Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of histochemical, histoenzymological, and fluorescence microscopy studies of the conductive tissue of the heart in acute myocardial infarction in 30 fatal cases are presented. Focal decrease in redox and hydrolytic enzymes, monoaminoxidase, and cholinesterase in elementa of the conduction system as well as changes in the pattern of fluorescence of the specific muscle cells were found. The intensity of metabolic lesions was more pronounced at early stages of myocardial infarction in those cases where the conducting pathways were proximal to the foci of necrosis.
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PMID:[Functional morphology of the heart conduction system in acute myocardial infarct]. 21 11

Enhanced electrical stability of acutely ischemic myocardium with vagal stimulation and acetylcholinesterase inhibition has been demonstrated experimentally. To extend these findings clinically, within 24 hours of acute myocardial infarction, 11 patients underwent continuous 10 hour Holter monitoring: 2.5 hour control before and after 5 hour constant edrophonium infusion (0.25 to 2.00 mg./minute). Continuous infusion of the agent lowered heart rate 92 to 78 b.p.m. (p less than 0.01). Although mean total ventricular extrasystoles (PVC's) per 5 hours per patient (131) and PVC's per 1,000 beats (4.7) were unchanged (p greater than 0.05), potentially lethal tachyarrhythmias (malignant PVC's: multifocal, R on T, paried, greater than 5 per minute or ventricular tachycardia) were terminated in six of 10 patients by edrophonium. However, serious ventricular arrhythmias continued in three patients and appeared in four despite the agent. Ventricular fibrillation did not occur during the 10 hour period of study. In addition, the patients were evaluated hemodynamically and by His bundle electrograms before and after a 10 mg. bolus of edrophonium prior to the 10 hour constant infusion: heart rate declined (88 to 72 b.p.m., p less than 0.01), while mean arterial pressure (98 mm. Hg), left ventricular filling pressure (14 mm. Hg), cardiac index (2.4 L. per minute per square meter), and stroke work index (36 Gm.m./M.2) were unchanged (p greater than 0.05). The edrophonium bolus prolonged the A-H interval (117 to 135 msec., p less than 0.01) while the H-Q interval was unaltered (48 msec; p greater than 0.05). It is concluded that increased vagal tone with edrophonium did not reduce the over-all presence of premature ventricular contractions in the entire study group; however, the malignant nature of PVCs and ventricular tachycardia appeared to be lessened by the parasympathomimetic agent in certain patients. In addition, no adverse hemodynamic or intraventricular conduction effects were produced by edrophonium administration.
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PMID:Clinical evaluation of the enhancement of vagal tone in acute myocardial infarction by edrophonium hydrochloride: effects on ventricular arrhythmias, His bundle electrography, and left ventricular function. 83 66

The aim of the present work was to determine experimentally the prognostic value of reduced activity of serum acetylcholinesterase (ACE) in cases of acute myocardial infarction (AMI). In the first part of the research we studied the mechanism of this reduction by comparing the serum results with the levels of the enzyme in cardiac tissue in such cases. It was found that ACE activity is reduced in serum and also in cardiac tissue in AMI, in contrast to creatine kinase (CK) that is augmented in serum but reduced in cardiac tissue. This fact was interpreted as a "reduced cardiac flow of ACE," in contrast to the "augmented cardiac clearance of CK" in similar cases. In the second part of our research, 50 patients, admitted in our hospital for AMI, were examined and their blood analysed mainly for ACE and CK at brief intervals (every 2-3 days), during hospitalization, and thereafter every 1-2 weeks for 1-4 months. From the results of ACE activity it was possible to classify these variations into four groups, each of them having a defined prognostic value for the evolution of the AMI, a persistent reduced serum activity being interpreted as a bad, severe prognosis, with high morbidity or mortality (groups II and III). We suggest, therefore, that the determination of ACE in serum in cases of AMI, especially before discharge home of such patients, may be an additional useful laboratory test in such cases.
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PMID:The prognostic value of serum acetylcholinesterase in myocardial infarction. Theoretical and clinical considerations. 716 46

A complex of enzymatic tests, characterizing the liver function and cellular cytolysis in patients with acute myocardial infarction of various severities (without complications and with various types of complications and outcomes) was used in examinations over the first week of the disease. Significant changes in five of the seven tested enzymes were found: aspartate aminotransferase, glutamate dehydrogenase, sorbitol dehydrogenase, cholinesterase, alanine aminotransferase, the degree and incidence of changes in their activities being the lowest in the patients with acute myocardial infarction without complications, higher in those with this condition with isolated complications, still higher in those with combined complications and a favorable outcome, and the highest in those with combined complications and a lethal outcome. Secondary hepatopathy in patients with acute myocardial infarction augments as the complications develop, particularly in arrhythmia, disordered conductivity, and combined complications. Measurements of glutamate dehydrogenase and sorbitol dehydrogenase are recommended starting from the first day of the disease, of cholinesterase from the third day of the disease for a dynamic monitoring of the liver status in order to timely detect and correct hepatopathy and assess the status of patients with complicated acute myocardial infarction.
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PMID:[Enzyme diagnosis of liver dysfunction in acute myocardial infarct and its complications]. 800 Jul 90

In order to clarify the relationship between thyroid function and left ventricular function in acute myocardial infarction (AMI), 52 patients (63.3 +/- 11.0 years old) admitted to the coronary care unit within 24 hours after the onset were studied. Both FT3 and FT4 levels measured at 48-72 h after the onset (1.66 +/- 0.59 pg/ml, 1.02 +/- 0.37 ng/dl) were significantly lower than those on admission (2.99 +/- 0.76 pg/ml; p < 0.01, 1.14 +/- 0.25 ng/dl; p < 0.05) and controls (3.27 +/- 0.66 pg/ml; p < 0.01, 1.22 +/- 0.23 ng/dl; p < 0.05). The decline of these thyroid hormone levels correlated well with the severity of AMI (Killip's classification), hemodynamic deterioration and liver function (low levels of albumin and cholinesterase). Low thyroid hormone levels were also associated with the elevation of catecholamine and alpha-hANP levels on admission. Low cortisol and impaired renal function were recognized as factors which might prolong the condition of low thyroid hormones. Non-survivors showed significantly lower levels of FT3 and FT4 48 hours after onset, and a lower level of FT4 in aged patients was consistent with a poor prognosis. In conclusion, the measurement of thyroid hormones in AMI is important in evaluating the severity of the condition and waking a prognosis.
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PMID:[The prevalence and significance of abnormal thyroid hormone metabolism in acute myocardial infarction]. 804 96

Dysfunction of the autonomic nervous system is of prognostic value for sudden death after acute myocardial infarction. Although the use of beta-blockers to counteract the adrenergic hyperactivity has been shown to decrease mortality in these patients, there have been no reports on the role of cholinomimetic drugs in the prognosis of patients after myocardial infarction. The present study was designed to investigate the effect of the administration of pyridostigmine bromide, a reversible anti-cholinesterase agent, on cardiac cholinergic activity assessed by the resting and reflex heart rate responses. Eight healthy volunteers were submitted to a conventional 12-lead electrocardiogram to obtain resting heart rate, and to three non-invasive cardiovascular tests: respiratory sinus arrhythmia, Valsalva maneuver and 4-sec exercise test. On two different days and following a randomized cross-over double-blind protocol, the experiments were performed before and 120 min after oral administration of either pyridostigmine bromide (30 mg) or placebo. Pyridostigmine increase (P < 0.05) the duration of the R-R intervals at rest (pre: 898 +/- 30 msec; post: 1019 +/- 45 msec; pre-placebo: 916 +/- 26 msec; post: 956 +/- 28 msec; P > 0.05). Although the duration of the R-R intervals during the autonomic tests was also increased (P < 0.05), the derived indexes of maximal fluctuation during the maneuvers did not change. These results indicate that oral pyridostigmine produces tonic cardiac cholinergic stimulation while exerting no effect on its reflex changes. Further studies are needed to address the potential role of the administration of pyridostigmine in the prognosis of patients with acute myocardial infarction.
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PMID:Resting and reflex heart rate responses during cholinergic stimulation with pyridostigmine in humans. 919 46

The authors used 2 national Veterans Health Administration databases to identify outpatient medications and all 30 Elixhauser comorbidities for 2579 unique patients, age 65+ years, hospitalized for syncope in fiscal year 2004. For comparison, we identified other elderly patients hospitalized with acute myocardial infarction (N = 4491), fracture (N = 2797), or pneumonia (N = 9473). The categories of medications included drugs that affect the cardiovascular, central nervous, or the muscular skeletal system. The most notable differences between syncope compared to acute myocardial infarction patients occurred in central nervous system drugs in anticonvulsants/barbiturates, antidepressants, antihistamine/antinauseants, antipsychotics, and cholinesterase inhibitors (P < .0018). Comparing syncope patients with fracture patients, the central nervous medication profile was similar, but the cardiovascular medication profile differed (P < .0018); their hypertension comorbidities also differed (60.45% vs 46.34%); (P < .0016). These findings indicate significant potential associations that warrant further study. Studies linking national outpatient medications to hospitalizations for specific conditions can foster the development of more proactive pharmacovigilance systems.
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PMID:National Veterans Health Administration hospitalizations for syncope compared to acute myocardial infarction, fracture, or pneumonia in community-dwelling elders: outpatient medication and comorbidity profiles. 1670 7

We report the first case of ocular myasthenia gravis (OMG) in a patient with complete tetraplegia, highlighting diagnostic and management challenges. Spinal multidisciplinary rural clinic and specialised inpatient Spinal Cord Injury Unit, NSW, Australia. A 61-year-old man with established C5 AIS A tetraplegia, presented with sudden onset of diplopia and bilateral ptosis, later diagnosed as OMG, in context of other complex co-morbidities, including a cervical cord syrinx, obstructive sleep apnoea and labile blood pressure. Clinical findings were consistent with fluctuating bilateral partial third and sixth nerve palsies. Acetylcholine receptor antibodies were negative, but electromyography demonstrated muscle fatigue. The ocular signs responded well to pyridostigmine. Medications taken before diagnosis, including solifenacin for neurogenic bladder overactivity, were ceased to avoid attenuating the anti-cholinesterase effect. However, the unopposed anti-cholinesterase activity led to frequent and painful abdominal spasms, associated with uncontrolled detrusor hyperreflexia and worsening autonomic dysreflexia (AD). A trans-vesical phenol block to treat this provided only short-lasting benefit. Pyridostigmine was ceased to avoid provoking his abdominal spasms and his regular medications were recommenced. It was decided that the most appropriate treatment for his distressing diplopia was an eye patch. After discharge home, he continued to experience problems with recurrent urinary tract infections, abdominal spasms, episodic postural hypotension and AD. After 5 months, the patient died from an acute myocardial infarction. This case report contributes new knowledge about the rare presentation of OMG in a person with chronic tetraplegia.
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PMID:Ocular myasthenia gravis in a person with tetraplegia presenting challenges in diagnosis and management. 3126 10

Cardiovascular diseases remain a major cause of morbidity and mortality worldwide. Cardiovascular diseases such as acute myocardial infarction, ischaemia/reperfusion injury and heart failure are associated with cardiac autonomic imbalance characterized by sympathetic overactivity and parasympathetic withdrawal from the heart. Increased parasympathetic activity by electrical vagal nerve stimulation has been shown to provide beneficial effects in the case of cardiovascular diseases in both animals and patients by improving autonomic function, cardiac remodelling and mitochondrial function. However, clinical limitations for electrical vagal nerve stimulation exist because of its invasive nature, costly equipment and limited clinical validation. Therefore, novel therapeutic approaches which moderate parasympathetic activities could be beneficial for in the case of cardiovascular disease. Acetylcholinesterase inhibitors inhibit acetylcholinesterase and hence increase cholinergic transmission. Recent studies have reported that acetylcholinesterase inhibitors improve autonomic function and cardiac function in cardiovascular disease models. Despite its potential clinical benefits for cardiovascular disease patients, the role of acetylcholinesterase inhibitors in acute myocardial infarction and heart failure remediation remains unclear. This article comprehensively reviews the effects of acetylcholinesterase inhibitors on the heart in acute myocardial infarction and heart failure scenarios from in vitro and in vivo studies to clinical reports. The mechanisms involved are also discussed in this review.
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PMID:The effects of acetylcholinesterase inhibitors on the heart in acute myocardial infarction and heart failure: From cells to patient reports. 3159 11