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Valproic Acid Overdose Review of a Case With Electrocardiographic Changes.
Muñiz, AE
The Journal of emergency medicine. 2017;(3):333-338
Abstract
BACKGROUND Valproic acid (VPA) is increasingly used to treat a variety of medical disorders, such as seizures, psychiatric disorders, and headaches. Therefore, accidental and intentional ingestions with valproic acid are increasing. OBJECTIVES A case is presented in an adolescent with ischemic electrocardiographic changes after an acute overdose with VPA. DISCUSSION Major features of a valproic acid overdose include respiratory depression, progressive coma, hepatotoxicity, thrombocytopenia, and hemodynamic instability. Electrocardiographic abnormalities usually consist of tachycardia and nonspecific changes. Supportive care is indicated in most overdoses and involves the monitoring and correction of electrolyte abnormalities, coagulopathies, and acid-base imbalances. Treatment may include activated charcoal, naloxone, l-carnitine, and extracorporeal detoxification. CONCLUSIONS Valproic acid overdose is a relatively rare and electrocardiographic changes usually consist of tachycardia and nonspecific changes, but ischemic changes may occur and usually transient and require only recognition.
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Modeling of Amiodarone Effect on Heart Rate Control in Critically Ill Patients with Atrial Tachyarrhythmias.
Salem, JE, El-Aissaoui, M, Alazard, M, Hulot, JS, Aissaoui, N, Le-Heuzey, JY, Funck-Brentano, C, Faisy, C, Urien, S
Clinical pharmacokinetics. 2016;(8):991-1002
Abstract
AIMS: Amiodarone is the gold-standard medication to control heart rate in critically ill patients with atrial tachyarrhythmias (ATs); however, effective doses and covariates influencing its efficacy remain unknown. We therefore performed pharmacodynamic modeling of heart rate reduction induced by amiodarone in these patients. METHODS AND RESULTS This observational study included 80 consecutive severely ill patients receiving amiodarone to treat ATs. A total of 1348 time-heart rate observations with 361 amiodarone dose administrations were analyzed during a period of up to 6 days after hospital treatment initiation using a nonlinear mixed-effect model. Pretreatment with amiodarone before intensive care administration, paroxysmal versus persistent AT, catecholamine infusion, and fluid and magnesium loading were among the covariates assessed in the model. In case of paroxysmal AT in a patient not pretreated with amiodarone, a 300 mg intravenous loading dose combined with an 800 mg oral dose on the first day, followed by 800 mg/day orally for 4 days was effective in achieving a heart rate between 80 and 115 bpm within the first day, and to maintain it during the next 4 days. Corresponding doses were twice as high in patients with persistent AT. Use of intravenous magnesium (p < 0.02) and fluid loading (p < 0.02) was associated with an earlier and greater heart rate decrease, while use of dobutamine had an opposite influence (p < 0.05). CONCLUSIONS In critically ill patients with AT, the dose of amiodarone required to control heart rate is influenced by the type of AT and by other easily measurable conditions which may allow better individualization of amiodarone dosing.
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Toxicities associated with NBOMe ingestion-a novel class of potent hallucinogens: a review of the literature.
Suzuki, J, Dekker, MA, Valenti, ES, Arbelo Cruz, FA, Correa, AM, Poklis, JL, Poklis, A
Psychosomatics. 2015;(2):129-39
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Abstract
BACKGROUND A new class of synthetic hallucinogens called NBOMe has emerged as drugs of abuse. OBJECTIVE Our aim was to conduct a systematic review of published reports of toxicities associated with NBOMe ingestion. METHODS We searched PubMed for relevant English-language citations that described adverse effects from analytically confirmed human NBOMe ingestion. Demographic and clinical data were extracted. RESULTS A total of 10 citations met the criteria for inclusion, representing 20 individual patients. 25I-NBOMe was the most common analogue identified, followed by 25B-NBOMe and 25C-NBOMe. Fatalities were reported in 3 (15%) cases. Of all the patients, 7 (35%) were discharged after a period of observation, whereas 8 (40.0%) required admission to an intensive care unit. The most common adverse effects were agitation (85.0%), tachycardia (85.0%), and hypertension (65.0%). Seizures were reported in 8 (40.0%) patients. The most common abnormalities reported on laboratory tests were elevated level of creatinine kinase (45.0%), leukocytosis (25.0%), and hyperglycemia (20.0%). CONCLUSION NBOMe ingestion is associated with severe adverse effects. Clinicians need to have a high index of suspicion for NBOMe ingestion in patients reporting the recent use of hallucinogens.
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Safety of intravenous ivabradine in acute ST-segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention: a randomized, placebo-controlled, double-blind, pilot study.
Steg, P, Lopez-de-Sà, E, Schiele, F, Hamon, M, Meinertz, T, Goicolea, J, Werdan, K, Lopez-Sendon, JL, ,
European heart journal. Acute cardiovascular care. 2013;(3):270-9
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Abstract
AIMS: Rapid heart rate lowering may be attractive in acute ST-segment elevation myocardial infarction (STEMI). Accordingly we studied the effect of intravenous ivabradine on heart rate in this setting. METHODS AND RESULTS This was a multicenter randomized double-blind placebo-controlled trial: patients aged 40-80 years were randomized after successful primary percutaneous coronary intervention (PCI) performed within 6 h of STEMI symptom onset. Patients were in sinus rhythm and with heart rate >80 bpm and systolic blood pressure >90 mm Hg. They were randomly assigned (2:1 ratio) to intravenous ivabradine (n=82) (5 mg bolus over 30 s, followed by 5 mg infusion over 8 h) or matching placebo (n=42). The primary outcome measure was heart rate and blood pressure. In both groups, heart rate was reduced over 8 h, with a faster and more marked decrease on ivabradine than placebo (22.2 ± 1.3 vs 8.9 ± 1.8 bpm, p<0.0001). After treatment discontinuation, heart rate was similar in both groups. Throughout the study, there was no difference in blood pressure between groups. There was no difference in cardiac biomarkers (creatine kinase (CK-MB), troponin T and troponin I). On echocardiography performed at baseline and post treatment (median 1.16 days), final left ventricular volumes were lower in the ivabradine group both for left ventricular end-diastolic volume (LVEDV) (87.1 ± 28.2 vs 117.8 ± 21.4 ml, p=0.01) and left ventricular end-systolic volume (LVESV) (42.5 ± 19.0 versus 59.1 ± 11.3 ml, p=0.03) without differences in volume change or left ventricular ejection fraction. CONCLUSION This pilot study shows that intravenous ivabradine may be used safely to slow the heart rate in STEMI. Further studies are needed to characterize its effect on infarct size, left ventricular function and clinical outcomes in this population.
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Reversible heart failure: toxins, tachycardiomyopathy and mitochondrial abnormalities.
Morris, PD, Robinson, T, Channer, KS
Postgraduate medical journal. 2012;(1046):706-12
Abstract
Heart failure is usually a relentless condition associated with a poor prognosis. Triggered by a physiological insult, maladaptive neurohumoral processes result in an ever-spiralling deterioration of cardiovascular function. However, there are certain underlying conditions which are associated with a temporary reduction in contractile function leading to reversible heart failure. These conditions affect a relatively small number of patients when compared with heart failure secondary to inherited cardiomyopathies and ischaemic heart disease. There are two broad mechanisms responsible for reversible myocyte dysfunction: acute inflammatory activation in which cytokines depress myocyte function, and toxic effects in which there is impairment of intra-cellular energetics. In this review, we discuss reversible heart failure caused by toxic effects. These effects can be caused by drugs (prescribed and illicit) and by tachycardic arrhythmia (tachycardiomyopathy), and are caused by abnormalities of mitochondrial function and myocytic calcium processing. The underlying pathological mechanisms, clinical features and management options are discussed, illustrated by clinical case studies.
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Resting heart rate and the risk of microvascular complications in patients with type 2 diabetes mellitus.
Hillis, GS, Hata, J, Woodward, M, Perkovic, V, Arima, H, Chow, CK, Zoungas, S, Patel, A, Poulter, NR, Mancia, G, et al
Journal of the American Heart Association. 2012;(5):e002832
Abstract
BACKGROUND A higher resting heart rate is associated with an increased probability of cardiovascular complications and premature death in patients with type 2 diabetes mellitus. The impact of heart rate on the risk of developing microvascular complications, such as diabetic retinopathy and nephropathy, is, however, unknown. The present study tests the hypothesis that a higher resting heart rate is associated with an increased incidence and a greater progression of microvascular complications in patients with type 2 diabetes mellitus. METHODS AND RESULTS The relation between baseline resting heart rate and the development of a major microvascular event was examined in 11 140 patients who participated in the Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation (ADVANCE) study. Major microvascular events were defined as a composite of new or worsening nephropathy or new or worsening retinopathy. Patients with a higher baseline heart rate were at increased risk of a new major microvascular complication during follow-up (adjusted hazard ratio: 1.13 per 10 beats per minute; 95% confidence interval: 1.07-1.20; P<0.001). The excess hazard was evident for both nephropathy (adjusted hazard ratio: 1.16 per 10 beats per minute; 95% confidence interval: 1.08-1.25) and retinopathy (adjusted hazard ratio: 1.11 per 10 beats per minute; 95% confidence interval: 1.02-1.21). CONCLUSION Patients with type 2 diabetes mellitus who have a higher resting heart rate experience a greater incidence of new-onset or progressive nephropathy and retinopathy. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT00145925. http://www.advance-trial.com/static/html/prehome/prehome.asp.
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[Progress for treating tachyarrhythmia by corydaline].
Zhang, P, Xu, FQ, Ma, XC
Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine. 2012;(5):713-6
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Pilsicainide.
Plosker, GL
Drugs. 2010;(4):455-67
Abstract
Pilsicainide is a class Ic antiarrhythmic agent used for the treatment of supraventricular and ventricular tachycardia. The pharmacodynamic effects of pilsicainide are achieved via selective sodium channel blockade. In randomized, multicentre trials in patients with atrial fibrillation, restoration of sinus rhythm was achieved in significantly more patients treated with a single oral dose of pilsicainide than those who received placebo, and in a numerically higher proportion of oral pilsicainide than intravenous disopyramide recipients. In another well designed trial in patients with persistent atrial fibrillation, the proportion of patients whose arrhythmia converted to normal sinus rhythm was significantly higher among those randomized to receive 2 weeks of oral pilsicainide therapy than among patients who received placebo. Over a 1-year period, both pilsicainide and cibenzoline (another class Ic agent) were effective in preventing recurrence of atrial fibrillation in a substantial proportion of patients in a single-centre crossover trial. There were no between-group differences in the subgroup of patients with shorter-duration atrial fibrillation, but actuarial results over 1 year significantly favoured cibenzoline over pilsicainide in patients with longer-duration atrial fibrillation. Both oral and intravenous pilsicainide have demonstrated efficacy in ventricular tachyarrhythmias, including ventricular extrasystole. Clinical trial and postmarketing surveillance data indicate that pilsicainide is generally well tolerated in most patients.
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Best evidence topic report. Intravenous magnesium in shock-resistant tachyarrhythmias.
Sen, A, Gidwani, S
Emergency medicine journal : EMJ. 2006;(3):220-1
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Amiodarone-induced neonatal hypothyroidism: a unique form of transient early-onset hypothyroidism.
Lomenick, JP, Jackson, WA, Backeljauw, PF
Journal of perinatology : official journal of the California Perinatal Association. 2004;(6):397-9
Abstract
Amiodarone is an iodine-rich drug used to treat cardiac dysrhythmias. The structure of amiodarone resembles that of thyroxine, and treatment with amiodarone may alter thyroid function. The effects of antenatal amiodarone use on fetal/neonatal thyroid function have only been addressed in a limited number of patient reports. We describe two cases of transient neonatal hypothyroidism due to in utero amiodarone exposure, followed by a brief review of the available literature.