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Review
. 2022 Mar 15:13:20420188221083530.
doi: 10.1177/20420188221083530. eCollection 2022.

Role of inflammation in diabetic cardiomyopathy

Pranav Ramesh  1 , Jian L Yeo  1 , Emer M Brady  1 , Gerry P McCann  1
Affiliations
Review

Role of inflammation in diabetic cardiomyopathy

Pranav Ramesh et al. Ther Adv Endocrinol Metab. .

Abstract

The prevalence of type 2 diabetes (T2D) has reached a pandemic scale. Systemic chronic inflammation dominates the diabetes pathophysiology and has been implicated as a causal factor for the development of vascular complications. Heart failure (HF) is regarded as the most common cardiovascular complication of T2D and the diabetic diagnosis is an independent risk factor for HF development. Key molecular mechanisms pivotal to the development of diabetic cardiomyopathy include the NF-κB pathway and renin-angiotensin-aldosterone system, in addition to advanced glycation end product accumulation and inflammatory interleukin overexpression. Chronic myocardial inflammation in T2D mediates structural and metabolic changes, including cardiomyocyte apoptosis, impaired calcium handling, myocardial hypertrophy and fibrosis, all of which contribute to the diabetic HF phenotype. Advanced cardiovascular magnetic resonance imaging (CMR) has emerged as a gold standard non-invasive tool to delineate myocardial structural and functional changes. This review explores the role of chronic inflammation in diabetic cardiomyopathy and the ability of CMR to identify inflammation-mediated myocardial sequelae, such as oedema and diffuse fibrosis.

Keywords: cardiovascular magnetic resonance imaging; diabetic cardiomyopathy; heart failure; inflammation; type 2 diabetes.

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Conflict of interest statement

Conflict of interest statement: The authors declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article.

Figures

Figure 1.
Figure 1.
Prevalence of cardiovascular complications in type 2 diabetes collected from the National Diabetes Audit 2018–2019, United Kingdom.
Figure 2.
Figure 2.
A summary of the inflammatory pathways leading to pathological cardiac remodelling and dysfunction in diabetic cardiomyopathy. Diabetes-associated cytokine release is primarily released via two mechanisms: NF-κB activation and AGE accumulation. The resulting mediators directly stimulate fibroblasts resulting in fibrosis, inhibit calcium movement causing impaired contractility and directly stimulate cardiomyocyte apoptosis and hypertrophy. AGE, advanced glycation end products; IL, interleukin; miR, micro-ribonucleic acid; NF-κB, nuclear factor-enhanced light chain activator of B cells; NO, nitric oxide; RAAS, renin–angiotensin–aldosterone system; T2D, type 2 Diabetes; TGF-β, tumour growth factor-beta; TNF-α, tumour necrosis factor-alpha.
Figure 3.
Figure 3.
Type 2 diabetes and associated subclinical inflammation causes oedema, myocardial fibrosis and macrophage infiltration which are detectable using CMR parametric mapping. A raised ECV is associated with increased adverse cardiac events. CMR, cardiac magnetic resonance; CV, cardiovascular; ECV, extracellular volume; USPIO, ultrasmall superparamagnetic iron oxide.
Figure 4.
Figure 4.
Multi-parametric tissue characterisation at mid-slice in inflammatory diseases involving the myocardium. On ECV maps, red areas represent abnormal ECV (greater than 30%). (a) Images of a healthy volunteer. (b) Acute myocarditis with higher native T1 values in the inferolateral wall of the left ventricle (B1, black arrow) consistent with LGE in the mid inferior-lateral wall (B2, yellow arrow). The ECV map demonstrates diffusely increased extracellular space. (c) Established rheumatoid arthritis with some rise in native T1 (C1) and ECV (C3). (d) Established systemic sclerosis with rise in native T1 predominantly in the septum (D1, black arrows) and widespread increase in ECV (D3). Images adapted from Haaf et al. ECV, extracellular volume; LGE, late gadolinium enhancement.
See this image and copyright information in PMC

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