Aggravation of Arrhythmia by Antiarrhythmic Drugs (Proarrhythmia).

Arrhythmia aggravation by antiarrhythmic drugs (proarrhythmia) can be caused by worsening or a change of a preexisting arrhythmia, development of a new arrhythmia, or development of a bradyarrhythmia. Aggravation of arrhythmia usually occurs within several days of beginning an antiarrhythmic drug or increasing the dose of the drug. The time of occurrence is based on the particular drug and its pharmacokinetic properties. Although there are no ways to predict the patient at risk for developing arrhythmia aggravation with any specific agents, risk factors include QT interval prolongation, elevated serum levels of the drug, electrolyte abnormalities, presence of heart failure, a history of a sustained ventricular tachyarrhythmia, and underlying myocardial ischemia.

Epidemiology and stratification of risk for sudden cardiac death.

Sudden cardiac death (SCD) is a major cause of mortality in the United States. Approximately 65% of cases of SCD occur in patients with underlying acute or chronic ischemic heart disease. The incidence of SCD increases 2- to 4-fold in the presence of coronary disease and 6- to 10-fold in the presence of structural heart disease. Ventricular fibrillation (VF) precipitated by ventricular tachycardia (VT) is a common mechanism of cardiac arrest leading to SCD. Triggers for SCD include electrolyte disturbances, heart failure, and transient ischemia. Although a large percentage of patients with out-of-hospital SCD do not survive, successful resuscitation to hospitalization has improved in recent years. One of the challenges for preventing SCD lies in identifying individuals at highest risk for SCD within a lower-risk population. The progression from conventional risk factors of coronary artery disease to arrhythmogenesis and SCD can be represented as a cascade of changes associated with levels of increasing risk. At the first level is atherogenesis, followed by changes in atherosclerotic plaque anatomy, which may be mediated by inflammatory processes. Disruption of active plaque formed during a transitional state initiates the thrombotic cascade and acute occlusion, after which acute changes in myocardial electrophysiology become the immediate trigger for arrhythmogenesis and SCD. Each level of the cascade offers different opportunities for risk prediction. Among the classes of risk predictors are clinical markers, such as ECG measures and ejection fraction. Transient risk markers, such as inflammatory markers, are potentially useful for identifying triggers for SCD. In the future, genetic profiling is expected to allow better assessment of individual risks for SCD.

Arritmias cardíacas / Arrhythmias

O campo das arritmias cardíacas vem mudando rapidamente, à medida que cresce o conhecimento dos mecanismos envolvidos. A enorme quantidade de informações reflete-se ao tamanho do nosso livro-texto, Arritmias cardíacas, mecanismos, diagnóstico e tratamento. Considerando-se que a quantidade e a profundidade da informação contida naquele livro ultrapassa em muito o que a maioria dos médicos, estudantes de medicina, enfermeiros, técnicos e outros profissionais da área de saúde necessita em sua prática diária da medicina, nos condensamos substancialmente os capítulos, sem, com isso, comprometer o conteúdo básico. Assim sendo, este Manual tenta servir como uma revisão condensada, porém completa, sobre os mecanismos e condutas envolvendo as diferentes arritmias cardíacas. Foi nossa intenção lidar com uma área extremamente complexa da medicina interna de forma direta e bastante simples. Esperamos ter obtido sucesso nessa tentativa e que todos aqueles que venham a utilizar este manual o achem útil em sua prática médica diária