Assuntos
Ensaios Clínicos como Assunto/normas , Desfibriladores Implantáveis/efeitos adversos , Remoção de Dispositivo/normas , Determinação de Ponto Final/normas , Marca-Passo Artificial/efeitos adversos , Falha de Prótese , Infecções Relacionadas à Prótese/cirurgia , Sistema de Registros/normas , Projetos de Pesquisa/normas , Ensaios Clínicos como Assunto/métodos , Consenso , Remoção de Dispositivo/métodos , Humanos , Infecções Relacionadas à Prótese/diagnóstico , Infecções Relacionadas à Prótese/microbiologiaRESUMO
Either central or peripheral baroreceptor reflex abnormalities, and/or alterations in neurohumoral mechanisms play a pivotal role in the genesis of neurally mediated syncope. Thus, improving our knowledge of the biochemical mechanisms underlying specific forms of neurally mediated syncope (more properly termed "neurohumoral syncope") might allow the development of new therapies that are effective in this specific subgroup. A low-adenosine phenotype of neurohumoral syncope has recently been identified. Patients who suffer syncope without prodromes and have a normal heart display a purinergic profile which is the opposite of that observed in vasovagal syncope patients and is characterized by very low-adenosine plasma level values, low expression of A2A receptors and the predominance of the TC variant in the single nucleotide c.1364 C>T polymorphism of the A2A receptor gene. The typical mechanism of syncope is an idiopathic paroxysmal atrioventricular block or sinus bradycardia, most often followed by sinus arrest. Since patients with low plasma adenosine levels are highly susceptible to endogenous adenosine, chronic treatment of these patients with theophylline, a non-selective adenosine receptor antagonist is expected to prevent syncopal recurrences. This hypothesis is supported by results from series of cases and from two controlled studies.