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

A survey is presented on the results of 100 consecutive patients who underwent mitral valve (78 patients) or mitral and aortic and/or tricuspid valve replacement (22 patients) with ball or disc valve prosthesis. The patients were followed-up from 6 to 54 months postoperatively. The mortality for mitral valve replacement was 13 (17%) early deaths (up to one month from operation) and 5 (6%) late deaths. The corresponding figures for multiple valve replacements were 9 (41%) and 3 (14%). A direct correlation was found between early mortality and preoperative functional class IV of the New York Heart Association (30% dead). Pulmonary hypertension combined with multiple valve disease resulted in an early mortality of 42%. No significant differences in early mortality figures after MVR were found between ball and disc valve prostheses. Predominant complications were respiratory infection and atelectasis (13%), acute myocardial infarction (11%) and haemorrhage (9%). Haemolysis was found in 9 patients and three other patients had haemolytic anaemia attributable to paravalvular leak which in two indicated the reapplication of the prosthesis. The main causes of death were heart failure, 8 early and 4 late deaths, and myocardial infarction, 5 and 4 respectively.
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PMID:Mitral valve replacement with ball and tilting disc valve prosthesis. A clinical and haemodynamic study. 127 55

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

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

A rapidly growing body of data supports the concept of in situ regulation of vascular tone: the ability of vasoactive substances to regulate vascular tone at their site of production within the wall of the vasculature. Sufficient data exist to suggest that ineffective production or response to endothelium-dependent vasodilator substances, or excessive production or responsiveness to endothelium-dependent vasoconstrictor substances may play an important role in cardiovascular disorders such as hypertension, coronary artery spasm, restenosis following coronary angioplasty, and congestive heart failure. The present review summarizes data which support the concept that endothelin, a potent vasoconstrictor produced by the endothelium, may play a role in the excessive vasoconstriction of heart failure. Increased circulating plasma endothelin may be particularly relevant to the range of pulmonary vasoconstriction encountered in congestive heart failure, with a correlation revealing that the greatest increase of plasma endothelin occurs in patients with marked pulmonary hypertension within the congestive heart failure patients studied.
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PMID:The potential role of endothelin as a vasoconstrictor substance in congestive heart failure. 146 46

Extracorporeal membrane oxygenation (ECMO) has been used at the Prince of Wales Children's Hospital, Sydney for the treatment of newborn infants with life-threatening respiratory or cardiac failure since August 1989. The main indications are that the disease is reversible, the surviving infant is likely to be normal and there is an 80% likelihood of death without ECMO. Eighteen of 19 newborn infants have survived at least 2 months after ECMO. The 15 infants receiving ECMO (nine with meconium aspiration, six with persisting pulmonary hypertension) who did not have a congenital diaphragmatic hernia were normal survivors. One death occurred at 5 months of age from chronic lung disease. Three of four infants with congenital diaphragmatic hernia were discharged following ECMO and appeared normal at 6, 9 and 18 months of age. These results are similar to results from other centres internationally. It appears that ECMO is a useful therapy for near-term newborn infants with otherwise fatal cardiorespiratory failure.
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PMID:ECMO in newborn infants: the New South Wales experience. 146 36

Non-invasive measurements of right and left ventricular ejection fraction (RVEF, LVEF) by multiple-gated equilibrium radionuclide ventriculography were performed in 19 control subjects, 55 patients with COPD and cor pulmonale, simultaneous right heart catheterizations were performed in 10 patients with cor pulmonale to determine the mean pulmonary artery pressure (mPAP), and then, the acute hemodynamic and functional effects of nifedipine were evaluated. The mean RVEFs are different significantly among the various groups. With the development of the diseases, the RVEFs reduce gradually. The mean LVEF reduces significantly in cor pulmonale patients with heart failure. The RVEF correlated negatively to mPAP (r = -0.7047, P < 0.01). After nifedipine (20mg), the RVEF and mPAP do not change significantly (P > 0.05), but the artery blood pressure reduces significantly. We conclude that the equilibrium radionuclide ventriculography may be a useful and accurate method in diagnosing early cor pulmonale and cor pulmonale with right heart failure, and nifedipine may not be a good vasodilator for pulmonary hypertension.
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PMID:[Measurement of right and left heart function of COPD and cor pulmonale by radionuclide ventriculography]. 147 86

Patients with chronic heart failure frequently have pulmonary hypertension. Because severe preoperative pulmonary hypertension predicts a poor outcome after orthotopic transplantation, pulmonary vasoreactivity is evaluated frequently in the pretransplantation screening of heart failure patients. We prospectively evaluated the utility of the direct pulmonary vasodilator, prostaglandin E1, and compared it to the nonspecific vasodilators, nitroglycerin and sodium nitroprusside, in the evaluation of pulmonary hypertension in 39 heart transplantation candidates. Prostaglandin E1 significantly lowered pulmonary artery pressure, transpulmonary pressure gradient, and pulmonary vascular resistance. An adequate pulmonary vasodilator response (defined as a decline in transpulmonary pressure gradient to less than 15 mm Hg) occurred in 31 patients (79%). In a subgroup of nine patients also tested with nitroglycerin, greater reductions (p less than 0.01) in both transpulmonary pressure gradient and pulmonary vascular resistance occurred with prostaglandin E1, compared to nitroglycerin. Five of six patients who did not respond to nitroglycerin responded to prostaglandin E1. In another subgroup of 12 patients who were also evaluated with sodium nitroprusside, prostaglandin E1 produced a larger decline (p less than 0.05) in transpulmonary pressure gradient and pulmonary vascular resistance than did sodium nitroprusside. Six of eight patients who did not respond to sodium nitroprusside responded to prostaglandin E1. Based on pulmonary vasodilator response to prostaglandin E1, 27 patients were accepted on the transplantation waiting list, and eight patients underwent orthotopic transplantation. Postoperatively, acute right ventricular failure of the donor heart developed in none of these patients. Significant hemodynamic improvement occurred by 24 hours and persisted through 4 weeks of postoperative follow-up in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Utility of prostaglandin E1 in the pretransplantation evaluation of heart failure patients with significant pulmonary hypertension. 824 Dec 36

Aortic valve lesions in progressive systemic sclerosis (PSS) are very uncommon. To our knowledge, aortic regurgitation (AR) associated with PSS has not been reported previously. We would like to report the case of a 58-year-old woman who had PSS with AR due to Raynaud's symptom, fever, positive ANA, accelerated ESR, and diastolic blowing murmur along the left sternal border. After treatment with adreno-cortico steroid and an immunosuppressive agent, the patient improved serologically and symptomatically. However, she was later admitted to our hospital again due to heart failure with progressive AR. She died of refractory heart failure with severe AR and tricuspid regurgitation (TR). The former was caused by aortic cusp lesions and the latter by pulmonary hypertension. An autopsy confirmed the diagnosis of PSS, which was found to have involved the heart, lungs and pancreas. Vasculitis with infiltration and fibrotic changes were noted in these organs. Moreover, there were fibrotic thickenings and shortenings in the aortic cusps with cell infiltration. There were no indications of rheumatic disease. These results suggest that the cause of our patient's aortic valve disease may have been PSS vasculitis.
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PMID:[Report of a case with aortic regurgitation in progressive systemic sclerosis]. 151 78

Obstructive sleep apnea may contribute to the development of pulmonary hypertension and RVF primarily through pulmonary vasoconstriction secondary to hypoxia. Several recent studies indicate, however, that intermittent apnea-related hypoxia is not sufficient to cause sustained pulmonary hypertension. These studies have been consistent in showing that pulmonary hypertension and RVF are almost invariably seen in the presence of diurnal hypoxia. Sustained pulmonary hypertension, therefore, appears to be associated with sustained hypoxia as is the case in COPD. Patients with OSA who have hypoxia while awake are, as a rule, obese and have mild-to-moderate diffuse obstructive airways disease. Thus, most cases of pulmonary hypertension in association with OSA result from a combination of OSA, obesity, and diffuse obstructive airways disease, a so-called overlap syndrome. However, from the therapeutic viewpoint, it is apparent that treatment of OSA by NCPAP or tracheostomy, in such cases, is usually sufficient to reverse pulmonary hypertension and RVF. More recent work has provided strong evidence that OSA can play a role in the pathogenesis of LV heart failure in patients with CHF of otherwise unknown etiology. It is likely that this occurs through a combination of increased LV afterload related to exaggerated negative Pit swings during obstructive apneas, to intermittent hypoxia, and to chronically elevated sympathoadrenal activity. Reversal of OSA by NCPAP in these patients may relieve LV heart failure. These findings add a new dimension to our understanding of the pathophysiologic effects of OSA on the cardiovascular system by demonstrating that the LV is a structure that may suffer functional impairment secondary to the stresses imposed by OSA. Finally, it has now become apparent that CSR in patients with CHF can cause symptoms of a sleep apnea syndrome when associated with intermittent hypoxia and arousals from sleep. Reversal of CSR during sleep by NCPAP can lead to alleviation of these symptoms and possibly to reduced cardiac dyspnea and LV systolic function as well. Taken together, this suggests that much more extensive use of polysomnography may be warranted in the investigation of cardiovascular disease. The reasons are compelling: sleep apnea disorders are common and eminently treatable conditions whose reversal can result in improved right and left heart function and symptomatic improvement in patients with impaired myocardial function.
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PMID:Right and left ventricular functional impairment and sleep apnea. 152 13


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