The morbidity of myocarditis demonstrates an upward tendency by years, is commonly defined as the
inflammation of myocytes and is caused by multiple factors. With the development of the molecular biological
technique, great breakthroughs in the diagnosis and understanding of pathophysiological mechanisms of myocarditis
have recently been achieved. Several questions remain unresolved, however, including standard treatment
approaches to myocarditis, which remain controversial and ambiguous. Heart rate, as an independent risk factor,
has been shown to be related to cardiac disease. Recent studies also show that the autonomic nervous system is
involved in immunomodulatory myocarditis processes. Heart rate reduction treatment is recommended in myocarditis
based on a number of animal experiments and clinical trials. It is possible that heart rate-lowering treatments
can help to attenuate the inflammatory response and myocyte injury and reverse ventricular remodeling.
However, how to execute the protective effects of heart rate reduction on myocarditis is still not clear. In this
review, we discuss the pathogenesis and pathophysiological process of viral myocarditis and propose heart rate
lowering as a therapeutic target for myocarditis, especially in light of the third-generation β-blockade carvedilol
and funny channel blocker ivabradine. We also highlight some additional beneficial effects of such heart rate
reduction agents, including anti-inflammatory, antioxidation, anti-nitrosative stress, anti-fibrosis and antiapoptosis
properties.
Stabilin-1 mediates beneficial monocyte recruitment and tolerogenic macrophage programming during CVB3-induced viral myocarditis
