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 case of 25-year-old woman with glycogen storage myopathy is reported here. She was hospitalized for acute heart failure after alcohol drinking. The electrocardiogram on admission showed marked ST elevation. Laboratory data showed elevated levels of serum myogenic enzymes but no rise in cardiomyogenic enzyme: CK 3862 IU/l CK-MB 35 IU/l, LDH 427 IU/l, GOT 203 IU/l. After several days, she recovered from acute heart failure and could walk without supporting. ST elevation in ECG and elevated myogenic enzymes were also normalized. The occurrence of acute myocardial infarction was ruled out because a coronary angiogram and 99 Tcm scintigram were normal. Physical examination revealed proximal muscular weakness and mental retardation (WAIS, total 72). Venous lactate response was normal after semi-ischemic forearm exercise. PAS staining of muscle specimen showed an excess deposit of glycogen. Ragged-red fibers were not seen on Gomori-trichrome stain. By electron microscopy, a large amount of glycogen particles were demonstrated in the subsarcolemma, but there were no abnormal mitochondrial changes. Biochemical analysis showed accumulation of glycogen in muscles: 28.7 mg/g muscle (normal 11.4 +/- 4.2 mg/g muscle). The activities of enzyme in the pathway of glycogen and glycogenosis (alpha-glucosidase, amylo-1,6-glucosidase, phosphorylase a, phosphorylase kinase, phosphofructokinase, etc.) were within normal limits. The spectrum of glycogen iodine complex was normal. Our case was different from any type of muscle glycogen storage disease previously reported. The etiology of an excess of glycogen deposit in muscles is unknown.
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PMID:[A case of glycogen storage myopathy with acute heart failure]. 220 34

There are several indications that the oxygen supply to the myocardium is inadequate in chronic heart failure. This is due to an increased intramyocardial vascular resistance, elevated filling pressures, and a shortened diastolic perfusion time. In parallel, the myocardial oxygen demand is heightened due to elevated wall stress, heart rate and contractility. This imbalance between myocardial oxygen supply and demand might be the cause of the adaptive metabolic changes seen in severe chronic heart failure. We showed increased LDH 5, decreased LDH 1 and increased ADP/ATP-carrier concentration in the myocardium from patients with chronic heart failure. After ACE-inhibitor treatment in 33 patients with chronic heart failure, LDH 1 increased from 38.7 +/- 6.7% to 42.3 +/- 5.5% (P less than 0.005) paralleled by a decrease in LDH 5 from 20.8 +/- 7.0% to 15.8 +/- 4.7% (P less than 0.001). The ADP/ATP-carrier concentration also decreased significantly within the normal range. This shift in the LDH isoenzyme pattern and decrease in the ADP/ATP-concentration can be interpreted as an indication for an improvement of myocardial energy balance in chronic heart failure under ACE-inhibitor therapy. This might help interrupt the self-perpetuation of chronic heart failure which is partially caused by a progressive subendocardial perfusion deficit.
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PMID:The effect of ACE inhibition on myocardial energy metabolism. 236 54

The primary cause of death following i.v. injection of the basic phospholipase A2 (PLA2) from Naja nigricollis venom has been attributed to its direct cardiotoxicity. In view of our recent findings that cardiac failure caused by the basic PLA2 from Naja m. mossambica is primarily due to hyperkalemia resulting from cellular damage and possibly also from hemolysis, the cause of death due to the basic PLA2 from Naja nigricollis was re-investigated. In the anesthetized mice and rats, the PLA2 (0.3 micrograms/g, i.v.) produced a transient hypotension followed by recovery and subsequently by cardiac failure with ECG changes suggestive of hyperkalemia, such as P-R prolongation, tall T-wave, biphasic QRS-T complex, low voltage of QRS, A-V block, etc. Analysis of blood chemistry revealed marked increases in the plasma levels of K+, CPK, LDH, GOT, GPT, inorganic phosphate and hemoglobin (probably a mixture of hemoglobin and myoglobin). In the atrial preparation, however, no marked cardiotoxicity was observed except for a slight negative inotropic effect at 30 micrograms/ml. When 200 micrograms of the enzyme was injected into the coronary circulation in the Langendorff preparation, also no marked cardiotoxic effect was observed except for a decrease (about 40%) of coronary flow. From these results, it is concluded that the primary cause of death following i.v. injection of the basic PLA2 from Naja nigricollis is apparently cardiac failure due to hyperkalemia, resulting from cellular damage and possibly also from hemolysis, rather than direct cardiotoxicity.
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PMID:Is direct cardiotoxicity the primary cause of death following i.v. injection of the basic phospholipase A2 from Naja nigricollis venom? 252 Mar 58

A 24-year-old woman was admitted to our hospital with acute paracetamol poisoning, and severe hepatic injury. The peak blood level of GOT, GPT and LDH were 32,600 U, 119,200 U and 36,500 U respectively. Glucagon-insulin and glutathione were administered to save the liver function. On the third hospital day, hemodialysis was administered to treat acute renal failure. On the 16th hospital day, when the liver and renal functions recovered, severe pulmonary congestion occurred and right heart catheterization revealed high pulmonary pressure. Echocardiography showed left ventricular enlargement accompanied by a severe diffuse impairment of left ventricular wall motion. Multi-focal ventricular arrhythmia was frequent during this period. Hemodialysis and artificial respiration were carried out for the treatment of heart failure. Three months after admission, myocardial perfusion scintigram showed patchy reduction in the uptake of Tl-201 throughout the myocardium, and left ventriculography showed mild diffuse impairment of the LV wall motion (ejection fraction: 49%). In this case, acute heart failure appeared approximately 2 weeks after the severe hepatic injury. Apparently myocardial damage following paracetamol overdosage is caused not only by direct toxicity but by severe metabolic derangement.
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PMID:A case of myocardial damage following acute paracetamol poisoning. 252 40

The effects of i.v. nitroglycerin were studied by ECG and enzymatically in 16 patients (mean age 57.9 +/- 1.4 years) (NTG) in comparison with a control lot (c) of 17 patients (mean age 62.7 +/- 2.1 years) treated with dipyridamole and/or nifedipine (N), admitted in the first 4-10 hours after the onset of the first symptoms. The patients with heart failure and those with Q waves and CPK or LDH values greater than 2 x n were not admitted. NTG was administered in doses of 20 micrograms--60 microgram/hour for 24-96 hours and systolic AT (s) was kept under 10% of the basic values but not under 100 mmHg. Myocardial infarction appeared in 9 N-treated patients (54.86%) and 11 controls (58.25%) (p = 0.07). The size of myocardial necrosis was reduced in the N-treated patients. Peak serum CPK levels had considerably less increases in N (from 72.9 U to 73.4 U) (p greater than 00.5) versus C from 34.2 U to 364.5 U) (p less than 0.001). The sum of segmentary depression failed from 9.13 mm to 3.19 mm (p less than 0.05) in N, whereas in C the decrease was not significant (6.12 mm as against 9.38 mm; p greater than 0.05). The evolution was severe in C, as the angina crises (14 cases versus 2 cases, p less than 0.01) and the extension of the infarction (8 cases versus, 0; p 0.05) less than 0.05) appeared more frequently than in N. Only two patients in C died (p less than 0.05). Therefore, i.v. NTG administration in small doses in acute myocardial infarction leads to immediate disappearance of the anginal pain, lowers the extent of the myocardial necrosis and improves the clinical evolution.
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PMID:[The effects of nitroglycerin administered intravenously in acute myocardial ischemia]. 257 23

Among various biochemical indices measured in 93 patients with ascites, ascitic LDH estimation was proved to be indiscreminatory, while ascites/serum LDH ratio has shown a diagnostic accuracy of 85 per cent. Ascitic total protein levels and ascites/serum total protein ratio (accuracy rates of 72 and 77% respectively) were limited, especially in differentiating the ascites due to heart failure. Serum ascites albumin gradient, showed a strong correlation to portal pressure (r, + 0.83 + 0.88), and was found to be the best diagnostic index (with an overall accuracy of 97 per cent) in distinguishing the 'transudative' from 'exudative' ascites. However, no index could discreminate the 'mixed' cases and provide the etiological diagnosis of the ascites.
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PMID:Differential diagnosis of ascitic fluid: evaluation and comparison of various biochemical criteria with a special reference to serum ascites albumin concentration gradient and its relation to portal pressure. 271 55

A 61-year-old man was admitted to our hospital with complaints of cough and left back and chest pain. He had suffered from left tuberculous pleurisy at the age of 20 years. Chest X-ray film and CT revealed atelectasis of the left lung, a left hilar mass and an irregular left atrial wall. Depressed P-Ta segment in the inferior limb and anterior chest leads and an abnormal P wave were found on ECG. Transbronchial lung biopsy showed squamous cell carcinoma. After radiation therapy, the patient complained of chest oppression. ECG revealed a normalized P-Ta segment deviation, markedly elevated ST segment in the inferior limb and lateral chest leads and a depressed ST segment in the anterior chest leads. These findings persisted until his death. An obscure appearance of the pericardium and an echogenic intramyocardial mass in the posteroinferior and lateral wall were evident by echocardiography. The patient died due to heart failure. Postmortem needle biopsy showed scattered intramyocardial tumor cell nests with keratinization. CPK, GOT and LDH were within normal limits throughout the course, but CPK-MB was slightly increased. Cardiac metastasis with an ECG appearance similar to that of acute myocardial infarction has been rarely reported. Our present case showed peculiar feature including 1) ECG findings similar to atrial and ventricular myocardial infarction, and 2) an echogenic intramyocardial mass and an ill-defined pericardium on echocardiography. These findings suggested direct invasion of squamous cell carcinoma of the lung to the ventricular myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Report of a case of lung cancer with metastasis to the myocardium which showed electrocardiographic findings similar to acute myocardial infarction and intramyocardial mass on echocardiography]. 274 Jun 46

The proper classification of pleural effusions into transudates and exudates has great clinical significance. It is believed that the treatment of congestive heart failure may convert an associated transudative pleural effusion into a "pseudoexudate." We studied eight patients with congestive heart failure during nine episodes of decompensation with pleural effusion, which was bilateral in five and right-sided in three. Thoracocentesis was done on identification of the patient and at 6 +/- 2 days after treatment of heart failure resulting in diuresis and a mean weight loss of 5.8 +/- 3.2 kg. The mean protein level of the pleural fluid was 2.2 +/- 0.7 g/dL at the initial study and increased to 3.2 +/- 1.08 g/dL at the final study (p less than 0.01). The LDH level of the pleural fluid increased from 116 +/- 69 to 183 +/- 117 units/L (p less than 0.01). The fluid/serum ratio for protein increased from 0.34 +/- 0.09 to 0.47 +/- 0.13 (p less than 0.01) and for LDH from 0.39 +/- 0.16 to 0.64 +/- 0.28 (p less than 0.01). In three patients, pleural fluid was classified as a transudate at the initial study but met the criteria for an exudate after treatment of heart failure. Effectiveness of diuresis was measured by weight loss; a significant correlation between weight loss per day and change in the protein level of the pleural fluid was noted (r = 0.715; p less than 0.05). We conclude that the treatment of congestive heart failure causes significant changes in the pleural fluid's chemistry; in some cases, a transudate may be converted into a "pseudoexudate."
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PMID:Treatment of congestive heart failure. Its effect on pleural fluid chemistry. 292 9

Isolated rabbit hearts were perfused normoxically or ischemically using the technique of Langendorff. The hearts were perfused with a modified Krebs-Henseleit solution, perturbated with 95% O2/5% CO2 or in case of ischemia with N2 which replaced the O2. The perfusion rate was 25 ml/min under normoxic and 2.5 ml/min under ischemic conditions. The oxygen pressure was about 65 kPa in the normoxic and about 6 kPa in the ischemic medium. Reperfusion of ischemic hearts was realized in some cases normoxically. During the ischemic perfusion and reperfusion LDH was released time depended into the perfusion medium and the aortic inflow pressure increased. The LDH release and the increase of the inflow pressure are strong correlated. Both parameters direct to ischemic myocardial lesions. Amrinone applied as bolus in the start period of ischemia or as an infusion during the ischemic and reperfusion time limited the release of LDH and the increase of the inflow pressure. The results were discussed as a direct protecting effect of amrinone against a myocardial ischemic lesion, which is in correspondence with the improving effects of amrinone on the ischemia caused heart failure of canines in vivo, shown by Campbell et al.
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PMID:The effect of amrinone on LDH release and perfusion pressure in isolated ischemic rabbit hearts. 322 85

Methods of clinico-instrumental investigation and biochemical monitoring (CPK and its membranous fraction) were employed for examination of 432 patients with acute myocardial infarction (AMI). Among them there were patients with an uncomplicated course of disease (19.4%), recurrences (13.7%) and AMI spreading (9%). Lung edema, a cardiogenic shock, ventricular fibrillation and complicated cardiac rhythm disorders were not detected on the 1st day of disease. Clinico-anamnestic data provided no opportunity for defining factors promoting AMI recurrences whereas AMI spreading frequently developed in patients with repeated AMI, suffering from essential hypertension, obesity and heart failure. Higher diastolic pressure in the pulmonary artery, an increase in the cardiac volume, a decrease in the ejection fraction and left ventricular stroke work--changes which were most pronounced in AMI spreading, were noted in patients with AMI lingering forms. Signs of disseminated intravascular blood coagulation were noted in the venous and arterial blood of patients with lingering AMI forms. A high blood enzyme level was shown to be accompanied by a low level of antibodies to LDH and CPK.
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PMID:[Clinico-pathogenetic variants of protracted forms of acute myocardial infarct]. 361 39


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