Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ECGs obtained on arrival at the hospital from 277 patients with acute myocardial infarction were analyzed retrospectively for PR displacements, which were classified as major or minor criteria for atrial infarction and related to the later occurrence of supraventricular arrhythmia in the hospital. Major criteria were (1) PR segment elevation greater than 0.5 mm in leads V5 and V6 with reciprocal PR segment depression in leads V1 and V2, (2) PR segment elevation greater than 0.5 mm in lead I with reciprocal PR segment depression in leads II and III, and (3) PR segment depression greater than 1.5 mm in precordial leads and greater than 1.2 mm in leads I, II, and III. Abnormal P waves were classified as minor criteria. Major and minor criteria were found in 15 (5.4%) and 19 (6.9%) patients, respectively. Eight (53.3%) patients with major and six (31.6%) with minor criteria had supraventricular arrhythmias, giving odds ratios of 9.9 and 3.7, respectively. Enzyme-estimated infarct size, the occurrence of heart failure, and mortality rates did not differ in patients with or without major criteria for atrial infarction. We conclude that the occurrence of PR segment displacements on the admission ECG may predict the risk of developing supraventricular arrhythmias during hospitalization for myocardial infarction.
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PMID:The relationship between ECG signs of atrial infarction and the development of supraventricular arrhythmias in patients with acute myocardial infarction. 172 51

Much recent attention has been focused on the tachycardia-induced heart failure model. We hypothesized that sustained tachycardia would lead to myocardial depression in rabbits, as it does in dogs and swine. We evaluated the passive and active length-tension relations and postrest contraction behavior in right ventricular papillary muscles from 22 New Zealand White rabbits, 11 controls, and 11 subjected to ventricular pacing at a rate of 400 beats/min for 29.4 +/- 10.6 days. Studies were performed in oxygenated buffer at 22 degrees C. Active tension was significantly reduced at muscle lengths of 0.95.Lmax and above; at Lmax it was 4.7 +/- 0.2 g/mm2 for the control group and 3.3 +/- 0.2 g/mm2 for the paced group (P less than 0.005). Both groups showed increased force development when the concentration of calcium in the buffer was increased. There were no differences between the groups in the passive length-tension relations. Of note, postrest contraction data showed that the second postrest beat was smaller for the paced animals for rest intervals up to 2 min, suggesting that beat-to-beat trans-sarcolemmal calcium handling may differ from normal in this model. We conclude that sustained tachycardia will lead to myocardial depression in rabbits; the extension of this model to a small animal species may offer new ways to explore its causative mechanisms.
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PMID:Myocardial depression produced by sustained tachycardia in rabbits. 173 23

Poisoning is a significant problem in the elderly. The majority of poisonings in older people are unintentional and may result from dementia and confusion, improper use of the product, improper storage or mistaken identities. Depression is also common in the elderly and suicide attempts are more likely to be successful in this age group. The elderly patient's recuperative abilities may be inadequate as a result of numerous factors including impaired hepatic or renal function as well as chronic disease processes. General management of poisoning in the elderly parallels management of younger adults, but it is especially important to ascertain underlying medical conditions and concurrent medications. In most poisonings, activated charcoal and cathartic are sufficient. Haemodialysis or haemoperfusion may be required at lower plasma drug concentrations in elderly patients. While the specific indications for antidotes are the same for all age groups, dosage alterations and precautions may need to be considered in the elderly. Drugs most often implicated in poisonings in the elderly include psychotherapeutic drugs, cardiovascular drugs, analgesics and anti-inflammatory drugs, oral hypoglycaemics and theophylline. Cardiovascular and neurological toxicities occur with overdoses of neuroleptic drugs and, more frequently and severely, with cyclic antidepressants. Patients with pre-existing cardiovascular disease are at particular risk of worsening ischaemic heart disease and congestive heart failure. Benzodiazepines only appear to produce significant toxicity during long term administration or in combination with other CNS depressants. Digoxin can cause both chronic and acute intoxication, most seriously cardiac toxicity including severe ventricular arrhythmias, second or third degree heart block or severe refractory hyperkalaemia. Immune Fab antibody is indicated for the management of digoxin toxicity, although patients dependent on the inotropic effect of digoxin may develop heart failure after digoxin Fab antibody administration. Nitrates can cause toxicity including headache, vomiting, hypotension and tachycardia from excessive sublingual, transdermal or intravenous doses. Conduction disturbances and hypotension occur with overdoses of antihypertensive drugs; these effects are mild with angiotensin converting enzyme (ACE) inhibitors, occasionally severe with beta-blockers and of significant concern with calcium channel antagonists. The elderly commonly use aspirin and other salicylates, are more likely to develop chronic intoxications to these agents, and are more susceptible to severe complications such as pulmonary oedema. Salicylate poisoning, recognition of which is often delayed, should be considered in elderly patients with neurological abnormalities or breathing difficulties, especially in the setting of acid-base abnormalities. The clinical effects of NSAID overdose are mild and usually involve the central nervous system and gastrointestinal tract.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Poisoning in the elderly. Epidemiological, clinical and management considerations. 179 7

Diastolic dysfunction is an important cause of the clinical syndrome of congestive heart failure. Traditionally, the syndrome of pulmonary congestion due to the elevation of left heart filling pressure has been attributed to the depressed ability of the heart to eject blood during systole, with a secondary increase in left ventricular volume. However, heart failure can also occur when the left ventricle fails to receive blood during diastole at low filling pressures. With a mild degree of resistance of the left ventricle to diastolic filling, the initial hemodynamic manifestation may just be the elevation of left ventricular diastolic pressure and pulmonary venous pressure. More severe resistance to left ventricular filling may cause an inadequate extent of diastolic filling and insufficient myofiber stretch, which results in the depression of stroke volume. In this review, the factors contributing to diastolic dysfunction are discussed, with a particular focus on the role of diastolic heart failure in patients with ischemic heart disease or hypertrophy.
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PMID:Significance of diastolic dysfunction of the heart. 182 70

The prognosis is poor for patients with left ventricular enlargement associated with large infarcts. We studied 78 patients using gated single-photon emission computed tomography (SPECT, to assess left ventricular volumes), right heart catheterization (to measure pulmonary wedge pressure and cardiac output), and conventional planar radionuclide ventriculography (to estimate ejection fraction), 2-6 days, 3-5 weeks, and 5-8 months after their first myocardial infarction. Patients were assigned to a large or small infarct-size group based on creatine kinase analysis. In 37 patients with large infarcts, left ventricular volume increased and was greater than 27% after 5-8 months than after 2-6 days (p less than 0.05). Although ejection fraction remained significantly depressed, stroke volume, which initially declined, was restored as a result of dilation and thus returned to normal by 3-5 weeks, indicating that enlargement of the left ventricle compensated for the loss of contractile myocardium and depression of global ejection fraction. The progressive nature of left ventricular dilation suggested that this process is of major pathophysiologic importance and that it plays an etiologic role in the genesis of heart failure and perhaps of sudden death following myocardial infarction. Dilation preceded hemodynamic deterioration, which became evident on exercise after 5-8 months in patients with large infarcts.
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PMID:Serial changes in left ventricular size after acute myocardial infarction. 183 92

Since the discovery of cyclic nucleotide phosphodiesterase 30 years ago, there have been major advances in our knowledge of this group of isoenzymes. Five families, each composed of several isoforms and having differing tissue distributions, have been described. David Nicholson and colleagues compare the tissue distribution of phosphodiesterase isoenzymes and discuss the differential effects of inhibition of particular isoenzymes, with differing subcellular localization, on tissue function. They also review the potential use of isoenzyme selective phosphodiesterase inhibitors in a range of clinical disorders such as heart failure, asthma, depression and dementia.
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PMID:Differential modulation of tissue function and therapeutic potential of selective inhibitors of cyclic nucleotide phosphodiesterase isoenzymes. 184 33

The phenomenon of postexcitatory depression (PED) of baroreceptors is related to augmentation of Na(+)- K(+) -adenosinetriphosphatase (ATPase) activity. To provide additional evidence to support the hypothesis that dogs with chronic heart failure have augmented Na(+) -K(+) -ATPase activity in baroreceptor endings, the present study was undertaken to compare the duration of the PED of carotid sinus baroreceptors from normal and heart failure dogs. The effect of perfusion of the carotid sinus with a cardiac glycoside was also investigated. Eight normal and six dogs with experimental heart failure induced by ventricular pacing (250 beats/min for approximately 5 wk) were used in this study. Dogs were anesthetized, and the carotid sinus was isolated and perfused. Single baroreceptor units from the carotid sinus nerve were recorded, and the duration of the PED was measured. The relationship between the magnitude of the pressure steps and the duration of PED was determined. Duration of PED was significantly prolonged in the heart failure group at each pressure step (range from 2.7 to 9.0 s compared with 0.5 to 2.9 s in normal dogs). For the relationship between the duration of the pressure step and duration of PED, the heart failure dogs exhibited a markedly longer duration of PED than the normal dogs (range from 2.3 to 12.4 s compared with 0.5 to 5.3 s in normal dogs). Perfusion of the carotid sinus with very low doses of ouabain decreased the duration of PED in the heart failure dogs; however, there was no such effect in the normal dogs. These data are consistent with the view that baroreceptor membranes have increased Na(+) -K(+) -ATPase activity in heart failure(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postexcitatory depression of baroreceptors in dogs with experimental heart failure. 184 69

A reduction in exercise capacity is a common feature of congestive heart failure. We hypothesized that depressed aerobic enzyme activity of skeletal muscle may contribute to this exercise intolerance. Biopsy samples of vastus lateralis muscle were obtained from seven patients with severe chronic heart failure and analyzed for aerobic enzyme activity. Compared with normal laboratory controls, the patients with heart failure had a moderate reduction (greater than 60%) in skeletal muscle citrate synthase and a marked reduction (greater than 90%) in succinate dehydrogenase and cytochrome oxidase (all p less than 0.001). Depression of aerobic enzyme activity of skeletal muscle is associated with severe chronic heart failure and is likely one of the contributory factors for impaired exercise capacity seen in the advanced stages of this condition.
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PMID:Depressed aerobic enzyme activity of skeletal muscle in severe chronic heart failure. 185 Apr 46

Isovolumic left ventricular (LV) preparations were used to assess myocardial failure associated with dietary taurine deficiency in cats. Adult female cats (n = 12) were fed a purified diet devoid of taurine for 6-8 mo. Six of the cats received 1,000 mg of crystalline taurine orally once daily. The remaining six cats were not provided taurine replacement. Compared with control preparations, hearts isolated from taurine-deficient cats generated significantly lower values for developed LV systolic pressure (107 +/- 6 vs. 66 +/- 15 mmHg; P less than 0.05), maximal rate of LV pressure rise (+dP/dtmax; 1,103 +/- 38 vs. 718 +/- 172 mmHg/s; P less than 0.05), and fall (-dP/dtmax; 930 +/- 46 vs. 587 +/- 129 mmHg/s; P less than 0.05). LV function curves generated by hearts from taurine-deficient cats were shifted downward and to the right of control curves, demonstrating inotropic depression. In addition, end-diastolic pressure-volume (compliance) relationships in hearts from taurine-deficient cats were shifted downward and to the right of controls in the direction of increased chamber compliance or distensibility. Ten millimolar taurine significantly improved inotropic indexes only in hearts from taurine-deficient cats but failed to affect diastolic compliance. Myocardial contractile dysfunction and LV chamber dilatation in hearts from taurine-deficient cats verify a causal association between dietary deficiency of this amino acid and dilated cardiomyopathy in this species.
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PMID:Systolic and diastolic dysfunction of the left ventricle induced by dietary taurine deficiency in cats. 185 11

Overnight studies were performed in 10 patients with severe chronic left heart failure (New York Heart Association grades III and IV) without pulmonary disease and in eight controls. Transcutaneous oxygen (Po2) and carbon dioxide tensions (Pco2) and oxygen saturation were measured and the electro-cardiogram was recorded. During sleep mean oxygen saturation fell to 92.7% (minimum 86.1%) from 95.1% when awake. During the night oxygen saturation was below 95% for 62% of the time, below 90% for 6% of the time, and below 85% for 1% of the time. In four patients there were oxygen desaturation dips (a fall of greater than 4% in oxygen saturation from a stable baseline that lasted greater than 30 s) with concurrent increases in Pco2. Two patients had bradycardia during the dips: in one there was non-sustained ventricular tachycardia during the dips and in the other there was ST depression (greater than 0.1 mV at 80 ms after the J point) during a dip. In the controls the fall in mean oxygen saturation from 95.4% when they were awake to 94.4% when they were asleep was less than the fall in patients with heart failure and there were no desaturation dips or arrhythmias. Thus patients with severe heart failure had episodes of oxygen desaturation during sleep, some of which were associated with arrhythmia. Such episodes may be related to the increased risk of sudden death in chronic heart failure.
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PMID:Overnight studies in severe chronic left heart failure: arrhythmias and oxygen desaturation. 190 36


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