‘How I do’ CMR in DCM

1. ‘How I do’ CMR in DCM Dr Sanjay Prasad, Royal Brompton Hospital London, UK. For SCMR August 2006 This presentation is posted for members of scmr as an educational guide – it represents the views and practices of the author, and not necessarily those of SCMR. s.prasad@rbht.nhs.uk

2. Cine

3. Dilated Cardiomyopathy • Unexplained dilatation and impaired contractile performance of the left ventricle in the absence of significant coronary artery disease • Prevalence – 38/ 100 000 • Variable onset • A familial basis is seen in around 15% of patients

4. Dilated Cardiomyopathy: Causes • Idiopathic — 50 % • Myocarditis — 9 % • Infiltrative disease — 5 % • Peripartum cardiomyopathy — 4 % • Hypertension — 4 % • HIV infection — 4 % • Connective tissue disease — 3 % • Other — 10 percent Felker et al, NEJM 2000

5. DCM: Diagnosis • Often late presentation • Annual mortality ~4% (>SCD) • Opportunity for detection at an early/preclinical stage

6. CMR Evaluation of DCM • The first important aspect is determining LV and RV volumes, ejection fractions and mass • We recommend the modified Simpson’s method rather than biplanar assessment since it makes no assumptions on cardiac morphology and is both more accurate and reproducible. • After piloting the 4ch and VLA views, retrospectively gated gradient echo cine slices are taken from the base to apex • Typically 7mm slices with a 3mm gap. • Usually myocardial coverage is achieved in 9-10 slices

7. CMR Quantification See the presentation ‘how I do’ LV volumes Downloadable from www.scmr.org

8. T2 Imaging • In patients with an acute presentation of DCM, T2-weighted imaging is recommended to look for evidence of active inflammation/oedema. • The most likely cause for increased signal in the absence of infarction will be due to myocarditis • Occasionally other conditions such as sarcoidosis may also manifest in this way.

9. T2 Imaging Patient with a dilated LV and evidence of increased mid-wall/subepicardial signal on T2-weighted images in the anterolateral wall. The underlying diagnosis was DCM post-myocarditis.

10. T2 Imaging • If the T2-weighted triple-inversion recovery sequence is used, typical sequence parameters are :- • Slice thickness of 8mm • Surface and body coils • TR – 2x RR • TE- 65ms • TI – 170ms • Images are taken in the VLA, 4ch view, plus a full SA stack

11. Assessment of Fibrosis • The presence of replacement fibrosis can be detected using the inversion recovery late enhancement technique following gadolinium-DTPA administration. • In several recent studies, about 60% of patients with DCM showed no detectable fibrosis. • 30% showed mid-wall enhancement that correlates with fibrosis on histology. • 10% showed a typical pattern of infarction with subendocardial rather than mid-wall enhancement. In the presence of normal coronaries, this is likely to represent recannalisation, an embolic episode or coronary spasm. McCrohon J et al, Circulation 2003

12. Detection of Fibrosis: Inversion Recovery Sequence • Dosage of Gd-DTPA: 0.1-0.2mmol/kg • At 0.1mmol/kg, images are usually acquired after about 5 minutes with a TI starting at ~340ms (every other heart beat). • At 0.2 mmol/kg, scans are acquired after about 15 minutes with a TI starting at ~250ms.

13. Detection of Fibrosis: Inversion Recovery Sequence • Tips to confirm mid-wall fibrosis and ensure that artefact is not being detected are:- • Phase swap each slice • If mid-wall enhancement is seen, ensure that the TI is optimal and if need be, repeat the slice with a different TI • Cross-cut through any areas of suspected mid-wall enhancement • If subendocardial enhancement is seen, reconsider the diagnosis or assess if this reflects ‘bystander’ coronary disease • It is normal to see some fibrosis around the LVOT and at the RV/LV septal insertion points

14. Assessment of Fibrosis In this example, no late enhancement is seen reflecting the absence of detectable fibrosis

15. Assessment of Fibrosis In this patient, there is evidence of mid-wall fibrosis (arrows)

16. Why assess fibrosis • It may be prognostically significant • It may indicate aetiology of LVF • It may indicate response to treatment • (beta-blockers/device therapy) Assomull et al, JACC 2006 (In press)

17. Assessment of Fibrosis • Although the prescan diagnosis was of DCM (normal coronary angiogram), the CMR study shows extensive subendocardial enhancement reflecting an ischaemic aetiology

18. Follow-Up • This will be clinically determined • In a stable patient where the question is of determining reverse remodelling, a reasonable interscan interval would be about 12 months