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Cardiomyocyte mitochondrial dysfunction in diabetes and its contribution in cardiac arrhythmogenesis.
El Hadi, H, Vettor, R, Rossato, M
Mitochondrion. 2019;:6-14
Abstract
Cardiovascular disease is the leading cause of diabetes-related morbidity and mortality. It is widely accepted that heart failure risk is increased in diabetic patients even after adjusting for coronary artery disease and hypertension. Mitochondria are the center of fatty acid (FA) and glucose metabolism and thus are likely to be impacted by impaired metabolism associated with diabetes. Although the cause of this increased heart failure risk is multifactorial, increasing evidence points toward a crucial role for cardiomyocyte mitochondria dysfunction. Altered energy metabolism, defects in mitochondrial dynamics, increased oxidative stress, impaired calcium (Ca2+) handling and mitochondria-induced cell death are observed in mitochondria of diabetic myocardium. In addition, mitochondrial dysfunction appears to contribute substantially to the origin of arrhythmias in diabetic hearts. The current review will describe these mitochondrial abnormalities in cardiomyocytes attempting to provide an overview of underlying mechanisms. Finally, we briefly discuss the potential link between mitochondrial malfunction and arrhythmogenesis.
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2.
Cardiac Alternans: Mechanisms and Clinical Utility in Arrhythmia Prevention.
Kulkarni, K, Merchant, FM, Kassab, MB, Sana, F, Moazzami, K, Sayadi, O, Singh, JP, Heist, EK, Armoundas, AA
Journal of the American Heart Association. 2019;(21):e013750
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3.
[Jervell and Lange-Nielsen syndrome].
Zhang, WJ, Sun, Y, Kong, WJ
Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology, head, and neck surgery. 2019;(9):825-829
Abstract
Summary Jervell and Lange-Nielsen syndrome(JLNS) is an autosomal recessive hereditary disease characterized by congenital severe sensorineural hearing loss in both ears and severe arrhythmias with QT interval prolongation. Children with JLNS often exhibit sensorineural hearing loss and are easily misdiagnosed as non-syndromic hearing loss before attack of cardiac event. When a cochlear implant is performed, a fatal arrhythmia is likely to occur during the perioperative period, which seriously threatens the life of the child. It is currently found that the pathogenic genes of JLNS are mainly KCNQ1 and KCNE1. This article reviews the clinical manifestations, pathogenic genes, diagnosis and differential diagnosis, intervention measures of JLNS to further draw the attention to the disease, reduce misdiagnosis, improve the survival rate and quality of life of children with JLNS.
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4.
Anorexia nervosa and heart disease: a systematic review.
Giovinazzo, S, Sukkar, SG, Rosa, GM, Zappi, A, Bezante, GP, Balbi, M, Brunelli, C
Eating and weight disorders : EWD. 2019;(2):199-207
Abstract
Anorexia nervosa (AN) is an eating disorder that most frequently afflicts females in adolescence. In these subjects, cardiovascular complications are the main cause of morbidity and mortality. Aim of this review is to analyze the hemodynamic, pro-arrhythmic and structural changes occurring during all phases of this illness, including re-feeding. A systematic literature search was performed on studies in the MEDLINE database, from its inception until September 2017, with PUBMED interface focusing on AN and cardiovascular disease. This review demonstrated that the most common cardiac abnormalities in AN are bradycardia and QT interval prolongation, which may occasionally degenerate into ventricular arrhythmias such as Torsades des Pointes or ventricular fibrillation. As these arrhythmias may be the substrate of sudden cardiac death (SCD), they require cardiac monitoring in hospital. In addition, reduced cardiac mass, with smaller volumes and decreased cardiac output, may be found. Furthermore, mitral prolapse and a mild pericardial effusion may occur, the latter due to protein deficiency and low levels of thyroid hormone. In anorectic patients, some cases of hypercholesterolemia may be present; however, conclusive evidence that AN is an atherogenic condition is still lacking, although a few cases of myocardial infarction have been reported. Finally, refeeding syndrome (RFS), which occurs during the first days of refeeding, may engender a critically increased risk of acute, life-threatening cardiac complications.
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5.
Proton pump inhibitor-induced hypomagnesemia complicated with serious cardiac arrhythmias.
Chrysant, SG
Expert review of cardiovascular therapy. 2019;(5):345-351
Abstract
Introduction: Magnesium is the third most common intracellular ion after potassium and calcium and is an important element in the functions of the body, since it participates in more than 300 enzyme systems. It also, plays a significant role in the transport of calcium and potassium across the cell membranes and protects against cardiac arrhythmias and is useful for their treatment due to hypomagnesemia induced from the proton pump inhibitors (PPIs). Areas covered: PPIs are used for the treatment of peptic ulcer disease (PUD) and gastroesophageal reflux disease (GERD), but have been associated with hypomagnesemia with serious cardiac arrhythmias including torsades de pointes (TdP). To better understand the magnitude of this problem, a Medline search of the English language literature was conducted from 2010 to 2018 and 35 papers with pertinent information were selected. Expert commentary: The review of these papers suggests that PPIs cause hypomagnesemia, which could be associated with serious cardiac arrhythmias including TdP. However, its incidence is not very common considering the millions of people taking PPIs, but the FDA has advised the physicians to be watchful about this serious adverse effect of PPIs and check the magnesium levels before initiation of PPI treatment.
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6.
Imaging cardiac innervation in amyloidosis.
Slart, RHJA, Glaudemans, AWJM, Hazenberg, BPC, Noordzij, W
Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology. 2019;(1):174-187
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Abstract
Cardiac amyloidosis is a form of restrictive cardiomyopathy resulting in heart failure and potential risk on arrhythmia, due to amyloid infiltration of the nerve conduction system and the myocardial tissue. The prognosis in this progressive disease is poor, probably due the development of cardiac arrhythmias. Early detection of cardiac sympathetic innervation disturbances has become of major clinical interest, because its occurrence and severity limits the choice of treatment. The use of iodine-123 labelled metaiodobenzylguanidine ([I-123]MIBG), a chemical modified analogue of norepinephrine, is well established in patients with heart failure and plays an important role in evaluation of sympathetic innervation in cardiac amyloidosis. [I-123]MIBG is stored in vesicles in the sympathetic nerve terminals and is not catabolized like norepinephrine. Decreased heart-to-mediastinum ratios on late planar images and increased wash-out rates indicate cardiac sympathetic denervation and are associated with poor prognosis. Single photon emission computed tomography provides additional information and has advantages for evaluating abnormalities in regional distribution in the myocardium. [I-123]MIBG is mainly useful in patients with hereditary and wild-type ATTR cardiac amyloidosis, not in AA and AL amyloidosis. The potential role of positron emission tomography for cardiac sympathetic innervation in amyloidosis has not yet been identified.
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7.
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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8.
Arrhythmogenic triggers associated with Sudden Cardiac Death.
Abdelsayed, M, Peters, CH, Ruben, PC
Channels (Austin, Tex.). 2018;(1):76-77
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9.
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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10.
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.