RESUMO
Atherosclerosis is a chronic inflammatory disease. Pathophysiological similarities between chronic infections and atherosclerosis triggered interest in a clinical association between these conditions. Various infectious microbes have been linked to atherosclerotic vascular disease in epidemiological studies. However, this association failed to satisfy the Koch's postulates of causation with multiple clinical trials demonstrating inefficacy of anti-infective therapies in mitigating atherosclerotic cardiovascular events. Identification of underlying pathophysiological mechanisms and experience with vaccination against various infectious agents has ushered a new avenue of efforts in the development of an anti-atherosclerotic vaccine. Studies in animal models have identified various innate and adaptive immune pathways in atherosclerosis. In this review, we discuss the patho-biological link between chronic infections and atherosclerosis, evaluate existing evidence of animal and human trials on the association between infections and cardiovascular disease and introduce the concept of an anti-atherosclerotic vaccine.
Assuntos
Aterosclerose/etiologia , Doença das Coronárias/etiologia , Infecções/complicações , Animais , Anti-Infecciosos/uso terapêutico , Aterosclerose/tratamento farmacológico , Aterosclerose/prevenção & controle , Movimento Celular/fisiologia , Proliferação de Células/fisiologia , Doença Crônica , Citocinas/fisiologia , Modelos Animais de Doenças , Progressão da Doença , Endotélio Vascular/fisiologia , Proteínas de Choque Térmico/fisiologia , Humanos , Inflamassomos/fisiologia , Leucócitos/fisiologia , Metabolismo dos Lipídeos/fisiologia , Mimetismo Molecular/fisiologia , Placa Aterosclerótica/etiologia , Ruptura Espontânea/etiologia , VacinaçãoRESUMO
PURPOSE OF REVIEW: This paper aims to discuss the interactions between inflammatory cytokines, immune cells, and heart failure (HF). The association of heart failure with inflammation has led to multiple studies on anti-inflammatory agents in acute and chronic heart failure. RECENT FINDINGS: Recent findings have implicated leukocytes subclasses and multiple inflammatory mediators in the progression of heart failure and cardiovascular disease. Studies have discovered further details on the interaction between immune cells-particularly macrophages and lymphocytes-and inflammation. There are both cell-mediated and cytokine-mediated pathways of inflammation, which are interconnected. Additionally, a number of markers have been used and studied in heart failure disease progression. In this review, we discuss inflammatory biomarkers and immune cell mediators involved in HF. We will focus on the correlations and role of these inflammatory mediators in the genesis of HF. We will also discuss the evidence on beneficial effects of anti-inflammatory agents in the setting of chronic HF.
Assuntos
Insuficiência Cardíaca/etiologia , Inflamação/imunologia , Animais , Antialérgicos/uso terapêutico , Citocinas/imunologia , Humanos , Inflamação/complicações , Inflamação/tratamento farmacológico , Leucócitos/imunologiaRESUMO
BACKGROUND: The autonomic nervous system (ANS) is a key regulator of the cardiovascular system. The two arms of the ANS, sympathetic and parasympathetic (vagal) have co-regulatory effects on cardiac homeostasis. ANS modulation and dysfunction are also believed to affect various cardiac disease states. Over the past decade, there has been increasing evidence suggesting gender differences in ANS activity. METHODS: In multiple previous studies, ANS activity was primarily assessed using heart rate variability, muscle sympathetic nerve activity, coronary blood flow velocity, and plasma biomarkers. Heart rate variability is a non-invasive measure, which can be analyzed in terms of low frequency and high frequency oscillations, which indicate the sympathetic and parasympathetic tone, respectively. These measures have been studied between women and men in states of rest and stress, and in cardiac disease. CONCLUSION: Studies support the concept of a significant gender difference in ANS activity. Further studies are indicated to elucidate specific differences and mechanisms, which could guide targeted therapy of various cardiovascular disease states.