The systemic spillover of pro-inflammatory mediators (IL-6, IL-8, tumor necrosis factor α) from the lungs, prompting platelet activation, endothelial inflammation and atherosclerosis has been considered the major pathogenic mechanism of exalted cardiovascular risk after acute exacerbated COPD [42,43,44]. Here, CXCL8 is linked to chronic obstructive pulmonary disease.