Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 expression of the Na,K-ATPase was studied in both normal and failing human myocardium which was collected within 5 min of cardiac explantation in preparation for orthotopic transplantation or at the time of organ harvest. Abundance of mRNA for all three catalytic alpha subunits of the Na,K-ATPase was analyzed in samples from patients with end-stage heart failure due to either ischemic or dilated cardiomyopathy, as well as from normal controls. Vanadate facilitated 3H-ouabain binding before and after a Digibind wash was analyzed on tissue from a subset of these patients. mRNA analysis demonstrated that all three catalytic Na,K-ATPase alpha subunits were expressed in human heart and that there was no evidence for change in relative expression or abundance induced by disease. The specific digitalis receptor concentration was 760 +/- 58 and 614 +/- 47 pmol/g wet weight in the samples from normal and failing hearts, respectively (p = NS). From these studies it can be concluded that, whereas there is a tendency for a decrease in the number of ouabain receptors in heart failure, there is no significant alteration in the expression of Na,K-ATPase message or protein caused by chronic heart failure.
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PMID:Na,K-ATPase expression in normal and failing human left ventricle. 132 67

In 100 patients 12 to 60 months after cardiac transplantation, the influence of transplant coronary vasculopathy and of the pretransplantation disease (end-stage heart failure caused by coronary artery disease or dilated cardiomyopathy) on the beta-adrenergic receptor (AR) numbers and beta 1/beta 2-AR ratio of right ventricular biopsies was determined. Patients with coronary vasculopathy (CVP) after cardiac transplantation had lower absolute numbers of beta 1-AR compared with patients without CVP. Since patients with CVP had increased left ventricular (LV) end-diastolic pressure and LV muscle mass, it is suggested that decreased beta 1-AR may be the result of an altered hemodynamic situation of the transplanted heart after development of CVP. Patients with dilated cardiomyopathy (DCM) before cardiac transplantation showed a decrease in total beta-AR and of the beta 1/beta 2-AR ratio as a result of an increase in beta 2-AR and a decrease in beta 1-AR numbers. The decreased beta 1/beta 2-AR ratio in patients with previous DCM may indicate that the beta-AR system of the transplanted heart might be influenced (at least in part) by pathophysiologic factors that are characteristic of the pretransplantation disease ultimately leading to cardiac transplantation and persisting after cardiac transplantation.
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PMID:Changes in cardiac beta 1- and beta 2-adrenoceptor densities after human cardiac transplantation: relation to transplant coronary vasculopathy and pretransplantation disease. 132 8

To explore the possible relationship between acute viral myocarditis and dilated cardiomyopathy (DCM), 35 acute diffuse viral myocarditis (ADVM) patients with cardiac enlargement were studied for 6 years on average. The results showed that: (1) In 22 ADVM patients, the dilated hearts had returned to normal on X-ray films. The other 13 cases still had cardiac enlargement complicated with various degrees of cardiac insufficiency (NYHA II/III) and ECG abnormalities. The manifestation of these 13 patients resembled those seen in the early stage of DCM. (2) Serum neutralizing antibody titres of Coxsackie B virus (CBV) in 35 ADVM patients after 6 years observation on average were significantly higher than those cases with cardiac enlargement induced by other causes (P less than 0.01). High neutralizing antibody titres (greater than or equal to 320) to CBV were more common among the patients with ADVM 65.7% vs 25.7% (P less than 0.05). The results indicate that some cases of ADVM might develop into DCM.
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PMID:[Possible relationship between acute viral myocarditis and dilated cardiomyopathy]. 132 6

This report is on three double aortic arch cases. They were diagnosed in our department between 1982 and 1992. The first case was complicated by dilated cardiomyopathy whose diagnosis was delayed due to a lack of clinical experience. Corrective surgery relieved the airway obstruction and his breathing improved postoperatively. The patient finally died of heart failure due to concurrent progressive dilated cardiomyopathy one and half years later. The second and third cases were diagnosed on the day of admission by a barium esophagogram and echocardiogram. MRI (Magnetic resonance image) of the cardiovascular system on these two patients revealed no other associated abnormalities. No angiography was done on the third case. They underwent surgery with excellent results. In any infant younger than 3 months with dyspnea and dysphagia, double aortic arch should be suspected. The esophagogram can show extrinsic compression. An echocardiogram can reveal two aortic arches. Both procedures can be performed easily and safely at the bedside. We recommend that these to be considered as routine examinations in such patients.
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PMID:[Double aortic arch-three cases report and operative treatment]. 133 31

Idiopathic dilated cardiomyopathy (IDCM) is a primary myocardial disease of unknown cause. We tested the hypothesis that IDCM was associated with a myocardial metabolic defect by determining a comprehensive biochemical profile of metabolite concentrations and enzyme activities for the major metabolic pathways of the myocardium. We used the Doberman pinscher breed as a naturally occurring canine model of IDCM and compared its myocardial profile with that of healthy adult mongrels. Compared with controls, myocardium in IDCM had markedly reduced mitochondrial electron transport activity and myoglobin concentration, in association with acidosis and energy depletion following anoxic challenge: 60% decreased NADH dehydrogenase and 50% decreased ATP synthetase activities; 90% decreased myoglobin concentration; and 30% reduced ATP and 50% increased lactate and proton concentrations. Sarcoplasmic reticulum Ca(2+)-transport ATPase was decreased by 42%. There was a 15% compensatory increase in fatty acid oxidation and Krebs cycle activity. Other biochemical changes were mild by comparison with the mitochondrial defects. We conclude that IDCM is associated with a marked impairment of mitochondrial production of ATP, arising from decreased activity of the mitochondrial electron transport system, including myoglobin. These changes may be secondary to an underlying genetic defect or may indicate a deficiency of the mitochondrial respiratory chain that predisposes this breed to heart failure.
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PMID:Respiratory chain defect of myocardial mitochondria in idiopathic dilated cardiomyopathy of Doberman pinscher dogs. 133 76

Patients with different heart diseases, dilated cardiomyopathy, valvular heart disease, hypertension, ischemic heart disease or myocarditis showed manifestations of autoimmunity and down-regulation of beta-adrenergic receptors. Autoantibodies against beta-adrenergic receptors in these patients were detected with radioligand binding inhibition assay. The results suggested that the down-regulation of cardiac beta-adrenergic receptors in these patients may be mediated by autoimmunity. Autoantibodies against beta-adrenergic receptor were not related to any specific heart diseases, but to the severity of heart failure irrespective of its etiology. The significance of these autoantibodies in heart failure was discussed.
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PMID:[Circulating autoantibodies against beta-adrenergic receptors in patients with heart diseases]. 133 2

A long-term follow-up study was performed for 110 patients with idiopathic dilated cardiomyopathy (DCM) for 34 +/- 12 months (range 3-122 months). Thirteen patients died of heart failure, 15 of sudden death and one of non-cardiac death. The 3- and 5-year survival rates were 78 and 62%, respectively. The important factors in predicting the 3-year survival rate were left ventricular end-diastolic volume index (LVEDVI > or = 150 ml/m2 = 66%, < 150 ml/m2 = 93%, p < 0.01), myocardial cell diameter (> 25 microns = 42%, < or = 25 microns = 87%, p < 0.05) and sustained ventricular tachycardia (VT present = 32%, absent = 85%, p < 0.01). In a prospective study, 26 patients with DCM were given a beta 1-partial agonist, xamoterol (200 mg daily) and were followed for 35 +/- 15 months (6-53 months). The cardiothoracic ratio, left ventricular end-diastolic dimension and exercise heart rate decreased, and the exercise duration, fractional shortening and ejection fraction increased after xamoterol therapy. The 3-year survival rate was 83%. These results suggest that the important factors in predicting the survival rate of DCM patients were LVEDVI, myocardial cell diameter and the occurrence of VT. Adjunctive xamoterol therapy in DCM had a beneficial effect on hemodynamics and symptoms.
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PMID:Risk factors and the effects of xamoterol in idiopathic dilated cardiomyopathy. 133

The case of a 19-year-old young man with clinical picture of congestive heart failure and supraventricular tachycardia is reported. Heart failure got better with conventional treatment, but the tachycardia persisted in spite of antiarrhythmic drugs. Echocardiogram showed dilated cardiomyopathy of important degree and the endomyocardial biopsy, mild interstitial infiltration. Scintigraphy with gallium 67 was normal. Twenty days after the patient leaving the hospital, suffered sudden death. It is discussed the hypothesis that patient had developed a tachycardiomyopathy secondary to the incessant tachycardia. The importance of the diagnosis is reinforced by possibility of reversion of the cardiomyopathy by the resection of the anomalous pathway.
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PMID:[Sudden death and tachycardiomyopathy in a young man with incessant tachycardia]. 134 Jul

In this study, the acute hemodynamic effects of pimobendan (2.5 mg), a new drug, was compared with that of captopril (12.5 mg) in the same 8 patients with chronic heart failure (NYHA class II-III); 3 with dilated cardiomyopathy and 5 with regurgitant valvular heart disease. The hemodynamics were serially assessed before and after drug administration for at most 6 hours. Pimobendan reduced mean blood pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure, right atrial pressure, total systemic vascular resistance, and total pulmonary vascular resistance but it increased heart rate. By contrast, captopril reduced mean blood pressure and double product. No significant changes were noted in the cardiac index, stroke volume index, AV-O2 difference or the arterial oxygen pressure between the 2 drugs. In conclusion, pimobendan seems to function as a strong arterio-veno-dilator rather than as an inotropic agent in patients with chronic heart failure.
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PMID:[Acute hemodynamic effects of pimobendan and captopril: a comparative study in the same patients with chronic heart failure]. 134 39


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