Heavy Snoring: Time to Take it More Seriously?

Abstract

WE ARE PLEASED THAT DRAGER AND LORENZI-FILHO1 RECOGNIZE OUR STUDY AS REPRESENTING AN EXCITING NEW AREA OF RESEARCH. A MAJOR CONCERN related to the title of our manuscript,2 “Heavy Snoring as a Cause of Carotid Artery Atherosclerosis.” We indeed hoped that the slightly provocative nature of this title might generate interest in a relatively novel hypothesis whereby snoring vibrations may contribute to the development of early carotid artery atherosclerosis. However, we agree that the demonstration of an independent association between snoring and carotid atherosclerosis in a cross-sectional study certainly does not establish a cause-effect relationship. Drager and Lorenzi-Filho1 are also concerned that our study did not exclusively involve patients with “primary snoring,” and included patients with OSA. This raises the important issue of how “primary snoring” is defined. There are no consensus guidelines, validated questionnaires, or measurements of snoring that define a “primary snorer.” Previous clinical studies have depended upon a snoring history (undefined characteristics) associated with an apnea-hypopnea index (AHI) below a certain threshold (Principles and Practice of Sleep Medicine3 recommends an AHI of <10 events/hour). In addition, there are no agreed technical specifications during polysomnography for identification of snores, and no accepted rules for the scoring of snoring.4 As acknowledged by Drager and Lorenzi-Filho,1 an important strength of our current study is the quantification of snoring during polysomnography, which we believe was partially responsible for our ability to demonstrate an independent association between snoring and carotid atherosclerosis. It is clear that better standardized definitions, agreed technical specifications for snore measurement and scoring rules for snoring are urgently required for future research. In our study, we used a relatively liberal definition of hypopnea which did not require an oxygen desaturation.5 In contrast, the study of Marin et al6 as quoted by Drager and Lorenzi-Filho,1 defined simple snorers as having a history of reported snoring and an AHI <5 events/hour, but where all events were required to be accompanied by an oxygen desaturation of ≥4%. If this latter criterion were applied to our data,2 91% of participants would be classified as simple snorers. This figure rises to 96% if an AHI cut-off <10 events/hour is used. Consequently, the degree to which our study represents findings in “primary snorers” depends largely on the definitions employed. Finally, our logistic regression analyses all included the AHI, the arousal index, and the 3% oxygen desaturation index (together with snoring measures). In our patient population, none of these factors (apart from snoring) provided significant associations with carotid atherosclerosis.2 As discussed in our paper, this clearly supports an independent association between heavy snoring and carotid atherosclerosis in our population with minimal OSA, but does not exclude significant associations related to arousals and oxygen desaturation in other patient populations. Given the high prevalence of snoring in the community, it would now seem important to seek increased understanding of linkages between snoring and carotid vascular disease. We look forward to further clarifying studies and further challenges to current scientific hypotheses.