**Indications for Hospitalization of Patients with Acute Pericarditis**


Table 3. Indications for Hospitalization of Patients with Acute Pericarditis. (adapted from reference 26)

There are certain scenarios when perimyocarditis present with focal EKG signs suggestive of STEMI. This can be challenging especially in developing countries where thrombolytic therapy is the mainstay of management of STEMI. In patients with acute pericarditis, thrombolytic therapy can be detrimental because of the risk of cardiac tamponade [52, 53]. Although the use of anticoagulants in patients with acute pericarditis is deemed

unfavorable, in their study on 274 consecutive cases of idiopathic or viral acute pericarditis, Imazio and colleagues concluded that neither the use of heparin, anticoagulants nor glycoprotein IIb/IIIa inhibitors is associated with an increased risk of cardiac tamponade. [54] Risk factors for complications in that study included the lack of complete response to aspirin or NSAID (OR = 14.6, 95% CI 6.1 to 35.1; P = 0.001), or corticosteroid use (OR = 3.0, 95% CI 1.1 to 8.9; P = 0.048).

The mainstay of therapy for acute pericarditis is NSAID (class 1 recommendation in 2004 ESC guidelines). The goal of NSAID is to reduce pain and inflammation. Ibuprofen might be preferred because of its rare side effects, favorable impact on coronary artery blood flow and large dose range from 1200 to 1800 mg daily [55]. Aspirin can also be used in antiinflammatory doses (up to 800 mg every 6 hours). Dose tapering is preferred to avoid recurrence. Gastric protection is mandatory and should be commenced in all patients. In perimyocarditis, NSAID should be used cautiously because in animal models they were shown to enhance the myocarditic process and may increase mortality [56-58]. Lower antiinflammatory doses should therefore be considered whenever possible in perimyocarditis and its main use is to control symptoms. Failure to respond to NSAID within one week

Perimyocarditis 115

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(indicated by persistence of fever, new pericardial effusion, or continuing chest pain) indicates that a cause other than viral is responsible and should be searched for. Although colchicines can be used alone or in conjunction with NSAID in treatment and prevention of recurrent pericarditis, there is lack of data regarding its benefit in perimyocarditis [59].

The use of corticosteroids was found to be an independent risk factor for recurrence of acute pericarditis [60, 61] because of their ability to promote viral replication [62, 63]. Its use should therefore be restricted for those with autoimmune disease or in cases refractory to NSAID and colchicine and a specific cause has not been found. Despite the long list of pathogens, in most cases, a specific etiology for acute perimyocarditis can't be determined. In instances where an underlying treatable cause is confirmed, treatment of the target organism should be commenced. After hospital discharge, patient should be followed for several weeks to rule out the development of heart failure or subclinical left ventricular dysfunction. All patients should be advised to avoid strenuous exercise during the recovery phase (4-6 weeks) which can increase the risk of ventricular arrhythmias.

#### **11. References**


(indicated by persistence of fever, new pericardial effusion, or continuing chest pain) indicates that a cause other than viral is responsible and should be searched for. Although colchicines can be used alone or in conjunction with NSAID in treatment and prevention of recurrent pericarditis, there is lack of data regarding its benefit in perimyocarditis [59]. The use of corticosteroids was found to be an independent risk factor for recurrence of acute pericarditis [60, 61] because of their ability to promote viral replication [62, 63]. Its use should therefore be restricted for those with autoimmune disease or in cases refractory to NSAID and colchicine and a specific cause has not been found. Despite the long list of pathogens, in most cases, a specific etiology for acute perimyocarditis can't be determined. In instances where an underlying treatable cause is confirmed, treatment of the target organism should be commenced. After hospital discharge, patient should be followed for several weeks to rule out the development of heart failure or subclinical left ventricular dysfunction. All patients should be advised to avoid strenuous exercise during the recovery

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**6** 

*Argentina* 

**Pathogenesis and Pathology of** 

**Chagas' Chronic Myocarditis** 

Julián González, Roberto Guerri-Guttenberg, Daniel Grana, Francisco Azzato and José Milei

*Instituto de Investigaciones Cardiológicas Prof. Dr. A. Taquini – UBA – CONICET* 

Chronic chagasic cardiomyopathy (CCC) is the most serious manifestation of the chronic phase of Chagas' disease and constitutes the most common type of chronic myocarditis in the world (Guerri-Guttenberg, et al., 2008, Milei, et al., 1996a, Milei, et al., 2009, Milei, et al., 1992a, Storino, et al., 1992). Chagas' disease, a chronic illness caused by the flagellate parasite *Trypanosoma cruzi* (*T. cruzi*), was first described in 1909 by the Brazilian physician Carlos Chagas (Chagas C, 1909). The insect vectors of the disease are present throughout most of South and Central America, and their zone of distribution extends across the southern United States (Rassi, et al., 2010). It was estimated by year 2000, that in endemic areas 40 million people were considered to be at risk of infection, being 20 million already infected. Every year near 200,000 new cases are expected to happen, and 21,000 deaths per

Although always considered to be confined to Latin America, due to migratory movements from endemic countries to Europe and North America, Chagas' disease is being detected more frequently in developed countries. Europe is estimated to have from 24,001 to 38,708 (lower or upper limit of estimate, respectively) immigrants with *T. cruzi* infection (Guerri-Guttenberg, et al., 2008). In the United States, six autochthonous cases, five transfusion related cases and five transplant related cases have been reported, but migratory movements still remain the main source of Chagas' disease. It has been estimated that around 89,221 to 693,302 infected Latin Americans migrated to the United States in the

Two phases of the disease can be distinguished: (1) acute phase, with transiently high concentration of parasites in tissue and blood, nonspecific symptoms, and a 5% myocarditis incidence, lasting 4 – 8 weeks; and (2) chronic phase, lasting lifelong. Chronic phase can be presented as indeterminate form, characterized by lack of symptoms and normal ECG and normal radiographic examination of the chest, esophagus and colon. Approximately 60 – 70% of patients remain in this form for the rest of their lives. Only 20-40% of infected individuals, 10-30 years after the original acute infection, will develop cardiac, digestive or mixed form of the disease, characterized by the appearance of megavicera (dilated cardiomyopathy, megaesophagus and/or megacolon). It poses a substantial public health burden due to high morbidity and mortality (Milei, et al., 2009, Rassi, et al., 2000, Rassi, et

**1. Introduction** 

year occur (WHO, 2005).

al., 2010).

period 1981 to 2005 (Milei, et al., 2009).

