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The significant change in EAT accumulation early after a myocardial injury suggest a bidirectional cross-talk between EAT and the myocardium, and different possible EAT responses to similar stimuli (myocardial ischemia). Many studies reported that EAT thickness, being a marker of EAT inflammatory status, is associated to increased cardiovascular risk, but this is the first evidence of EAT remodeling following myocardial injury. In the present population a EAT > 0 was associated with higher LV volumes and lower LV systolic function, independently from the troponin peak, which has been used to estimate the infarct size. Cardiac troponins provide very useful information in this respect, especially in patients with STEMI (Halln, 2012). Troponin peak has been demonstrated to be an independent predictor of infarct size measured at SPECT in a community-based cohort of patients with first myocardial infarction (Arruda-Olson et al., 2011). Thus, we can hypothesize that the myocardial ischemia drives EAT phenotypic changes which in turn regulate post-infarct LV remodeling. This hypothesis is also supported by the evidence that neither basal nor at follow-up EAT thickness were associated by themselves to LV post-infarct remodeling. EAT may transduce systemic inflammation to the myocardium and have a crucial role in the balance between inflammatory and anti-inflammatory cytokines. IL-13 is an anti-inflammatory cytokine that promotes polarization of macrophages toward an M2 phenotype (Gause et al., 2013; Wynn, 2015). IL-13 directly acts on target tissues to promote cell cycle activity during regenerative wound healing (Kasaian and Miller, 2008). Previous evidence demonstrated a role for endogenous IL-13 in neonatal cardiomyocytes cell cycle and heart regeneration and suggested recombinant IL-13 as therapeutic approach for activating pro-regenerative and survival pathways in the heart (Wodsedalek et al., 2019). Furthermore, IL-13 could be particularly involved in post-ischemic myocardial remodeling by suppressing fibrinogen production and inhibiting dendritic cell and/or macrophage function (Vasse et al., 1996; Davidson et al., 2007; Shao et al., 2007). Jafarzadeh et al. (2009) reported higher circulating levels of IL-13 in control subject compared to infarcted patients. In the current study, our data are consistent with a protective role of IL-13, as its increase after myocardial infarction is associated to recovery of LV systolic function at 3 months. We also observed that changes in IL-13 circulating levels at 3 months are inversely associated to EAT thickening. In the surgical group (Supplementary Material) we also observed that EAT and its cell subtypes are a source of IL-13. We also observed a significant correlation between EAT and serum levels of IL-13. This evidence supports the hypothesis that serum levels mirror EAT inflammatory status. However, we cannot exclude that the relationship between local and systemic inflammation could be bidirectional and circulating levels of inflammatory mediators could concur to EAT phenotypic and functional remodeling. The possible link between IL-13 and EAT remodeling has been explored in the context of valvular heart disease, were EAT thickness is associated to adverse LV remodeling (Vianello et al., 2019). In patients with valvular heart disease, IL-13 expression by EAT is involved in molecular up-regulation of genes encoding for fat mediators associated with adipose tissue remodeling (Vianello et al., 2019). The finding that only the EAT thickness, and not EAT at T0 or T1, is associated to LV adverse remodeling in our study population, can be explained by the acute nature of the pathology considered. While in valvular heart disease, the progression of the disease goes parallel with the increase of EAT thickness, STEMI is an acute event affecting both myocardial and EAT remodeling.

Unit 10 is 90 cm thick, comprising interbedded matrix and clast-supported beds that lie conformably on unit 9, dipping ~20 north. Matrix supported beds consist of >95% ash and < 5% 2 mm pumice and lithic clasts. Matrix-supported beds are indurated and the outer surface stained reddish-brown. Clast-supported beds comprise 90% juvenile material including < 3% bombs: lithic clasts constitute 10% of the unit. Pumice lapilli are generally angular or sub-angular to sub-rounded with a modal diameter of 1 cm, but some clast-supported beds contain clasts up to 4 cm diameter. Abundances of the five pumice lapilli types were not quantified for this unit, but pumice lapilli tend towards denser vesicle textures. Angular banded and breadcrust bomb types are present: maximum bomb diameter is 33 cm. Lithic clasts are angular, comprising a phenocryst bearing purple-red lava and grey phenocryst bearing lava. Modal lithic clast diameter is 0.5 cm, but clasts up to 4 cm diameter occur in beds containing the 4-cm pumice clasts. The upper contact with a thick clast-supported unit is slightly undulating (Fig. 14F) but sharply defined, while the lower contact is sharp and planar only disrupted by larger bombs protruding into the base of Unit 10 from Unit 9. Unit 10 is continuous across the exposed EC canyon wall, extending another ~70 m SSW until covered by alluvial canyon debris.

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