Myocardial Inflammation-Are We There Yet?

Abstract

Several exogenous or endogenous factors can lead to inflammatory heart disease. Beside infectious myocarditis, other systemic inflammatory disorders such as sarcoidosis, systemic lupus erythematosus (SLE), systemic sclerosis (SSc), Churg-Strauss syndrome, and rheumatoid arthritis can affect the myocardium. Myocardial inflammation may have a major impact on the outcome of these patients, resulting in sudden cardiac death, severe arrhythmias, or end-stage heart failure. The current gold standard for definite confirmation of inflammatory heart disease is endomyocardial biopsy (EMB), but is invasive and suffers low sensitivity and specificity due to sampling errors. Thus, non-invasive methods for detecting the extent and changes over time of the inflammatory myocardial disease are needed. Cardiac magnetic resonance (CMR) is such a non-invasive method. We will describe and discuss different approaches for CMR assessment of inflammatory myocardial disease including early gadolinium enhancement (EGE), T2-weighted imaging, late gadolinium enhancement (LGE), the newer mapping proton relaxation techniques (T1 pre-contrast, T1 post-contrast, T2 mapping), and the hybrid PET/MRI technique.

Keywords: Cardiovascular magnetic resonance; Edema; Gadolinium; Mapping; Myocardial inflammation; Tissue characterization.

Fig. 1

CMR of a 28-year-old male presenting with dyspnea and chest pain 5 days after flu-like symptoms. Due to ST elevation and elevated cardiac enzymes, the patient underwent coronary angiography where coronary stenosis could be excluded. Cine images reveal global preserved left ventricular ejection fraction (LVEF = 60 %) with discrete hypokinesia at the lateral wall. LGE is present in multiple locations (white arrows), suggestive of myocarditis. The acute nature of the disease is demonstrated by positive dark-blood T2W images displaying a clear bright signal in the lateral wall, in an area consistent with LGE findings. Note that on the correspondent T2-weighted images in the long-axis, these lesions are not well delineated. This patient received state of the art heart failure medication (betablocker, ARB); in the next few months, the initial extensive LGE lesions decreased in size (which could be observed at a subsequent CMR scan) and the patients complaints resolved completely

Fig. 2

A 61-year-old female presenting with chest pain and elevated cardiac enzymes. Coronary artery disease (CAD) was ruled out by coronary angiography. a Cine images showed a slightly diminished left ventricular ejection fraction (LVEF = 53 %). b LGE images revealed an almost transmural LGE inferoseptal from midventricular to the apex, from epicardial origin. This pattern could indicate cardiac manifestation of a systemic disease such as sarcoid. c T2-weighted images demonstrate hyperintense regions (edema) in the inferoseptal wall (white arrows), corresponding to LGE. Biopsies were taken, which confirmed the diagnosis of sarcoidosis, and steroid therapy was initiated

Fig. 3

A 72-year-old woman was referred with increasing shortness of breath and intermittent chest pain. Echocardiography revealed a diminished left ventricular ejection fraction (35 %); significant CAD could be ruled out by coronary angiography. Biopsy of an enlarged scalene lymph node showed non-caseating granulomas, so cardiac sarcoid was considered, and a hybrid PET/MRI was scheduled. In the upper row T2-weighted images are displayed in cine short axis views. Middle row shows the concomitant LGE images; the presence of LGE is indicated by the white arrows. In the bottom row, there are fused images (MRI and PET): note that PET images show an increased uptake in the border zones of the LGE, suggesting that the process of inflammation affects more regions than displayed solely by LGE. Far right, CMR images showing splenic nodules with enhancement on both LGE sequences and by PET. Reprinted with permission from LWW [42]

Fig. 4

Cardiac magnetic resonance images from a 48-year-old patient with systemic sclerosis (SSc), with a normal left ventricular (LV) ejection fraction of 63 %. a LGE imaging with no focal areas of enhancement. b T2 map. c Native T1 map (acquired using ShMOLLI at 1.5 T) showed significantly elevated average LV myocardial T1 values of 1009 ± 47 ms (normal 962 ± 25 ms). d Post-contrast T1 map acquired at 15 min after gadolinium administration. Average post-contrast T1 values were 479 ± 18 ms. Extracellular volume (ECV) quantification using pre- and post-contrast T1 mapping and adjusting for the hematocrit demonstrated a significant expansion of interstitial space at 40 % (normal 27 ± 3 %). Images courtesy Dr. Ntobeko Ntusi, University of Oxford