From the Guidelines
Septic myocarditis is caused by an inflammatory response to infectious agents, leading to the destruction of myocytes.
Pathogenesis of Septic Myocarditis
The pathogenesis of septic myocarditis involves the infection of the myocardium by various agents, including viruses, bacteria, fungi, and protozoans 1. This infection triggers an inflammatory response, which can lead to the destruction of myocytes and subsequent cardiac dysfunction. The inflammatory response can be caused by the direct effects of the infectious agent on the myocardial tissue or by triggering an immune response that presents as an acute inflammatory myocarditis 1.
Key Factors in the Pathogenesis of Septic Myocarditis
- Infectious agents: A wide range of infectious agents can cause septic myocarditis, including enteroviruses, adenoviruses, parvovirus B19, and human herpes virus type 6 1.
- Inflammatory response: The inflammatory response to the infectious agent can lead to the destruction of myocytes and subsequent cardiac dysfunction.
- Immune response: The immune response to the infectious agent can also contribute to the pathogenesis of septic myocarditis, with autoimmune responses playing a role in some cases 1.
Diagnosis of Septic Myocarditis
The diagnosis of septic myocarditis can be made using a combination of clinical presentation, laboratory tests, and imaging studies. Endomyocardial biopsy remains the gold standard for the diagnosis of myocarditis, but CMR is becoming a increasingly useful non-invasive test for confirming the diagnosis 1. ECG, transthoracic echocardiogram, and biomarker concentrations can also be used to support the diagnosis 1.
From the Research
Pathogenesis of Septic Myocarditis
The pathogenesis of septic myocarditis is a complex process that involves multiple mechanisms, including:
- Inflammatory response: Sepsis-induced myocardial dysfunction is associated with an inappropriate immune response to invading microorganisms, leading to the activation of inflammation and the release of cytokines and other mediators 2, 3.
- Nitric oxide production: Excessive nitric oxide production has been implicated in the development of cardiac dysfunction in sepsis 4.
- Mitochondrial dysfunction: Mitochondrial dysfunction has been shown to contribute to the development of sepsis-induced cardiomyopathy 4.
- Disturbances in calcium homeostasis: Alterations in calcium homeostasis have been implicated in the development of cardiac dysfunction in sepsis 4.
- Myocardial edema: Myocardial edema has been shown to play a significant role in the pathogenesis of sepsis-induced cardiomyopathy, particularly in association with cardiac remodeling in septic shock patients 4.
Key Mechanisms
The key mechanisms underlying the pathogenesis of septic myocarditis include:
- Activation of the immune system: The activation of the immune system in response to invading microorganisms leads to the release of cytokines and other mediators, which can cause cardiac dysfunction 5.
- Release of damage-associated molecular patterns (DAMPs): The release of DAMPs, such as extracellular histones and high-mobility group box 1, can contribute to the development of myocardial dysfunction in sepsis 3.
- Alterations in myocardial microvascular permeability: The alteration of myocardial microvascular permeability, particularly through the activation of the bradykinin receptor B1, can contribute to the development of myocardial edema in sepsis 4.
Underlying Factors
The underlying factors that contribute to the pathogenesis of septic myocarditis include:
- Sepsis: Sepsis is a major risk factor for the development of myocardial dysfunction, and the severity of sepsis is associated with the severity of cardiac dysfunction 2, 3.
- Infection: Infection is a major trigger for the development of sepsis and subsequent myocardial dysfunction 3.
- Inflammatory response: The inflammatory response to invading microorganisms is a key factor in the development of cardiac dysfunction in sepsis 2, 3.