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The study design was an observational cohort study, among university hospital DCM patients. The study group comprised 184 consecutive patients with DCM. Individuals with signs or symptoms of ongoing myocarditis or diagnosed with significant coronary artery disease were excluded. CE-CMR was performed on a 1.5 T clinical scanner. LGE was evaluated by two independent observers. For quantification of fibrosis, LGE was defined as areas with a signal intensity >2 SD above the mean signal intensity. Areas were measured by manual planimetry and expressed as percentage of myocardial mass. Those who had been initially diagnosed as having DCM and displaying a subendocardial or transmural pattern of late gadolinium enhancement suggestive of myocardial infarction were excluded from final analysis.
The composite end point included cardiac death, hospitalization for decompensated heart failure, or appropriate implantable cardioverter defibrillator discharge for a mean + SEM of 685+ 30 days.
The authors found LGE in 72/184 patients (39%). LGE associated with a significantly lower left ventricular (LV) ejection fraction (31% (20.9-42.2%) vs 44% (33.1-50.9%), p < 0.001), higher LV end-diastolic volume index and higher LV mass. Individuals with LGE were more likely to experience the composite end point (15/72 vs 6/112, p= 0.002). The receiver operating characteristic curve (ROC) showed that a LGE of >4.4% of LV mass was optimal discriminator for the composite end point. LGE retained its independent predictive value also in multivariate Cox regression analysis. Importantly, the prognostic significance of LGE was dependent on the degree of LV dysfunction so that those with severely impaired LV function had more unfavorable outcome.
The authors discussed that LGE probably reflects the segmental replacement fibrosis whereas the diffuse interstitial fibrosis is not visualized by contrast-enhanced cardiac MRI. They concluded that in this DCM patient cohort LGE was associated with pronounced LV remodelling, functional impairment and adverse outcome. The possible mechanisms could be the arrhythmogenicity of local fibrotic areas and loss of ventricular compliance due to fibrosis. The role of LGE in clinical decision making has not yet been clarified.
This was so far the largest DCM cohort studied with CE-CMR. Examining the relationships between patterns and amount of LGE and adverse cardiac remodelling may increase our understanding of the mechanisms of heart failure. Data from genetically characterized DCM populations could possibly in the future reveal whether some of the LGE patterns might reflect different ethiologies of DCM.
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