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

Cardiac beta-adrenoceptor density and beta 1- and beta 2-subtype distribution were examined in human left ventricular myocardium from transplant donors serving as controls and from patients with mitral valve stenosis, aortic valve stenosis, idiopathic dilated cardiomyopathy, and ischaemic cardiomyopathy respectively. The total beta-adrenoceptor density was similar in transplant donors and patients with moderate heart failure (NYHA II-III) due to mitral valve stenosis, but was markedly reduced in all forms of severe heart failure (NYHA III-IV) studied. A reduction of both beta 1- and beta 2-adrenoceptors was found in patients with severe heart failure due to mitral valve stenosis or ischaemic cardiomyopathy. In contrast, a selective down-regulation of beta 1-adrenoceptors with unchanged beta 2-adrenoceptors and hence a relative increase in the latter was observed in idiopathic dilated cardiomyopathy and aortic valve stenosis. It is concluded that the extent of total beta-adrenoceptor down-regulation is related to the degree of heart failure. Selective loss of beta 1-adrenoceptors is not specific for idiopathic dilated cardiomyopathy but also occurs in aortic valve stenosis. Changes in beta 1- and beta 2-subtype distribution are rather related to the aetiology than to the clinical degree of heart failure.
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PMID:Distinct down-regulation of cardiac beta 1- and beta 2-adrenoceptors in different human heart diseases. 164 74

Excess fatigue is a common symptom of many chronic cardiovascular disorders with low cardiac output. Impairment of skeletal muscle function due to metabolic alterations seems to play a major role. In heart failure fatigue is a predominant symptom. It may be an early symptom on diseases with slow but progressive inhibition of blood flow, i.e. in constrictive pericarditis, pulmonary hypertension or mitral valve stenosis. Excess fatigue as a precursor of myocardial infarction is being discussed. Finally fatigue may be a limiting side effect of diuretic and beta-blocking agents.
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PMID:[Cardiovascular causes of abnormal fatigability]. 175 69

Catheter-balloon mitral valvuloplasty was performed in 7 females with rheumatic mitral stenosis on the 19th-32nd week of pregnancy. Four patients were operated on with signs of cardiac insufficiency, two--in a state of pulmonary pre-edema. Edema of the lungs in one patient continued developing on the operating table. The results of the treatment were good in all cases. The area of the mitral orifice increased from 0.9-1.75 to 2.4-3.5 cm2. The pressure gradient between the left atrium and the left ventricle dropped from 25-40 to 2-8 mm Hg. This was attended by the disappearance of the diastolic murmur and the clinical manifestations of stasis in pulmonary circulation in all patients. The development of mitral regurgitation after the operation was not encountered in any of the patients. The period of roentgenoscopy lasted 17.5 min. on the average. Screens were used to protect the fetus from the direct effect of the X-rays. Pregnancy ended in delivery in 6 patients; spontaneous labor at term occurred in 4, cesarean section had to be performed in one patient with placenta previa; one woman gave birth to twins on the 36th week of pregnancy. All the babies were healthy. Catheter-balloon valvulotomy does not yield to closed mitral commissurotomy in efficacy. The fact that it is only mildly injurious and does not need general anesthesia make this intervention preferable for pregnant women suffering from mitral stenosis.
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PMID:[Treatment of mitral valve stenosis in pregnant women by the method of balloon valvuloplasty]. 179 21

Interventional cardiology has become an alternative to surgery in the treatment of coronary artery and stenotic valvular diseases. Percutaneous transluminal coronary angioplasty is a method of treating severe coronary stenoses under simple local anaesthesia with a primary success rate of 90% and a mortality of about 1%--nearly zero in single vessel disease. These results have to be tempered by the relatively common occurrence of restenosis (30 to 40%) which are treatable by repeat angioplasty. Amongst the new techniques under evaluation at present, coronary endoprostheses (stents) seem to be the most effective in reducing the rate of restenosis. Percutaneous mitral valvuloplasty with an inflatable balloon catheter is associated with excellent results in cases of mitral stenosis when the valvular and subvalvular apparatus is not stiff and not calcified. On the other hand, the results of aortic valve dilatation are often inadequate and temporary, and this technique is now reserved for very elderly patients with severe aortic stenosis and irreducible cardiac failure, inoperable, and for patients with symptomatic calcific aortic stenosis who have to undergo urgent extracardiac surgery and who could benefit from valvular replacement at a later date. Interventional cardiology may replace or postpone surgery and allows effective treatment of patients too old or too ill to undergo cardiac surgery.
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PMID:[Interventional cardiology in adults]. 180 82

Gangrene of the left upper limb was found to complicate severe mitral stenosis presenting with heart failure in a sixty-eight-year-old woman with a documented left atrial thrombus. Arterial obstruction as the cause of gangrene was excluded by Doppler-assisted assessment of the peripheral pulses. Venous gangrene can complicate severe mitral stenosis and must be distinguished from arterial embolization, in which urgent surgical treatment is imperative.
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PMID:Venous gangrene (phlegmasia caerulea dolens) complicating heart failure from severe mitral stenosis--a case history. 189 41

A 60-year-old female with mitral stenosis developed prosthetic valve endocarditis due to methicillin resistant staphylococcus aureus septicemia 3 weeks after mitral valve replacement. In vitro test disclosed susceptibility to minocycline and clindamycin. Despite large amount of intravenous administration, progressive heart failure due to massive perivalvular leakage occurred as a consequence of persisting infection. An emergent operation revealed valve detachment of the posterior portion resulting from ring abscess formation. A mitral prosthesis with a Gore-Tex flange was implanted partially in the left atrium just above the mitral ring and sutured to the atrial wall. Postoperative relapse was not detected even after discontinuing antibiotics. Prosthetic valve endocarditis due to methicillin resistant staphylococcus aureus is highly resistant to antibiotic therapy and likely to develop valve ring abscess. Prompt surgical treatment is mandatory in this situation.
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PMID:[A case report of early prosthetic valve endocarditis due to methicillin resistant Staphylococcus aureus infection--an experience of intraatrial implantation of mitral prosthesis with a Gore-Tex flange]. 196 Apr 64

We reported a case with left atrial giant thrombus (LAGT) which appeared over a period of six months. The patient was a 65-year-old woman who came to our hospital complaining of syncopal attack. Her electrocardiogram showed atrial fibrillation with very slow ventricular response, and there was cardiac arrest for 1500 ms, mitral stenosis and regurgitation, aortic and tricuspid regurgitations were recognized in the echocardiogram. By coronary angiography, 90% stenosis in the left circumflex artery (LCX) was found, and using transseptal left atrium heart catheterization, pressure gradient from the left atrium to the left ventricle was also measured. We diagnosed that her valvular diseases were mild. To protect her from unconsciousness and heart failure, a permanent pacemaker was implanted and PTCA for LCX lesion was performed. After six months, we found LAGT by echocardiography. It is very rare that LAGT is formed in a short period. We suggested that the changes of hemodynamics caused by transseptal left atrial catheterization or the permanent pacemaker implantation effected the formation of the LAGT.
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PMID:[A case of left atrial giant thrombus which appeared in a short period]. 204 11

Diastolic heart failure is characterized by increased resistance to diastolic filling of one or both cardiac ventricles. Although some degree of diastolic failure exists in most patients presenting clinically with heart failure, a substantial subset of patients have relatively pure diastolic heart failure with normal systolic function. Diastolic heart failure can be due to structural abnormalities that increase resistance to ventricular inflow, and these structural abnormalities can be extramyocardial (e.g., constrictive pericarditis and mitral stenosis) or intramyocardial (e.g., fibrosis and amyloidosis). In addition to structural abnormalities, physiological derangement of myocardial inactivation and relaxation can contribute importantly to diastolic dysfunction in patients with heart failure. There is mounting evidence that advanced myocardial hypertrophy is associated with increased resistance to ventricular diastolic inflow due to both structural alteration (increased wall thickness and altered collagen matrix) and impaired diastolic relaxation of the hypertrophied myocardium. Physiological mechanisms for impaired relaxation in advanced hypertrophy remain controversial but can include disordered function of myocardial sarcoplasmic reticulum, subendocardial ischemia, and altered adenylate cyclase function. Diastolic dysfunction can play an important role in the genesis of flash pulmonary edema seen in patients with ischemic heart disease because myocardial ischemia is associated with a decline in relaxation rate, increased resistance to early diastolic filling, and in some cases, a striking upward shift in the left ventricular diastolic pressure-volume relation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diastolic dysfunction and congestive heart failure. 213 51

The atrial natriuretic factor (ANF) is a hormone whose effects and mode of secretion have been determined. But its exact role in the regulation of volemia in comparison with that of the renin-angiotensin system is still to be defined. Studies of human diseases associated with an increase of ANF plasma concentration may help reach this goal. The mechanisms resulting in elevated ANF plasma concentrations (increase of secretion, decrease of catabolism of the hormone) and the effects of these high levels of ANF on renal functions and circulation are analysed in chronic cardiac failure, mitral stenosis, pulmonary artery hypertension, acute tachycardias, chronic and acute renal failures and in the course of cardiac transplantation. The therapeutic usefulness of drugs inhibiting ANF catabolism (blockers of the clearance receptors for ANF and inhibitors of the enzymes degrading ANF) is also considered.
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PMID:[Atrial natriuretic factor. Role in the physiopathology of cardiac and renal diseases]. 213 35

Lungs of 37 patients with pulmonary hypertension (PHT), 5 normal human lungs, and 30 normal rat lungs, were studied using immunohistochemical stainings for actin, alpha-smooth muscle (alpha-SM) actin and desmin. The type of PHT was determined on clinicopathologic grounds (in 17 cases by catheterism); 20 patients had precapillary and 17 postcapillary PHT. In normal lungs, myofibroblasts, ie, contractile interstitial cells (CIC), distributed in alveolar septa, were not stained by alpha-SM actin antibodies. Only around the venules, were cells labeled by this antibody present. Furthermore, there were bundles of alpha-SM actin-positive cells around the openings of air sacculi into the alveolar ducts. In precapillary PHT, the distribution and immunostaining properties of interstitial cells remained unchanged; alpha-SM actin-positive cells were observed in thickened arterial intima and in plexiform lesions. In postcapillary PHT secondary to heart failure, to mitral stenosis, or in veno-occlusive disease, many interstitial cells in the alveolar septa were decorated by alpha-SM actin antibodies but not with desmin. The authors propose that, in postcapillary PHT, mechanical stretch due to capillary congestion may be responsible for the generation of cells that express an actin isoform associated with smooth muscle.
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PMID:Modulation of actin isoform expression in alveolar myofibroblasts (contractile interstitial cells) during pulmonary hypertension. 218 26


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