Abstract
Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide and encompasses chronic bronchitis and emphysema. It has been shown that vascular wall remodeling and pulmonary hypertension (PH) can occur not only in patients with COPD but also in smokers with normal lung function, suggesting a causal role for vascular alterations in the development of emphysema. Mechanistically, abnormalities in the vasculature, such as inflammation, endothelial dysfunction, imbalances in cellular apoptosis/proliferation, and increased oxidative/nitrosative stress promote development of PH, cor pulmonale, and most probably pulmonary emphysema. Hypoxemia in the pulmonary chamber modulates the activation of key transcription factors and signaling cascades, which propagates inflammation and infiltration of neutrophils, resulting in vascular remodeling. Endothelial progenitor cells have angiogenesis capabilities, resulting in transdifferentiation of the smooth muscle cells via aberrant activation of several cytokines, growth factors, and chemokines. The vascular endothelium influences the balance between vaso-constriction and -dilation in the heart. Targeting key players affecting the vasculature might help in the development of new treatment strategies for both PH and COPD. The present review aims to summarize current knowledge about vascular alterations and production of reactive oxygen species in COPD. The present review emphasizes on the importance of the vasculature for the usually parenchyma-focused view of the pathobiology of COPD.
Highlights
Chronic Obstructive Pulmonary Disease and the Cardiovascular System: Vascular Repair and Regeneration as a Therapeutic Target
Various studies have shown that pulmonary vascular remodeling and endothelial dysfunction occurs in animal models of lung emphysema [78], in patients with mild Chronic obstructive pulmonary disease (COPD) not suffering from hypoxemia, and in smokers with normal lung function [72, 79]
Vascular remodeling and pulmonary hypertension (PH) can occur in cases of COPD, in severe cases and in mild-to-moderate forms of the disease and even in smokers with no airflow limitations
Summary
Respiratory diseases are a major cause of morbidity and mortality worldwide. COPD is caused by a persistent obstruction of the airflow in the lungs, which has profound effects on cardiac function and gas exchange, with systemic consequences. Present studies describing patients with mild-to-moderate COPD demonstrated reduced RV volumes compared with healthy controls [47] This discrepancy can be explained by the fact that majority of the patients with severe COPD primarily suffer from increased intrathoracic pressures due to hyperinflation and airway obstruction, but not from right heart failure. The high prevalence of left ventricular systolic dysfunction in individuals with COPD can be explained by the acceleration of the progression of coronary atherosclerosis by systemic inflammation, which leads to the development of ischemic heart disease. The remodeling of all vessel layers cannot be reversed by supplemental oxygen, either in cases of acute [74] or chronic COPD [75]
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