Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042510 (ventricular fibrillation)
 10,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antiarrhythmic efficacy of mexiletine in acute myocardial infarction (AMI) was studied in 99 patients randomized to mexiletine or placebo treatment. The loading dose was 250 mg i.v. and 400 mg orally followed by 200 mg orally 2 h later, and thereafter 200 mg t.i.d. up to 42 h. Arrhythmias occurring during 48 h were analysed from continuous electrocardiographic recordings. AMI was verified in 35 of 50 mexiletine patients and in 38 of 49 placebo patients. No deaths or instances of ventricular fibrillation occurred in the AMI patients. The number of patients who had any event of accelerated idioventricular rhythm (AIVR; P less than 0.05) runs of ventricular premature beats (VPBs; P less than 0.01), ventricular tachycardia (P less than 0.01) and Ron T beats (P less than 0.05) was smaller in the mexiletine group than in the placebo group. The number of all VPBs (P less than 0.05), hours with occurrence of AIVR (P less than 0.05), runs (P less than 0.01) and Ron T beats (P less than 0.05) was smaller in the mexiletine than in the placebo group. Serum levels of mexiletine tended to be low throughout the study. The half-life of the elimination was 13.7 +/- 7.2 h (means +/- S.D.). Adverse effects were infrequent, and the treatment was well-tolerated. Combined iv. and oral mexiletine prophylaxis significantly suppressed repetitive ventricular tachyarrhythmias and Ron T beats. However, no clinical benefit from mexiletine treatment could be shown in a coronary care unit with a low frequency of primary ventricular fibrillation.
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PMID:Antiarrhythmic efficacy of combined intravenous and oral mexiletine in acute myocardial infarction. A double blind placebo-controlled study. 638 36

Aconite poisoning was examined in five patients (four males and one female) aged 49 to 78 years old. The electrocardiogram findings were as follows: ventricular tachycardia and ventricular fibrillation in case 1, premature ventricular contraction and accelerated idioventricular rhythm in case 2, AIVR in case 3, and nonsustained ventricular tachycardia in cases 4 and 5. The patient in case 1 was given percutaneous cardiopulmonary support because of unstable hemodynamics, whereas the other patients were treated with fluid replacement and antiarrhythmic agents. The main aconitine alkaloid in each patient had a half-life that ranged from 5.8 to 15.4 h over the five cases, and other detected alkaloids had half-lives similar to the half-life of the main alkaloid in each case. The half-life of the main alkaloid in case 1 was about twice as long as the half-lives in the other cases, and high values for the area under the blood concentration-time curve and the mean residence time were only observed in case 1. These results suggest that alkaloid toxicokinetics parameters may reflect the severity of toxic symptoms in aconite poisoning.
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PMID:Five cases of aconite poisoning: toxicokinetics of aconitines. 1757 59

Accelerated idioventricular rhythm is defined as a ventricular rhythm of 60-100 beats per minute or a ventricular tachycardia that does nor exceed 120 beats per minutes. Although, it rarely converts to a fatal arrhythmia like ventricular fibrillation, it needs to be differentiated from AIVR, which is from another origin. AIVR may occur due to ischemic heart disease (ST elevated myocardial infarction), cardiomyopathy, rheumatic fever and digitalis intoxication. We report here on a case of AIVR that was related to desflurane administration.
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PMID:Accelerated idioventricular rhythm associated with desflurane anesthesia :A case report. 3062 90