**2.4.2 Invasive techniques**

156 Myocarditis

Myocarditis is often associated with pericarditis, and many patients present with signs (pericardial friction rub) and symptoms that suggest concurrent myocarditis and

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

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

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

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

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

Cyanosis may occur. Murmurs of mitral or tricuspid regurgitation may be present due to

In cases where a dilated cardiomyopathy has developed, signs of peripheral or pulmonary

Diffuse inflammation may develop leading to pericardial effusion, without tamponade, and pericardial and pleural friction rub as the inflammatory process involves surrounding

ventricular compliance, as in CHF [Smiterman TC and Willerson JT, 2007].

damage (troponin or creatine kinase cardiac isoenzymes) are elevated.

radiation, and their cost [Subinas et al. 2005].

**2.4.1 Physical examination** 

ventricular dilation [Howes 2010].

structures [Howes 2010].

thromboembolism may be found [Howes 2010].

to fever [Howes 2010].

pericarditis.

**2.4 Diagnostic** 

the myocardium alone.

**Cardiac angiography:** This is often indicated to rule out coronary ischemia as a cause of new-onset heart failure, especially when clinical presentation mimics acute myocardial infarction. It usually shows high filling pressures and reduced cardiac outputs [Tang et al., 2009].

The gold standard is still **biopsy of the myocardium**, generally done in the setting of angiography. A small tissue sample of the endocardium and myocardium is taken, and investigated by a pathologist by light microscopy and—if necessary—immunochemistry and special staining methods [Cunningham et al., 2006]. Histopathological features are: a myocardial interstitium with abundant edema and inflammatory infiltrate, rich in lymphocytes and macrophages. Focal destruction of myocytes explains the myocardial pump failure. The need for routine myocardial biopsy in patients with HIV is controversial and associated risks are significant – sensitivity is low, especially in patchy lesions, and beyond research protocols, its use is limited to patients with extensive cardiac damage with no identifiable cause [Wu et al., 1990].

Myocarditis identified at autopsy or on endomyocardial biopsy in HIV-infected patients is most often nonspecific and manifested as focal, inflammatory lymphocytic infiltrates without myocyte necrosis. Other reported histopathologic findings include lymphocytic infiltration with myocyte necrosis fulfilling the Dallas criteria or myocyte damage without associated cellular inflammatory infiltrate [Anderson et al., 1988, Barbaro et al., 1998]. The autopsy finding of focal myocarditis in many patients who die of AIDS-related complications, but have no known premortem heart disease, suggests that focal lymphocytic infiltration may have no clinical significance. By comparison, diffuse lymphocytic myocarditis meeting the Dallas criteria appears rare [Anderson et al., 1988].

The prevalence of nonspecific myocarditis is related to the stage of HIV infection and the presence of structural heart disease. In one study of HIV-infected patients with a premortem diagnosis of dilated cardiomyopathy*,* histologic findings consistent with lymphocytic myocarditis by the Dallas criteria were identified in 63 of 76 patients (83%) [Barbaro et al., 1998].
