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

Pulmonary hypertension results from many causes: left cardiac failure, increased pulmonary blood flow, proximal vascular obstruction, decrease of the distal vascular bed (by loss of vessels, narrowing of their luminal diameter, or endoluminal obstruction). A part from passive hemodynamic responses, active processes contribute to pulmonary hypertension by vasomotricity and remodeling of the vascular wall. The biopathology of vasomotor mediators, as well as of endothelial and smooth muscle cell interactions just begins to be understood.
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PMID:[Etiology and physiopathology of pulmonary artery hypertensions (PAHT)]. 185 21

Deformability of erythrocytes and hematological parameters in white leghorn and broiler chickens were measured at age 7, 14, 21, 28, and 35 days. For deformability testing, a simple vertical apparatus containing a polycarbonate membrane with 5-microns pores was used. This technique assesses erythrocyte deformability by measuring the filtration time of an erythrocyte suspension through the pores. There was a significant difference in filtration time between the leghorns and broilers at all sampling times. These results indicate that reduced erythrocyte deformability in broilers may be one of the predisposing factors that increase resistance to blood flow and alter the rheology of blood in the microcirculation in the lung. Increased resistance to flow may result in pulmonary hypertension, heart failure, and ascites in broiler chickens.
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PMID:Reduced erythrocyte deformability as a possible contributing factor to pulmonary hypertension and ascites in broiler chickens. 185 19

Twenty five infants with truncus arteriosus underwent complete surgical correction in the first year of life between January 1984 and June 1990 at Marie Lannelongue Hospital. All had cardiac failure and pulmonary hypertension. Another severe cardiac malformation was present in 6 cases. Complete repair was carried out under cardiopulmonary bypass with moderate hypothermia. After closing the ventricular septal defect the continuity of the right ventricle and pulmonary artery was reestablished by a valved Dacron conduit with a bioprosthesis (13 patients), by an autologous pericardial conduit with the same type of prosthesis (5 patients), by a valveless conduit (1 patient) or by direct insertion of the pulmonary artery (6 patients). Eight children (32%) died shortly after surgery. Seventy one per cent of children operated in the first month of life died compared with only 17% of those operated after one month of life (p less than 0.05). The seventeen survivors have been followed up for an average of 21 +/- 22 months. Three secondary deaths were observed at 33 days, 2 and 10 months after surgery: the first child died of left ventricular failure and pulmonary vascular disease related to the complexity of the associated cardiac malformations; the other 2 deaths were unexpected. The one and three year survival rate is 54%. Pulmonary stenosis with a systolic pressure gradient of more than 30 mmHg was found in 7 patients of whom 6 had valved Dacron conduits (p less than 0.01). One child was successfully operated 60 months after the total correction and another child is on the waiting list for reoperation 69 months after the total correction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immediate and mid-term results of complete repair of truncus arteriosus during the first year of life]. 189 4

More than 10 years ago, thrombolytic therapy with urokinase and streptokinase for pulmonary embolism was found to have considerable advantages over standard heparin therapy. After the introduction of alteplase, a recombinant tissue plasminogen activator, further studies confirmed this benefit. However, thrombolytic therapy for pulmonary embolism has not gained universal acceptance, even though it now has U.S. Food and Drug Administration approval. Clear advantages of thrombolytic therapy over conventional heparin therapy are improved pulmonary capillary blood volume, accelerated clot lysis and accelerated pulmonary perfusion. Earlier reversal of right-sided heart failure, a lower incidence of recurrent pulmonary embolism, a reduced risk of chronic pulmonary hypertension and reduced mortality have been claimed as advantages, but these have not been adequately proved. A recent survey suggests that about half of all patients with pulmonary embolism are potential candidates for thrombolytic therapy. In a subset of patients with hemodynamic compromise, thrombolysis has definite advantages over heparin therapy.
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PMID:Thrombolysis for pulmonary embolism. 192 47

Between 1972 and 1987, 43 patients underwent isolated mitral valve replacement with mean pulmonary arterial pressures greater than 50 mmHg. The valve disease was stenosis in 13 cases, regurgitation in 15 cases and mixed mitral valve disease in 15 cases. Forty-one patients (95 %) had invalidating cardiac failure (Stages III and IV of the NYHA Classification). The hospital mortality was 2.3%. Thirteen patients died during follow-up, 8 of cardiac failure, 3 of sudden death and 2 died of non-cardiac causes. The 8 year actuarial survival was 82 +/- 7% with an average postoperative follow-up of 96 +/- 41 months. No patients were lost to follow-up. Eighty six per cent of survivors (25/29) are asymptomatic or paucisymptomatic. Doppler studies were performed in 22 patients, showing normal prosthetic function in 18 cases and an obstructive prosthesis in 4 cases. Seventeen patients had tricuspid regurgitation showing normal pulmonary artery systolic pressures in 9 cases and less than 55 mmHg in 5 cases. On average, systolic pulmonary artery pressure fell from 88 +/- 11 mmHg before to 33 +/- 9 mmHg after surgery (p = 0.01). These results show that severe pulmonary hypertension is not prohibitive for mitral valve replacement. The long-term results are good with functional improvement and reduction of pulmonary hypertension.
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PMID:[Mitral valve replacement in severe pulmonary hypertension. Long-term results]. 195 13

Reports in the literature have suggested that a complex alteration in beta-receptor pathway takes place in failing human myocardium. The purpose of our study was to evaluate the beta-adrenergic receptor system in an experimental model of heart failure induced by monocrotaline in rats. Monocrotaline, administered with a single intraperitoneal injection (50 mg/Kg), causes pulmonary hypertension and right ventricular hypertrophy, associated with congestive heart failure. beta 1 and beta 2-receptors were characterized in the right ventricle by direct radioligand binding utilizing [125I] Iodocyanopindolol and selective beta 1-(CGP 20712A) and beta 2-(ICI 118551) antagonists. Adenylate cyclase was measured in basal condition and in the presence of different stimulators as isoproterenol with ICI 118551 (beta 1-receptor-stimulated activity), isoproterenol with CGP 20712A (beta 2-receptor-stimulated activity), Gpp(NH)p, NaF and forskolin. In the right ventricle of the failing hearts the beta 1-receptor density decreased selectively (-55.8%) while the beta 2-receptor density was unchanged. Modifications in the adenylate cyclase system were demonstrated: a reduction in the basal and beta 1- and beta 2-stimulated adenylate cyclase activity; a decrease in adenylate cyclase activation elicited by Gpp(NH)p, but not by forskolin and NaF. In conclusion, these data suggest that in monocrotaline-induced heart failure in the rat there is a selective beta 1-receptor down-regulation and an impaired coupling efficiency of G proteins. These results are in line with biochemical changes found in patients with heart failure.
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PMID:[The adrenergic beta system in an experimental model of heart failure]. 196 56

In this study three groups of four adult beagle dogs were irradiated with a 12-Gy single dose to the thorax. The fields used were the entire thorax, the entire thorax with a heart block in place, and the heart with one-third of the lung volume. The response of the lung was evaluated by cellular and biochemical analysis of sequential bronchoalveolar lavage fluids, blood gas analysis, physical examination, and histopathology. Sparing a small volume of lung improved survival. Cardiac function was evaluated by right heart catheterization, echocardiography, physical exam, and histopathology. Pulmonary artery pressure was increased in all dogs, mean systemic artery pressure was decreased in all dogs, and no difference could be shown among the groups. These effects are likely secondary to a reduced pulmonary capillary volume. Stroke volume was significantly deceased in dogs that had their hearts included in the field but not in dogs with their hearts shielded. This effect was not thought to be secondary to lung injury. The influence of lung irradiation on cardiac function was limited to pulmonary hypertension. Pulmonary hypertension may be enhanced by the release of vasoactive compounds. Pulmonary hypertension may contribute to radiation-induced heart failure.
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PMID:Early radiation response of the canine heart and lung. 198 99

Primary pulmonary hypertension is a clinical syndrome characterized by pulmonary hypertension in the absence of sufficient underlying cardiac, parenchymal pulmonary, or systemic disease to account for it. The population of patients with primary pulmonary hypertension is a heterogeneous one, both clinically and histologically. As the etiologic mechanisms are unknown, therapy is directed toward the consequences of the pulmonary vascular process. Oxygen supplementation, the use of digoxin and diuretics for symptomatic heart failure, and anticoagulation all may have a role in treating primary pulmonary hypertension, although vasodilator therapy has been the main area of investigation. Screening for vasodilator responsiveness, defining a favorable vasodilator effect, predicting long-term effectiveness, and deciding who to treat have all been controversial. New approaches, such as use of high-dose calcium channel-blocking agents and continuous intravenous infusion of prostacyclin (an investigational agent), have recently been proposed. When medical therapies are exhausted, heart-lung or lung transplantation has increasingly become an option for selected patients.
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PMID:The management of primary pulmonary hypertension. 199 95

A-59-year old woman died from heart failure associated with tricuspid regurgitation and pulmonary hypertension. Necropsy revealed that her tricuspid valve was composed of six leaflets. We found no previous report of this type of tricuspid valve abnormality.
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PMID:A case of congenital tricuspid valve abnormality showing six leaflets. 200 1

The patient responded to treatment at the first onset of heart failure but gradually became irresponsive to treatment, experiencing fatigue and malaise as the chief complaints and suffering from gradually progressive decrease in exercise capacity and body weight. Dose of DOA gradually increased to maintain well clinical state of the patient. Unusual for heart failure, he had bradycardia as the basal rhythm without showing a tendency for tachycardia. Cardiac catheterization revealed pulmonary hypertension and low cardiac output, however, left ventricular ejection fraction was 37%. There were no notable changes in ultrasonic cardiogram or CTR through the clinical course. Tl-201 myocardial images and pulmonary perfusion images showed gradual worsening corresponding to progressive worsening of clinical state. From these findings, the patient was determined as a candidate for heart transplantation.
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PMID:[Tl-201 myocardial images in a patient with dialated cardiomyopathy, who finally received heart transplantation]. 202 Jan 39


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