Key result
Epicarditis is linked to significantly higher intramyocardial vascular CML accumulation versus controls.
Why the study?
Increased deposition of the advanced glycation end-product N(e)-(carboxymethyl)lysine (CML) had been observed in intramyocardial vasculature in acute myocardial infarction and myocarditis, prompting exploration of CML presence in the hearts of patients with epicarditis.
Is epicarditis without myocarditis or myocardial infarction associated with increased accumulation of N(e)-(carboxymethyl)lysine (CML) in the intramyocardial vasculature compared to controls without heart disease?
Case-Control (n=20)
No
Is epicarditis without myocarditis or myocardial infarction associated with increased accumulation of N(e)-(carboxymethyl)lysine (CML) in the intramyocardial vasculature compared to controls without heart disease?
Patients with isolated epicarditis have significantly increased accumulation of the advanced glycation endproduct N(e)-(carboxymethyl)lysine in the intramyocardial vasculature, indicating coronary microvascular inflammation and dysfunction that may contribute to increased cardiovascular risk.
Answers are grounded in this paper and cite their sources.
Epicarditis was associated with greater CML accumulation; hypothesis-generating for microvascular dysfunction in isolated epicarditis.
Advanced glycation end-products (AGEs) are implicated in the pathogenesis of vascular disease. In previous studies we have found increased deposition of N(e)-(carboxymethyl)lysine (CML) in intramyocardial vasculature in the heart in acute myocardial infarction and myocarditis. It is known that the process of inflammation plays a role in the formation of AGEs. In this study we have explored the presence of CML (a major AGE) in the heart of patients with epicarditis using a monoclonal anti-CML antibody. Nine patients with epicarditis (n = 9) died and their hearts were used for this study, control were hearts from patients who died from conditions unrelated to heart disease and without signs of myocarditis or epicarditis CML deposition and complement were significantly increased in patients with epicarditis compared to control hearts. Thus epicarditis increases CML depositions in the intramyocardial vasculature.
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Baylan et al. (2023) conducted a case-control in Epicarditis (n=20). Epicarditis vs. Control patients who died of causes unrelated to heart disease without epicarditis was evaluated on N(e)-(carboxymethyl)lysine (CML) immunohistochemical (IH) score in the intramyocardial vasculature (p=0.0003). Epicarditis significantly increased N(e)-(carboxymethyl)lysine (CML) accumulation in the intramyocardial vasculature compared with control patients without heart disease (p = 0.0003).
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