Assuntos
Força da Mão , Mãos , Voluntários Saudáveis , Humanos , Movimento , Reprodutibilidade dos TestesRESUMO
Heart rate is a major determinant of cardiac output, myocardial oxygen consumption and coronary blood flow under physiological and pathological conditions. Experimental and clinical data have demonstrated that heart rate reduction is the main mechanism for reducing ischemia, improving left ventricular function, decreasing the risk of plaque rupture and post myocardial infarction mortality. Nowadays betablockers are the best class of drugs that can lower heart rate in patients with cardiovascular diseases, but sometimes their use is limited by some contraindications. Ivabradine is a new drug that reduces the firing rate of pacemaker cells in the sinoatrial node through a different mechanism with respect to betablockers. The purpose of this review is to investigate the main trials that support Ivabradine adoption in clinical practice.
Assuntos
Benzazepinas/farmacologia , Fármacos Cardiovasculares/farmacologia , Doenças Cardiovasculares/fisiopatologia , Frequência Cardíaca/efeitos dos fármacos , Isquemia Miocárdica/prevenção & controle , Nó Sinoatrial/efeitos dos fármacos , Antagonistas Adrenérgicos beta/farmacologia , Angina Pectoris/tratamento farmacológico , Angina Pectoris/fisiopatologia , Ensaios Clínicos como Assunto , Canais de Cátion Regulados por Nucleotídeos Cíclicos/efeitos dos fármacos , Canais de Cátion Regulados por Nucleotídeos Cíclicos/fisiologia , Insuficiência Cardíaca/tratamento farmacológico , Frequência Cardíaca/fisiologia , Humanos , Ivabradina , PrognósticoRESUMO
In the last years, a considerable number of studies have been performed on the relationship between infection from Helicobacter Pylori and atherosclerotic diseases, like stroke and ischemic heart disease. In particular, some infections could have a role on the genesis and development of damage to the vascular wall and of atheromatous plaque. It has been suggested that HP could influence the development of IHD through different pathways, such as endothelial cells colonization, changes in the lipid profiles, increased coagulation and platelet aggregation levels, induction of molecular mimicry mechanisms and the promotion of a low-grade systemic inflammation. Based on this hypothesis, it has been performed a considerable number of studies in order to investigate the role of HP in the development and pathogenesis of CAD. Most of this trials gave conflicting results, some denying the presence of a possible relationship between HP infection and increased risk of CAD. Despite of that, results from these studies have raised new interesting perspectives on coronary heart disease, especially regarding the possibility of modifying the clinical history of the disease through eradication of these microorganisms. The results are contradictory and require further investigation.
