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QTc prolongation after ADHD medication.
Snircova, E, Marcincakova Husarova, V, Ondrejka, I, Hrtanek, I, Farsky, I, Nosalova, G
Neuro endocrinology letters. 2018;(8):549-554
Abstract
OBJECTIVE Multicenter studies have shown that cardiovascular risks of ADHD medication are extremely low. However, QTc length has been shown to be increased in smaller samples of patients or case reports after stimulant and atomoxetine medication. Based on recent studies of genetic polymorphisms associated with drug-induced QTc prolongation and polymorphisms linkage to regional populations, we hypothesized that the drug-induced QTc prolongation could be a factor of particular polymorphisms linked to specific regional populations undistinguished in multicenter studies. METHODS We included 69 patients from a region of central Slovakia, 36 patients were taking atomoxetine and 33 patients methylphenidate. QTc, heart rate, potassium levels and BMI were examined before and after 8 weeks of treatment. Therapeutic effect was measured by ADHD-RS-IV. RESULTS We found QTc prolongation after 8 weeks of treatment both with atomoxetine and methylphenidate that was neither followed by the significant changes in BMI and potassium levels nor the significant increase of heart rate. CONCLUSION This is the first study revealing QTc prolongation in the group of ADHD children from the same region after 8-week treatment with atomoxetine and methylphenidate, indicating the potential discrete abnormalities in cardiac functioning associated with polymorphisms in genes of dopaminergic and noradrenergic system.
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2.
Arrhythmogenic triggers associated with Sudden Cardiac Death.
Abdelsayed, M, Peters, CH, Ruben, PC
Channels (Austin, Tex.). 2018;(1):76-77
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3.
Tips for management of arrhythmias in endocrine disorders from an European Heart Rhythm Association position paper.
Özcan, EE, Dural, M, Görenek, B
Anatolian journal of cardiology. 2018;(4):241-245
Abstract
In endocrine diseases, hormonal changes, electrolyte abnormalities, and the deterioration of heart structure can lead to various arrhythmias. In diabetic patients, hypoglycemia, hyperglycemia, and hypokalemia can trigger arrhythmias, and diabetic cardiomyopathy can also cause electrical and structural remodeling to form substrates for arrhythmias. The risk of atrial fibrillation (AF) increases in hyperthyroidism; however, the prevalence of ventricular arrhythmias in hypothyroidism is higher. Besides AF and ventricular tachycardias, bradycardias and atrioventricular blocks can also be seen in pheochromocytoma due to the desensitization of adrenergic cardiovascular receptors. The correction of metabolic and electrolyte disturbances in patients with adrenal cortex disease should be the main approach in the prevention and treatment of arrhythmias. Early initiation of treatment in patients with acromegaly seems to decrease the development of cardiac remodeling and ventricular arrhythmia. Early and late after depolarizations due to hypercalcemia in hyperparathyroidism can lead to life-threatening ventricular arrhythmias. This elegant position paper provides important recommendations regarding prevention and treatment of arrhythmias for specific endocrine disorders.
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4.
Ventricular Arrhythmic Storm after Initiating Sacubitril/Valsartan.
Vicent, L, Juárez, M, Martín, I, García, J, González-Saldívar, H, Bruña, V, Devesa, C, Sousa-Casasnovas, I, Fernández-Avilés, F, Martínez-Sellés, M
Cardiology. 2018;(2):119-123
Abstract
OBJECTIVES Sacubitril/valsartan was approved recently for the treatment of patients with heart failure and reduced ejection fraction. We present 6 cases of ventricular arrhythmia, that occurred shortly after sacubitril/valsartan initiation, that required drug withdrawal. Other potential triggering factors of electrical storm were ruled out and, from the arrhythmic perspective, all of the patients were stable in the previous year. Our aim is to describe the possible association of sacubitril/valsartan with arrhythmic storm. METHODS This was an observational monocentric study performed in the first 7 months of sacubitril/valsartan commercialization in Spain (October 2016). All patients were included in the SUMA (Sacubitril/Varsartan Usado Ambulatoriamente en Madrid [Sacubitril/Valsartan Used in Outpatients in Madrid]) registry. Patients were consecutively enrolled on the day they started the drug. Ventricular arrhythmic storm was defined as ≥2 episodes of sustained ventricular arrhythmia or defibrillator therapy application in 24 h. RESULTS From 108 patients who received the drug, 6 presented with ventricular arrhythmic storm (5.6%). Baseline characteristics were similar in the patients with and without ventricular arrhythmic storm. The total number of days that sacubitril/valsartan was administered to each patient was 5, 6, 44 (8 since titration), 84, 93, and 136 (105 since titration), respectively. CONCLUSIONS Our data are not enough to infer a cause-and-effect relationship. Further investigations regarding a potential proarrhythmic effect of sacubitril/valsartan are probably needed.
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5.
[Genetically determined abnormal electrical activity of the brain and the heart].
Mańka-Gaca, I, Łabuz-Roszak, B, Machowska-Majchrzak, A
Wiadomosci lekarskie (Warsaw, Poland : 1960). 2018;(2 pt 2):413-416
Abstract
Mutations leading to disorders within ion (mainly potassium and sodium) channels, have different degrees of expression in the brain and in the heart, which can cause simultaneous occurrence of disorders in both organs. This is manifested by the occurrence of epileptic seizures and cardiac electrical disturbances, further exacerbated by stimulation of autonomic structures within the central nervous system. In all patients with unclear paroxysmal disorders, and in those with unexplained sudden cardiac death, consideration should be given to the possibility of occurrence of genetically determined disorders in the ion channels. This article concerns the most common genetically determined epilepsy syndromes and genetically determined cardiac diseases.
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6.
Antiarrhythmic drug therapy during cardiopulmonary resuscitation: should we use it?
Soar, J
Current opinion in critical care. 2018;(3):138-142
Abstract
PURPOSE OF REVIEW The optimal antiarrhythmic drug therapy (amiodarone or lidocaine) in the treatment of ventricular fibrillation/pulseless ventricular tachycardia (VF/pVT) cardiac arrest that is refractory to defibrillation is uncertain. This article reviews the evidence for and against these drugs, alternatives treatments for refractory VF/pVT and aims to define the role of antiarrhythmic drugs during cardiopulmonary resuscitation (CPR). RECENT FINDINGS A large randomized controlled trial that compared amiodarone, lidocaine and saline 0.9% sodium chloride for the treatment of refractory VF/pVT out-of-hospital cardiac arrest reported no difference in survival to hospital discharge or neurological outcome. In patients with witnessed arrest, survival was improved with antiarrhythmic drugs compared to saline. SUMMARY The benefit of antiarrhythmic drugs appears to be for those patients in whom initial early CPR and defibrillation attempts fail and the antiarrhythmic drug is given early. There does not appear to be any clear survival benefit for any one particular drug and other factors such as availability and cost should be considered when deciding which drug to use. Furthermore, other interventions (e.g. percutaneous coronary intervention and extra-corporeal CPR) may provide additional survival benefit when defibrillation attempts and antiarrhythmic drugs are not effective.
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7.
Apheresis on aged patients/donors with complicated backgrounds like ischemic heart disease, arrhythmia, and others.
Yokohama, A, Yokote, K, Maruhashi, T
Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis. 2018;(5):619-622
Abstract
Peripheral blood stem cells (PBSCs) are currently one of the most important stem cell sources for hematopoietic stem cell transplantation as well as cell therapy for ischemic heart disease or critical limb ischemia. Thus, it is sometimes necessary to collect autologous PBSCs from donors who have comorbidities. In terms yield, a sufficient number of PBSCs can be collected from donors with comorbidities for performing cell therapy if their age is < 60 years or up to a maximum of 70 years, although the number of PBSCs collected from older donors would probably be lower than that obtained from younger donors. On the other hand, granulocyte colony-stimulating factor (G-CSF) administration sometimes results in severe adverse events (AEs), such as ischemic heart disease and vascular thrombosis. Therefore, it is very important to perform strict medical check-ups according to the standards for donor operations in each country before apheresis. The apheresis procedure and G-CSF administration should be performed after administering the appropriate treatment. There is very less information available regarding AEs related to citrate administration during apheresis in aged donors with complicated medical histories. Medical staff should have knowledge of the electrocardiogram (ECG) QTc prolongation that occurs during apheresis owing to hypocalcemia caused by citrate administration, necessitating electrocardiographic monitoring of patients. Calcium should be administered during apheresis to prevent citrate related symptoms.
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8.
The Role of Radiopharmaceuticals in Amiodarone-Induced Thyroid Pathology.
Irimie, A, Piciu, D
Current radiopharmaceuticals. 2017;(3):146-154
Abstract
BACKGROUND AND OBJECTIVE The use of amiodarone for the treatment of ventricular and supraventricular dysrhythmias brings in organism an increased amount of iodine, interfering with thyroid function. If the treatment needs to be interrupted, iodine remains at abnormal levels for months or even years. The aim of the study was to review the literature regarding the optimal tests for early diagnostic and to analyze the role of nuclear medicine tests in the differential and correct assessment of the amiodarone-induced thyroid pathology. METHODS We made a review of available publications in PUBMED referring the amiodaroneinduced thyroid pathology, focusing on the differential diagnosis, made by nuclear medicine tests, of hypothyroidism (AIH) and hyperthyroidism expressed as: type I amiodarone induced thyrotoxicosis (AIT I), type II amiodarone induced thyrotoxicosis (AIT II), and less frequently as a mixt form, type III amiodarone induced thyrotoxicosis (AIT III). We presented cases from the database of a tertiary center in Cluj-Napoca, Romania. RESULTS Despite the frequent complication of thyroid function, this pathology is underestimated and diagnosed. There is a limited number of studies and clear protocols, especially in the mixed forms cases. This increase in iodine uptake interferes seriously with thyroid hormone production and release. The nuclear medicine tests are essential in the correct assessment and differential diagnosis of different forms of induced thyroid dysfunction. The destruction of the follicular cells can result in the release of excessive thyroid hormone into the circulation, with potential development of atrial fibrillation, worsening the cardiac disease, so any benefic therapeutic procedure should be known; the use of radioiodine as therapy alternative, despite the known limitations induced by blockade was clear benefic in the case presented. A special attention needs to be addressed to those patients with differentiated thyroid cancer, which will be submitted to radioiodine therapy and are under chronic therapy with amiodarone. CONCLUSION The nuclear medicine procedures are essential in the correct assessment and differential diagnosis of different forms of induced thyroid dysfunction. The radioiodine is not recommended in AIT, due to stunning effect induced by iodine excess, but in some special, lifethreatening condition, radioiodine I-131 might be a treatment option.
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9.
Effects of Long-Acting Loop Diuretics in Heart Failure With Reduced Ejection Fraction Patients With Cardiac Resynchronization Therapy.
Asami, M, Aoki, J, Tanimoto, S, Horiuchi, Y, Watanabe, M, Furui, K, Yasuhara, K, Sato, T, Tanabe, K, Hara, K
International heart journal. 2017;(2):211-219
Abstract
There have been no reports evaluating the impact of long-acting loop diuretics (LLD) on the outcome of heart failure (HF) and arrhythmia treatment in HF with reduced ejection fraction (HFrEF) patients implanted with a cardiac resynchronization therapy (CRT) device.This was a prospective, single-blind, randomized crossover study. We allocated 21 consecutive CRT implanted patients into 2 groups. The furosemide group received furosemide as a first treatment and azosemide as a second treatment. The azosemide group received this treatment in the reverse order. The first treatment was given to each group for 6 months and the second treatment continued for an additional 6 months. We combined the data of each medication regimen in each group and analyzed it at baseline, 6 months, and 1 year. The primary endpoints were the variation of fluid index and thoracic impedance measured by CRT at 6 months.The baseline characteristics were similar for both groups. The difference in the primary endpoints was not statistically significant between the 2 medication arms (fluid index: -29.6 ± 64.4 versus 16.2 ± 48.2; P = 0.22, thoracic impedance: -0.49 ± 17.8 versus 2.45 ± 12.5; P = 0.56). Likewise, the clinical outcome of HF and the CRT derived parameters in both arms were comparable.HFrEF patients taking LLD after CRT implantation might be comparable to those taking short-acting loop diuretics in the treatment of HF and HF-associated arrhythmias.
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10.
Channelopathies as Causes of Sudden Cardiac Death.
Schwartz, PJ, Ackerman, MJ, Wilde, AAM
Cardiac electrophysiology clinics. 2017;(4):537-549
Abstract
This article reviews the main clinical aspects of 3 channelopathies: the long QT syndrome, the catecholaminergic polymorphic ventricular tachycardia, and the Brugada syndrome. The text summarizes our views on clinical presentation and diagnosis, on risk stratification, and on therapy. Special attention is given to the progress in the understanding of the genetic bases and on the growing impact of genetics on therapy, which, at least in the case of long QT syndrome, now allows gene-specific management.