The paper aimed to present evidence of the effect of some pathophysiological features of chronic obstructive pulmonary disease (COPD) on cardiac remodeling in patients free of overt cardiovascular diseases, traditional cardiovascular risk factors and pulmonary hypertension. Contrary to traditional beliefs that cardiac abnormalities in COPD have been mainly associated with the right ventricle, several recent studies have shown an independent effect of pulmonary hyperinflation and emphysema on left ventricular (LV) diastolic filling and LV hypertrophy. Pulmonary hyperinflation and emphysema cause intrathoracic hypovolemia, low preload, small end-diastolic dimension and mechanical compression of LV chamber which could worsen end-diastolic stiffness. Interestingly, that the presence of LV hypertrophy in COPD patients is important but currently poorly understood area of investigation. Pulmonary hyperinflation, increased arterial stiffness and sympathetic activation may be associated with LV hypertrophy. Two-dimensional ultrasound speckle tracking studies have shown the presence of sub-clinical LV systolic dysfunction in patients even with moderate COPD and free of overt cardiovascular diseases. Sarcopenia related to the inflammatory-catabolic state in COPD and hypoxia could play an important role regarding LV systolic dysfunction. Recent data reported the effects of long-acting bronchodilators on reducing lung hyperinflation (inducing lung deflation). Further studies are required to evaluate the effects of pharmacological lung deflation therapy on cardiac volume and function.
Regional lung deflation with increased airway volume underlies the functional response to bronchodilators in chronic obstructive pulmonary disease
