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

One to two per cent of children and up to 11% of adolescent have arterial hypertension. In most cases children and adolescent are not recognized to be hypertensive because physicians do not routinely measure blood pressure. Often the diagnosis is recognized only when the pediatric patients develop a complication: seizure, stroke, heart failure or paraplegia. Renovascular hypertension in children and adolescents is more common than all of the other causes combined, except for coarctation of the aorta. The diagnosis is not so easy and includes the usual history, physical examination (signs and symptoms of coarctation of the isthmic or abdominal aorta or of an abdominal mass or of one of the adrenal causes of hypertension), laboratory studies, abdominal ultrasound study and chest x-ray. Sometime a CAT can be usefull. The next steps are the early and rapid-sequence IVP, renal angiography and peripheral and renal renin activity. The management of renovascular hypertension in children and adolescent includes a conservative approach (percutaneous transluminal renal angioplasty or renal embolization), rarely used in pediatric age, and the surgical treatment. This latter includes all the surgical procedures of renal revascularization and, in unilateral renal parenchymal diseases, the nephrectomy or a partial nephrectomy. The postoperative results are very good in a high percentage of cases. In bilateral cases, the revascularization surgical procedures improve or normalize also the impaired renal function.
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PMID:[Renovascular hypertension in childhood]. 182 81

A case of cardiac failure in a 54 year old man with a diffuse total arteriovenous aneurysm of the liver is reported. The aneurysm was arteriolarvenous, without a wide bore localised fistula. It occupied the whole hepatic mass, including the territories of the right subphrenic and anterior collateral of the gastroduodenal artery. The cause of cardiac failure was the elevated cardiac output, 15 1/min, which fell to 6 1/min at each peroperative occlusion of the hepatic artery. After ligature of this vessel, the cardiac output stabilised at 9 1/min and remained at this value 4 months after surgical cure. This case is comparable to the neonatal cardiac failure due to multinodular hepatic angioma with respect to the clinical, angiographic and CAT scan characteristics, and the surgical cure of the high cardiac output syndrome. Some of the histological features were suggestive, in places, of the structure of hepatic cavernoma, which makes the exact pathological classification of this diffuse aneurysm difficult; the closest possibility being an involuted from of diffuse capillary hemangioma of childhood allowing such long survival and, occasionally taking on the appearances of a cavernoma. Permanent surgical cure by ligature of the hepatic artery was an additional rare feature of this case.
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PMID:[Curable asystole in an adult caused by a diffuse and complete arteriovenous aneurysm of the liver. Cure by ligation of the hepatic artery]. 640 47

Two cases of aortocaval fistula are described in patients with an otherwise asymptomatic abdominal aortic aneurysm. Both presented because of cardiac symptoms, one with chest pain and acute heart failure and electrocardiogram signs of acute coronary ischaemia, the other with a long history of chronic cardiac failure resistant to therapy. In the first case the fistula was proven by means of a CAT scan. Positive proof of a fistula or leakage is important because asymptomatic aneurysms should not be operated on in cardiac compromised patients. On the other hand, if an aortocaval fistula is present, operation is necessary to prevent fatal cardiac failure.
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PMID:"Asymptomatic" ruptured aneurysm: a report of two cases of aortocaval fistula presenting with cardiac failure. 851 21

Phospholamban, through modulation of sarcoplasmic reticulum calcium-ATPase activity, is a key regulator of cardiac diastolic function. Alterations in phospholamban expression may define parameters of muscle relaxation. In experimental animals, phospholamban is differentially expressed in various striated and smooth muscles, and within the four chambers of the heart. Decreased phospholamban expression within the heart during heart failure has also been observed. Furthermore, regulatory elements of mammalian phospholamban genes remain poorly defined. To extend these studies to humans, we (1) characterized phospholamban expression in various human organs, (2) isolated genomic clones encoding the human phospholamban gene, and (3) prepared human phospholamban promoter/luciferase reporter constructs and performed transient transfection assays to begin identification of regulatory elements. We observed that human ventricle and quadriceps displayed high levels of phospholamban transcripts and proteins, with markedly lower expression observed in smooth muscles, while the right atria also expressed low levels of phospholamban. The human phospholamban gene structure closely resembles that reported for chicken, rabbit, rat, and mouse. Comparison of the human to other mammalian phospholamban genes indicates a marked conservation of sequence for at least 217 bp upstream of the transcription start site, which contains conserved motifs for GATA, CP1/NFY, M-CAT-like, and E-box elements. Transient transfection assays with a series of plasmids containing deleted 5' flanking regions (between -2530 and -66 through +85) showed that sequences between -169 and the CP1-box at -93 were required for maximal promoter activity in neonatal rat cardiomyocytes. Activity of these reporters in HeLa cells was markedly lower than that observed in rat cardiomyocytes, suggesting at least a partial tissue selectivity of these reporter constructs.
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PMID:The human phospholamban gene: structure and expression. 1019 97

Brain natriuretic peptide (BNP) gene expression and chronic activation of the sympathetic nervous system are characteristics of the development of heart failure. We studied the role of the beta-adrenergic signaling pathway in regulation of the human BNP (hBNP) promoter. An hBNP promoter (-1818 to +100) coupled to a luciferase reporter gene was transferred into neonatal cardiac myocytes, and luciferase activity was measured as an index of promoter activity. Isoproterenol (ISO), forskolin, and cAMP stimulated the promoter, and the beta(2)-antagonist ICI 118,551 abrogated the effect of ISO. In contrast, the protein kinase A (PKA) inhibitor H-89 failed to block the action of cAMP and ISO. Pertussis toxin (PT), which inactivates Galpha(i), inhibited ISO- and cAMP-stimulated hBNP promoter activity. The Src tyrosine kinase inhibitor PP1 and a dominant-negative mutant of the small G protein Rac also abolished the effect of ISO and cAMP. Finally, we studied the involvement of M-CAT-like binding sites in basal and inducible regulation of the hBNP promoter. Mutation of these elements decreased basal and cAMP-induced activity. These data suggest that beta-adrenergic regulation of hBNP is PKA independent, involves a Galpha(i)-activated pathway, and targets regulatory elements in the proximal BNP promoter.
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PMID:Isoproterenol and cAMP regulation of the human brain natriuretic peptide gene involves Src and Rac. 1082 15

Patients with chronic renal and heart failure present with hypertension and widespread vasoconstriction, respectively. Although systemic release of nitric oxide (NO) may be elevated in both pathological syndromes, enhanced production of NO fails to overcome endothelial dysfunction. Plasma concentrations of L-arginine, a cationic amino acid precursor for NO synthesis, are reduced whilst levels of the endogenous L-arginine analogues, asymmetric and symmetric dimethyl arginine and N(G)-monomethyl-L-arginine, seem to be elevated. We have reported that transport of L-arginine via the cationic amino acid transporters y(+)/CAT and/or y(+)L are up-regulated in erythrocytes, peripheral blood mononuclear cells and platelets from both patients with either chronic renal or heart failure. A possible explanation why NO serves as a failing counter-regulatory mechanism in both these pathologies is that availability of L-arginine for NO production is reduced despite the observed increase in membrane transport. This review examines the mechanisms underlying alterations in NO production in chronic renal and heart failure, and the possible role of L-arginine transport in vascular and platelet dysfunction observed in both syndromes.
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PMID:Abnormalities in L-arginine transport and nitric oxide biosynthesis in chronic renal and heart failure. 1123 Sep 69

Several randomized clinical trials have been designed to evaluate the usefulness of prophylactic implantable cardioverter defibrillator (ICD) therapy in patients with nonischemic cardiomyopathy. In 2 trials, CAT and AMIOVIRT, no survival benefit was reported for patients with dilated cardiomyopathy and prophylactic ICD therapy. The major limitation of both trials is the small sample size of 104 patients in CAT and 103 patients in AMIOVIRT. Another limitation of both trials is the lack of a run-in phase on optimized medical therapy. Since LV function may improve considerably on optimized medical therapy, LV function should be reevaluated 3 to 4 months after initiation of ACE inhibitors, ss-blockers and aldosterone antagonists before prophylactic ICD therapy is considered. Two additional trials, DEFINITE and SCD-HEFT, are still ongoing. Particularly SCD-HEFT will follow a sufficient number of patients with nonischemic cardiomyopathy to give a more definitive answer with regard to the clinical usefulness of prophylactic ICDs in patients with nonischemic cardiomyopathy. Recently, the Marburg Cardiomyopathy study (MACAS) was finished. The results of MACAS strongly suggest that reduced LV ejection fraction is the most important arrhythmia risk predictor in idiopathic dilated cardiomyopathy, whereas signal-averaged ECG, baroreflex sensitivity, heart rate variability and T wave alternans do not appear to be helpful for arrhythmia risk stratification. In addition, MACAS showed that total mortality in patients with idiopathic dilated cardiomyopathy and an ejection fraction <30% is only about 5% per year on optimized medical therapy after exclusion of patients with end stage heart failure and after exclusion of patients with sustained ventricular arrhythmias. Thus, any future study designed to demonstrate a mortality benefit by prophylactic ICD therapy with an 80% power in this patient population needs to enroll more than 1000 patients.
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PMID:Clinical trials of prophylactic implantable defibrillator therapy in patients with nonischemic cardiomyopathy: what have we learned and what can we expect from future trials? 1507 Dec 76

Studies on the lipid peroxidation and antioxidant changes and their significance during myocardial injury have provided a new insight into the pathogenesis of heart disease. The heart failure subsequent to myocardial infarction may be associated with an antioxidant deficit as well as increased myocardial oxidative stress. The present study was designed to evaluate the effect of the combination of ferulic acid and ascorbic acid on antioxidant defense system and lipid peroxidation against isoproterenol (ISO)-induced myocardial infarction in rats. Induction of rats with isoproterenol (150 mg/kg body weight daily, i.p.) for 2 days resulted in a marked elevation in lipid peroxidation, serum marker enzymes (LDH, CPK, GOT, and GPT), and a significant decrease in activities of endogenous antioxidants (SOD, GPx, GST, CAT, and GSH). Pre-co-treatment with the combination of ferulic acid (20 mg/kg body weight/day) and ascorbic acid (80 mg/kg body weight/day) orally for 6 days, significantly attenuated these changes when compared to the individual treatment groups. Histopathological observations were also in correlation with the biochemical parameters. Thus, ferulic acid and ascorbic acid significantly counteracted the pronounced oxidative stress effect of ISO by the inhibition of lipid peroxidation, restoration of antioxidant status, and myocardial marker enzymes levels. In conclusion, these findings indicate the synergistic protective effect of ferulic acid and ascorbic acid on lipid peroxidation and antioxidant defense system during ISO-induced myocardial infarction and associated oxidative stress in rats.
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PMID:Synergistic interactions of ferulic acid with ascorbic acid: its cardioprotective role during isoproterenol induced myocardial infarction in rats. 1644 96

Primary and secondary prevention of sudden cardiac death is not sufficiently assured by medication. The (automatic) implantable cardioverter/defibrillator ((A)ICD) is able to terminate life-threatening arrhythmias (ventricular fibrillation/flutter, ventricular tachycardia) reliably. The identification and care of risk patients is of crucial importance. Initially, only survived resuscitation for ventricular fibrillation or ventricular tachycardia was regarded as a confirmed indication. Several studies (CABG patch, MADIT, MADIT II, MUSTT, DINAMIT, CAT AMIOVIRT, DEFINITE, COMPANION, SCD-HeFT) have examined the prophylactic indication for ICD therapy in risk groups. Patients with chronic state after myocardial infarction with markedly impaired left ventricular function and/or spontaneous, non-sustained ventricular tachycardia have been documented to benefit. Patients with moderately severe or severe heart failure also profit from ICD implantation, where appropriate in combination with cardiac resynchronization therapy in conduction disorders. There is divergent data on dilated cardiomyopathy. ICD is not indicated in patients with acute infarctions or undergoing elective bypass surgery.
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PMID:AICD treatment in 2004--state of the art. 1710 77

Previous in vivo study demonstrated that betagamma-CAT, a newly identified non-lens betagamma-crystallin and trefoil factor complex from frog Bombina maxima skin secretions, possessed potent lethal toxicity on mammals resulted from hypotension and cardiorespiratory arrest. However, the mechanism of cardiac dysfunction induced by the protein is unknown. Here, we report that betagamma-CAT, with dosages of 0.8-3.0 nM, elicited an acute negative inotropic effect in isolated rabbit heart Langendorff preparations, which mimicked acute heart failure. In addition, the effect of betagamma-CAT on the hearts was mediated by endothelium-dependent coronary vasoconstriction (P<0.01, compared between endothelium-intact and removal hearts). After betagamma-CAT (3.0 nM) treatment, the positive signal of tumor necrosis factor-alpha (TNF-alpha) was detected mainly around the endothelial cell layer as detected by in situ indirect immunofluorescence, indicating that the release of TNF-alpha occurred. At the same time, a rapid TNF-alpha release was detected in primary cultured rabbit endocardial endothelial cells (REECs) treated with betagamma-CAT. After addition of betagamma-CAT (3.0 nM) for 10 min and 30 min, the TNF-alpha levels were increased to 57.33+/-3.22 pg/ml and 60.00+/-5.35 pg/ml (P<0.05, compared with the control values of 21.67+/-3.45 pg/ml and 33.70+/-6.24 pg/ml, respectively). At high concentrations, betagamma-CAT interfered with the cell viability of REECs (CC(50) about 25 nM). Taken together, betagamma-CAT was able to induce acute myocardial depression and the toxic effect might be partially explained by the release of TNF-alpha. The finding provides new information to understand the patho-physiological roles of non-lens betagamma-crystallins and trefoil factors.
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PMID:Betagamma-CAT, a non-lens betagamma-crystallin and trefoil factor complex from amphibian skin secretions, caused endothelium-dependent myocardial depression in isolated rabbit hearts. 1860 41


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