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

Pulsus alternans of the pulmonary artery without systemic pulsus alternans is uncommon and is associated with multiple diseases. Two cases of pulmonary hypertension with pulmonary arterial pulsus alternans and right-sided heart failure are described. Primary pulmonary hypertension was demonstrated at autopsy in both cases. These two case reports constitute another previously unreported cause for pulsus alternans in the pulmonary circuit.
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PMID:Pulmonary arterial pulsus alternans secondary to primary pulmonary hypertension. 13 88

The abnormalities of the receptor-G protein-adenylyl cyclase (RCG) system in failing human myocardium as the result of 1) idiopathic dilated cardiomyopathy (IDC), 2) ischemic dilated cardiomyopathy (ISCDC), and 3) primary pulmonary hypertension (PPH) were investigated. Depending on the etiology of heart failure, abnormalities of the RCG system result from a reduced number of beta 1 receptors, uncoupling of beta 1 or beta 2 receptors, alteration of G protein function, or decreased catalytic subunit activity of adenylyl cyclase. Compared to IDC, beta 1 receptor down-regulation is less pronounced in ISCDC, and slightly more pronounced in PPH. Preliminary data suggest that beta 1 receptor down-regulation results from alteration in steady-state receptor mRNA levels. Increased functional activity of Gi protein, which seems to result from posttranslational modification, is observed in IDC and ISCDC. Altered Gi protein function may be the basis for beta-receptor uncoupling in IDC and ISCDC, whereas in PPH, this phenomenon may result from altered adenylyl cyclase function. Catalytic subunit activity of adenylyl cyclase is decreased in order of increasing pulmonary hypertension in right-ventricular preparations from PPH greater than IDC greater than ISCDC. However, catalytic subunit activity is similar in LV preparations from all three groups. The decrease in adenylyl cyclase catalytic subunit activity may be the result of the marked cellular injury produced by pressure overload. In summary, numerous desensitization phenomena occur in the failing human heart that are etiology- or model-dependent. To a certain extent, these changes are teleologically beneficial, as they are able to partially protect the failing heart from potentially toxic adrenergic stimuli.
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PMID:Changes in the receptor-G protein-adenylyl cyclase system in heart failure from various types of heart muscle disease. 132 59

The possibilities of the classification developed by Lang, Strazhesko, Vasilenko and that of heart failure functional classes, which has been adopted by the New York Heart Association (NYHA), to evaluate the status of patients with severe heart failure are compared in this communication. A total of 1619 patients with Stages IIB-III heart failure of various origin (coronary heart disease, dilated cardiomyopathy, rheumatic heart disease, myocarditis, primary pulmonary hypertension) were studied. To assess the patients' status the attending physicians used 7 grades: (1) satisfactory; (2) close to moderate; (3) moderate; (4) close to severe; (5) severe; (6) close to critical; (7) critical. Each patient was independently evaluated for grade and functional class by experts by using a specially developed schedule. An analysis of the distribution of the patients by grade and functional class demonstrated that the 4-graded functional class classification has advantages over the 7-graded one due to more settled, reproducible, recurrent and less scattered opinions (in case of the common source of information), the functional class, unlike the grade, was found to be unassociated with the nature of the disease. A simple grade summing-up (regrouping the patients from 7 to 4 grades) unenables one to adequately go over to the NYHA functional class. It is concluded that the tested NYHA classification should be used to evaluate the status of patients with severe heart failure.
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PMID:[Use of functional classes to assess the status of patients with severe heart failure]. 152 34

Four years after an HIV infection and without any preceding illness characteristic of AIDS, a 24-year-old woman developed dyspnoea on exertion and peripheral oedema. She had for several years been an intravenous drug addict and contracted hepatitis A and B. There were no symptoms of the HIV infection. Clinical, radiological and echocardiographic examination demonstrated right ventricular failure caused by pulmonary hypertension not due to pulmonary embolism or another known aetiology. The patient died suddenly 9 months after the diagnosis from heart failure. Autopsy established primary pulmonary hypertension with pathognomonic plexogenic pulmonary arterial disease which had led to cor pulmonale with overload myocarditis. Although there had been no clinical signs of renal failure, there was histological evidence of mesangioproliferative glomerulonephritis and non-destructive interstitial nephritis. This case demonstrates that, in addition to the typical AIDS-associated diseases, other rarer syndromes may, in uncertain ways but connected with the HIV infection, decide the prognosis of such patients.
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PMID:[Primary pulmonary hypertension and mesangioproliferative glomerulonephritis in HIV infection]. 158 15

Primary pulmonary hypertension (PPH) is a rare disease, which almost inevitably leads to right-sided heart failure and death. This is to our knowledge the first report of ophthalmological complications. A 43-year-old woman in the late stage of PPH who had been continuously treated with oxygen developed an uveal effusion syndrome, which manifested as bilateral central serous retinal detachment and ciliochoroidal swelling. The serous detachment improved promptly after interruption of the oxygen therapy and again worsened when it was resumed because of massive dyspnea. Systemic blood pressure was 115/95. Right-sided cardiac catheterization revealed a systolic pulmonary arterial pressure of 110 mmHg. Pulmonary function tests showed a normal PO2 with oxygen and a light hypoxia without therapy. We came to the following conclusions: First, the central serous retinal detachment and peripheral choroidal swelling were induced by the striking increase in pulmonary arterial pressure, which almost equaled the systemic arterial pressure. Although the same ophthalmological findings have been reported in experimental animals after exposure to pure oxygen, pulmonary function tests disproved high oxygen concentration as the causative agent in our patient. Second, the improvement of pigment epithelial function after the interruption of oxygen therapy could be explained by the following hypotheses. Hypoxia induced a dilation of the choroidal arteries, followed by an improved supply of nutritive material for the pigment epithelium. There is experimental evidence that glucose might be the limiting metabolite of pigment epithelial function.
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PMID:[Serous retinal detachment in O2 therapy of primary pulmonary hypertension]. 178 18

Familial primary pulmonary hypertension was found in two siblings (sister and brother). The woman noted exertional dyspnea at the age of 28 yr. The younger brother noticed exertional dyspnea, cough with bloody sputum and pretibial edema at the age of 38 yr. We diagnosed them as primary pulmonary hypertension as based on hemodynamic and histopathological findings. Regardless of the treatment, both patients died of right-sided heart failure with a short time course. We examined their family members, but there were no other members with primary pulmonary hypertension.
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PMID:Familial primary pulmonary hypertension--report of two siblings. 183 76

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

Four young horses of various breeds and suffering from atrial fibrillation died of heart failure. All had markedly high pulmonary arterial pressure, right-sided cardiomegaly, and lack of histologic lesions in the right atrium or pulmonary parenchyma. Three horses had hypertrophy and/or necrosis of the tunica media of the pulmonary vasculature. Clinical signs of disease, physiologic data, and pathologic findings indicated that these horses had primary pulmonary hypertension with secondary right-sided cardiac ventricular hypertrophy and dilatation, atrial fibrillation, and heart failure.
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PMID:Pulmonary hypertension as a cause of atrial fibrillation in young horses: four cases (1980-1989). 201 43

Since Shumway carried out the first successful heart-lung transplant (HLT) in Stanford in 1981, HLT has become a new therapeutic means for patients with end-stage pulmonary disease or arterial hypertension. However, it is still rarely carried out because of a lack of donors and the complexity of the surgery and postoperative course. This review described the criteria for proper donor and recipient selection, as well as the anaesthetic and postoperative management of HLT patients at Marie Lannelongue Hospital. The lack of suitable organ grafts results, at least in part, from improper donor management. Pulmonary oedema by fluid overloading and excessive haemodilution should be carefully prevented. Low doses of catecholamines and vasopressin maintain circulatory stability and convenient organ function. The indications for HLT (primary pulmonary hypertension, Eisenmenger's complex, and end-stage bronchopulmonary disease) are all characterized by severe pulmonary hypertension, hypoxaemia and cardiac failure. Careful anaesthetic induction is required to avoid circulatory collapse. Cardiopulmonary bypass (CPB) should be started early, so that mediastinal dissection may be carried out in satisfactory haemodynamic conditions. After unclamping the aorta, circulatory support with fluid and catecholamine infusion is often required. High inspired oxygen fraction and end-expiratory positive pressure may be required because of reperfusion pulmonary oedema. Blood transfusion is often needed as there are major blood losses due to dissection of the posterior mediastinum during CPB. Postoperative catecholamine administration is prolonged over several days. Negative fluid balance is often necessary to reduce pulmonary oedema. Improvement in surgical technique, early extubation, and late prescription of steroids have reduced the incidence of tracheal complications. Acute renal failure often occurs as a result of prolonged CPB, hypovolaemia, drug nephrotoxicity and sepsis. Bacterial complications (pneumonia, mediastinitis) are the main causes of early death. After the 15th postoperative day, opportunistic infections and allograft rejection are the main complications. Since 1981, major advances in HLT recipient management resulted in improved survival rates (70-80% at 1 year, and 60-70% at 2 years for the best teams). Despite the complexity of management, and the longterm threat of obliterative bronchiolitis, HLT is, at present time, the only possibility for these young patients to recover a normal quality of life.
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PMID:[Anesthesia and intensive care for heart-lung transplantation]. 205 32

Clinical experience with long-term nifedipine treatment in 23 patients aged between 1 1/12 and 14 8/12 years is reported. The cardiopulmonary diseases comprised primary pulmonary diseases with pulmonary hypertension (n = 4), congenital heart defects with intracardiac shunts and pulmonary hypertension which either were inoperable as a result of an Eisenmenger reaction (n = 7) or presented a high surgical risk (n = 5), or defects in which pulmonary hypertension did not regress despite corrective (n = 1) or palliative surgery (n = 3), and congenital defects without pulmonary hypertension (n = 3). Subjective improvement with an increase in physical performance was clearly observed in 15 cases. Echocardiography and cardiac catheter examinations showed no progression of the pulmonary arterial diseases, except in 1 patient with severe primary pulmonary hypertension and an 11-year observation period with nifedipine treatment during the last 4 years. No complications occurred during the 4 corrective operations. A patient aged 14 8/12 years with the Down syndrome and atrioventricular septal defect developed easily controllable heart failure during 7-day administration of nifedipine without additional cardiotherapy. 4 children initially suffered from flushed face and scalp, in one case with headache; 2 children reported fatigue. Long-term treatment with nifedipine should begin with strict 7-day supervision in hospital and possibly additional digitalization. Success of the treatment was determined by an improved quality of life in patients with primary pulmonary hypertension and inoperable defects, and by a reduced perioperative risk and postoperative regression of pulmonary hypertension in patients with operable defects.
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PMID:Experience with long-term nifedipine therapy in paediatric cardiological patients. 211 16


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