By PD Dr Manuel Richter, MD, on behalf of the Pulmonary Vascular Research Institute.
Pulmonary hypertension (PH) is a multifactorial chronic pulmonary disease. During the past decade, various pathophysiological pathways eventually leading to progressive pulmonary vascular remodelling have been detected. Of note, there is increasing evidence that environmental and/or life-style factors may promote initiation and/or progression of the disease. Along this line, animal studies have shown that tobacco smoke exposure impairs pulmonary endothelial function and drives elevation of pulmonary arterial pressure, beside the well-known detrimental impact on the lung parenchyma itself. Pre-clinical studies indicate that tobacco smoke mediates airway inflammation and proliferation due to overexpression of various inflammatory mediators, cytokines and growth factors, which may be causally linked with endothelial dysfunction. Moreover, tobacco smoke is affecting endothelial cells themselves, inducing among other effects a disbalance in endothelial vasodilators and vasoconstrictors.
These pre-clinical data provide strong evidence for an impact of smoking on PH not only in those patients suffering from pulmonary hypertension due to smoking related chronic lung disease, but probably in all PH patients. Specific treatments targeting (smoking induced) endothelial injury may be considered, albeit there is only one overall message: stop smoking.