Expert review of respiratory medicine
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Expert Rev Respir Med · Aug 2015
ReviewShould we treat chronic obstructive pulmonary disease as a cardiovascular disease?
Chronic obstructive pulmonary disease (COPD) is characterized by largely irreversible airflow limitation and is associated with several extrapulmonary manifestations and co-morbidities. Cardiovascular diseases are among the most frequent co-morbid conditions affecting patients with COPD and have important prognostic implications for hospitalization and mortality. In turn, COPD shares common risk factors with several cardiovascular diseases (i.e., smoking habit), while several features of COPD can predispose to cardiovascular disease (i.e., gas exchange abnormalities, polycythemia, systemic inflammation and sedentary lifestyle). ⋯ This review will discuss the increased prevalence and prognostic implications of cardiovascular co-morbidities in patients with COPD. The effect of COPD on the outcomes in cardiovascular disease will also be highlighted and the pathogenic mechanisms that underlie cardiovascular co-morbidities in patients with COPD will also be reviewed. Finally, options for the management of cardiovascular co-morbidities in patients with COPD will be discussed.
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Expert Rev Respir Med · Aug 2015
Permanent alveolar collapse is the predominant mechanism in idiopathic pulmonary fibrosis.
Alveolar epithelial cell loss and impaired epithelial cell regeneration are currently accepted as central initiating events in idiopathic pulmonary fibrosis (IPF), but subsequent downstream effects remain uncertain. The most accepted downstream effect is aberrant and dysregulated mesenchymal cell proliferation and excess extracellular matrix (ECM) accumulation. ⋯ Loss of tissue aeration is a consequence of alveolar collapse, which occurs in IPF as a result of apposition and septal incorporation of denuded basal lamina. Permanent alveolar collapse is well-documented following epithelial injury, has the ability to mimic interstitial fibrosis radiologically and histologically, and is a better supported explanation than dysregulated fibroblast proliferation and excess ECM accumulation for the constellation of findings in patients with IPF.