**2.4 Diagnostic**

Myocarditis refers to an underlying process that causes inflammation and injury of the heart. It does not refer to inflammation of the heart as a consequence of some other insult. Many secondary causes, such as a heart attack, can lead to inflammation of the myocardium and therefore the diagnosis of myocarditis cannot be made by evidence of inflammation of the myocardium alone.

Myocardial inflammation can be suspected on the basis of electrocardiographic (ECG) results, elevated C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR) and increased IgM (serology) against viruses known to affect the myocardium. Markers of myocardial damage (troponin or creatine kinase cardiac isoenzymes) are elevated.

The difficulty in diagnosing myocarditis lies in the known absence of specificity and sensitivity of the various diagnostic techniques used. Systematic biochemical measurements are not diagnostic and an increase in cardiotropic virus antibodies only reflects the response to a recent viral infection, but does not indicate active myocarditis. Endomyocardial biopsy, considered to be the diagnostic gold standard, is associated with a not inconsiderable risk of injury, as well as with sampling errors due to the focal involvement of the myocardium, which therefore reduces its diagnostic sensitivity. Radioactive isotope studies, widely used for the diagnosis of myocarditis, are limited by their low specificity, the exposure to radiation, and their cost [Subinas et al. 2005].

#### **2.4.1 Physical examination**

Physical findings of myocarditis can range from a normal examination, through all classes of congestive heart failure (CHF) to cardiovascular collapse and shock. Patients with mild cases of myocarditis have a nontoxic appearance and simply may appear to have a viral syndrome. Tachypnea and tachycardia are common. Tachycardia is often out of proportion to fever [Howes 2010].

More acutely ill patients have signs of circulatory impairment due to left ventricular failure. A widely inflamed heart shows the classic signs of ventricular dysfunction including the following: jugular venous distention, bibasilar crackles, ascites and peripheral edema.

Third heart sound (S3) or a summation gallop may be noted with significant biventricular involvement. Intensity of the first heart sound (S1) may be diminished. S3 generally occur between 0.12 and 0.24 second after the aortic component of the second heart sound. Clinically, the third heart sound (S3 gallop) may be a physiologic sound in children and young adults. It may be produced by factors that generate increased rate or volume of flow with high cardiac output or by conditions associated with cardiac dilatation and altered ventricular compliance, as in CHF [Smiterman TC and Willerson JT, 2007].

Cyanosis may occur. Murmurs of mitral or tricuspid regurgitation may be present due to ventricular dilation [Howes 2010].

In cases where a dilated cardiomyopathy has developed, signs of peripheral or pulmonary thromboembolism may be found [Howes 2010].

Diffuse inflammation may develop leading to pericardial effusion, without tamponade, and pericardial and pleural friction rub as the inflammatory process involves surrounding structures [Howes 2010].
