Cardiac > Adultdz > Myocarditis

Myocarditis:

Clinical:

Myocardial inflammation (myocarditis) can be secondary to a number of etiologies including infection (typically viral or HIV), cardiotoxic agents (drugs, chemotherapy- anthracyclines), autoimmune (SLE), or post-transplant rejection [7]. The most common viral agents are coxsackie B virus (accounts for 50% of cases [7]), noncoxsackie enterovirus, herpes virus 6, adenovirus, and parvovirus B19 [6,7]. The incidence of myocarditis in HIV patients is reported to be between 6-52% and no specific pathogen is found in more than 80% of cases [10]. It is a lymphocytic myocarditis in about half of the cases [10]. Common pathogens indentified in HIV myocarditis include toxoplasma gondii, mycobactrium tuberculosis, and cryptococcus neoformans [10].

The level of troponin I is more often elevated than that of CK-MB in patients with myocarditis [8]. For viral myocarditis, spontaneous recovery within a few weeks to months is common [3,4]. However, chronic myocarditis (dilated cardiomyopathy) occurs in 10-21% of cases [3,11]. Sudden cardiac death can occur in up to 12% of young adults [6].

X-ray:

MR: The diagnosis of myocarditis is made on the basis of two of three "Lake Louise" criteria: 1- regional or global signal intensity increase on T2 images; 2- increased global myocardial early gadolinium enhancement ratio (EGEr ≥4.0); 3- at least one focal, nonischemic lesion at inversion-recovery late gadolinium enhancement imaging [12].

Focal or global areas of increased signal can be seen within the myocardium on T2 images [7]. Cine balanced steady-state free precession (SSFP) sequences (which yield high contrast between blood and myocardium) can also be used to detect acute inflammation [9]. Owing to the T1 component of the signal, SSFP MRI sequences following contrast administration correlate well with areas of enhancement on delayed contrast imaging [9]. In areas of myocardial inflammation, the increased T2 relaxation time- due to edema- combined with the decrease in T1 relaxation after contrast administration allows detection of myocardial abnormalities [9].

Delayed myocardial enhancement can be seen in 24-88% of cases of acute viral myocarditis [7]. With acute myocarditis, delayed hyperenhancement is generally scattered, nodular and subepicardial (or midmyocardial as opposed to vascular disease that produces subendocardial abnormalities), without respect for vascular territories, and often with an inferolateral/lateral and apical distribution [1,2,4,8]. The changes may be subtle and focal acutely, becoming more diffuse over the next 10 days [1].

Although subepicardial enhancement is seen in the majority of cases, focal transmural areas of enhancement can occur in severe cases [5]. In myocarditis, myocardial damage is more diffuse than damage due to infarction. Islands of necrotic cells are scattered throughout the focus of acute myocarditis [2]. Therefore, contrast enhancement in acute myocarditis may not be as intense as in myocardial infarction [2].  With herpes 6 infection, it has been suggested that the septum is primarily involved, and that with parvovirus 19, there is a predilection for the inferolateral wall [7].

 During healing, inflammatory cells infiltrate the myocardial regions of myocarditis, and eventually necrotic myocytes are replaced by areas of fibrous tissue and delayed contrast enhancement can persist in the chronic phase [2]. The area of myocarditis diminishes in size as it is replaced by scar and this can explain the observation that contrast enhancement typically decreases over time [2].

REFERENCES:

(1) AJR 2007; Lim RP, et al. Non-ischemic causes of delayed myocardial hyperenhancement on MRI. 188: 1675-1681

(2) Radiographics 2006; Vogel-Claussen J, et al. Delayed enhancement MR imaging: utility in myocardial assessement. 26: 795-810

(3) Radiology 2008; Gutberlet M, et al. Suspected chronic myocarditis at cardiac MR: diagnostic accuracy and association with immunohistologically detected inflammation and viral persistence. 246: 401-409

(4) AJR 2009; Goitein O, et al. Acute myocarditis: noninvasive evaluation with cardiac MRI and transthoracic echocardiography. 192: 254-258

(5) Radiographics 2009; Cummings KW, et al. A pattern-based approach to assessment of delayed enhancement in nonischemic cardiomyopathy at MR imaging. 29: 89-103

(6) Radiographics 2009; Sparrow PJ, et al. CT and MR imaging findings in patients with acquired heart disease at risk for sudden cardiac death. 29: 805-823

(7) AJR 2011; Hoey ETD, et al. Cardiovascular MRI for assessment of infectious and inflammatory conditions of the heart. 197: 103-112

(8) Radiographics 2011; James OG, et al. Utility of FDG PET/CT in inflammatory cardiovascular disease. 31: 1271-1286

(9) AJR 2011; Deux JF, et al. Acute myocarditis diagnostic value of contrast-enhanced cine steady-state free precession MRI sequences. 197: 1081-1087

(10) AJR 2012; Nakazono T, et al. HIV-related cardiac complications: CT and MRI findings. 198: 364-369

(11) Radiology 2012; O'Donnell DH, et al. Cardiac MR imaging of nonischemic cardiomyopathies: imaging protocols and spectra of appearances. 262: 403-422

(12) Radiology 2014; Acute myocarditis: multiparametric cardiac MR imaging. 273: 383-392

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