Asthma and chronic obstructive pulmonary disease (COPD) represent the leading chronic respiratory diseases of interest in the word, owing to their high prevalence and burden on the health system. Care of these patients, undergoing frequent exacerbations, is a heavy burden on healthcare systems. In the last few years, large improvements in the management of asthma and COPD have been made, owing to new drugs and management strategies, and to the improvement of the nonpharmacologic treatment of COPD.

There are still many unmet needs in the treatment of these diseases. In asthma, strategies to improve control should be implemented. There is a need to use more biomarkers to tailor treatment, in the assessment and choice of appropriate therapy, especially in severe patients. In COPD, there is growing evidence of individual differences in lung function decline rate and associated differences in appropriate management strategies. Early effective and prolonged bronchodilation can slow disease progression and reduce the frequency of exacerbations.

New perspectives include the use of biologic drugs (anticytokine monoclonal antibodies) in selected categories of severe asthmatics, potential new inhibitors of chemokines and cytokines involved in the pathobiology of asthma and COPD, and a further improvement of current drugs and better implementation of management strategies, particularly in COPD patients.

The natural course of chronic obstructive pulmonary disease (COPD) is complicated by the development of systemic consequences and comorbidities. COPD has been associated with an increased risk for cardiovascular disease, osteoporosis, cachexia and skeletal muscle weakness. In several large prospective cohort studies, the degree of airflow limitation was an independent predictor of both fatal and nonfatal cardiovascular events, implying a causal relationship between airflow obstruction and vascular disease.

The pathomechanisms responsible for this association are mostly unknown. It has been proposed that systemic inflammation, oxidative stress, hypoxia and sympathetic activation may be mechanisms in COPD leading to vascular dysfunction and cardiovascular disease. However, the current evidence of a causal relationship between COPD and vascular dysfunction is insufficient and more data from well-designed studies are urgently needed, hopefully leading to novel therapeutic and preventive approaches in the care of patients with COPD.