Abstract
BackgroundSystemic inflammatory processes plausibly contribute to the development of cardiovascular complications, causing increased morbidity and mortality in type 2 diabetes. Circulating inflammatory markers, i.e., interleukin (IL)-6 and tumour necrosis factor-α, are associated with neurocardiac measures. We examined a broad panel of various inflammatory and inflammation-related serum markers to obtain more detailed insight into the possible neuro-immune interaction between cardiovascular regulation and systemic level of inflammation.MethodsSerum samples from 100 participants with type 2 diabetes were analysed. Heart rate variability, cardiovascular autonomic reflex tests, and cardiac vagal tone tests were performed based on electrocardiographic readings. Data regarding covariates (demographic-, diabetes-, and cardiovascular risk factors) were registered.ResultsIncreased serum levels of IL-12/IL-23p40 (p < 0.01) and intercellular adhesion molecule (ICAM)-1 (p < 0.007) were associated with diminished heart rate variability measures. After all adjustments, the associations between IL-12/23p40, SDANN and VLF persisted (p = 0.001). Additionally, serum levels of vascular endothelial growth factor (VEGF)-C were associated with response to standing (p = 0.005).DiscussionThe few but robust associations between neurocardiac regulation and serum markers found in this study suggest systemic changes in proinflammatory, endothelial, and lymphatic function, which collectively impacts the systemic cardiovascular function. Our results warrant further exploration of IL-12/IL-23p40, ICAM-1, and VEGF-C as possible cardiovascular biomarkers in T2D that may support future decisions regarding treatment strategies for improved patient care.
Highlights
Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in type 2 diabetes (T2D), accounting for approximately 50% of all deaths [1]
E.g., in Alzheimer’s disease [8], such systemic inflammation is known to associate with neuronal loss, resulting in widespread disruption of neuronal function, and over the last decade, accumulating evidence suggests that underlying chronic inflammation contributes to the development of diabetes complications including neuropathy and CVD [9]
No associations between any of the chemokines and neurocardiac function were found. In this cohort of adults with T2D, we found that increased levels of IL-12/IL-23p40 and intercellular adhesion molecule (ICAM)-1 were associated with diminished cardiac-derived time-domain measures of heart rate variability, suggesting parasympathetic withdrawal on autonomic regulation
Summary
Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in type 2 diabetes (T2D), accounting for approximately 50% of all deaths [1]. E.g., in Alzheimer’s disease [8], such systemic inflammation is known to associate with neuronal loss, resulting in widespread disruption of neuronal function, and over the last decade, accumulating evidence suggests that underlying chronic inflammation contributes to the development of diabetes complications including neuropathy and CVD [9] In both in recent-onset and long-term T2D, associations between cardiac measures and inflammatory markers highlight changes in proinflammatory cytokines like interleukin-6 [10,11,12], TNF-α [13], and IL-18 [10, 14], as well as intercellular adhesion molecule (ICAM)-1 [14, 15], and C-reactive protein (CRP) [10, 14] as potential contenders for investigating modulation of neurocardiac function. We examined a broad panel of various inflammatory and inflammation-related serum markers to obtain more detailed insight into the possible neuroimmune interaction between cardiovascular regulation and systemic level of inflammation
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