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67±6%), while in DCM patients LV end-diastolic volume (102±17 ml/m2) and ejection-fraction (49±5%) were worse than both controls and LM carriers (p<0.001). Moreover, DCM patients presented worse diastolic dysfunction (9±3 vs 7±1, p<0.01), NT-proBNP plasma levels (438±416 vs 108±139 ng/l, p<0.01) and Doppler-estimated pulmonary pressure (33±7 vs 30±5 mmHg, p<0.01) than LM carriers. Six (43%) DCM patients presented DE, representing 9±3% of LV mass; similarly, seven (42%) LM carriers had DE, but with a larger extension (11±5% of LV mass, p<0.03). In LM carries DE distribution was patchy (2 pts) or midwall (5 pt), similarly to DCM patients (patchy in 1 pt, midwall in 4 pts, subendocardial in 1 pt). GPC reached a steady state 5 minutes after gadolinium injection. In DCM patients GPC was slightly higher than controls (0.42±0.05 vs 0.38±0.06, p=0.04), while in LM carriers it was much higher (0.45±0.07) than controls (p<0.01). Even excluding hyperenhanced myocardium, in LM carriers GPC remained higher than controls, while in DCM patients only slightly higher than controls. Conclusions

Myocardial fibrosis as a early cardiac marker of disease in patients with lamin A/C mutations