Response

Abstract

We are grateful to Dr Burtscher for his interest in our article “Protective Cardiovascular Effect of Sleep Apnea Severity in Obesity Hypoventilation Syndrome” published in CHEST (July 2016).1Masa J.F. Corral J. Romero A. et al.Protective cardiovascular effect of sleep apnea severity in obesity hypoventilation syndrome.Chest. 2016; 150: 68-79Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar Dr Burtscher poses two main questions: (1) Is the term ischemia preconditioning used appropriately in our study or rather should we be referring to hypoxic preconditioning? and (2) does hypoxemia and hypercapnia during wakefulness in obesity hypoventilation syndrome (OHS) evoke a protective cardiovascular effect in contrast to patients with severe OSA who experience hypoxemia only during sleep? Regarding the first question, we think the final pathway of the so-called ischemia preconditioning phenomenon is tissue hypoxia caused by reduction in blood flow, arterial hypoxemia, or both. Patients with OSA and OHS experience a reduction in blood flow after each obstructive event because of cyclic surges in sympathetic activity that lead to vasoconstriction. Furthermore, it is plausible that the degree of myocardial dysfunction is greater when tissue hypoxia is caused by vasoconstriction combined with arterial hypoxemia than by arterial hypoxemia alone.2Shizukuda Y. Mallet R.T. Lee S.C. Downey H.F. Hypoxic preconditioning of ischaemic canine myocardium.Cardiovasc Res. 1992; 26: 534-542Crossref PubMed Scopus (122) Google Scholar Ischemic preconditioning seems to occur more readily with sustained hypoxemia than with intermittent hypoxemia.3Ryan S. Taylor C.T. McNicholas W.T. Selective activation of inflammatory pathways by intermittent hypoxia in obstructive sleep apnea syndrome.Circulation. 2005; 112: 2660-2667Crossref PubMed Scopus (735) Google Scholar Patients with OHS are exposed to both types of hypoxemia; therefore, it is likely that there is an additive effect. In fact in our study, the prevalence of cardiovascular morbidity was lowest in patients with OHS who also had the most severe form of OSA. This finding supports the notion that sustained and intermittent hypoxemia may result in a more powerful angiogenic stimulation than either one alone. Clearly these findings are hypothesis generating, and further research is necessary. In summary, we do not think sustained hypoxemia is the only reason for the protective cardiovascular effect we observed in our patients with OHS and the most severe form of OSA, but rather it is a combination of cumulative exposure to significant hypoxemia during wakefulness due to hypoventilation plus intermittent hypoxemia during sleep due to very severe OSA. It remains unclear whether hypercapnia modulates the effect of hypoxemia, since experiments involving hypoxic preconditioning did not include exposure to hypercapnia. Protective Cardiovascular Effect of Sleep Apnea Severity in Obesity Hypoventilation SyndromeCHESTVol. 150Issue 1PreviewObesity hypoventilation syndrome (OHS) is associated with a high burden of cardiovascular morbidity (CVM) and mortality. The majority of patients with OHS have concomitant OSA, but there is a paucity of data on the association between CVM and OSA severity in patients with OHS. The objective of our study was to assess the association between CVM and OSA severity in a large cohort of patients with OHS. Full-Text PDF Potential Effects of Hypoxia Preconditioning in Obesity Hypoventilation Syndrome?CHESTVol. 150Issue 6PreviewI have read with the greatest interest the article by Masa et al1 published in CHEST (July 2016) who demonstrated that severe oxygen desaturation was associated with reduced cardiovascular morbidity in patients with obesity hypoventilation syndrome (OHS). The authors discussed a putative role of ischemia preconditioning (IP) potentially contributing to the beneficial effects observed in these patients. In my opinion, this point should be addressed in greater detail. Full-Text PDF