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 24-year-old woman presented with right-sided infectious endocarditis due to methicillin-resistant Staphylococcus aureus (MRSA). This is the first report of right-sided infectious endocarditis caused by MRSA in Japan. The patient was admitted to the Jichi Medical School Hospital because of fever of unknown origin and disturbance of consciousness. Several months before, she had discontinued treatment for hyperthyroidism. Antibiotics effective against MRSA, vancomycin and flomoxef, were given intravenously, but a new heart murmur was detected. Echocardiographic study revealed vegetations attached to the tricuspid valve and abscess formation on the ventricular septum. The vancomycin dosage was increased and arbekacin sulfate was also given from the sixth hospital day. However, these antibiotics had very little effect and the abscess rapidly increased in size. Color flow mapping finally demonstrated intracardiac shunt flow through the ruptured abscess of the ventricular septum and sinus of Valsalva. She died suddenly, probably from heart failure. The prognosis of infectious endocarditis due to MRSA is poor and drug therapy often fails. Thus, surgery should be considered in the early stage.
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PMID:[Right-sided infectious endocarditis due to methicillin-resistant Staphylococcus aureus resulting in ruptured abscess of the ventricular septum and sinus of Valsalva]. 777 96

Iron poisoning is the most common cause of overdose mortality in children under six years of age and there are no reports of survival with iron levels > 2687 mumol/L (> 15,000 micrograms/dL). A 22-month-old male was brought to the emergency department by his parents after ingesting an estimated 50 ferrous sulfate tablets (60 mg elemental iron/tablet) several hours earlier. Despite spontaneous emesis and gastric lavage his condition deteriorated and he was found to have a serum iron of 2992 mumol/L (16,706 micrograms/dL). During the first four days in the intensive care unit, he developed coma, metabolic acidosis, hypovolemic and cardiogenic shock, liver failure, coagulopathy and adult respiratory distress syndrome. He was treated with a unique deferoxamine dosage schedule (25 mg/kg/h for 12 h/d x 3 d), mechanical ventilation, Swan-Ganz catheter monitoring, dopamine/nitroprusside therapy, blood product, bicarbonate, electrolyte and volume replacement. After a prolonged hospital course complicated primarily by gastric outlet obstruction he was dismissed on full oral feedings, gaining weight, and neurologically intact. Swan-Ganz catheter monitoring guided the management of this patient's shock, iron-induced cardiac failure, and deferoxamine mesylate induced adult respiratory distress syndrome. Further experience and research is required to determine the most appropriate deferoxamine mesylate dosing schedule and our experience expands the range for possible survival after massive iron overdose.
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PMID:Survival after a severe iron poisoning treated with intermittent infusions of deferoxamine. 783 15

The use of protamine sulfate in patients has been associated with severe circulatory collapse and myocardial failure. However, the exact mechanisms responsible for these reactions to protamine remain unclear. Accordingly, we examined the effect of protamine on isolated myocyte contractile function. Indexes of isolated myocyte contractile function, percent shortening, and velocity of shortening were examined using videomicroscopy. Porcine cardiocytes (n = 75) were studied at baseline and in the presence of 80 micrograms/mL protamine. In addition, myocyte function was examined sequentially, first during treatment with 8 IU/mL heparin and then after the addition of a protamine dose sufficient to completely bind the heparin. The binding of heparin and protamine resulted in the formation of a heparin-protamine complex. The protamine concentration of 80 micrograms/mL is approximately equal to the serum concentration of protamine obtained in patients when administered in a dose of 5 mg/kg. In the presence of 80 micrograms/mL protamine, both percent shortening and velocity of shortening fell by more than 32% from baseline values (p < 0.05). The presence of either heparin alone or the heparin-protamine complex resulted in no change in baseline myocyte contractile measurements. Furthermore, to examine the effect of protamine on myocyte beta-adrenergic responsiveness a second series of experiments were performed. Myocyte contractile function was measured when 25 nmol/L isoproterenol was added to each of the protocols above. The presence of 80 micrograms/mL protamine resulted in a significant blunting of myocyte beta-adrenergic responsiveness. The presence of either heparin alone or the heparin-protamine complex resulted in no change in myocyte beta-adrenergic responsiveness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of protamine on myocyte contractile function and beta-adrenergic responsiveness. 817 66

Magnesium has previously been used in the treatment of various arrhythmias, but few randomized and prospective studies are available. In a single-blind study, the efficacy and safety of intravenous magnesium sulfate (bolus doses of 5 + 5 mmol followed by infusion of 0.04 mmol/min) versus verapamil (5 + 5 mg followed by 0.1 mg/min) was evaluated in 57 patients with supraventricular arrhythmias (supraventricular tachycardia, atrial fibrillation, and atrial flutter) of recent onset (less than 1 week). Fifteen (58%) of the patients receiving magnesium (n = 26) converted to sinus rhythm within 4 h, and 16 (62%) within 24 h. Verapamil caused a lower ventricular rate, but only six (19%) of the patients (n = 31) converted to sinus rhythm within 4 h (p < 0.01) and 16 (52%) within 24 h (NS). No side effects were observed during magnesium infusion, whereas six patients receiving verapamil had to be withdrawn from further study medication due to symptomatic side effects (hypotension in three, cardiac failure in three). Magnesium appears to be an effective and safe drug for the treatment of supraventricular arrhythmias. The overall efficacy for conversion to sinus rhythm is at least as effective as with verapamil, and its action is more rapid.
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PMID:The effect of magnesium versus verapamil on supraventricular arrhythmias. 850 78

Sulfoconjugated catecholamines have been regarded simply as metabolites of free catecholamines. However, a conjugated form of the catecholamine, dopamine has recently attracted much attention because it is present at high levels in the plasma of humans and experimental animals. We carried out experimental and clinical studies to determine the physiological significance of this large amount of dopamine conjugate in the plasma. Clinical studies showed that the plasma level of dopamine sulfate decreased significantly during the acute phase of heart failure, whereas that of free dopamine increased. Moreover, the plasma level of conjugated dopamine in patients with essential hypertension was higher than that in control subjects, and being highest in patients with renal hypertension. In experimental studies, we examined the activity for deconjugating DA sulfate in homogenates of organs from dogs. The kidney and liver exhibited the highest activities, and in the heart, the activity was higher in the atrium than the ventricle. We also examined the effect of dopamine sulfate on isolated perfused rat heart. Dopamine sulfate was found to be converted to free dopamine, which was responsible for the positive inotropic action, in atrial tissue. Moreover, deconjugation of DA sulfate to the free form was accelerated by a high work lord on the heart. From these results, we conclude that the formation of dopamine sulfate plays a role in regulating the level of plasma free dopamine and that plasma dopamine sulfate may be a storage or reserve form of dopamine. Free (or active) dopamine may be formed through a deconjugation reaction when necessary.
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PMID:Physiological significance of plasma sulfoconjugated dopamine: experimental and clinical studies. 852 36

The purpose of this study was to examine the activity and expression of sarcoplasmic reticulum (SR) Ca(2+)-ATPase in left ventricular (LV) myocardium of dogs with chronic heart failure (HF). LV and right ventricular (RV) tissue specimens were obtained from six normal (NL) control dogs and six dogs with chronic HF (LV ejection fraction, 23 +/- 2%) produced by multiple sequential intracoronary microembolizations. Thapsigargin-sensitive Ca(2+)-ATPase activity was measured in isolated SR membrane fractions prepared from LV and RV myocardium. Ca(2+)-ATPase expression, using a specific dog myocardium monoclonal antibody, was measured in sodium dodecyl sulfate (SDS) extract prepared from LV and RV myocardium. Ca(2+)-ATPase activity in both ventricles of NL or HF dogs increased with increasing Ca2+ concentration and reached a plateau at 3 microM Ca2+. The maximal velocity (Vmax, mumol Pi released.min-1.mg-1) of Ca(2+)-ATPase activity was significantly lower in LV of HF dogs compared with NL (0.15 +/- 0.01 vs. 0.23 +/- 0.01, P < 0.05), whereas the affinity of the Ca2+ pump for Ca2+ was unchanged. LV tissue levels of Ca(2+)-ATPase (densitometric units/5 micrograms noncollagen protein) were also significantly lower in LV myocardium of HF dogs compared with NL (3.52 +/- 0.43 vs. 5.53 +/- 0.47, P < 0.05). No significant differences in Ca(2+)-ATPase activity or expression were observed in RV myocardium of HF dogs compared with NL. We conclude that SR Ca(2+)-ATPase activity and protein levels are reduced in LV myocardium of dogs with chronic HF. This abnormality of the SR Ca2+ pump of the failed LV can result in impaired Ca2+ uptake and ultimately to Ca2+ overload and global LV dysfunction.
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PMID:SR Ca(2+)-ATPase activity and expression in ventricular myocardium of dogs with heart failure. 924 69

This study in rats investigated the effects of 0.5 mEq/1 kg body weight of magnesium sulfate solution upon hypoxic left cardiac ventricular pressure (Part 1), optimal timing for injection of magnesium sulfate solution for successful resuscitation (Part 2) and survival benefits of magnesium sulfate after 8 or 12 min of hypoxia (Part 3) in rats resuscitated by single bolus arterial reperfusion using 2 ml of arterial blood and 6-9 micrograms epinephrine. A total of 153 pentobarbital anesthetized rats were subjected to 8 or 12 min 0.75% O2:99.25% N2 hypoxia in order to induce cardiac arrest. In Part 1, 13 rats (six control and seven injected with magnesium sulfate solution) were subjected to 12 min hypoxia and cardiac left ventricular pressure (LVP) was measured. In Part 2, 47 rats were exposed to 12 min of hypoxia. Normal saline or magnesium sulfate solution was injected prior to hypoxia, at 2 or 4 min of hypoxia, to find the optimal timing of magnesium sulfate injection for successful resuscitation by arterial reperfusion. In Part 3, 90 rats were studied to determine 7-day survival. Two control groups were injected with saline during 8 min (29 rats) or 12 min (18 rats) of hypoxia and two groups received magnesium sulfate solution during 8 min (14 rats) and 12 min (29 rats) of hypoxia. Magnesium sulfate fully reversed the hypoxic increase of LVP and improved survival after 12 min of hypoxia from approximately 15 (control) to 100% if given during the first 2.5 min of hypoxia. The main cause of the progressive resuscitation failure after 8 or 12 min control hypoxia was a progressive increase in acute cardiac failure. Although magnesium sulfate solution significantly improved immediate recovery after hypoxia (8 and 12 min), mortality due to reperfusion injury (para or tetraplegia) was observed in 62% of rats surviving longer than 1 day after 8 min and 100% after 12 min hypoxia (in control rats-50 and 100%, respectively). The overall survival after hypoxia, with or without reperfusion injury, was relatively low: 28% in control groups after 8 min and 17% after 12 min. In the magnesium sulfate groups these numbers were only slightly higher, 36 and 21%, respectively. It is concluded that in conjunction with arterial reperfusion magnesium sulfate infusion is very effective in improving acute cardiac recovery after 8-12 min of hypoxia. The likely mechanism of magnesium sulfate action is decreased incidence of ventricular fibrillation (VF) and asystole, and possibly myocardial relaxation during and after hypoxia, a property which may qualify MgSO4 as an ischemic preconditioning agent. Poor long-term survival rates of rats exposed to hypoxia and resuscitated by intraarterial reperfusion do not support its use in resuscitation.
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PMID:Magnesium sulfate solution dramatically improves immediate recovery of rats from hypoxia. 925 61

In order to address the role that the ambient air pollution mix, comprised of gaseous pollutants and various physical and chemical measures of particulate matter, plays in exacerbating cardiorespiratory disease, daily measures of fine and coarse particulate mass, aerosol chemistry (sulfates and acidity), and gaseous pollution (ozone, nitrogen dioxide, sulfur dioxide, and carbon monoxide) were collected in Toronto, Ontario, Canada, in the summers of 1992, 1993, and 1994. These time series were then compared with concurrent data on the number of daily admissions to hospitals for either cardiac diseases (ischemic heart disease, heart failure, and dysthymias) or respiratory diseases (tracheobronchitis, chronic obstructive long disease, asthma, and pneumonia). After adjusting the admission time series for long-term temporal trends, seasonal variations, the effects of short-term epidemics, day of the week effects, and ambient temperature and dew point temperature, positive associations were observed for all ambient air pollutants for both respiratory and cardiac diseases. Ozone was least sensitive to adjustment for the gaseous and particulate pollution measures. However, the association between the health outcomes and carbon monoxide, fine and coarse mass, sulfate levels and aerosol acidity could be explained by adjustment for exposure to gaseous pollutants. Increases in ozone, nitrogen dioxide, and sulfur dioxide equivalent to their interquartile ranges corresponded to an 11% and 13% increase in daily hospitalizations for respiratory and cardiac diseases, respectively. The inclusion of any one of the particulate air pollutants in multiple regression models did not increase these percentages. Particle mass and chemistry could not be identified as an independent risk factor for the exacerbation of cardiorespiratory diseases in this study beyond that attributable to climate and gaseous air pollution. We recommend that effects of particulate matter on health be assessed in conjunction with temporally covarying gaseous air pollutants.
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PMID:The role of particulate size and chemistry in the association between summertime ambient air pollution and hospitalization for cardiorespiratory diseases. 928 96

Dynamic changes in the reduction-oxidation (redox) state of the tissue lead to the pathophysiological condition. Reduced homocysteine causes dysfunctions in endothelium. The proliferation of smooth muscle cells may lead to occlusive vascular disease, ischemia, and heart failure, but whether fibrosis and hypertension are a consequence of smooth muscle proliferation is unclear. Redox changes during hyper-homocyst(e)inemia may be one of the causes of premature atherosclerotic heart disease. To examine the effect of homocystine on human vascular smooth muscle cells (HVSMC), we isolated HVSMC from idiopathic dilated cardiomyopathic hearts. Coronaries in these hearts were apparently normal. HVSMC numbers in culture were measured by hemocytometer in the presence and absence of homocystine. Results show that homocystine induced cellular proliferation. This proliferation was reversed by the addition of the antioxidant N-acetylcysteine (NAC). Homocystine induces collagen expression in a dose- and time-dependent manner, as measured by Northern blot (mRNA) analysis. The 50% inhibitory concentration of 5 microM for collagen was estimated. The induction of collagen was reversed by the addition of NAC and reduced glutathione. To localize the receptor for homocystine on HVSMC, we synthesized fluorescamine-labeled homocystine conjugate. Incubation of labeled homocystine with HVSMC demonstrated membrane and cytosol localization of homocystine binding. The receptor-ligand binding was disrupted by NAC. Based on sodium dodecyl sulfate-polyacrylamide gel electrophoresis fluorography, we observed a 40- to 25-kDa homocystine redox receptor in HVSMC. Our results suggested that the redox homocysteine induces HVSMC proliferation by binding to the redox receptor and may exacerbate atherosclerotic lesion formation by inducing collagen expression.
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PMID:Homocysteine redox receptor and regulation of extracellular matrix components in vascular cells. 948 29

The first case of chronic cardiac toxicity due to an antimalarial agent was reported in 1971 and since then several cases of heart failure, restrictive cardiomyopathy or atrioventricular block have been ascribed to this family of drugs. We report the case of a 43-year-old woman who developed juvenile chronic arthritis at the age of ten, followed in adulthood by sero-positive rheumatoid arthritis. In 1980 she was put under chloroquine sulfate (hydroxychloroquine was not available) in a dose of 200 mg/d (152.66 mg of chloroquine), with 10 mg/day of prednisone. She developed myalgia and increased skin pigmentation, but disregarded recommendations that these symptoms required discontinuation of chloroquine therapy. She was lost to follow-up, but continued the chloroquine therapy of her own accord. In December 1993, she developed a third-degree atrioventricular block with syncopes requiring implantation of a pacemaker. The rare but well-documented myopathy induced by antimalarial agents can produce early severe lesions of the cardiac muscle, which may have a predilection for the interventricular septum, explaining the risk of atrioventricular block. Although histologic studies were not performed in our patient, the clinical evidence of toxicity, absence of underlying heart disease and fairly young age of the patient pointed to chloroquine toxicity. Periodic cardiac investigations including electrocardiography may be warranted in patients under antimalarial therapy.
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PMID:Third-degree atrioventricular block in a patient under chloroquine therapy. 952 87


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