cardiomyopathies of atrial origin in children. Myth or reality?]. 135 26

A review over adrenergic transmembrane signalling in human heart muscle cells, changes in this signalling in patients with heart failure and the influence of medical treatment of heart failure, is presented. In heart failure, the myocardial contractibility is decreased, although the plasma level of catecholamines is elevated. This can be due to changes in the transmembrane signalling. In heart failure, the numbers of beta-receptors are decreased, the amount of Gs-protein is probably unchanged and the amount of Gi-protein is probably increased. Changes in signalling are described in more detail in patients with heart failure based on idiopathic dilated cardiomyopathy (DCM), where a selective down regulation of beta 1-receptors is seen. In heart failure of other origin, there is probably a concomitant reduction in beta 1- and beta 2-receptors. The selective regulation in patients with DCM, can be based on autoantibodies. A 30% reduction in maximal response on selective beta 2 stimulation is additionally seen in patients with DCM, probably based on an increase in the amount of Gi-protein. beta-antagonists increase and beta-agonists decrease the numbers of beta-receptors. The regulation is selective when selective antagonists and agonists are used, and nonselective when nonselective drugs are used. How other drugs affect the transmembrane signalling is still to be elucidated.
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PMID:[Adrenergic signal transduction in heart failure]. 135 1

Central sympathetic stimulation results in direct vascular vasoconstriction mediated by activation of alpha-adrenergic receptors. However, it is unknown whether this vasoconstriction is mediated by alpha 1 or alpha 2-adrenoceptor subtypes. In patients with congestive heart failure (CHF), both circulating and neuronally released catecholamines produces vasoconstriction via alpha-adrenergic stimulation. This vasoconstriction produces detrimental hemodynamic effect in CHF patients since it increases right and left ventricular filling pressures and pulmonary and systemic vascular resistances. While the myocardial alpha 1-adrenoceptors seems not to be down-regulated in heart failure, the functional integrity of vascular alpha 1 and alpha 2-adrenoceptors in CHF remains to be elucidated. Accordingly, the present study was designed to assess whether the limb vascular response to alpha 1 or alpha 2-adrenoceptor stimulation is impaired in patients with CHF. We studied 25 control subjects and 19 patients with CHF due to primary dilated cardiomyopathy. Forearm blood flow was measured by venous occlusion plethysmography. Sympathetic stimulation was produced by cold. The intraarterial pump-infusions of BHT 933 (a selective alpha 2-adrenoceptors agonist agent, 0.1, 1, 10 micrograms/kg/min for 5 min) produced the same peripheral vasoconstriction in CHF and in control subjects: 32 +/- 23.9%, 47.3 +/- 20% and 55 +/- 26.1% respectively at I, II, and III dose in CHF and 28.7 +/- 38.6%, 36 +/- 14.5%, and 57 +/- 13.8% respectively at I, II, and III dose in control subjects. The dose response to BHT 933 was not different in the 2 groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of alpha-adrenergic receptor blockade on peripheral vasoconstriction induced by the cold pressor test. Evidence for functional integrity of alpha 1 and alpha 2 adrenergic receptors in patients with congestive heart failure]. 136 84

In the past 50 years, an increased understanding of the pathophysiologic mechanisms associated with the development of heart failure has produced a more precise treatment of this syndrome. The effects of the agents used for the treatment of patients with advanced heart failure have been summarized in this article and demonstrate the importance of vasodilatory drugs on the survival and progression of dilated cardiomyopathy.
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PMID:Current issues in advanced heart failure. 138 96

Myoglobin is known to protect the mechanical function of the heart from hypoxia by acting as a sarcoplasmic oxygen reservoir and shuttle. We postulated a role for myoglobin in the pathogenesis of congestive heart failure. Several models of congestive heart failure were employed to test the hypothesis, including spontaneous inherited dilated cardiomyopathy in Doberman Pinschers, and heart failure produced by rapid ventricular pacing in dogs, volume overload in chickens and furazolidone toxicity in turkeys. Myocardial myoglobin was decreased by approximately 50% for all models (P less than 0.05). In Doberman Pinschers dogs which are predisposed to the development of dilated cardiomyopathy and have mild subclinical depression of cardiac performance, myocardial myoglobin (1.05 +/- 0.22 mg/g) is approximately 50% decreased compared to healthy mongrel dogs (2.15 +/- 0.52 mg/g), approximately twice as much as dobermans with heart failure (0.47 +/- 0.25 mg/g) but similar to the concentration found in dogs paced to heart failure (1.09 +/- 0.34 mg/g). Myocardium from poultry had remarkably decreased myoglobin compared to mammals (34 +/- 4 micrograms/g) with heart failure produced either by furazolidone or salt toxicity causing a further 50% reduction. In the canine models of heart failure, myocardial myoglobin concentration was demonstrated to be correlated with biochemical and physiological indicators of myocardial performance, namely, mitochondrial and sarcoplasmic reticular ATPase activities, and cardiac output, systemic vascular resistance, pulmonary capillary wedge pressure and mean arterial pressure, respectively. Our data implicates a role for myoglobin deficiency in the pathogenesis of congestive heart failure and in the predisposition of doberman pinschers to dilated cardiomyopathy.
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PMID:Myocardial myoglobin deficiency in various animal models of congestive heart failure. 140 11

The study was undertaken to examine the efficacy of beta-adrenoblockers used in 26 patients with chronic heart failure which had been caused by coronary heart disease in 12 patients, by rheumatic heart disease in 8 patients, by dilated cardiomyopathy in 5 patients, and by chronic myocarditis in 1 patient. beta-Blockers such as oxprenolol, propranolol, and metoprolol were supplemented to the therapy of the patients with chronic heart failure who were resistant to cardiac glycosides, diuretics, and vasodilators. This resulted in functional class improvement by the New York Heart Association from 3.67 +/- 0.1 to 2.29 +/- 0.1. The authors defined the following predictors of the efficacy of beta-blockers in chronic heart failure: duration of the disease, diastolic pressure, cardiac rhythm, and left ventricular ejection fraction and discussed the mechanisms responsible for their positive effect in chronic heart failure.
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PMID:[Potential possibilities of using adrenergic beta blockers in chronic heart failure]. 140 23

We report a case of renal cell carcinoma with pulmonary metastases treated with recombinant alpha interferon and subsequently presenting as congestive heart failure due to a dilated cardiomyopathy. A 66-year-old man presented himself to the department of internal medicine at our hospital with a complaint of persistent cough with sputum on August 27, 1988. Ultrasonogram, computed tomography and angiography showed a right renal cell carcinoma and chest x-ray films disclosed bilateral multiple nodular shadows, probably representing metastases of the renal tumor. After being transferred to our department, the patient underwent the ligation of the right renal artery and vein and the postoperative treatment with recombinant alpha interferon, achieving a complete response for pulmonary metastases and a partial response for the primary region. On February 14, 1990 the patient was admitted to our hospital with a complaint of dyspnea to be diagnosed as congestive heart failure due to dilated cardiomyopathy. The interferon therapy was suspected to have caused the heart disease, and four months after discontinuation of interferon therapy the heart failure symptoms had improved, but hypokinesis of the cardiac wall still persisted. To our knowledge, this may be the first case of alpha interferon-related cardiomyopathy in Japan.
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PMID:[Dilated cardiomyopathy following alpha interferon therapy of renal tumor with pulmonary metastases: a case report]. 141 58


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