Diagnosis of Acute Global Myocarditis Using Cardiac MRI with Quantitative T1 and T2 Mapping: Case Report and Literature Review
A 28-year-old male was presented to the emergency department complaining of dyspnea, dizziness, and chest tightness over the preceding 24 hours. He had no significant past medical history. His body temperature was 37.2℃, blood pressure was 104/72 mm Hg, heart rate was 95 beats per minute (bpm), and his physical examination was gernally normal. Laboratory studies showed a WBC count of 16.2 × 103/µL (reference range, 4.0-10.8 × 103/µL) and platelets of 219 × 103/µL (reference range, 150-400 × 103/µL). Additionally, troponin T was found to be 0.958 mcg/L (reference range, 0-0.014 mcg/L), and C-reactive protein (CRP) was 14.7 mg/L (reference range, 0.1-6.0 mg/L). Chest X-ray showed mild pulmonary congestion and cardiomegaly. ECG on admission revealed normal sinus rhythm at a rate of 79 bpm with T-wave abnormalities. Transthoracic echocardiography showed reduced global left ventricular systolic function with an ejection fraction (EF) of 34%, diffusely increased myocardial echogenicity, and a small pericardial effusion. Based on these results, acute myocarditis was suggested as a clinical diagnosis.\nA cardiac MRI was performed on the third day of admission using a 1.5-T MR scanner (Magnetom Avanto; Siemens Medical Solutions, Erlangen, Germany). After scout images were taken, the cine MRI was performed with balanced steady-state free precession (b-SSFP) to obtain horizontal long-axis, vertical long-axis, 3-chamber view, and contiguous short-axis images. T2-weighted images were obtained by using a triple inversion recovery black-blood turbo spin-echo sequence along the contiguous short-axis planes from the apex to the base of the left ventricle (LV). Quantitative T2 mapping with a T2-prepared SSFP pulse sequence and pre-T1 mapping with a modified Look and Locker technique were performed during the mid-diastolic phase along the same short-axis planes as the T2-weighted images. The acquisition parameters for T2 mapping were: T2 preparation times = 0 ms, 24 ms, and 55 ms; repetition time (TR) = 3 × R-R ms; echo time (TE) = 0 ms, 24 ms, and 55 ms; acquisition matrix = 126 × 192; acquisition time = 7 × R-R; single-shot acquisition; flip angle = 70°; and bandwidth = 916 Hz/pixel. The acquisition parameters for T1 mapping were: TR = 740 msec, TE = 1.06 msec, flip angle = 35°, acquisition matrix = 192 × 124, field of view = 320 × 400 mm, slice number = 10 slices. Late gadolinium enhancement-MRI (LGE-MRI) was performed using a magnitude and phase-sensitive inversion recovery (PSIR) prepared by fast gradient echo sequence with the inversion time adjusted to null the normal myocardium. LGE-MR images were obtained along the same axis plane and with the same slice thickness as in the cine-MRI, 10 minutes after the administration of 0.2 mmol/kg of a gadoterate meglumine (Dotarem®; Guerbet, France). The acquisition parameters were: TR = 600 ms, TE = 3.4 ms, flip angle = 25°, acquisition matrix = 156 × 256, field of view = 320 × 400 mm, slice number = 10 slices, cardiac phase = middiastole. After obtaining the LGE-MR images, the post-T1 mapping was performed 15 minutes after the contrast media injection, using the same slice axis and parameters as pre-T1 mapping. T2-pixel maps and pre-post T1-pixel maps were generated after motion corrections using commercially available software on the scanner's workstation (Syngo; Siemens Medical Solutions, Erlangen, Germany).\nOn cine images, global systolic dysfunction resulted in an EF of 30%. Bilateral pleural effusions and a pericardial effusion were also noted (). On T2WI, there was not a patchy region of increased signal intensity (SI) in the LV myocardium, but global edema was presented with a ratio of myocardium to skeletal muscle of > 2.0 (). On the TI scout images, it was difficult to determine the optimal nulling time for the LV. We ultimately selected 270 ms as the nulling time (). On LGE images with a magnitude and PSIR (), global hyper SI throughout the LV myocardium was suggested, though it was uncertain whether the increased SI was due to incomplete myocardial nulling or diffuse myocardial delayed enhancements. The T2 and T1 values were measured according to AHA myocardial segmentation with the exception of the apex () (). On quantitative T2 map images, myocardial T2 values remarkably increased to about 91.4 ± 6.1 milliseconds (ms) (reference value, 55.5 ± 2.3) () (). The precontrast T1 value of the myocardium also increased to 1276.6 ± 32.4 ms (reference value, 1034.1 ± 53.1) () (). On post-T1 mapping images, the mean myocardial T1 value was 625 ± 12.4 ms, which was similar to the T1 value of the LV cavity (623 ms) (). The myocardial extracellular volume (ECV) fraction was calculated as follows: ECV fraction = (ΔR1 of myocardium / ΔR1 of LV blood pool) × (1 - hematocrit), R1 = 1 / T1, ΔR1 = Post-contrast R1 - Pre-contrast R1 (). The pre-T1 value of the LV cavity was approximately 1520 ms. The patient's hematocrit was 43.6%. The calculated mean ECV fraction for the LV myocardium was 45.9 ± 1.9% (range: 43-49.7%). Thus, it was concluded that diffusely high myocardial SI on the LGE-MR images was not caused by incomplete nulling of the myocardium, but rather by ECV expansion of the myocardium.\nThe patient's final diagnosis was myocarditis based on clinical symptoms, ECG results, biomarkers, echocardiogram results, and cardiac MR findings. Follow-up echocardiography was performed one week after initiating conservative care, revealing improved global LV systolic function with an EF of 67%. CRP peaked on the fourth day of admission at 156.1 mg/L, but decreased thereafter and normalized to 1.1 mg/L on the fourteenth day of admission.