Myocarditis

In the ED, suspecting acute myocarditis in HIV-infected patients is important as this condition may evolve to include life-threatening congestive heart failure and arrhythmias.

Fever and infection of the upper respiratory tract or flu-like symptoms may precede exertional dyspnea by as little as hours or days. Signs and symptoms may occur at rest and include palpitations, atypical chest pain, and electrocardiographic alterations (ST-segment elevation followed by T-wave inversion in different leads). Laboratory alterations may include elevated cardiac troponin I (cTnI) and myoglobin levels with or without increased levels of myocardial fraction of creatine kinase (CK-MB). A clinical diagnosis of myocarditis or congestive heart failure in an HIV-infected patient may be difficult to make due to the masking of symptoms by concomitant bronchopulmonary disease and/or wasting syndromes. Differentiating myocarditis from myocardial infarction may also be difficult. A careful clinical history and physical examination, electrocardiogram (ECG) review, and analysis of traditional risk factors expanded to include HIV-specific therapies (i.e., PIs in the context of HAART regimens) may direct the diagnosis.

Myocardial enzyme testing will help to detect myocardial injury rapidly with high sensitivity and specificity. Markers of cardiac injury should be interpreted in relation to the timing of the onset of the patient’s symptoms. An elevation of myoglobin in the absence of an elevated cTnI level in subsequent samples may be related to an inflammatory muscle disease. Myositis is more likely to occur in HIV-infected patients, making myoglobin a much less specific marker for cardiac injury.

An isolated positivity of cTnI suggests a minimal myocardial damage of small areas of the myocardium (micronecrosis). In HIVpositive patients, micronecrosis may be caused by an inflammatory process secondary to myocarditis or pericarditis with extended epicarditis (perimyocarditis) or secondary to autoimmune mechanisms induced by infections or antiviral drugs.

In case of a positive CK-MB and/or cTnI in patients with a nondiagnostic ECG (e.g., presence of left bundle-branch block, chronic ischemic alterations), clinical skills and echocardiography should help guide the differential diagnosis of myocarditis (absence or reversible hypokinesia) or acute myocardial infarction (with or without ST-segment elevation). However, endomyocardial biopsy represents the gold standard in the diagnosis of myocarditis. According to the Dallas criteria, myocarditis is defined as “a process characterized by a lymphocytic infiltrate of the myocardium with necrosis and/or degeneration of adjacent myocytes not typical of the ischemic damage associated with coronary artery disease” [3].

Intravenously administered immunoglobulins may be useful in improving the clinical outcome and the echocardiographic measurements of cardiac mass and function. The apparent efficacy of immunoglobulin therapy may be the result of immunoglobulins inhibiting cardiac autoantibodies (i.e., anti- a-myosin autoantibodies) by competing for Fc receptors or dampening the secretion or effects of cytokines and cellular growth factors [4]. Serial therapy in children has been shown to improve fractional shortening and left ventricular mass and to stabilize the disease process. Immunomodulatory therapy may be helpful in HIV-infected adults and children with declining left ventricular function, but further study is needed to evaluate the efficacy of this therapy and its impact on mortality.

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Source: Barbaro Giuseppe, Boccara Franc (eds.). Cardiovascular Disease in AIDS. 2nd edition. — Springer,2009. — 169 p.. 2009

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Myocarditis

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