Bronchiectasis-COPD Overlap Syndrome: A Comprehensive Review of its Pathophysiology and Potential Cardiovascular Implications
- PMID: 39655338
- PMCID: PMC11626662
- DOI: 10.1177/29768675241300808
Bronchiectasis-COPD Overlap Syndrome: A Comprehensive Review of its Pathophysiology and Potential Cardiovascular Implications
Abstract
Bronchiectasis-Chronic Obstructive Pulmonary Disease Overlap Syndrome (BCOS) is a complex pulmonary condition that merges bronchiectasis and chronic obstructive pulmonary disease (COPD), presenting unique clinical challenges. Patients with BCOS typically exhibit a range of symptoms from both conditions, including a chronic productive cough, reduced lung function, frequent exacerbations, and diminished exercise tolerance. The etiology of BCOS involves multiple factors such as genetic predisposition, respiratory infections, tobacco smoke, air pollutants, and other inflammatory mediators. Accurate diagnosis requires a comprehensive approach, incorporating pulmonary function tests to evaluate airflow limitation, radiographic imaging to identify structural lung abnormalities, and blood eosinophil counts to detect underlying inflammation. Treatment strategies are tailored to individual symptom profiles and severity, potentially including bronchodilators, inhaled corticosteroids, and pulmonary therapy to improve lung function and quality of life. Patients with BCOS are also at an increased risk for cardiovascular complications, such as stroke, ischemic heart disease, and cor pulmonale. Additionally, medications like beta-agonists and muscarinic antagonists used in COPD treatment can further affect cardiac risk by altering heart rate. This paper aims to provide a thorough understanding of BCOS, addressing its development, diagnosis, treatment, and associated cardiovascular complications, to aid healthcare providers in managing this multifaceted condition and improving patient outcomes.
Keywords: alpha 1 antitrypsin; aspergillus fumigatus; bronchiectasis; chronic obstructive lung disease; hypoxic vasoconstriction; inflammatory mediators; pseudomonas aeruginosa; pulmonary hypertension; tobacco exposure; vascular remodeling.
© The Author(s) 2024.
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