**4. Clinical features**

As stated previously, clinical picture of myocarditis is extremely variable, ranging from asymptomatic ECG abnormalities to heart failure (Dec et al., 1985, Bowles et al., 2003). The term ''*Acute* fulminant myocarditis'' is used for cases with severe congestive heart failure or cardiogenic shock (Amabile et al., 2006). Age of child influences clinical presentation of myocarditis (Dec et al., 1985). Viral prodrome of flu-like illness, respiratory symptoms or gastroenteritis may precede symptoms of heart failure. Neonates and infants present with poor feeding, irritability or listlessness, diaphoresis, apnea and episodic pallor. Usual symptoms of congestive heart failure, as well as mild cyanosis and pallor are observed on physical examination. It should be emphasized that neonates and affected younger infants may have intrauterine myocarditis with chronic course (Bowles et al., 2003). For very young infants acquiring myocarditis in the peripartal period, the prognosis is very poor, with more than 90% of children dying. Previous studies have implicated the myocarditis as the cause of sudden death (Friedman et al., 1998, Bowles et al., 2003). In the retrospective study of Krous et al., they evaluated the infants who died of sudden death infant syndrome in a safe sleep environment, accidental suffocation or myocarditis were assessed, and they have noticed the manifestation of scattered inflammatory cells and necrotic myocyte were noticed (Krous et al., 2009). From this observation, they suggested that few scattered inflammation and necrotic myocyte were normal finding in the developing heart exposed to new environmental pathogens. However, degree of cardiac infiltration was found to be greater in infants who died of myocarditis. In German study published in 2004, researchers found that viral myocardial affection is the cause of death in cases with SIDS (Dettmeyer et al., 2004). Besides, it was proposed by authors that PVB19 seems to play a more significant role than presumed so far.

Recent history of viral disease 10 to 14 days preceding presentation typically occurs in older children and adolescents (Friedman et al., 1998). Nonspecific gastrointestinal and respiratory complaints are more common than chest pain (Vashist&Singh, 2009). Jugular venous distension and pulmonary rales may be seen, and the resting tachycardia may be obvious, unlike in neonates. Since symptoms of myocarditis vary considerably in children, diagnosis can be challenging. Durani and colleagues, documented that most patients present with complaints of shortness of breath having tachypnea at presentation (Durani et al., 2009). Vomiting (48%) and poor feeding (40%) are also commonly seen in myocarditis. The authors also observed that the diagnosis of myocarditis was missed on the first presentation to a physician in 83% of cases. In a retrospective review, of 31 children with probable and definite myocarditis, 57% were initially diagnosed as suffering pneumonia or asthma (Freedman et al., 2007). One point that deserves attention in these studies is the absence of other signs of congestive heart failure in the majority of cases with myocarditis. Only 50% of children had hepatomegaly and 34% had abnormal chest radiography. The electrocardiographic changes include sinus tachycardia with low voltage QRS complexes, inverted T waves typically occur in the clinical setting of myocarditis (Durani et al., 2009). Wide Q waves and ST segment changes as a pattern of myocardial infarction also may be observed. Supraventricular tachycardia, ventricular tachycardia or atrial fibrillation, as well as atrioventricular block may occur (Friedman et al., 1994). Of note, the sensitivity of electrocardiography in myocarditis is only 47% (Morgera et al., 1992). However, Freedman and colleagues found that sensitivity of electrocardiography as a screening test was 93% (Freedman et al., 2007). Additional interesting finding that is worth to mentioning that the presence of axis deviation (%37) in children with myocarditis. Although ventricular tachycardia is a rare initial manifestation of myocarditis, it may often develops in long-term follow up and may occasionally result in sudden death (Drory et al., 1991).

Myocarditis imitating an acute coronary syndrome has also been defined. Viral genomes were demonstrated in 71% of adult cases with normal coronary anatomy, clinically mimicking myocardial infarction. Parvovirus B19 was most common agent identified in this study (Kuhl et al., 2003). ECG criteria (wide Q waves in I, avL, V5 and V6, ST segment change > 2 mm, ventricular arrhythmias) was described for the diagnosis of myocardial infarction in children (Towbin et al., 1992). However, similar ECG findings can occur in myocarditis (Durani et al., 2009). Most common ECG findings in adult patients with myocarditis include ST segment elevation(55%), T wave inversion (27%), ST segment depression (27%) and pathological Q waves (%18) (Dec et al., 1992, Angelini et al., 2000). Myocardial infarction and myocarditis in neonates overlap and mimic each other (deVetten et al., 2011). Despite angiographically normal coronary anatomy, global or segmental wall motion abnormalities are commonly obvious (Angelini et al., 2000). Physicians should always bear in mind the possibility of acute myocarditis in younger cases who present with acute coronary syndromes when coronary risk factors are lacking, global rather than segmental left ventricular dysfunction is evident on echocardiography or ECG abnormalities encompass beyond a single coronary artery zone (Magnani&Dec, 2006).
