Inflammation refers to immune cells and proteins released into the bloodstream by immune cells, like CRP and IL-6 which are used by clinicians as an indicator of inflammation. CRP and IL-6 are measured in the blood (i.e., sera). Myocarditis is defined by the presence of inflammation or immune cells in the heart muscle, called myocardium, by histology when a heart biopsy is obtained. Research in animal models has revealed that it is not just the presence of inflammation that causes a problem leading to heart failure, but it depends on the “type” of inflammation in the heart. There are many types of immune cells and some of them are good at fighting off infections like the viral infections that commonly cause myocarditis, and so are “protective”. However, other immune cells can exacerbate disease by increasing inflammation and promoting scarring (i.e., fibrosis) that can lead to heart failure and dilated cardiomyopathy (a chronic heart disease where the heart becomes very large and stops pumping usually requiring a heart transplant). Immune cells that research has identified as being “bad” for the heart include mast cells (allergy cells that release histamine and the reason we take anti-histamines when having allergic reactions) and eosinophils (important in eosinophilic and giant cell myocarditis). Mast cells and eosinophils release proteins that increase inflammation and the risk for developing heart failure and promote fibrosis and scarring that lead to dilated cardiomyopathy. Studies in animal models suggest that it is likely that many people get inflammation in the heart following common viral infections or other triggers, but they respond to the infection with mainly “protective” types of immune cells and so do not develop heart failure or dilated cardiomyopathy. Researchers studying myocarditis are searching for markers in the blood (called biomarkers) that will indicate the patients most at risk for developing heart failure and dilated cardiomyopathy following a viral infection or other trigger.
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