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)

Using a standardized porcine CPR-model (3 min of cardiac arrest induced by ventricular fibrillation) the effects of epinephrine (10 micrograms/kg iv, 50 micrograms/kg iv, 100 micrograms/kg endobronchially, eb) and norepinephrine (10 micrograms/kg iv, 100 micrograms/kg eb) on resuscitability and early post-resuscitation haemodynamics were compared. Success rate was 100% after epinephrine 10 micrograms/kg iv and 100 micrograms/kg eb, 75% after epinephrine 50 micrograms/kg iv, 80% after norepinephrine iv and 60% after norepinephrine eb. In an unmedicated control group 50% of all animals were successfully resuscitated. Early post-resuscitation haemodynamics in the high dose epinephrine group were characterized by tachycardia and progredient myocardial failure, while in the norepinephrine groups a low cardiac output was accompanied by small cardiac stroke volumes and an increased vascular resistance. It is concluded that iv or eb epinephrine given in standard doses has still to be considered as the drug therapy of choice after short term cardiac arrest or in the presence of ventricular fibrillation. Before different drugs or dosing strategies can be recommended, further experimental and clinical validation is required.
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PMID:[New standards for catecholamine therapy in cardiopulmonary resuscitation? Results of a modified application in a resuscitation model]. 163 6

A 5-month-old boy died of progressive heart failure that started at the age of 3 months. Autopsy revealed a mitochondrial cardiomyopathy and a mitochondrial myopathy of the limb muscle and diaphragm. Cytochemically random defects of cytochrome c oxidase were visualized by light and electron microscopy in the diaphragm and especially the heart muscle, the limb muscle showing a diffuse attenuation whereas the liver and kidneys reacted normally. The activities of NADH-dehydrogenase (complex I) and cytochrome c oxidase (complex IV) were severely diminished (20% residual activity of controls) in the skeletal and heart muscle. In the heart, succinate cytochrome c reductase (complex II/III) was additionally decreased to the same degree. Loss of cytochrome c oxidase activity was based on a reduction of both mitochondrial and nuclear derived subunits in the heart and diaphragm as revealed by immunohistochemical analysis, whereas the limb muscle showed a normal immunoreactive protein content. The results illustrate heterogeneous tissue expression of respiratory chain enzyme defects and demonstrate that a cardiomyopathy may be the leading presentation of a mitochondrial disorder in early infancy.
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PMID:Fatal infantile mitochondrial cardiomyopathy and myopathy with heterogeneous tissue expression of combined respiratory chain deficiencies. 165 34

We describe a cardiac arrest which occurred during general anaesthesia in the prone position for surgical correction of lumbar kyphosis in a patient with Marfan's syndrome. Peroperative monitoring was routine with ECG, non-invasive arterial pressure, oximetry, PETCO2 and central venous pressure, plus aortic blood flow and and systolic time intervals via an oesophageal echo-Doppler device. Forty-five minutes after the start of surgery, a sudden decrease in aortic blood flow followed by a decrease in PETCO2 suggested acute cardiac failure despite continuation of the ECG signal. Initial CPR in the prone position produced a slight increase in PETCO2. When the patient was turned to the supine position and the legs elevated, chest compression was more efficient and spontaneous circulation was rapidly restored. Circulatory arrest could be explained by incompletely treated hypovolaemia, or by myocardial depression (decrease in aortic blood flow and lengthened pre-ejection period) combined with excessive hypotension in a patient with Marfan's syndrome, thus compromising coronary blood flow producing ST segment depression. Continuous non-invasive aortic blood flow and PETCO2 monitoring proved valuable in the early detection and treatment of circulatory arrest and in the evaluation of the efficiency of peroperative CPR.
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PMID:Non-invasive continuous haemodynamic and PETCO2 monitoring during peroperative cardiac arrest. 870 1

To better characterize the role of skeletal muscle in chronic heart failure we studied energetic charge, metabolites and enzyme activity in the energy production pathway. We selected 15 males with severe chronic heart failure (NYHA class III, stable clinical conditions and in normal nutritional status) and seven controls. Controls and patients were submitted to biopsy of the vastus lateralis muscle in resting and fasting conditions. Hormone profiles were also evaluated. Our results showed near normal ATP, ADP and AMP concentrations, but there were substantially more reductions in glycogen (46 +/- 5 vs 77 +/- 6 mumoles glycosidic units.g-1 fresh tissue) and creatine phosphate (5 +/- 1 vs 13 +/- 1 mumoles.g-1 fresh tissue) in patients than in controls. We also found a reduction in glycolytic activity (pyruvate kinase 1009 +/- 79 vs 1625 +/- 26 nmoles. min-1.mg protein-1), despite normal tricarboxylic acid cycle velocity, an increase in alanine amino-transferase (964 +/- 79 vs 425 +/- 34 nmoles. min-1.mg protein-1) and in aspartate aminotransferase (515 +/- 44 vs 291 +/- 56 nmoles.min-1.mg protein-1). An increase was also observed in total NADH cytochrome c reductase (128 +/- 14 vs 68 +/- 5 nmoles.min-1.mg protein-1), while cytochrome oxidase activity was normal. The cortisol/insulin ratio was slightly elevated (77 +/- 4 vs 32 +/- 12). In conclusion, normonutritive patients with severe heart failure show an imbalance in the energy production/utilization ratio. The impairment is probably due both to a decrease in production and an increase in consumption of energy owing to greater cellular workload and/or a hypercatabolic state.
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PMID:Biochemical analysis of muscle biopsy in overnight fasting patients with severe chronic heart failure. 892 17

The clinical case of a 45-year-old patient referred to us for chest pain and with clinical examination and ECG negative for ischaemic damage, is reported. The patient, hospitalised in a bed without an ECG monitor, presented heart failure due to ventricular fibrillation. He was re-examined first with ventilation and EMC and then with defibrillation. Reanimation continued for about 70 minutes. Administration of high doses of adrenalin (0.2 mg/kg) and 9 defibrillations failed to resolve the refractory VF; nor did i.v. lidocaine administration resolve the situation. Echocardiogram did not reveal cardiac tamponade. Administration of 4 g of magnesium sulphate followed by adrenalin and defibrillation, led to asystole with subsequent restoration of sinus rhythm. The patient was then transferred to Intensive Care where he was sedated and curarized for 48 hours. The clinical course was characterised from the start by positive aspects that excluded the need to carry out instrumental investigations such as evoked somatosensory potentials, in the formulation of a prognosis. The patient was transferred to the Hospital Cardiology Unit 72 hours after admission. Two weeks later the patient was discharged with a complete recovery of neurological functions and with no metabolic or thoracopulmonary changes. It can be concluded from this experience that prognosis during CPR may not be reliable. So the factors that should lead us to carry out prolonged reanimation are the age of the patient, his pre-existing clinical conditions, the speed of our actions and correct performance of reanimation.
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PMID:[Complete neurologic recovery after prolonged cardiac arrest caused by refractory ventricular fibrillation. Clinical case]. 907 13

Chronic cobalt exposure is characterized by severe cardiac insufficiency. Since the mechanisms of cobalt toxicity are not yet clear, we analysed the effects of chronic cobalt exposure on antioxidant enzyme activities and myocardial mitochondrial ATP production rate in a rat model. One group of rats was fed a conventional diet and another a cobalt supplemented diet for 24 weeks. The manganese-superoxide dismutase activity was markedly reduced in the cobalt rats (18+/-4.7 U/mg protein) compared to the control rats (100+/-22 U/mg protein; p <0.001). Activity in the respiratory chain enzymes succinate-cytochrome c reductase, NADH-cytochrome c reductase and cytochrome c oxidase was also reduced in the cobalt rats (p<0.01). Glutamate dehydrogenase activity, located in the mitochondrial matrix, was unchanged. The mitochondrial ATP production rate in relation to myocardial mass was lower in the cobalt rats for all substrates tested except palmitoyl-l-carnitine + malate. In conclusion, 24 weeks of chronic cobalt exposure induces a marked decrease in manganese-superoxide dismutase activity, a moderate decrease in mitochondrial ATP production rate and a general reduction in the capacity of the respiratory chain. The impairment in mitochondrial ATP production might be secondary to the decreased manganese-superoxide dismutase activity, causing inactivation of mitochondrial factors susceptible to superoxide radicals.
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PMID:Chronic cobalt exposure affects antioxidants and ATP production in rat myocardium. 1176 20

The recommended targeting of the elderly, those with heart conditions and their family members for CPR education remains unaccomplished. Little is known about cardiac patients' knowledge of and attitude towards CPR and CPR education. This study aimed to investigate cardiac care patients' attitude towards CPR and interest in CPR education. An interview, based on a questionnaire, was conducted with 401 consecutive patients admitted to a coronary care unit. Most participants had heard about the concept of CPR and 64% were aware of its content. In the event of an emergency, 96% were willing to undergo CPR. Age, previous myocardial infarction and heart failure were significantly associated with the willingness or lack of willingness to undergo CPR. Forty percent of the participants had attended one or more courses but only a few within the last two years. The major reasons for not being educated in CPR were a lack of awareness of the availability of CPR training for the public, lack of interest or lack of enterprise. Among those not educated in CPR, 46% would like to attend a course. A hospital was the preferred location for the course, often due to the perceived higher competence of the instructors, but sometimes, because it offered a safe environment. The primary health care centre was preferred because of its location near the participants' homes. In order to increase the proportion of people trained in CPR in target groups such as cardiac care patients and their family members, healthcare professionals should provide patients with information and opportunities to attend locally situated, professionally led courses.
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PMID:The attitude of cardiac care patients towards CPR and CPR education. 1513 93

The combination of spironolactone with an ACE inhibitor for patients with heart failure may cause severe hyperkalemia. We report the case of a female patient, who developed hyperkalemic (11.4 mmol/l) cardiac arrest probably induced by combined spironolactone and ACE-inhibitor therapy. She was treated successfully by hemodiafiltration under on-going resuscitation which resulted in restoration of spontaneous circulation within 30 min of starting CPR. She was discharged 2 weeks later without any residual neurological effects.
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PMID:[Successful resuscitation of a patient with hyperkalemic cardiac arrest by emergency hemodiafiltration]. 1591 33

Hemodynamic monitoring has been used extensively during the last decades for risk stratification and guiding treatment of patients with cardiovascular destabilization, especially in the scenario of acute heart failure and cardiac shock. Every cardiac pump has its own maximum performance, which denotes its pumping capability. The heart is a muscular mechanical pump with an ability to generate both flow (cardiac output) and pressure. The product of flow output and systemic arterial pressure is the rate of useful work done, "or the cardiac power" (CP). Cardiac pumping capability can be defined as the cardiac power output achieved by the heart during maximal stimulation, and cardiac reserve is the increase in power output as the cardiac performance is increased from the resting to the maximally stimulated state (CPR). Resting CP for a hemodynamically stable average sized adult is approximately 1 W. However, during stress or exercise, CPR can be recruited to increase the heart's pumping ability up to 6 W. In acute heart failure, the patient becomes hemodynamically unstable, and most of the cardiac pumping potential is recruited in order to sustain life. Hence, cardiac power measurements in patients with acute heart failure or with cardiogenic shock at rest represent most of the recruitable reserve available during the acute event, and their measurement reflects the severity of the patient's condition. It has been found that a cutoff value for CP of 0.53 W accurately predict in-hospital mortality for cardiogenic shock patients. Others investigators observed cutoff for increased mortality of CP < 1 W, data that were obtained at doses of maximal pharmacologic support yielding the individual maximal CP. In our experience, the cutoff value for CP that accurately predicts in-hospital mortality for cardiogenic shock patients is 0.7 W, but its impact on short-term prognosis is clearer if the patient achieves a CP equal or higher than 1 W after an optimal myocardial revascularization with interventional cardiac procedures. According to the data collected from the literature, CP deserves a place in the evaluation of the patient with cardiogenic shock due to an acute myocardial infarction, but a more profound analysis of this parameter an further evaluation are required in order to better understand its prognostic meaning in this acute cardiac syndrome.
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PMID:["Cardiac power output" an old tool, possibly a modern tool for assessing cardiac pumping capability, as well as for a short-term prognosis in cardiogenic shock due to acute myocardial infarction]. 1674 10

Chronic hemodynamic overload on the heart results in pathological myocardial hypertrophy, eventually followed by heart failure. Phosphatase calcineurin is a crucial mediator of this response. Little is known, however, about the role of calcineurin in response to acute alterations in loading conditions of the heart, where it could be mediating beneficial adaptational processes. We therefore analyzed proteome changes following a short-term increase in preload in rabbit myocardium in the absence or presence of the calcineurin inhibitor cyclosporine A. Rabbit right ventricular isolated papillary muscles were cultivated in a muscle chamber system under physiological conditions and remained either completely unloaded or were stretched to a preload of 3 mN/mm(2), while performing isotonic contractions (zero afterload). After 6 h, proteome changes were detected by two-dimensional gel electrophoresis and ESI-MS/MS. We identified 28 proteins that were upregulated by preload compared to the unloaded group (at least 1.75-fold regulation, all P < 0.05). Specifically, mechanical load upregulated a variety of enzymes involved in energy metabolism (i.e., aconitase, pyruvate kinase, fructose bisphosphate aldolase, ATP synthase alpha chain, acetyl-CoA acetyltransferase, NADH ubiquinone oxidoreductase, ubiquinol cytochrome c reductase, hydroxyacyl-CoA dehydrogenase). Cyclosporine A treatment (1 micromol/l) abolished the preload-induced upregulation of these proteins. We demonstrate for the first time that an acute increase in the myocardial preload causes upregulation of metabolic enzymes, thereby increasing the capacity of the myocardium to generate ATP production. This short-term adaptation to enhanced mechanical load appears to critically depend on calcineurin phosphatase activity.
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PMID:Myocardial adaptation of energy metabolism to elevated preload depends on calcineurin activity : a proteomic approach. 1827 99


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