From the Guidelines
The pathogenesis of infectious myocarditis is a complex process involving direct viral infection, host immune response, and inflammatory destruction of myocytes.
Key Mechanisms
- Viral infection: The initial injury is often caused by a virus, which can lead to an inflammatory response and myocardial damage 1.
- Host immune response: The host's innate and acquired immunologic response plays a crucial role in the pathogenesis of myocarditis, with excessive activation of innate immune pathways and a surge of proinflammatory cytokines 1.
- Inflammatory destruction of myocytes: The inflammatory response can lead to the destruction of myocytes, resulting in myocardial damage and potentially progressing to dilated cardiomyopathy (DCM) 1.
Phases of Myocarditis
- Acute injury: The initial phase, often caused by a virus, which can lead to an inflammatory response and myocardial damage.
- Host immune response: The second phase, where the host's immune system responds to the infection, potentially leading to further myocardial damage.
- Recovery or transition to scar and DCM: The final phase, where the myocardium either recovers or transitions to scar tissue and potentially progresses to DCM.
Diagnostic Considerations
- Endomyocardial biopsy: Remains the gold standard for diagnosing myocarditis, but is not always required for clinical management 1.
- Cardiovascular magnetic resonance (CMR): A sensitive, non-invasive test for confirming acute myocarditis, and can provide insights into the severity and localization of myocardial inflammation 1.
From the Research
Pathogenesis of Infectious Myocarditis
The pathogenesis of infectious myocarditis is a complex process involving various factors, including:
- Viral infection, with coxsackievirus B3 being a dominant etiological agent 2
- Immune responses, both innate and adaptive, which contribute to the severity of myocardial damage 2
- Autoimmune mechanisms, with evidence suggesting the production of antibodies against self-antigens and the involvement of T helper cells, particularly Th17 cells 3
- Cytokines, such as tumor necrosis factor (TNF)-alpha and interleukin (IL)-1, which can modulate the outcome of cardiotropic virus infection and enhance its autoimmune sequela 4
Key Processes Governing Pathogenesis
The key processes governing the pathogenesis of infectious myocarditis include:
- Viral replication and persistence in the heart 5
- Immune-mediated damage to the myocardium, which can lead to chronic myocarditis and dilated cardiomyopathy 2
- Inflammation and injury of the myocardium, resulting in clinical manifestations such as lymphocytic, eosinophilic, or giant cell/granulomatous myocardial inflammation 5
Etiologies and Implications for Clinical Practice
The etiologies of myocarditis are diverse, including infectious and non-infectious agents, and the impact of certain clinical features on risk assessment, patient outcomes, and treatment options is not entirely clear 6. Understanding the pathogenesis and etiology of myocarditis is essential for personalizing patient care and implementing novel therapeutic strategies 6.