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1.
Pediatric patients' head-up-tilt-test with pharmacological challenge, it is safe?
García, A, Bustillos-García, GA, Rivera-Roodríguez, L
Archivos de cardiologia de Mexico. 2020;(2):163-172
Abstract
Syncope in pediatrics represents an important cause of visits to the emergency units. For this reason, excluding a cardiac or malignant origin is essential at the time of the initial approach to determine what is the next step in management, or if they need to be referred to a pediatric cardiologist and/or electrophysiologist. Vasovagal syncope is the most frequent cause of syncope in pediatrics, in which a detailed clinical history is enough to make the diagnosis. If no diagnosis is concluded by the history, or if it is necessary to define the hemodynamic response of the patients, the head-up-tilt-test is indicated; this will trigger syncope due to an orthostatic stress caused by the angulated table (passive phase). If a negative response remains, it can be followed by a pharmacologic challenge to trigger the hemodynamic response, which is still controversial in pediatrics. The pharmacologic challenge increases the sensitivity with a slight reduction in test specificity. Although there is not a specific drug for the challenge in pediatric patients yet, the most commonly drugs used are nitrates and isoproterenol, the latter related to a great number of adverse effects. Sublingual administration of nitrates in the challenge has been proven to be ideal, effective, and safe in this specific age group. The aim of this article is to make a literature search to demonstrate the effectiveness and safety of the pharmacologic challenge during the head-up-tilt-test in pediatrics, emphasizing a study conducted at the National Institute of Cardiology with isosorbide dinitrate.
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2.
Pediatrics patients head-up tilt test with pharmacological challenge, it is safe?
García, A, Bustillos-García, GA, Rivera-Rodríguez, L
Archivos de cardiologia de Mexico. 2020;(2):178-188
Abstract
Syncope in pediatrics represents an important cause of visits to the emergency units. For this reason, excluding a cardiac or malignant origin is essential at the time of the initial approach in order to determine what is the next step in management, or if they need to be referred to a pediatric cardiologist and/or electrophysiologist. Vasovagal syncope is the most frequent cause of syncope in pediatrics, in which a detailed clinical history is enough to make the diagnosis. If no diagnosis is concluded by the history, or if it is necessary to define the hemodynamic response of the patients, the head-up tilt test is indicated; this will trigger syncope due to an orthostatic stress caused by the angulated table (passive phase). If a negative response remains, it can be followed by a pharmacologic challenge in order to trigger the hemodynamic response, which is still controversial in pediatrics. The pharmacologic challenge increases the sensitivity with a slight reduction in test specificity. Although there is not a specific drug for the challenge in pediatric patients yet, the most commonly drugs used are nitrates and isoproterenol, the latter related to a great number of adverse effects. Sublingual administration of nitrates in the challenge has been proven to be ideal, effective and safe in this specific age group. The aim of this article is to make a literature search in order to demonstrate the effectiveness and safety of the pharmacologic challenge during the head-up tilt test in pediatrics, emphasizing a study conducted at the National Institute of Cardiology with isosorbide dinitrate.
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3.
Vasospastic Angina Presenting With Syncope and Chest Pain: A Case Report and Brief Literature Review.
Malik, SA, Porter, TT, Pavlides, G, Chatzizisis, Y
South Dakota medicine : the journal of the South Dakota State Medical Association. 2017;(11):498-502
Abstract
A 65-year-old male presented to the hospital with chest pain associated with recurrent syncope. He had a history of coronary artery disease and a long-standing history of smoking. While he was hospitalized, he had an episode of chest pain during which he was found to have transient ST segment elevation in the inferior leads. He was also noted to have a brief cardiac tachyarrhythmia. Coronary arteriography revealed vasospasm of the left anterior descending artery and right coronary artery, which were relieved to a significant extent after administration of intracoronary nitroglycerin. Subsequent angiograms and fractional flow reserve studies, demonstrated underlying non-obstructive coronary artery disease at the sites of spasm. No percutaneous coronary intervention was pursued. The patient was started on a calcium channel blocker on dismissal from the hospital. Upon follow up several months later, he remained free of symptoms that brought him to the hospital.
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4.
The effects of body weight status on orthostatic intolerance and predisposition to noncardiac syncope.
Christou, GA, Kiortsis, DN
Obesity reviews : an official journal of the International Association for the Study of Obesity. 2017;(3):370-379
Abstract
Orthostatic intolerance (OI) is frequently the mechanism underlying the occurrence of noncardiac syncope (NCS) and is associated with substantial risk for injury. Body weight status appears to be a modifier of orthostatic responses and possibly influences the propensity to NCS. The majority of cross-sectional studies have found that the lower the body mass index (BMI) the greater the predisposition to OI is, accompanied with both down-regulation of sympathetic nervous system activity and up-regulation of parasympathetic nervous system activity. These changes appear to occur across the whole spectrum of BMI values from underweight to obesity, while they may be associated more strongly with central body fat than total body fat. Weight loss following bariatric surgery has been consistently found to increase OI, attributed first to the effects of weight loss per se, second to the specific type of surgical procedure and third to the potential postoperative autonomic neuropathy due to vitamin deficiency. The increased OI following bariatric surgery renders this intervention not easily tolerable for the affected individuals, mandating increased fluid and salt intake, pharmacological measures or surgical adjustments to attenuate OI. All future studies investigating orthostatic responses and NCS should implement a matching of the population arms for BMI and ideally for body fat.
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5.
Pathophysiology of neurally-mediated syncope.
Malamud-Kessler, C, Bruno, E, Chiquete, E, Sentíes-Madrid, H, Campos-Sánchez, M
Neurologia (Barcelona, Spain). 2016;(9):620-627
Abstract
INTRODUCTION Neurally-mediated syncope (NMS) is defined as a transient loss of consciousness due to an abrupt and intermittent drop in blood pressure (BP). OBJECTIVES This study describes the putative pathophysiological mechanisms giving rise to NMS, the role of baroreflex (BR), and the interaction of its main haemodynamic variables: heart rate (HR) and BP. DEVELOPMENT Episodic dysregulation affects control over the haemodynamic variables (HR and BP) mediated by baroreflex mechanisms. During active standing, individuals experience a profound transient drop in systolic BP due to the effect of gravity on the column of blood and probably also because of reflex vasodilation. Abnormalities in the BR in NMS could be due to a more profound drop in BP upon standing, or to delayed or incomplete vasoconstriction resulting from inhibited or delayed sympathetic activity. CONCLUSIONS Sympathetic hyperactivity is present in patients with NMS at rest and before syncope. During active standing or passive tilting, excessive tachycardia may be followed by bradycardia and profound hypotension. Recovery of systolic BP is delayed or incomplete.
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6.
[Brugada syndrome].
Leenhardt, A, Hamdaoui, B, Di Fusco, S, Extramiana, F, Meddane, M, Denjoy, I, Milliez, P, Dejode, P, Cauchemez, B
Archives des maladies du coeur et des vaisseaux. 2003;:30-7
Abstract
The Brugada syndrome is characterised clinically by the occurrence of syncope or sudden death due to ventricular arrhythmias in patients with structurally normal hearts and electrocardiographic signs of right bundle branch block and ST elevation in the right precordial leads (V1 to V3). The transmission of the condition is autosomal dominant with variable penetration. Mutations have been identified in a gene coding for the alpha sub-unity of the sodium channel (SCN5A) on chromosome 3 in only 30% of cases. This mutation is responsible for a reduction of the density of the sodium current and explains the aggravation of the electrocardiographic anomalies by antiarrhythmic drugs which block the sodium channels. The prognosis is poor in symptomatic patients and depends on the prevention of sudden death by the implantation of an automatic defibrillator. The therapeutic decision is much more difficult in asymptomatic patients without a family history. The authors propose a decisional algorithm. The management may have to be modified in the months or years to come depending on advances in the understanding of this syndrome.
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7.
[Postprandial hypotension in the elderly].
Puisieux, F
Presse medicale (Paris, France : 1983). 2003;(26):1226-30, 1237
Abstract
A FREQUENT BLOOD PRESSURE DISORDER Falls and syncope are frequent accidents in the elderly and may be caused by a large variety of disorders. Over the past decade, postprandial hypotension (PPH), which is defined as a decrease in systolic blood pressure of 20 mmHg or more within two hours of ingestion of the meal, has been recognised as a common cause of syncope and falls in this population. It should therefore be searched for systematically in any assessment of syncope and falls. The PPH mechanism is not fully understood, but PPH is probably the consequence of an alteration in the compensatory mechanisms for meal-induced splanchnic blood pooling and the lowering of peripheral vascular resistance following ingestion of food. REGARDING TREATMENT Treatment of PPH, which may be non pharmacologic and pharmacologic, is not well codified, because too few rigorous studies has been conducted on symptomatic patients.
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8.
Brugada syndrome: a decade of progress.
Antzelevitch, C, Brugada, P, Brugada, J, Brugada, R, Shimizu, W, Gussak, I, Perez Riera, AR
Circulation research. 2002;(12):1114-8
Abstract
The Brugada syndrome has gained wide recognition throughout the world and today is believed to be responsible for 4% to 12% of all sudden deaths and approximately 20% of deaths in patients with structurally normal hearts. The incidence of the disease is on the order of 5 per 10 000 inhabitants and, apart from accidents, is the leading cause of death of men under the age of 50 in regions of the world where the inherited syndrome is endemic. This minireview briefly summarizes the progress made over the past decade in our understanding of the clinical, genetic, cellular, ionic, and molecular aspects of this disease.
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9.
[Long QT syndrome and Brugada syndrome: 2 aspects of the same disease?].
Cerrone, M, Crotti, L, Faggiano, G, De Michelis, V, Napolitano, C, Schwartz, PJ, Priori, SG
Italian heart journal. Supplement : official journal of the Italian Federation of Cardiology. 2001;(3):253-7
Abstract
In clinical cardiology, resort has recently been made to molecular genetics in order to explain some mechanisms that underlie sudden cardiac death in young people with structurally normal hearts. It has become evident that genetic mutations regarding cardiac ion channels may disrupt the delicate balance of currents in the action potential, thus inducing malignant ventricular tachyarrhythmias. The cardiac sodium channel gene, SCN5A, is involved in two of such arrhythmogenic diseases, the Brugada syndrome and one form of the long QT syndrome (LQT3). It is believed that these syndromes result from opposite molecular effects: Brugada syndrome mutations cause a reduced sodium current, while LQT3 mutations are associated with a gain of function. The effects of class I antiarrhythmic drugs have been used to differentiate these diseases. Intravenous flecainide is used as a highly specific test to unmask the electrocardiographic phenotype of the Brugada syndrome. On the other hand, on the basis of experimental and clinical studies, the possibility that the same drugs act as a gene-specific therapy in this disorder by contrasting the effect of mutations in LQT3 has been explored. Recent evidence shows that phenotypic overlap may exist between the Brugada syndrome and LQT3. One large family with a SCN5A mutation and a "mixed" electrocardiographic pattern (prolonged QT interval and ST-segment elevation) has been reported. Moreover, our recent data showed that flecainide challenge may elicit ST-segment elevation in some LQT3 patients. The presence of "intermediate" phenotypes highlights a remarkable heterogeneity suggesting that clinical features may depend upon the single mutation. Only deepened understanding of the genotype-phenotype correlation will allow the definition of the individual patient's risk and the development of guidelines for clinical management.
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10.
[Molecular genetics of the long QT syndrome. Genes causing syncope and sudden death].
Fosdal, I, Wettrell, G, Christiansen, M, Kanters, JK, Larsen, LA
Lakartidningen. 2001;(8):810-5
Abstract
Molecular genetic studies in congenital long QT syndrome have characterized genes and mechanisms of arrhythmias. At least six genes encoding cardiac potassium and sodium ionic channels have been described with several mutations in each gene. The altered function produces abnormal cardiac repolarization seen on ECG as prolongation of the QT-interval and T-wave abnormalities. This may increase the propensity for ventricular arrhythmias such as Torsade de Pointe, the cause of unexpected syncope and sudden death in young patients. Clinical manifestations vary depending on the genotype present. Gene-specific therapies have recently been tried. Initial therapy of choice for symptomatic and also asymptomatic children is administration of beta-blockers.