Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

A 15-year-old girl with a four-month history of cardiac failure from undetermined cause was admitted to the hospital with weakness, fatigue, and weight loss. During her hospitalization she was found to have abused diet aids, laxatives, and cathartics. Although an electrocardiogram revealed nonspecific T-wave abnormalities and laboratory studies showed supranormal enzyme test results for creatine kinase and lactate dehydrogenase, no definite explanation of the cardiomyopathy was forthcoming. Ipecac abuse leading to cardiomyopathy was suspected early in the hospitalization. HPLC analysis of a urine sample showed emetine, a principle component of ipecac, the presence of which was later confirmed by more-specific HPLC analysis with photodiode array detection.
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PMID:Emetine identified in urine by HPLC, with fluorescence and ultraviolet/diode array detection, in a patient with cardiomyopathy. 292 Apr 26

The present study was designed to examine the effects of two new angiotensin-converting enzyme (ACE) inhibitors, CGS 14831 and CGS 16617 (3 mg/kg i. v. 1 min prior to occlusion and 4 and 24 h after occlusion), on myocardial ischemic (MI) damage and left-ventricular hypertrophy in rats. Administration of CGS 14831 or CGS 16617 inhibited angio-tensin-I-induced pressor responses by 40-100% for 4 h after each dose. Myocardial creatine phosphokinase (CK) levels were 10.6 +/- 0.6 U/mg protein in sham-MI animals, and following coronary artery occlusion for 48 h were decreased to 4.1 +/- 0.2 U/mg protein in MI + vehicle animals (p less than 0.01). CGS 14831 and CGS 16617 attenuated the decrease in CK content and resulted in 47 and 40% sparing, respectively, of the left-ventricular free wall. Neither agent attenuated the left-ventricular hypertrophy which developed following coronary artery occlusion. These data indicate that the nonsulfhydryl ACE inhibitors CGS 14831 and CGS 16617 have a significant cardioprotective effect in rats surviving 48 h, and suggest a potential therapeutic usefulness of these agents for the treatment of ischemia-induced heart failure.
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PMID:Effects of two nonsulfhydryl angiotensin-converting enzyme inhibitors, CGS 14831 and CGS 16617, on myocardial damage and left-ventricular hypertrophy following coronary artery occlusion in the rat. 297 11

Rats were fed a diet containing beta-guanidinopropionic acid (GP), an inhibitor of creatine transport. After 6 to 8 weeks of feeding the myocardial creatine (Cr) and phosphocreatine (PCr) stores were severely depleted while ATP content was normal. Hearts of GP-treated rats perfused according to Neely's working heart model revealed clear cardiac contractile failure: the maximal work capacity at a stepwise increase in resistance as well as the maximal oxygen consumption were 32 to 40% less in the GP group. The cardiac failure in GP-treated working hearts was associated with a rise in the left ventricular diastolic pressure, which could cause a diminished cardiac output probably due to impaired LV filling. The extent of the contractile failure was found to depend on functional load and on the degree of Cr (PCr) substitution. The energy fluxes through creatine kinase measured by the 31P-NMR saturation transfer technique were diminished by a factor of two after substitution of 90% of creatine, but still exceeded the rate of ATP turnover. The results are compatible with the concept of phosphocreatine pathway for intracellular energy transport and show that PCr is an important high energy phosphate compound for cardiac contractile function.
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PMID:The cardiac contractile failure induced by chronic creatine and phosphocreatine deficiency. 321 3

The progression of clinical disease and serum creatine kinase (CK) levels in canine X-linked muscular dystrophy (CXMD) was studied in 7 dogs from birth to 12-14 months and in 18 dogs at varying intervals from birth to 8 weeks. One affected male was studied from age 3.5 to 6 years, and all pups were descendants of this dog. A lethal neonatal form was recognized in some pups. In the more typical form, clinical signs of stunting, weakness and gait abnormalities were evident by 6-9 weeks and were progressive, leading to marked muscle atrophy, fibrosis and contractures by 6 months. Serum CK levels were markedly elevated, such that affected pups could be identified by 1 week. CK values increased until 6-8 weeks, then plateaued at approx. 100 times normal. Affected females and beagle-cross dogs were less severely affected than large breed-cross dogs. In the 2 adult dogs with cardiac insufficiency CK levels had decreased to 5-15 times normal. These studies show that CXMD and Duchenne muscular dystrophy have striking phenotypic as well as genotypic similarities. In addition, these studies of CXMD suggest that in females and in smaller dogs the same genetic defect results in a less severe clinical disease.
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PMID:Canine X-linked muscular dystrophy. An animal model of Duchenne muscular dystrophy: clinical studies. 322 30

To determine the relative prognostic significance of location (anterior or inferior) and type (Q wave or non-Q wave) of infarction, the hospital course and follow-up outcome (mean duration 30.8 months) of 471 patients with a first infarction were analyzed. Analyses were performed grouping the patients according to infarct location (anterior, n = 253; inferior, n = 218), infarct type (Q wave, n = 323; non-Q wave, n = 148), and both location and type (inferior non-Q wave, n = 85; inferior Q wave, n = 133; anterior non-Q wave, n = 63; and anterior Q wave, n = 190). Patients with anterior infarction had a substantially worse in-hospital and follow-up clinical course compared with those with inferior infarction, evidenced by a larger infarct size (21.2 versus 14.9 g Eq/m2 creatine kinase, MB fraction [MB CK], p less than 0.001), lower admission left ventricular ejection fraction (38.1 versus 55.3%, p less than 0.001) and higher incidence of heart failure (40.7 versus 14.7%, p less than 0.001), serious ventricular ectopic activity (70.2 versus 58.9%, p less than 0.05), in-hospital death (11.9 versus 2.8%, p less than 0.001) and total cumulative cardiac mortality (27 versus 11%, p less than 0.001). Patients with Q wave infarction similarly experienced a worse in-hospital course compared with patients with non-Q wave infarction, evidenced by a larger infarct size (20.7 versus 12.7 MB CK g Eq/m2, p less than 0.001), lower admission left ventricular ejection fraction (43.7 versus 50.6%, p less than 0.001), and a higher incidence of heart failure (31.9 versus 21.6%, p less than 0.05) and in-hospital death (9.3 versus 4.1% p less than 0.05). However, there was no increased rate of reinfarction or mortality in hospital survivors with non-Q wave infarction compared with those with Q wave infarction, and total cardiac mortality was similar (16 versus 21%, p = NS). To evaluate the role of infarct location and type independent of infarct size, patients were grouped according to quartile of infarct size, and outcome was reanalyzed within each group. Patients with anterior infarction demonstrated a lower left ventricular ejection fraction on admission and after 10 days than did patients with inferior infarction, even after adjustment for infarct size, as well as a higher incidence of congestive heart failure and cumulative cardiac mortality.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Prognostic significance of location and type of myocardial infarction: independent adverse outcome associated with anterior location. 327 32

Serum myoglobin levels were studied in 178 consecutive patients admitted for chest pain due to ischemic cardiac injury. Serum myoglobin level was compared with the clinical condition, electrocardiographic changes, and serum creatine kinase levels. Elevated serum myoglobin concentration was present in all patients with acute myocardial infarction, as defined by World Health Organization, Geneva, criteria, and, in addition, in about 50% of patients with so-called acute coronary insufficiency. On this basis we could define two different groups of patients with acute coronary insufficiency: cases exhibiting elevated serum myoglobin levels (group 1) and those with normal levels (group 2). In group 1 although creatine kinase levels were in the normal range, they were significantly higher than in group 2. Four patients from group 1 developed heart failure and another a typical acute myocardial infarction during hospitalization, whereas no patients of group 2 had such complications. In patients with acute myocardial infarction, the elevation of serum myoglobin preceded that of creatine kinase in most cases. Myoglobin release appears to be related to infarct size, the highest levels were found in extensive myocardial infarction and less marked elevations in cases of subendocardial infarction and in half of the cases with acute coronary insufficiency. It is proposed that serum myoglobin is a reliable measure of myocardial necrosis and serves to detect a hitherto undefined population of small-size acute myocardial infarction, with its attendant clinical and prognostic implications.
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PMID:Serum myoglobin levels in patients with ischemic myocardial insult. 340 Oct 97

After prolonged ischemia followed by reperfusion of the isolated rat heart, irreversible heart failure is associated with creatine kinase leakage from the cells. The possible implications of MM creatine kinase leakage from myofibrillar compartments on the contractile properties of ventricular muscle have been studied in control versus ischemic hearts. Total creatine kinase activity decreased in ischemic cells while creatine kinase and ATPase activities were not modified in isolated myofibrils. The efficiency of creatine kinase and phosphocreatine in the relaxation of rigor tension in skinned ventricular preparations was not changed after ischemia. Furthermore, neither the pCa/tension relationship nor the rate of tension development following length changes were modified by ischemia. These results show that the contractile properties of myofilaments as well as the functional coupling between myosin ATPase and creatine kinase are preserved in ischemic hearts suffering irreversible contractile failure.
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PMID:Contractile properties and creatine kinase activity of myofilaments following ischemia and reperfusion of the rat heart. 343 83

Miscellaneous cardiac abnormalities can occur after electrical burns. The long term outcomes are still unknown. We studied 10 patients, 9 of whom suffered high-voltage electrocution, and one of whom was struck by lightning. Serial electrocardiograms (ECG) and serum MB creatine phosphokinase isoenzyme (MB-CPK) activities were obtained during their stay in hospital. ECG and thallium 201 cardiac scintigraphy at rest, as well as echocardiograms were obtained in all patients 4 to 48 months after discharge. In hospital, 9 patients showed one or more abnormal findings at physical examination (4 cases), ECG (8 cases), MB-CPK (1 case). At long term follow-up, 5 patients had one or more myocardial functions or conduction abnormalities, with or without symptoms. One patient had compensated heart failure. Nine patients were asymptomatic. Abnormal ECG findings persisted in 3 patients. Three cardiac scans showed evidence of regional myocardial hypoperfusion. Decreases in left ventricular indices measured by echocardiogram were found in 3 patients. We conclude that high-voltage electrocution is associated with a high incidence of cardiac abnormalities, which may persist. Long term evaluation, requiring cardiac T1 201 scintigraphy and echocardiogram, may be justified.
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PMID:Myocardial injury after electrical burns: short and long term study. 344 60

This study compares the effects of digoxin, placebo and ibopamine (SB-7505), the orally active 3,4-diisobutyryl ester of N-methyl-dopamine, on exercise tolerance and cardiac rhythm of 14 patients whose left ventricular heart failure (end-diastolic pressure, 26.3 +/- 5.9 mmHg; ejection fraction, 0.42 +/- 0.10%) depended on a previous myocardial infarction. Patients were admitted to the study while on chronic oral digoxin treatment (serum levels between 1.1 and 1.9 ng/ml). Placebo instead of digoxin was given for the following month. Thereafter ibopamine 50 mg t.i.d. for one month was given. A sequence of one-month treatments with digoxin, placebo and ibopamine was repeated, then ibopamine was administered continuously for the next two months. The concurrent treatment (diuretics in all patients, nitroderivates in twelve, calcium antagonists in two) remained unchanged during the observation period. Symptoms-limited exercise tests and 24-h Holter recordings were obtained at admission, at the end of each one-month treatment and at the end of the observation period. Two patients developed unstable angina without increase of serum creatine phosphokinase while on ibopamine and were withdrawn. Out of the 12 patients that concluded the trial, one required supplementary doses of diuretic at the end of the second period on placebo. The results obtained during the trial suggest that: a) therapeutic plasma levels of digoxin have no deleterious effect on cardiac rhythm nor significantly increase exercise tolerance as compared with placebo; b) diuretics and nitrates appear to sustain the clinical stability of these patients as a group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of digoxin, placebo and ibopamine on exercise tolerance and cardiac rhythm of patients with chronic post-infarct left ventricular failure. 370 53

This study examined the effects of ethanol and hereditary cardiomyopathy on sodium and water excretion by golden Syrian hamsters of both sexes. Ethanol (4 g/kg) or the isotonic saline vehicle were injected IP into 60-70-day-old hamsters of normal and cardiomyopathic (BIO 14.6) strains. Urine and blood were collected after 90 or 350 min in different groups. Cardiomyopathic hamsters more quickly lost their righting responses, eliminated ethanol more slowly, and had lower urine volume and sodium excretion than normal hamsters after ethanol injections. Plasma creatine kinase levels were normal in all animals tested, indicating no active skeletal or cardiac lesioning in the cardiomyopathic hamsters at the time of the experiment. Some factors which could contribute to the increased CNS and renal sensitivity to ethanol in cardiomyopathic hamsters include impaired ethanol metabolism, enhanced myocardial depression, and reduced atrial content of natriuretic peptides. The results do not owe to decompensated heart failure. Thus, the genetic mutation which causes skeletal and cardiac myopathy in these hamsters may also affect the metabolism and sensitivity to ethanol.
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PMID:Ethanol in cardiomyopathic hamsters: Na and water excretion and righting response. 371 87


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