Key result
Higher myocardial inflammation and fibrosis in DCM are linked to worse cardiac death or LVAD risk.
Why the study?
Myocardial inflammation and fibrosis are risk factors for poor outcomes in dilated cardiomyopathy, but the combined prognostic value of these two factors evaluated by myocardial biopsy required investigation.
Does combined assessment of myocardial inflammation and fibrosis using myocardial biopsy predict cardiac death or LVAD implantation in patients with dilated cardiomyopathy?
Cohort (n=255)
Yes
Does combined assessment of myocardial inflammation and fibrosis using myocardial biopsy predict cardiac death or LVAD implantation in patients with dilated cardiomyopathy?
p-value: p=<0.001
Combined assessment of myocardial inflammation and fibrosis from biopsy samples provides significant prognostic value for predicting cardiac death or LVAD implantation in patients with dilated cardiomyopathy.
May refine DCM risk stratification via biopsy; hypothesis-generating and should not yet change practice.
Background Among patients with dilated cardiomyopathy (DCM), myocardial inflammation and fibrosis are risk factors for poor clinical outcomes. Here, we investigated the combined prognostic value of these two factors, as evaluated using myocardial biopsy samples. Methods This retrospective and multicentre study included patients with DCM—defined as LVEF of ≤45% and left diastolic diameter of >112% of predicted value, without evidence of secondary or ischaemic cardiomyopathy. In myocardial biopsy samples, inflammatory cells were counted using immunohistochemistry, and Masson’s Trichrome staining was performed to quantify the myocardial fibrosis as collagen area fraction (CAF). Higher myocardial inflammation was defined as leucocytes of ≥14/mm², including ≤4 monocytes/mm², with CD3 + T lymphocytes of≥7/mm². Greater myocardial fibrosis was defined as CAF of>5.9% by the Youden’s index. The primary endpoint was cardiac death or left ventricular assist device implantation. Results A total of 255 DCM patients were enrolled (average age, 53.1 years; 78% males). Within this cohort, the mean LVEF was 28.0%, mean CAF was 10.7% and median CD3 + cell count was 8.3/mm 2 . During the median follow-up period of 2688 days, 46 patients met the primary endpoint. Multivariable Cox proportional hazard analyses revealed that CD3 + cell count and CAF were independent determinants of the primary endpoint. Kaplan–Meier analysis showed that patients with both higher myocardial inflammation and greater fibrosis had the worst prognosis (log-rank p<0.001). When myocardial inflammation was graded as one of three degrees: T lymphocytes of <13/mm² (low); 13 of 13.1–23.9/mm² (moderate); and T lymphocytes of ≥24 /mm² (high), patients with moderate inflammation exhibited a superior survival rate when CAF was ≤5.9%, but a worse survival rate when CAF was >5.9%. Conclusions Having both biopsy-proven higher myocardial inflammation and greater fibrosis predicted the worst clinical prognosis in patients with DCM.
No takes yet. Share an insight, caveat, or question.
Nakayama et al. (2025) conducted a cohort in Dilated cardiomyopathy (n=255). Combined assessment of myocardial inflammation and fibrosis was evaluated on Cardiac death or left ventricular assist device implantation (p=<0.001). Patients with dilated cardiomyopathy who had both biopsy-proven higher myocardial inflammation and greater fibrosis had the worst prognosis for cardiac death or LVAD implantation (log-rank p<0.001).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: