Be Gj Lo Qt What Are The Next Letters
Be Gj Lo Qt What Are The Next Letters – Revista Española de Cardiología is an international scientific journal dedicated to publishing research articles on the treatment of cardiovascular diseases. The magazine, which has been published since 1947, is the official publication of the Association of Spanish Artists and the founder of REC Publications. Articles are published in English and Spanish in the electronic edition.
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Be Gj Lo Qt What Are The Next Letters
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Figure 2. Genotype-phenotype correlation in the most common long QT syndrome. * Denotes cases that have the mutation and describe the phenotype.
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Figure 3. Model showing the distribution of cardiac-corrected QT interval (QTc) in patients with mutations in KVLQT1, HERG, or SCN5A, and their nondominant relatives. The curve to the left depicts the distribution of unaffected members and the curve to the right, the affected members.
Long QT syndrome (LQTS) is an arrhythmogenic ion channel disorder characterized by severe ventricular hypertrophy, resulting in prolonged electrocardiographic QT interval. The condition is associated with sudden cardiac death due to severe ventricular arrhythmias resembling torsade de pointes. Eleven years after the discovery of the rules of the heart channels in nature, hundreds of mutations in, to date, 10 genes have been associated with pain. Genetic research conducted so far has shown that, although the severity of the disease is high, there are common types of polymorphisms in genes that are associated with the condition that can be and easy to develop torsade de pointes in some people. especially if specific medications are administered. Additionally, some polymorphisms have been shown to have regulatory properties that either enhance or counteract the effects of the mutation. Understanding the molecular structure of the disease has allowed to improve the treatment and lead to a better life among the patients, thus showing the important interaction between genotype, phenotype and therapy. Despite these advances, a quarter of patients do not have mutations in the genes identified to date. As a result, LQTS remains an area of active research. This article contains a summary of the major clinical and genetic advances in cancer that have occurred over the past decade.
El síndrome de QT long (SQTL) is an arrhythmogenic channelopathy characterized by a serious alteration in ventricular repolarization, transduced electrocardiographically by a prolongation of the QT interval. Predispose to sudden death by malignant ventricular arrhythmias of the type of torsade de pointes. A 11 years from the identification of the main canals affected in this disease, hundreds of mutations have been described and so far 10 genes related to the syndrome have been described. El escrutinio genético realized since then has shown that, if the serious form of the disease is sporadic, there are polymorphisms comunes en los genes relacionados con la enfermedad que pueden genereta susceptibilidad person al desarrollo desarrollo des desarrollos to, pharmacos; más aún, polymorphisms with regulative qualities that can exacerbate or silence the severity of a mutation have been identified. The understanding of the molecular processes of the disease has allowed to optimize the treatment and improve the survival of the affected, thus generating an important genotype-phenotype-treatment correlation. Despite the advances, a quarter of the cases do not have mutations in the genes described so far, so the SQTL continues to be a research topic. The present article represents the analysis of the main clinical and genetic concepts developed in the last years about this singular disease.
Long QT syndrome (LQTS) is associated with altered ventricular repolarization, resulting in a prolonged QT interval on the electrocardiogram (ECG). The condition predisposes patients to severe ventricular arrhythmia (torsade de pointes) and sudden death. The clinical and electrocardiographic description of long QT syndrome was reported in 1957 by Anton Jervell and Fred Lange Nielsen, 1 who published their study on a family of unrelated parents with 6 children. Four of the children had birth pain and syncopal syndrome, and 3 presented sudden death. ECG studies of these patients showed an abnormally long QT interval. Both parents were asymptomatic, had a normal ECG, and did not present hearing problems. In 1964, Romano and Ward themselves reported a heart attack associated with recurrent syncope, a family history of sudden death, and prolonged QT interval without deafness. with congenital neuronal loss, corresponds to a homozygous mutation, with a severe phenotype and a high risk of sudden death. The condition known as Romano-Ward syndrome generally corresponds to a heterozygous mutation, patients do not show hearing loss, and the severity of the disease varies greatly. Almost half a century later, in 1995, 3, 4 the main genes associated with LQTS were described and the disease was recognized as an abnormality of the heart channel. It was the first coronary artery disease to be described and is perhaps the most studied arrhythmogenic ion channel disease to date. The clinical picture is very different: the patient can be asymptomatic, or show repeated syncope, seizures, or sudden death as the first manifestation of the disease. Initially, LQTS was considered to be a rare disease and, as a result, severe manifestations of the disease were rare. However, the incidence of the mutation is estimated at 1 / 3000-5000, 5 32% of asymptomatic carriers can have a corrected QT interval (QTc) in the heart within normal limits , the disease is transmitted to 50% of their offspring, they are more prone to arrhythmia compared to the general population, and up to 20% may be symptomatic.6
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Long QT syndrome shows a large genetic component. More than 500 mutations distributed in 10 genes were described in this case: KCNQ1, HERG, SCN5A, KCNE1, KCNE2, ANKB, KCNJ2, CACNA1, CAV3, and SCN4B. Despite the progress made in this area, the genetic diagnosis cannot be established in 25%-30% of patients.7, 8 The presentation of the disease is usually monogenic6; Polygenic or polysite compounds usually have more flavor. The prevalence, ie, patients who have the mutation and express the phenotype, ranges from 25% to 90%. 9 Less frequently, there can be differences in the expression of the disease, with different genotype many resulting from the same mutation. Genetic studies developed over the past 11 years have provided important genotype-phenotype relationships, which have helped guide the way of treatment. In addition, interesting observations have been made about the susceptibility of the individual to the development of arrhythmia in studies investigating frequent polymorphisms in this population, a phenomenon that has raised a lot of interest, especially in the field of medicine.
The previously used classification of LQTS was based on homozygous or heterozygous presentation of the disease, resulting in Jervell-Lange-Nielsen syndrome (with deafness) and Romano-Ward syndrome (without deafness). ), in turn. The current classification emphasizes genetic research, as described in Table 1. The 3 main genes associated with the disease were described in 1995-1996. These genes, which encode units to form units of potassium channels IKs and IKr, and the sodium channel Nav1.5, account for about 65% of cases. Although in the following years seven more genes were included in the list, they only account for 5% of cases.
Ion channels are transmembrane proteins that transport ions across the cell membrane. The channels in the LQTS are selective or specialized in the transport of a single ion and are voltage dependent, i.e. their activation occurs at a specific internal voltage, which varies according to the subtype of the channel. The electrical and contractile events that occur in the cardiomyocyte are controlled by these structures. Ion channels form a macromolecular complex that consists of a core that forms the channel cavity and auxiliary proteins that stabilize it (Figure 1). The dysfunction of the channel seen in LQTS can occur at these two sites: the main protein or the proteins that regulate it (Table 1). Entry into the pore forming unit, known as alpha, results in three types of LQTS: LQTS1 (affecting the IKs potassium channel), LQTS2 (affecting the IKr potassium channel ), and LQTS3 (affects sodium channel). Because these are the most common substeps, they are the best clinical characteristics and origins. The phenotype-genotype correlations in these three major features are illustrated in Figure 2. Currently, Jervell-Lange-Nielsen syndrome corresponds to LQTS types 1 and 5. In fact, these patients are and congenital deafness and homozygous or heterozygous combinations affecting current IKs. Romano-Ward syndrome includes types from LQTS 1 to