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

Previous studies showed increased growth hormone (GH) plasma levels in patients with severe heart failure. It has been hypothesized that the activation of adenohypophysis determines the enhanced release of GH. The present study was designed to verify whether impaired hepatic function, due to biventricular cardiac failure and hepatic stasis, by reducing synthesis and release of insulin-like growth factor-1 (IGF-1), may affect the negative feedback mechanism of the IGF-1 on GH secretion. We studied 20 normotensive, non diabetic patients without primitive liver disease; 10 patients in NYHA functional class IV with clinical signs of biventricular cardiac impairment and hepatic stasis (Group A); 10 patients in NYHA functional class III with prevalent left ventricular dysfunction (Group B). Blood samples for radioimmunologic determination of GH, IGF-1, atrial natriuretic factor (ANF), proteins, albumin plasma levels and transaminase plasma levels measurements, were collected 24 hours before hemodynamic study. Group A patients had clinical and hemodynamic signs of hepatic stasis with impaired liver function (SGOT 68 +/- 5.5 U/l; SGPT 89 +/- 4.3 U/1; proteins 4.56 +/- 0.4 g/dl with albumin/globulin ratio < 1; albumin plasma levels 2.8 +/- 0.7 g/dl). The parameters were normal in Group B (SGOT 16 +/- 3.7 U/l;SGPT 13 +/- 1.9 U/l; proteins 7.5 +/- 0.7 g/dl with albumin/globulin ratio > or = 1.5;albumin plasma levels 4.2 +/- 1.2 g/dl). ANF values, over normal range in both groups, were significantly higher in Group A (157.9 +/- 43.9 vs 65.6 +/- 14.6 fmol/ml.p < 0.0001). In Group A GH values were increased (4.9 +/- 4.5 vs 0.12 +/- 0.04 ng/ml); on the contrary IGF-1 values were lower (187.9 +/- 98.2 vs 260.4 +/- 141.4 ng/ml, p < 0.01). The comparison between IGF-1 and albumin plasma levels showed a high correlation either in Group A (r = 0.88, p < 0.001;) or in Group B (r = 0.81, p < 0.001). Our findings allow to hypothesize that the reduced hepatic synthesis and release of IGF-1 may be responsible for the lack of trophic action of GH on cardiac myocytes in patients with biventricular heart failure and hepatic stasis.
 ...
PMID:[Changes in growth hormone/insulin-like growth factor-1 axis in patients with normal pituitary function and biventricular cardiac failure and hepatic stasis]. 876 34

The two primary goals of mechanical circulatory support are to provide adequate perfusion of the vital organs and to decrease cardiac work. The support of the myocardium is in an effort to cause a reversal of cardiac damage. The recovery process apparently takes place in two stages. Initially, there is a rapid functional recovery of cells in marginally ischemia areas. Then there is a slower process of hypertrophy of normal and recovering myofibers. The process involves the reversal of interstitial and of intercellular myocardial edema in areas of viable myocardium while halting the extension of necrosis into reversibly ischemic areas. It appears that this process is extended from 3 to 5 days, and functional recovery can occur for up to 2 weeks. After a 2-week period, there appears to be little functional recovery of myocardial cells. In autopsy series of nonsurvivors, it appears that most of the patients had suffered from biventricular failure. Biventricular failure appears to be one of the more common complications of the support patient. Right ventricular failure will be attempted to be supported by right ventricular assist devices. The right ventricular assist device, unfortunately, adds a level of complication to the recovery process for the bridge-to-transplant or cardiomyopathy patient. The patients who are involved in support fall into three categories: (1) the bridge-to-transplant patient, (2) the patient recovering from postcardiotomy, and (3) the patient who recovers from an acute myocardial insult. It appears that after 2 weeks the recovery period for all of these groups demonstrates no further functional recovery. The bridge-to-transplant patients usually need to be supported until the transplant occurs. The postcardiotomy patient and the acute myocardial failure patient are the most disappointing support group, since they have a higher morbidity and mortality, and a lower chance of recovery. Salvage rates appear to be in approximately the 25% range in the acute insult category.
 ...
PMID:Cardiac assist devices. 879 47

The direct toxic effect of alcohol and its metabolite acetaldehyde has been demonstrated both in laboratory animals and in humans. Alterations in the mitochondrial ultrastructure and the dilatation of the sarcoplasmatic reticulum have been shown after an acute infusion of alcohol in the heart. These changes correlate with decreased mitochondrial function, defects in protein synthesis and the occurrence of arrhythmias. The risk of developing alcoholic cardiomyopathy is related to both the mean daily alcohol intake and the duration of drinking, but there is much individual susceptibility to the toxic effect of alcohol. Most patients, in whom alcoholic cardiomyopathy develops, have been drinking over 80 g/d for more than 5 years. The clinical diagnosis of alcoholic cardiomyopathy reflects the coexistence of global myocardial dysfunction in a heavy drinker in whom no other cause for myocardial disease was found. In studies focussing on alcoholic cardiomyopathy the surprising histologic findings in endomyocardial biopsy in about 30% of all cases was myocarditis with a lymphocytic infiltrate in association with myocyte degeneration or focal necrosis. In myocarditis, the network of microtubules and intermediate filaments is also disrupted by the inflammatory reaction which involves resident cells (myocytes, fibroblasts, endothel cells) and systemic cells (granulocytes, macrophages, monocytes, lymphocytes). Changes in the cardiac cytoskeleton and the extracellular matrix may affect contractile function, since the cytoskeleton organizes the intra- and intercellular architecture. After all, in patients with alcohol abuse and myocarditis the immune functioning appears to be compromised. Several studies suggest that heavy drinking alters both lymphocyte and granulocyte production and function. Alcohol consumption per se might harm the immune system. Furthermore, the myocardial damage due to alcohol consumption could initiate autoreactive mechanisms comparable to those in viral or idiopathic myocarditis. Patients with alcohol abuse and myocarditis have a poor prognosis: signs of biventricular failure including tachycardia, hepatomegaly, and peripheral and lung edema are observed. These symptoms are as nonspecific as are various echocardiographic and electrocardiographic changes such as atrial and ventricular arrhythmias which may be associated both with myocarditis, alcoholic cardiomyopathy and acute effects of drinking without hemodynamic alterations. For the management of patients with alcohol abuse the prevention of further alcohol intake is mandatory to reverse the myocardial damage and the unfavorable predisposition for infection. Specific treatment of myocarditis is the second important option, and treatment of heart failure by reducing the size of the dilated heart and alleviating the signs and symptoms of heart failure is a logical third step.
 ...
PMID:[Alcohol and myocarditis]. 880 5

A 73-yr-old woman with a 4 yr history of rheumatoid arthritis presented with the clinical features of congestive cardiac failure. She had a good early response to standard therapy although she subsequently developed recurrent biventricular failure. The preservation of good ventricular function on echocardiography in the face of clinical evidence of myocardial insufficiency raised the possibility of constrictive pericarditis, which was confirmed on cardiac catheterization. Constrictive pericarditis should be considered in patients with rheumatoid arthritis who develop unexplained cardiac failure. Early diagnosis requires a high index of suspicion and cardiac catheterization may be necessary to confirm the diagnosis. Medical treatment is largely ineffective and pericardiectomy should be considered.
 ...
PMID:Rheumatoid constrictive pericarditis. 911 46

The amount and location of intra- and extravascular fluids varies for the type and duration of heart failure. In some instances (acute LHF) pulmonary and systemic blood volume actually diminishes, and in others (chronic LHF) pulmonary blood volume diminishes at the bases while increasing in the upper lobes. It is only in right heart failure that clinically visible "congestion" occurs and the phrase congestive failure should be reserved for right heart failure. It is more valuable clinically for the film reader to analyze which compartments contain increased or diminished fluid and from this analysis, to decide whether the patient is in left, right or biventricular failure and whether this is acute or chronic. Upper lobe engorgement, (flow inversion) is not caused by basal edema, as previously hypothesized, but by reflex vasoconstriction secondary to chronic elevation of left atrial pressure. The mechanism is designed to improve left atrial function.
 ...
PMID:What is "congested" in cardiac failure? A newer approach to plain film interpretation of cardiac failure. 914 17

The critical cell signals that trigger cardiac hypertrophy and regulate the transition to heart failure are not known. To determine the role of Galphaq-mediated signaling pathways in these events, transgenic mice were constructed that overexpressed wild-type Galphaq in the heart using the alpha-myosin heavy chain promoter. Two-fold overexpression of Galphaq showed no detectable effects, whereas 4-fold overexpression resulted in increased heart weight and myocyte size along with marked increases in atrial naturietic factor ( approximately 55-fold), beta-myosin heavy chain ( approximately 8-fold), and alpha-skeletal actin ( approximately 8-fold) expression, and decreased ( approximately 3-fold) beta-adrenergic receptor-stimulated adenylyl cyclase activity. All of these signals have been considered markers of hypertrophy or failure in other experimental systems or human heart failure. Echocardiography and in vivo cardiac hemodynamic studies indeed revealed impaired intrinsic contractility manifested as decreased fractional shortening (19 +/- 2% vs. 41 +/- 3%), dP/dt max, a negative force-frequency response, an altered Starling relationship, and blunted contractile responses to the beta-adrenergic agonist dobutamine. At higher levels of Galphaq overexpression, frank cardiac decompensation occurred in 3 of 6 animals with development of biventricular failure, pulmonary congestion, and death. The element within the pathway that appeared to be critical for these events was activation of protein kinase Cepsilon. Interestingly, mitogen-activated protein kinase, which is postulated by some to be important in the hypertrophy program, was not activated. The Galphaq overexpressor exhibits a biochemical and physiologic phenotype resembling both the compensated and decompensated phases of human cardiac hypertrophy and suggests a common mechanism for their pathogenesis.
 ...
PMID:Transgenic Galphaq overexpression induces cardiac contractile failure in mice. 922 25

Perivalvular leaks following prosthetic valve replacement are associated with significant morbidity. Management has classically consisted of valve replacement or blind surgical repair. Our study examines the results of intraoperative transesophageal echo-guided repair of perivalvular leaks (ITEGR). Between November 24, 1987 and January 1st, 1996, 23 patients (10 men, 13 women) at the Montreal Heart Institute underwent ITEGR. Ninety percent were NYHA class III-IV preoperatively. Seventy to 85% had significant cardiac insufficiency preoperatively. Eighty-six percent of the leaks were in the mitral valve location, 90% of which were mechanic prosthesis. Eighty-nine percent of patients had hemolysis with an average LDH of 720. Mean bypass time was 125 minutes with a mean clamp time of 77 minutes. Most patients were undergoing a third operation at the time of repair. Operative mortality was 8%, all due to biventricular failure. A mean follow-up of 67 months showed a late death of 10%. Of the 19 survivors, 77% were NYHA class I-II. Overall mortality was 20%. In our institution valve re-replacement in similar circumstances was associated with an operative and long-term mortality of 7% and 26% respectively. We conclude that intraoperative transesophageal echo-guided repair is an excellent management alternative in patients with perivalvular leaks with decreased late and overall mortality.
 ...
PMID:[Clinical results of peroperative transesophageal echography in peri-valvular leaks of heart prosthesis]. 973 99

Left dominant biventricular failure is a common type of heart failure after cardiac surgery. We developed a biventricular bypass (BVB) system for treatment of postcardiotomy ventricular failure, and we previously reported that the clinical results of the BVB system were superior to those obtained with venoarterial bypass (VAB). The purpose of this study was to evaluate the effect of the BVB system on left ventricular (LV) performance in comparison to that of VAB by means of the LV pressure-volume relationship (PVR). Eight adult mongrel dogs (14-21 kg) underwent VAB with right atrial and aortic cannulation. Left atrial cannulation was added for BVB, and both atrial drainage tubes were joined with a Y-shaped connector. The bypass flow was maintained at half of the baseline cardiac output (0.7-1.0 L/min), and the hemodynamic parameters were monitored. A high fidelity microtip catheter and a conductance catheter were used to evaluate LV function. The slope of the LV end-systolic pressure-volume relation (Emax), the slope of the LV end-systolic pressure-stroke-volume relation (Ea), the LV stroke work (SW), LV potential energy (PE), LV pressure-volume area (PVA), the slope of the SW end-diastolic volume relation (PRSW), and an index of the LV energizing charge (ratio of PE/PVA) were assessed during transient occlusion of the inferior vena cava. LV contractility (Emax) showed no significant change during each experiment. Standardized LV work (PRSW) was reduced by BVB in comparison to the baseline and in comparison to VAB. The rate of LV energy charge (PE/PVA) significantly increased only during BVB. These results suggested that the BVB system might be an effective circulatory support for reducing LV work and improving the LV energizing charge in patients with severe heart failure after cardiac operation.
 ...
PMID:Effect of a balanced biventricular bypass system on left ventricular energies. 975 70

Juvenile haemochromatosis is a rare inborn error of iron metabolism with clinical manifestations before 30 years of age. Unlike adult haemochromatosis which principally affects men, juvenile haemochromatosis affects the sexes equally; it causes early endocrine failure, dilated cardiomyopathy and joint disease. We report four patients (two of each sex) from three pedigrees affected by juvenile haemochromatosis with a mean onset at 22 years (range 14-30). All had endocrine deficiency with postpubertal gonadal failure secondary to pituitary disease; two suffered near-fatal cardiomyopathy with heart failure. Mean time to diagnosis from the first clinical signs of disease was 9.8 years (range 0.5-20) but general health and parameters of iron storage responded favourably to iron-depletion therapy. A 24-year-old man listed for heart transplantation because of cardiomyopathy [left ventricular (LV) ejection fraction 16%] responded to intravenous iron chelation with desferrioxamine combined with phlebotomy (ejection fraction 31%). A 27-year-old woman with subacute biventricular heart failure refractory to medication required orthotopic cardiac transplantation before the diagnosis was established (LV ejection fraction 25%). Genetic studies showed that these two patients with cardiomyopathy from unrelated families were heterozygous for the HFE 845G-->A (C282Y) mutation and wild-type at the H63D locus: complete sequencing of the intron-exon boundaries and entire coding sequence of the HFE gene failed to identify additional lesions. Two siblings in a pedigree without cardiomyopathy were wild-type at the HFE C282Y locus; although the brother harboured a single copy of the 187C-->G (H63D) allele, segregation analysis showed that in neither sibling was the iron-storage disease linked to MHC Class I markers on chromosome 6p. Juvenile haemochromatosis is thus a genetically heterogenous disorder distinct from the common adult variant.
 ...
PMID:Hereditary juvenile haemochromatosis: a genetically heterogeneous life-threatening iron-storage disease. 1002 15

We report the case of a 23-year-old man with acute aortic valve insufficiency caused by endocarditis, who after emergency aortic valve replacement developed biventricular heart failure. The heart failure was treated with temporary assist devices. Subarachnoid bleeding and thrombus obstruction of the left ventricular outflow tract was detected. The postoperative course is presented with special emphasis on management of subarachnoid bleeding and the simultaneous use of anticoagulation necessary for ventricular assist devices.
 ...
PMID:Ventricular thrombus and subarachnoid bleeding during support with ventricular assist devices. 1039 Dec 92


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>