**8. Cardiac magnetic resonance imaging**

In perimyocarditis, gadolinium contrast MRI is useful to conrm the diagnosis by detecting an area of delayed contrast-enhancement, to evaluate the severity of inammation in the acute stage as well as to determine the extent of brosis in the pericardium and myocardium [42]. The normal pericardium is observed as an area of low intensity on T1-weighted images and T2-weighted images [43]. In acute pericarditis, the inflamed pericardium is thickened and appears as an area of medium to high intensity with delayed contrast-enhancement recognized in the swollen pericardium which extends to the subepicardial myocardium affected by myocarditis [42]. The delayed enhancement in cardiac magnetic resonance (CMR) is explained by the leaking of the contrast media into the interstitial space due to

Fig. 3. Echocardiogram 5 days after admission. Parasternal long axis view (A) and short axis (B) in diastole. Normalization of the myocardial thickness in the posterior wall and posterior papillary and resolution of the pericardial effusion can be seen. Adapted from reference 38

Another non-invasive diagnostic tool in patients presenting with chest pain, ST segment elevation and elevated cardiac biomarkers is the use of the 64-slice coronary CT angiography (CCTA) which is a reliable test that can be utilized in patients with low to intermediate pretest probability for coronary artery disease. Shturman et. al. used the 64 slice CCTA to rule out coronary artery disease in a case of perimyocarditis mimicking myocardial infarction [40]. This simple noninvasive test and can avert the unnecessary need for coronary angiography or thrombolytic therapy for a presumed STEMI. Recently, Computed tomographic angiography (CTA) "triple rule out" protocol has been utilized in the emergency department for patients presenting with acute chest pain to differentiate between pulmonary embolism, aortic dissection and acute coronary syndrome. Compared with the usual radiation dose of a standard 64-slice CCTA, the effective radiation dose of a "triple rule-out" scan is often increased by 50% which should limit its unrestricted use. Takakuwa et. al. reported the successful use of the "triple rule-out" scan in diagnosing acute perimyocarditis (figure 4) and excluding other serious etiologies as acute coronary

In perimyocarditis, gadolinium contrast MRI is useful to conrm the diagnosis by detecting an area of delayed contrast-enhancement, to evaluate the severity of inammation in the acute stage as well as to determine the extent of brosis in the pericardium and myocardium [42]. The normal pericardium is observed as an area of low intensity on T1-weighted images and T2-weighted images [43]. In acute pericarditis, the inflamed pericardium is thickened and appears as an area of medium to high intensity with delayed contrast-enhancement recognized in the swollen pericardium which extends to the subepicardial myocardium affected by myocarditis [42]. The delayed enhancement in cardiac magnetic resonance (CMR) is explained by the leaking of the contrast media into the interstitial space due to

syndrome, aortic dissection and pulmonary embolism [41].

**8. Cardiac magnetic resonance imaging** 

with permission.

**7. CT angiography** 

Fig. 4. Four chamber view (left). TRO study demonstrating mild-to-moderate pericardial effusion surrounding the heart. Left anterior oblique view (right) optimized to visualize the full length of the RCA. PE - pericardial effusion, RV - right ventricle, LV - left ventricle, LAD - left anterior descending coronary artery. Adapted with modification from reference number 41 with permission.

inammation. As it stays out of the vessel, it cannot be washed away and is held for a longer time allowing it to be seen in the delayed enhancement images (figure 5) [44].

Fig. 5. Four chamber long-axis views. (A) Cardiac magnetic gadolinium delayed enhancement showing subepicardial hyperenhancement (arrow). (B) Cardiac CT delayed enhancement (arrows). Adapted from reference 44 with permission from Elsevier.

Cardiac magnetic resonance can also be a tool to differentiate between acute perimyocarditis and myocardial infarction. In acute myocarditis, myocardial late gadolinium enhancement is present in up to 88% of cases [45,46] which characteristically has patchy distribution not conforming to any particular coronary artery territory and is usually in the subepicardial and not the subendocardial layer [47] differentiating it from myocardial infarction.

Perimyocarditis 113

As earlier described, perimyocarditis is a combination of both pericardial inflammation and myocardial damage. Treatment should therefore target both pathologies. Because myocarditis is a more serious diagnosis owing to the potential of serious ventricular arrhythmias and heart failure, the diagnosis of myocarditis is deemed more important. Acute pericarditis usually runs a smooth and benign course after empiric treatment with NSAID and routine hospitalization in most cases is not necessary. Perimyocarditis on the other hand has higher incidence of complications and is one of the indications for hospitalization. Checking the levels of cardiac biomarkers and echocardiography is therefore mandatory in any case of acute pericarditis. Imazio et. al. identified certain poor prognostic predictors that are more frequently associated with an increased risk of short term complications and therefore an indication for hospitalization [26]. Table 3 lists various

indications for hospitalization of patients presenting with acute pericarditis

4. Findings of cardiac tamponade (i.e., hypotension and neck vein distention)

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

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,

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

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

3. Echocardiographic findings of a large pericardial effusion

5. History of trauma and compromised immune system

2. Body temperature greater than 100.4° F (38° C)

**10. Management** 

1. Anticoagulation therapy

95% CI 1.1 to 8.9; P = 0.048).

6. Myopericarditis 7. Troponin I elevation

reference 26)
