The chronic obstructive pulmonary disease (COPD) is the chronic respiratory condition most prevalent in adults, caused mainly by smoking. Its burden is progressively increasing and, according to the World Health Organization, is one of the main causes of mortality and disability around the world. Patients with COPD present acute worsening of the disease, defined as acute exacerbations, which are the main cause of hospitalizations and deaths. Therefore, it is crucial to identify effective interventions focused in their prevention. Patients with COPD present dyspnoea and intolerance to exercise responsible for a progressive reduction in the level of physical activity, which is an independent risk factor for future exacerbations and mortality. On the other hand, it has been demonstrated that COPD patients with low level of physical activity present higher marker levels of systemic inflammation. Interventions able to increase the level of physical activity in COPD patients have demonstrated positive effects in quality of life and a few clinical trials suggest that improving physical activity is able to prevent exacerbations. We hypothesize that these effects could be explained by changes in systemic inflammation secondary to an increase of physical activity.

Cardiovascular disease (CVD) is the most frequent cause of premature death according to data from the American Heart Association and World Health Organization. Incidence and prevalence are on the rise. Rheumatoid Arthritis (RA) is the most common autoimmune disease. It is a chronic and systemic disease characterized by articular involvement with deformity ranging from persistent pain to premature disability. CVD is the most frequent cause of death in RA patients, even more than in diabetes mellitus 2 or chronic kidney disease. Multiple CVD risk scales have been tested in order to obtain a more accurate prediction of premature death by stroke or myocardial infarction in RA patients. Most of the scales, even those adjusted including RA features like inflammation and antibodies titles, have failed to properly predict the real CVD risk. Individually, RA specific autoantibodies have been related with increased CVD risk and multiple mechanistic explanations have arisen, generating even a new concept called “Autoimmune Atheromatosis”. Nevertheless, this association fails to give a full understanding of the accelerated and aggressive atheromatosis process that RA patients develop. New studies oriented to mechanistic explanations are necessary in order to develop new diagnostic targets and prevention strategies.