Résumé
Background: the pathophysiological mechanisms linking chronic obstructive pulmonary disease (COPD) and cardiovascular comorbidities remain poorly understood. Emphysema and COPD exacerbations are believed to play a key role in these interactions. However, it remains unclear whether exacerbation severity is influenced by associated cardiac decompensation. This study investigates the interactions between emphysema, COPD exacerbations, and cardiovascular function. Methods: the study has two parts; a retrospective analysis of patients hospitalized for COPD exacerbations at Montpellier University Hospital in 2017, collecting clinical, biological, and pulmonary function data. The second component uses an animal model of emphysematous rats, induced by increasing doses of intratracheal elastase (4U, 6U, or 10U per group), further exacerbated by LPS administration. Cardiac (echocardiography) and respiratory (plethysmography, pressure-volume curve) functions were assessed at 24 hours and 5 weeks post-exacerbation, alongside histological analysis of lung and heart analysis. Results: cardiac impairment, as indicated by the need for diuretics during exacerbation, is associated with the requirement for intensive care unit admission (p=0.027). The animal model demonstrated dosedependent emphysema with increasing elastase administration (p<0.0001). Exacerbation induced significant right ventricular dysfunction, evidenced by reduced TAPSE (p=0.01) and a heart failure profile with preserved ejection fraction, evidenced by an increased E/e' ratio in emphysematous rats (p=0.011), and reduced left ventricular end-diastolic area (p=0.03). At stable conditions, left diastolic dysfunction persisted, with a dose-dependent linear correlation between the E/e' ratio and the Mean Linear Intercept (R²=0.53, p=0.0003). Conclusion: cardiac decompensation during exacerbation influences its severity. Emphysema induces diastolic dysfunction during both exacerbation and stable phases in a COPD rat model.