Pathophysiology
Summary
Myocarditis occurs when myocardium undergoes inflammatory damage, precipitated by various causes such as infection, toxin exposure, or hypersensitivity reactions. Viruses, notably coxsackievirus B, enterovirus, adenovirus, HIV, parvovirus, HHV 6, are common culprits. Additionally, bacteria such as Borrelia burgdorferi, which causes Lyme disease, and others like Rickettsia & Mycoplasma have been implicated. Myocarditis can also stem from infections with protozoa like Trypanosoma cruzi, which is responsible for Chaga's disease and culminates in myocarditis and dilated cardiomyopathy. Trypanosoma cruzi infection of the myocardium shows dense collections of protozoa on histology. Fungal infections, including those by Candida, Mucor, and Aspergillus, are especially prevalent in immunocompromised patients.
Histologically, viral myocarditis displays an inflammatory infiltrate within the myocardium. A critical consequence of viral myocarditis is the release of cross-reactive antigens from damaged myocytes, which in turn elicits the formation of autoantibodies that target heart tissue. Complications like dilated cardiomyopathy and systolic heart failure may arise in viral myocarditis.
Clinically, patients may initially exhibit flu-like symptoms before the onset of myocarditis. Clinical presentation often mimics that of MI, featuring precordial chest pain, accompanied by constitutional symptoms such as fever, malaise, and dyspnea.
Toxin exposure can also cause myocarditis. Substances such as anthracyclines, notably doxorubicin and daunorubicin, alcohol, cocaine, carbon monoxide, and certain antibiotics have been identified. Additionally, the toxins from Corynebacterium diphtheriae can cause myocarditis. Hypersensitivity myocarditis can initiate a delayed type IV hypersensitivity reaction and is caused by drugs such as furosemide, HCTZ, sulfa drugs, ampicillin, azithromycin, and zidovudine. A hallmark of this condition on histology is the presence of lymphocytic & eosinophilic interstitial inflammatory infiltrates.
Autoimmune diseases such as SLE, scleroderma, RA, and acute rheumatic fever—particularly after a Strep pyogenes pharyngitis—can induce myocarditis.
Inflammatory damage frequently triggers the release of cardiac markers like troponins & CK MB. In severe cases, inflammation-induced abnormal cardiac conduction can culminate in life-threatening arrhythmias or even sudden cardiac death.
Lesson Outline
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FAQs
Myocarditis is characterized by inflammation of the myocardium and can arise from a variety of etiologies including infectious agents, toxins, and immune-mediated responses. Infectious causes may include viral, bacterial, fungal, or protozoal pathogens. Exposure to toxins such as alcohol, carbon monoxide, or certain pharmaceuticals like diuretics and antibiotics can also induce myocarditis. Moreover, autoimmune conditions and hypersensitivity reactions to drugs may contribute to the development of this cardiac disorder.
Myocarditis commonly manifests with systemic symptoms like fever, malaise, and shortness of breath. It may also elicit precordial chest pain, mimicking the clinical presentation of a myocardial infarction. Diagnostic indicators include elevated levels of cardiac-specific proteins such as troponins and CK-MB, which signal myocardial damage. Inflammation of the myocardium can also disrupt cardiac conduction, resulting in arrhythmias that may escalate to sudden cardiac death.
Certain medications, including sulfa drugs, furosemide, HCTZ, ampicillin, azithromycin, and zidovudine, can induce hypersensitivity myocarditis. This form of myocarditis is mediated by a delayed type IV hypersensitivity reaction, which involves helper T cells. The drug or its metabolites act as antigens that activate these T cells, resulting in inflammation of the myocardium. The pathological hallmark of hypersensitivity myocarditis is lymphocytic and eosinophilic interstitial inflammatory infiltrates within the cardiac tissue. Prompt recognition and discontinuation of the causative drug are essential for management.
If not promptly managed, myocarditis may progress to more serious cardiac conditions. Persistent myocardial inflammation and damage can lead to ventricular dilation and weakening, culminating in dilated cardiomyopathy. This compromised cardiac function may further deteriorate into systolic heart failure, characterized by the heart's inability to provide adequate blood flow to meet the body's demands.
The hallmark microscopic feature of myocarditis is myocardial inflammation. The presentation varies with the etiology: viral myocarditis often shows mixed inflammatory infiltrates, while infection with Trypanosoma cruzi reveals dense protozoal aggregates. Hypersensitivity myocarditis is typified by lymphocytic and eosinophilic interstitial inflammatory infiltrates. In certain instances, damaged myocytes release cross-reactive antigens, which can prompt the formation of autoantibodies that target cardiac tissue.
