Ebook Manual of electrophysiology: Part 2
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Ebook Manual of electrophysiology: Part 2
Long QT, Short QT and Brugada SyndromesCHAPTER10Seyed Hashemi, Peter J MohlerChapter Outline■ LQT Syndrome-Clinical Manifestations-Pathogenesis-Molecu Ebook Manual of electrophysiology: Part 2ular Genetics-Genotype-Phenotype Correlation Studies and Risk Stratification Strategies-Diagnosis-Genetic Testing-Therapy-ICD Therapy-Left Cardiac Sympathetic Denervation-Genotype-Specific Therapy■SQT Syndrome-Clinical Manifestations-Molecular Genetics-Pathogenesis-Diagnosis-Therapy■Brugada Syndrome Ebook Manual of electrophysiology: Part 2-Clinical Manifestations-Genetics-Pathogenesis-Diagnosis-Prognosis, Risk Stratification and TherapyINTRODUCTIONOver the past two decades, ample informEbook Manual of electrophysiology: Part 2
ation has been accumulated on cellular mechanisms and genetics of arrhythmias in structurally normal heart. The basic pathogenic mechanism for these aLong QT, Short QT and Brugada SyndromesCHAPTER10Seyed Hashemi, Peter J MohlerChapter Outline■ LQT Syndrome-Clinical Manifestations-Pathogenesis-Molecu Ebook Manual of electrophysiology: Part 2 death (especially in the young) due to congenital arrhythmias, coupled with the potential availability of preventive measures, mandate the need for higher awareness of the medical community of these potentially lethal arrhythmia syndromes. In this chapter, we will review the current state of unders Ebook Manual of electrophysiology: Part 2tanding of inherited arrhythmias including long QT (LỌT) syndrome, short QT (SQT) syndrome and Brugada syndrome. This review focuses on inherited arrhEbook Manual of electrophysiology: Part 2
ythmias andLong QT, Short QT and Brugada Syndromes311the most common forms of the LQT syndromes (types 1, 2 and 3) were identified.4-6 Since then, theLong QT, Short QT and Brugada SyndromesCHAPTER10Seyed Hashemi, Peter J MohlerChapter Outline■ LQT Syndrome-Clinical Manifestations-Pathogenesis-Molecu Ebook Manual of electrophysiology: Part 2ated arrhythmia syndromes.Clinical ManifestationsThe congenital LQT syndrome is a common identifiable cause of sudden death in the presence of structurally normal heart. The natural history of LQT syndrome is highly variable.8-12 The majority of patients may be entirely asymptomatic with the only ab Ebook Manual of electrophysiology: Part 2normality being ỌT prolongation in the ECG.8-12 Some gene variant carriers of LỌT syndromes may not even display the prolonged ỌT interval (silent carEbook Manual of electrophysiology: Part 2
riers).13’14 Symptomatic patients typically, present in the first two decades of life including the neonatal period, with recurrent attacks of syncopeLong QT, Short QT and Brugada SyndromesCHAPTER10Seyed Hashemi, Peter J MohlerChapter Outline■ LQT Syndrome-Clinical Manifestations-Pathogenesis-Molecu Ebook Manual of electrophysiology: Part 2e and, polarity of QRS complexes such that their peak appears to be twisting around an imaginary isoelectric baseline. Torsade de pointes may resolve spontaneously, however, it has a great potential to degenerate into ventricular fibrillation and is an important cause of sudden death.9PathogenesisAs Ebook Manual of electrophysiology: Part 2 the QT interval represents a combination of action potential (AP) depolarization and repolarization, variations in ỌT interval may arise from the dysEbook Manual of electrophysiology: Part 2
function of ion channel, responsible for the timely execution of the cardiac AP. A decrease in the outward repolarizing currents (mainly potassium curLong QT, Short QT and Brugada SyndromesCHAPTER10Seyed Hashemi, Peter J MohlerChapter Outline■ LQT Syndrome-Clinical Manifestations-Pathogenesis-Molecu Ebook Manual of electrophysiology: Part 2 u Vi en .comLong QT, Short QT and Brugada SyndromesCHAPTER10Seyed Hashemi, Peter J MohlerChapter Outline■ LQT Syndrome-Clinical Manifestations-Pathogenesis-MolecuGọi ngay
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