- Meeting abstract
- Open Access
2029 Systemic sclerosis: detection of myocardial fibrosis by contrast-enhanced MRI
© Nassenstein et al; licensee BioMed Central Ltd. 2008
- Published: 22 October 2008
- Systemic Sclerosis
- Pericardial Effusion
- Myocardial Fibrosis
- Late Enhancement
- Myocardial Edema
Systemic sclerosis (SSc) represents a complex disorder of obscure etiology which affects the skin as well as various organs. Cardiac manifestations of SSc may result in pericardial disease, valvular disease, conduction system abnormalities, and arrhythmias; however, myocardial fibrosis is the hallmark with major impact on treatment and patients' prognosis.
Thus, our study aimed to assess the potential of contrast enhanced cardiac MRI for early detection of cardiac involvement in patients with systemic sclerosis.
Our study included 35 patients (31 female, 4 male; mean age, 54 ± 14 years) with known systemic sclerosis and an age, sex and cardiovascular risk factors matched control group. Patients with known coronary artery disease (CAD) or a history of myocardial infarction were excluded from the study. All examinations were performed on a 1.5 T MR scanner (Magnetom Avanto, Siemens, Germany). The MRI protocol included Steady-State Free Precession cine sequences (TrueFISP, TR 3 ms, TE 1.5 ms, FA 60°) in long and short axis views for the assessment of myocardial function. Fat-suppressed T2-weighted turbo spin echo images (TR 2 heart beats, TE 49 ms, FA 180°) in standard orientations were acquired for the assessment of myocardial edema. Additionally, an inversion-recovery fast low angle shot sequence (turboFLASH, TR 8 ms, TE 4 ms, TI 180–240 ms, FA 20°) was applied in short and long axis views 10–15 min after injection of a 0.2 mmol/kg BW of Gd-DTPA (Magnevist™, Schering AG, Berlin, Germany).
The concept of myocardial late enhancement has been established for the assessment of myocardial viability. In chronic myocardial infarction, the accumulation of gadolinium-based contrast material reflects irreversible damage and scar formation. However, whereas LE is highly sensitive in characterizing myocardial scarring, it is not specific for ischemic damage since contrast agents generally accumulate in tissues with an increased interstitial space or areas with cell membrane damage. Thus, LE also occurs in myocardial areas of inflammation, edema, as well as fibrosis (Hunold, AJR 2005). Contrast-enhanced MRI must be considered as the imaging modality of choice for the detection of myocardial fibrosis in vivo. Our data show that late enhancement can be detected in 15% of SSc patients with no clinical evidence of myocardial involvement. Therefore, contrast-enhanced MRI seems to be well suited for screening of myocardial fibrosis, monitoring the progression and possibly evaluating therapeutic effects. However, long-term follow-up studies are mandatory to investigate the impact of late enhancement on patients' prognosis.
This article is published under license to BioMed Central Ltd.