Author + information
- Aibek E. Mirrakhimov, MD∗ ( and )
- Erkin M. Mirrakhimov, MD, PhD
- ↵∗Saint Joseph Hospital, Department of Internal Medicine, 2900 North Lake Shore, Chicago, Illinois 60657
We read the recently published report by Kasai et al. (1) with keen interest. The investigators performed a study comparing the application of lower body positive airway pressure and its effects on the neck circumference and partial pressure of carbon dioxide in patients with heart failure and sleep apnea. These researchers demonstrated that in all patients with sleep apnea, lower body positive airway pressure led to a reduction in leg volume and to an increase in neck circumference. Interestingly, despite such rostral fluid shift, patients with central sleep apnea (CSA) had a decrease in transpharyngeal resistance, increased minute ventilation and reduced partial pressure of carbon dioxide compared with patients with obstructive sleep apnea, who had opposite findings. We want to sincerely congratulate the investigators on these important results. However, there are some questions that need to be addressed in future research.
The investigators speculated that pulmonary congestion (although they did not monitor this parameter in the study) and subsequent stimulation of pulmonary irritant receptors might explain why patients with CSA had an increase in minute ventilation and reduced partial pressure of carbon dioxide via increased respiratory drive. Therefore, the question that arises is why more fluid goes to the lungs in patients with CSA compared with patients with obstructive sleep apnea (presumed to be the case because of opposite findings in the study): is it related to a greater fluid volume in cases of more advanced heart failure? It is well known that the prevalence of CSA increases with a greater severity of heart failure (2); thus, the presence of CSA may simply reflect the degree of cardiac dysfunction. Therefore, patterns of sleep apnea may change over time on the basis of the status of cardiac performance.
Alternatively, other mechanisms yet to be elucidated may be responsible for greater pulmonary congestion in patients with CSA. Fluid overload and pulmonary congestion may explain why patients with renal disease have a greater prevalence of CSA compared with the general population (3). Therefore, it is important to study whether pulmonary congestion and stimulation of pulmonary irritant receptors will explain the different response to rostral fluid shift in patients with CSA and obstructive sleep apnea (4).
- American College of Cardiology Foundation
- Kasai T.,
- Motwani S.S.,
- Yumino D.,
- et al.
- Tada T.,
- Kusano K.F.,
- Ogawa A.,
- et al.