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)

Characteristic alterations in the serum and urine biochemical profiles of Doberman Pinschers with congestive heart failure (CHF) resulting from idiopathic dilated cardiomyopathy were determined. We compared these alterations with those observed in 2 other models of CHF: rate overload induced by rapid ventricular pacing in dogs, and biventricular hypertrophy and dilatation induced in turkey poults by furazolidone toxicosis. Serum and urine biochemical changes in both models of CHF in dogs were mild to moderate in degree, and were moderately consistent. They could be attributed to secondary neurohumoral, hepatic, and renal effects of heart failure. The most marked and consistent changes observed were mildly decreased anion gap that developed, in part, because of decreased serum sodium concentration, moderately increased catecholamine concentrations, moderate lactaciduria, hyposthenuria, and mildly increased urea concentrations and liver enzyme activities. In birds with furazolidone cardiomyopathy, we observed mild increases in serum urate concentration, liver and muscle enzyme activities, but moderately increased sodium concentration with decreased chloride concentration. In the pacing and furazolidone models, in which CHF was rapidly induced, moderate to marked hypoproteinemia was attributable to decreases in albumin and globulin concentrations. Using the avian model we found that the hypoproteinemia could be largely attributed to blood volume expansion, and to a lesser extent, inanition. Development of hypoalbuminemia during rapid ventricular pacing and furazolidone treatment may contribute to the effects of rate overload or drug toxicity in the pathogenesis of CHF, because hypoalbuminemia may contribute to altered hemodynamics and neuroendocrine system activation. Our data indicate that clinical biochemical analysis of serum and urine may be useful for assessing progression of CHF.
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PMID:Clinical pathologic profiles of dogs and turkeys with congestive heart failure, either noninduced or induced by rapid ventricular pacing, and turkeys with furazolidone toxicosis. 842 73

NSAIDs pose little threat of renal insult in normal, healthy persons at therapeutic dosages. However, NSAID administration to susceptible persons may cause decrements in renal plasma flow and glomerular filtration rate within hours. Such acute noxious renal effects are mediated by products of arachidonic acid metabolism. Precipitous decrements in glomerular filtration and renal ischemia, manifested by increased serum creatinine and urea nitrogen, are possible. However, these effects are usually fully reversible with prompt discontinuation of the offending NSAID. Risk factors for the development of these acute renal effects are known. Acute interstitial nephritis with or without nephrotic syndrome is a rare form of renal toxicity that typically occurs between 2-18 months of use. Renal impairment may be so severe as to require temporary hemodialysis; however, renal function usually returns to normal upon discontinuation of the NSAID. The mechanism of acute interstitial nephritis is presumed to be of allergic origin but could also be caused by a reactive metabolite. Fenoprofen use appears to be associated with a much higher risk for its development. In contrast to the acute effects of NSAIDs, irreversible, analgesic-associated nephropathy manifested by papillary necrosis and chronic interstitial nephritis may occur following months to years of high doses of analgesic mixtures. The mechanism by which combination analgesics produce this form of renal injury is unknown and could be either a result of medullary ischemia or a direct effect of a reactive metabolite. An important issue to be resolved is the relationship between the acute, reversible, prostaglandin-mediated renal effects of the NSAIDs and chronic, irreversible destruction, if such a relationship exists. Theoretically, continual or repeated decrements in renal function in patients with predisposing risk factors could cause or contribute to progressive deterioration in renal function. Elevations in blood pressure or interference with the effects of antihypertensive medications could theoretically also contribute to long-term renal deterioration. In addition to renal syndromes caused by NSAIDs that result in renal impairment, other transient effects on electrolyte and water metabolism may also occur. Reduced secretion of sodium may result in formation of edema, exacerbation of heart failure, or increased blood pressure. Hyporeninemic-hypoaldosteronism may produce hyperkalemia. Finally, reduced excretion of water has rarely caused hyponatremia. It has been suggested that NSAIDs may be renoprotective in patients with nephrotic syndrome. Others have suggested that sulindac is "renal-sparing" because of a unique metabolic pathway that supposedly limits the exposure of the kidney to the active sulfide metabolite.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renal toxicity of the nonsteroidal anti-inflammatory drugs. 849 47

In a 43-year-old patient with Ebstein's anomaly and a history of acute myocardial infarction by means of duplex ultrasonography and aortography the diagnosis of thrombotic occlusion of the a aorta was established, starting above the insertion of the renal arteries and reaching as far as the bifurcation of the aorta and the common iliac arteries. In the clinical picture dominated complete anuria with uraemia and marked hyperkaliaemia as a result of ischaemic affection of the extremities due to thrombosis of the aorta; at the onset of hospitalization also left ventricular failure with hyperhydration and later also signs of the hyperviscous syndrome. The latter developed after repeated haemofiltrations which led to a rise of the originally high haemoglobin and haemotocrit values a result of a righ-left shunt in Ebstein's anomaly. After improvement of the clinical condition local fibrinolytic treatment of the aortal thrombosis with urokinase (total dose 2,160,000 u. administered within 24 hours) was provided. The thrombus with a total length of 13.5 cm was dissolved except for a residual portion of 10 mm located in the area of insertion of the right renal artery. After dissolution of the thrombus it proved possible to restore the blood flow into the left kidney a and lower extremities, but not into the right kidney because of the residual thrombus. Seventy-two hours after terminated fibrinolysis - and after 31 days of anuria - the diuresis was restored and after a polyuric stage normalization of mineral, urea levels was restored and the creatinine value was slightly above the upper normal range. Concurrently with fibrinolytic therapy angioplasty of the aorta was carried out and a stent was placed on the left iliac artery. The clinical condition of the patient was improving, the patient started to mount stairs. Death occurred suddenly and the cause was cardiac failure due to very serious congenital heart disease.
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PMID:[Subacute thrombosis of the abdominal aorta with suprarenal involvement and successful treatment with pharmacomechanical fibrinolysis]. 855 98

The relationship between baseline clinical, laboratory and auxiliary indicators on the one-year mortality was investigated in 125 patients with chronic heart failure caused by ischaemic heart disease or cardiomyopathy associated with dilatation. During the baseline examination all patients had cardiac symptoms-functional class NYHA II-IV- and their ejection fraction assessed by echocardiography was < 40% and/or their cardiothoracic index was > 50%. Within twelve months after the baseline examination 19 (15.2%) patients died. Signs of pulmonary congestion and the cardiothoracic index were the most significant prognostic indicator of the one-year mortality (p < 0.001). As to other indicators, the following were statistically significant: sodium level, urea level, the duration of the ergometric test and the patients' body weight. Statistical significance was not recorded in echocardiographic indicators and the NYHA classification. These data, in particular the newly introduced four-grade classification of pulmonary congestion, make it possible to assess a more accurate prognosis of high risk patients with chronic heart failure.
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PMID:[Non-invasive prognostic parameters in chronic heart failure]. 862 60

Dystrophin serves a variety of roles at the cell membrane through its associations, and defects in the dystrophin gene can give rise to muscular dystrophy and genetic cardiomyopathy. We investigated localization of cardiac dystrophin to determine potential intracellular sites of association. Subcellular fractionation revealed that while the majority of dystrophin was associated with the sarcolemma, about 35% of the 427-kDa form of dystrophin was present in the myofibrils. The dystrophin homolog utrophin was detectable only in the sarcolemmal membrane and was absent from the myofibrils as were other sarcolemmal glycoproteins such as adhalin and the sodium-calcium exchanger. Extraction of myofibrils with KC1 and detergents could not solubilize dystrophin. Dystrophin could only be dissociated from the myofibrillar protein complex in 5 M urea followed by sucrose density gradient centrifugation where it co-fractionated with one of two distinctly sedimenting peaks of actin. Immunoelectron microscopy of intracellular regions of cardiac muscle revealed a selective labeling of Z-discs by hystrophin antibodies. In the genetically determined cardiomyopathic hamster, strain CHF 147, the time course of development of cardiac insufficiency correlated with an overall 75% loss of myofibrillar dystrophin. These findings collectively show that a significant pool of the 427-kDa form of cardiac dystrophin was specifically associated with the contractile apparatus at the Z-discs, and its loss correlated with progression to cardiac insufficiency in genetic cardiomyopathy. The loss of distinct cellular pools of dystrophin may contribute to the tissue-specific pathophysiology in muscular dystrophy.
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PMID:The association of cardiac dystrophin with myofibrils/Z-disc regions in cardiac muscle suggests a novel role in the contractile apparatus. 864 39

Heart failure in hypertensive patients is known to be dependent not only on the absolute value of blood pressure but also on other factors, hence the prognosis varies. In this study, the effect of renal dysfunction on the development of heart failure in hypertensive patients was assessed. Fifty-five patients who were admitted in hypertensive heart failure (HHF) were compared with 55 hypertensive patients who had never been in heart failure (HT), in their renal function, assessed by serum creatinine and urea levels. The haemoglobin (Hb) and serum albumin (Alb) levels were also measured. The two groups were matched for age, sex, level of blood pressure and body mass index. The duration of hypertension was similar in both groups. Mean serum creatinine was higher in the HHF group: 4.50 +/- 0.90 vs. 0.97 +/- 0.06 mg/100ml (P < 0.001). Also the Hb and Alb levels were lower in the HHF than the HT group: 11.63 +/- 0.40 vs. 13.2 +/- 0.21 g/100 ml (P < 0.001) and 3.7 +/- 0.1 vs. 4.40 +/- 0.09 g/100 ml (P < 0.001), respectively. The proportion with abnormal renal function (creatinine > 1.5 mg%) was also significantly higher in HHF: 28/55 vs. 8/54, chi 2 = 16.3 (P < 0.001). When adjustment was made for low serum albumin, Hb and fundal changes by multivariate analysis, serum creatinine was significantly higher in the HHF group: F = 4.294 (P < 0.05). Low serum albumin was also independent of haemoglobin and creatinine: F = 19.52 (P < 0.001), but Hb was not significantly different after adjustment for Alb and creatinine. This study suggests that renal dysfunction is independently associated with the development of heart failure in HT patients.
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PMID:Heart failure in Nigerian hypertensive patients: the role of renal dysfunction. 878 84

The regulatory myosin light chain (MLC) is phosphorylated in cardiac muscle by Ca2+/calmodulin dependent myosin light chain kinase (MLCK) and is considered to play a modulatory role in the process of force generation. In order to determine changes in MLC phosphorylation in cardiac hypertrophy and heart failure, the relative content of MLCK and MLC phosphorylation in the cardiac muscle from both sham control and experimental rats were assessed at 4 and 8 weeks following ligation of the left coronary artery. Changes in the relative MLCK content were measured by electrophoresis and immunoblot assay whereas phosphorylated and unphosphorylated MLC were separated by non-denaturing 10% acrylamide/urea gel and identified by Western blotting. The relative amount of MLCK was increased by 20-35% in the viable left ventricle, right ventricle and septum from the 8-week experimental rats in comparison to the respective control values. The MLC phosphorylation increased significantly in the right ventricle and septum but decreased markedly in the viable left ventricle from 8-week experimental rats in comparison to the control values. No appreciable changes in the relative amount of MLCK and MLC phosphorylation were seen between control and experimental rats at 4 weeks. These results suggest duration and region specific changes in the levels of MLCK and MLC phosphorylation in cardiac hypertrophy and heart failure subsequent to myocardial infarction.
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PMID:Myosin light chain phosphorylation in cardiac hypertrophy and failure due to myocardial infarction. 882 82

The present study enrolled 214 patients, aged 26 to 83 years, with symptomatic New York Heart Association class II through IV congestive heart failure. Patients were continued on their previous therapeutic regimens, which included an angiotensin-converting enzyme (ACE) inhibitor and a loop diuretic with or without digitalis. Patients were randomized to 1 of 5 parallel treatment groups: placebo or spironolactone at a single daily dose of 12.5, 25, 50, or 75 mg for 12 weeks. Serum levels of creatinine, urea nitrogen, potassium, plasma renin activity, and N-terminal proatrial natriuretic factor (pro-ANF), as well as urinary aldosterone levels, were measured periodically. Measurements at 12 weeks versus baseline values indicated significant increases in plasma renin activity and aldosterone excretion and significant decreases in systolic and diastolic blood pressure and pro-ANF. Hypokalemia (serum potassium < 3.4 mmol/L) occurred in 10% of placebo-treated patients and in 0.5% of the spironolactone group. The incidence of hyperkalemia (serum potassium > or = 5.5 mmol/L) was 5% for the placebo group, whereas it was 5%, 13%, 20%, and 24% for the 12.5-, 25-, 50- and 75-mg spironolactone treatment groups, respectively. Predictors of hyperkalemia included the use of ACE inhibitors other than captopril, ACE inhibitor dose, and baseline elevation of serum creatinine or potassium levels. Thus, daily doses of 12.5 to 25 mg of spironolactone coadministered with conventional therapy of ACE inhibitors, loop diuretics, and digitalis are relatively safe (provided that serum potassium levels are monitored) and effective in blocking the effects of aldosterone, while reducing the potential for hypokalemia in patients with heart failure.
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PMID:Effectiveness of spironolactone added to an angiotensin-converting enzyme inhibitor and a loop diuretic for severe chronic congestive heart failure (the Randomized Aldactone Evaluation Study [RALES]). 888 63

Hyponatremia is the most frequent electrolyte disorder in clinical medicine. It is usually attributable to primary vasopressin excess, causing the syndrome of inappropriate antidiuresis (SIAD), or to secondary vasopressin stimulation, involving a baroreceptor mechanism. The latter is regularly found in the hyponatremia of liver cirrhosis, cardiac failure and volume contraction. In the first kind of setting the concentrations of creatinine, urea and urate in plasma will be low because of the associated volume expanded state. In the second type of setting they will be elevated because of the circulatory compromise of these patients. The hyponatremia of SIAD may be treated by water restriction, furosemide and substitution of the inadvertent sodium losses by giving 3% NaCl. Baroreceptor hyponatremia is best treated by fluid restriction together with judiciously administered saline. In correcting severe chronic hyponatremia, the rate of correction should not exceed 1 mM/l/h and the corrected serum sodium concentration should not be higher than 130 mM/l. In the foreseeable future oral non-peptide oral vasopressin antagonists will become available. They are expected to become new tools for the treatment of hyponatremia.
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PMID:Hyponatremia: pathophysiology, differential diagnosis and new aspects of treatment. 890 18

The prognosis and clinical findings related to prognosis were examined in 300 patients with congestive heart failure in a prospective study. The diagnosis was based on case history data (NYHA class II or III), depressed ejection fraction (< or = 40%) and/or increased cardiothoracic ratio (> or = 50%). Forty-eight (16%) patients died within 1 year after the entry examination. Non-invasive baseline parameters of survivors and non-survivors were compared. All necessary medication was allowed. At the entry of the study three parameters independently predicted an increased mortality on a high significance level (P < 0.01): cardiothoracic ratio, signs of lung congestion on the chest X-ray (four grade classification), and plasma urea level; other three parameters did so on a lower significance level (P < 0.05): plasma natrium, creatinine value and endsystolic volume. Other parameters such as age, ejection fraction, NYHA class or exercise tolerance duration were not statistically different in survivors and non-survivors. Our modification (a four grade classification) of the signs of lung changes on the chest X-ray enables a more accurate determination of the prognosis in patients with chronic heart failure.
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PMID:Non-invasive prognostic factors in chronic heart failure. One-year survival of 300 patients with a diagnosis of chronic heart failure due to ischemic heart disease or dilated cardiomyopathy. 891 74


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