MUSELLA, FRANCESCA (2021) Aetiology and prognostic significance of non-infarct pattern late gadolinium enhancement in patients with coronary artery disease: a cardiovascular magnetic resonance prospective outcome study. [Tesi di dottorato]

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Background: Patterns of late gadolinium enhancement typically associated with dilated cardiomyopathy (DCM) are increasingly being recognised in coronary artery disease (CAD) populations . Long-term prospective cardiovascular magnetic resonance (CMR) studies may enhance our understanding of the prognostic significance and aetiological background of this novel phenotype. Methods: Patients with chronic CAD were prospectively recruited into a CMR registry between 2009 and 2016. Non-infarct pattern late gadolinium enhancement (NI-LGE) was confirmed by two independent level 3 CMR readers and subcategorised as either mid-wall, subepicardial or in multiple patterns and present in the ventricular septum, left ventricular free wall or in both locations. The primary endpoint was all-cause mortality. Secondary endpoints included a composite of cardiovascular mortality, major heart failure event or major arrhythmic event. All clinical events were adjudicated by a panel of experienced cardiologists blinded to the imaging data. Univariable and multivariable analyses of the primary and secondary outcomes were examined using Cox regression modelling. Results: 453 patients (mean age 64 years, mean left ventricular ejection fraction [LVEF] 47%, 95% with evidence of severe CAD) were followed for a median of 6.4 years. 63 (14%) patients had evidence of NI-LGE with involvement of the ventricular septum in 55 (12%) individuals. Patients with NI-LGE had elevated indexed LV end-diastolic volumes (131mls vs 103mls, P<0.001), elevated indexed LV end-systolic volumes (82mls vs 50mls, P<0.001) and a lower LVEF (38% vs 48%, P<0.001) as compared to patients without this CMR biomarker. Additionally, patients with NI-LGE had a similar number of severely diseased coronary vessels (p=0.46) but a decreased prevalence of prior myocardial infarction diagnoses (56% vs 76%, P<0.001), lower number infarcted myocardial segments (3 vs 5, P<0.001) and reduced infarct pattern LGE mass (12g vs 19g, P=0.001). Cumulative incidence of the primary endpoint by presence or absence of NI-LGE suggested that patients with this CMR biomarker had an increased risk of the primary endpoint (10-year risk 64% vs 42% for patients with and without NI-LGE, P<0.001). Additionally, cumulative incidence of the primary and secondary endpoints by presence or absence of septal NI-LGE suggested that patients with this pattern of LGE had increased risk of both outcomes. On multivariable analyses however, neither NI-LGE or septal mid-wall LGE were associated with the primary endpoint. Conclusions: NI-LGE in patients with CAD is likely a marker of significant adverse LV remodelling but does not appear to be an independent prognostic indicator after adjustment for baseline covariates. The greater LV dilatation despite reduced burden of myocardial infarction in this group potentially suggests the presence of a concomitant non-ischaemic cardiomyopathic process however the aetiological ground truth remains unclear. In conclusion, patients with CAD and CMR evidence of non-infarct pattern myocardial fibrosis represent an advanced disease subgroup and intensive optimisation of prognostic therapies is likely indicated.

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