Next Article in Journal
Description of Thermochromic Offset Prints Morphologies Depending on Printing Substrate
Next Article in Special Issue
Respiratory and Cardiovascular Parameters Evaluation in OSA Patients Treated with Mandibular Advancement Device
Previous Article in Journal
A Machine Learning Model for Predicting Noise Limits of Motor Vehicles in UNECE R51 Regulations
Previous Article in Special Issue
Increasing Hypopnea in Sleep Breathing Disturbance Improves Postoperative Oxygen Saturation in Patients with Very Severe Obstructive Sleep Apnea
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
Applied Sciences
Volume 10
Issue 22
10.3390/app10228094
applsci-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles thumb_up
...
Endorse textsms
...
Comment
first_page
settings
Order Article Reprints
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Article

A Non-Framework Multilevel Surgery May Reduce Mean Heart Rate in Patients with Very Severe Obstructive Apnea Having Confined Retroglossal Space and Framework

by
Ethan I. Huang
1,2,3,*,
Shu-Yi Huang
2,4,5,
Yu-Ching Lin
2,3,4,6,
Chieh-Mo Lin
4,7,
Chin-Kuo Lin
4,7,
Ying-Chih Huang
8 and
Jian-An Su
9
1
Department of Otolaryngology, Chang Gung Memorial Hospital, Chiayi 61363, Taiwan
2
Sleep Center of Chang Gung Memorial Hospital, Chiayi 61363, Taiwan
3
School of Medicine, Chang Gung University, Taoyuan 33302, Taiwan
4
Division of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital, Chiayi 61363, Taiwan
5
Department of Nursing, Chang Gung University of Science and Technology, Chiayi 61363, Taiwan
6
Department of Respiratory Care, Chang Gung University of Science and Technology, Chiayi 61363, Taiwan
7
Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan
8
Department of Neurology, Chang Gung Memorial Hospital, Chiayi 61363, Taiwan
9
Department of Psychiatry, Chang Gung Memorial Hospital, Chiayi 61363, Taiwan
*
Author to whom correspondence should be addressed.
Appl. Sci. 2020, 10(22), 8094; https://doi.org/10.3390/app10228094
Submission received: 4 October 2020 / Revised: 8 November 2020 / Accepted: 13 November 2020 / Published: 15 November 2020
(This article belongs to the Special Issue State of the Art in Comorbidities and Complications Associated with Sleep-Related Breathing Disorders)
Browse Figures
Review Reports Versions Notes

Abstract

:
An elevated mean heart rate in untreated patients of obstructive sleep apnea (OSA) may lead to a higher risk of mortality and the development of various cardiovascular diseases. The elevation may positively relate to the severity of OSA and present in both wakefulness and sleep. A reduction in heart rate has been presented in reports of treating OSA patients with continuous positive airway pressure (CPAP). However, patients with very severe OSA may refuse use of CPAP devices and advocated surgeries, such as direct skeletal surgery or tracheostomy. It is unclear whether the non-framework multilevel surgery we reported previously can overcome the unfavorable anatomy and reduce mean heart rate, which serves as a risk factor of mortality. Here, we show that multilevel surgery reduced the mean heart rate from 68.6 to 62.7 with a mean reduction of 5.9 beats/min. The results suggest that the surgery may reduce the risk of consequences and mortality associated with an elevated mean heart rate, such as various cardiovascular diseases. We disclose these findings, along with the variations and possible risks to our future patients with very severe OSA who refuse or cannot use a CPAP device or reject direct skeletal surgery.

1. Introduction

An elevated heart rate is a risk factor of mortality for cardiovascular diseases [1,2]. Historically, it has been a risk factor of mortality in both the general population and in the population with cardiovascular disease [1,2,3,4,5,6,7,8]. In terms of gender, an elevated resting heart rate is an independent predictor of noncardiovascular mortality in both genders, and of cardiovascular mortality in men, independent of age and hypertension [6]. In terms of age, it is a risk factor for mortality from all causes in younger men and in middle-aged men and women [1]. Resting heart rate is a simple measurement with prognostic implications [7]. That is why drug-induced reductions in heart rate may be beneficial in several clinical conditions, such as myocardial infarction [2], congestive heart failure [2], and angina [7].
An elevated heart rate may be positively related to the severity of OSA [9,10,11]. It is associated with an increased risk of cardiovascular diseases, stroke, and all-cause mortality (e.g., the relative risks were 1.79, 2.15, and 1.92, respectively, compared to normal individuals [12]). Cicek et al. showed a higher mean heart rate in the severe OSA group than the other (mild or moderate) groups [9]. Kawano reported a positive Spearman correlation between apnea–hypopnea index (AHI) and mean heart rate in all three (24-h, wakefulness, and sleep) sections of time [10]. Konecny et al. reported that heart rate elevation is most easily noticeable during sleep for OSA patients with hypertrophic cardiomyopathy [13]. This association between elevated heart rate and the severity of OSA presents not only during the daytime but also at night-time during sleep [9,10]. An elevated heart rate seen during sleep suggests a high chance of the presence in mean daytime or 24-h heart rates.
Patients with very severe OSA usually have a confined retroglossal space and framework. They make up a distinct subgroup and show differences in several areas, from OSA of other severities. Their daytime awake partial pressure of oxygen may go as low as 77 mmHg [14]. Researchers classified very severe OSA in the literature into a general group of high AHI or respiratory disturbance index (RDI), from 40 [15,16], 50 [17,18,19,20,21], 60 [22,23,24,25,26], 70 [27], to 100 events/h [28]. These patients have minimal inspiratory movement of the lateral pharyngeal walls and a smaller cross-sectional area [20], more comorbidity due to hypertension [14], and associations with higher insulin resistance [29]. Patients with very severe OSA have a narrow retroglossal space and confined framework [30]. The narrow airway is difficult enlarge via conventional uvulopalatopharyngoplasty (UPPP) or non-framework surgeries [23,31]. They are not necessarily obese, nor do they have a high body mass index (BMI) (e.g., see [23,25]). For those who refuse to use or cannot benefit from continuous positive airway pressure (CPAP), the advocated surgical procedures include direct skeletal surgery [30], bariatric surgery [32], and tracheostomy in patients meeting the set criteria [15,33]. In this distinct subgroup, our earlier reports showed that multilevel surgery could reduce postoperative AHI [34,35], desaturation frequency (mean desaturation index) [34], and desaturation level (mean oxyhemoglobin saturation of pulse oximetry (SpO2) desaturation) [34] in order to improve mean SpO2. However, it is not clear whether multilevel surgery can decrease postoperative resting heart rate in order to lower the risk of associated consequences and mortality.
A reduction in heart rate has been presented in reports of treating OSA patients with CPAP [11,36,37]. Long-term CPAP therapy may lead to an intra-group decrease in resting heart rate [36,37] or a significant inter-group reduction (CPAP vs. non-CPAP using patients) [38]. Efficiently treated CPAP users showed lower incidence of cardiovascular diseases than incompletely treated cases (e.g., 6.7% vs. 56.8% in [39]). Nevertheless, CPAP withdrawal usually results in a rapid recurrence of OSA and a rebound in heart rate [40]. Accurate mean heart rate is easily obtained by the recording and analysis of a polysomnography (PSG). Unlike manually interpreted or reported data such as AHI, RDI, or Epworth Sleepiness Scale (ESS), mean heart rate can serve a clinical role as an objective predictor of mortality or an objective measurement of surgical success. Here, in patients of very severe OSA, we replicated studies in the literature to examine the correlation between preoperative AHI and mean heart rate in sleep. We found that multilevel surgery, as an alternative treatment to CPAP, can reduce mean heart rate in sleep. We tested the correlation between changes in mean heart rate and essential sleep parameters, then compared the results to other treatments available in the literature.

2. Materials and Methods

2.1. Patient Enrollment

The patients enrolled were the same as those in our earlier work on the improvement of oxygen saturation [34]. From Mar. 2015 to May 2020, we enrolled consecutive patients who met the criteria of: 1. 20 years old or older, 2. AHI ≥ 60 events/h, 3. refusal or unsuccessful CPAP (e.g., bad compliance or high on-CPAP AHI referred from a sleep medicine specialist), 4. received a multilevel surgery at the nose, palate, and tongue base [35], 5. PSGs with AHI and mean heart rate before and after the surgery. We had no specific exclusion criteria.

2.2. Evaluation and Surgeries

We evaluated each patient by endoscopies before and after the surgery and conducted each PSG overnight in the level-1 sleep laboratory of our hospital with a certified technician. The nasal procedure, routine septomeatoplasty, was carried out with oral intubation. We performed Z-palatoplasty as illustrated in our earlier report [35]. The open tongue-base procedure was performed with transoral robotic surgery or transoral laser microsurgery. Please see our earlier report [34] for postoperative care and other settings.

2.3. Data Collection and Analysis

Each patient completed a PSG 6 months (193 ± 67 days) after the surgery, when the postoperative anatomy was considered stable (as the period of 3 to 6 months was adopted in the past reports, e.g., see [41,42]). We measured the mean AHI reduction, as a cross-study standard recommended by Caples, S. M. et al. [43], to compare our results with others in the literature. We examined the scatter plot to find out whether there were outliers and computed the Pearson correlation to display the association between preoperative AHI and mean heart rate. We compared the individual pre- and postoperative mean heart rate in the PSGs, then calculated the mean heart rate reduction. We conducted a paired t-test to analyze the differences in mean heart rate reduction and AHI reduction, against no difference after the surgery. To discover the main contributors to the postoperative mean heart rate change, we computed a Spearman correlation to display the association between proportion difference in mean heart rate (i.e., postoperative–preoperative/preoperative fraction of mean heart rate) and proportion difference in one of the following sleep parameters: AHI, hypopnea in AHI ratio [34], desaturation index, and mean SpO2. Values of p < 0.05 were considered statistically significant.
We performed the statistical tests in MATLAB 9.4.0.813654 (MathWorks, Natick, Massachusetts, United States of America).

3. Ethical Statements

The study was approved by the Institutional Review Board of Chang Gung Medical Foundation, Taiwan.

4. Results

Twenty-seven very severe OSA patients were registered in this study. Twenty-four were male and three were female. A male prevalence (88.9%) confirmed the earlier reports on severe OSA patients (e.g., see [15,28,44]). The average BMI was 28.5 with a standard deviation (SD) of 3.5 kg/m2. Their ages ranged from 29 to 63 years (mean = 47.4 with a SD of 10.6). No patient reported a medication history of taking beta-blockers or a past history of cardiovascular diseases. All patients underwent Z-palatoplasty (ZPP) and partial open tongue-base glossectomy. One patient had UPPP at another hospital. Twenty-five received septomeatoplasty. One and three patients underwent regular adenoidectomy and endoscopic sinosurgery, respectively. Table 1 lists their results for comparisons with those of others. There was one instance of postoperative bleeding 10 days after the surgery, causing an unexpected return to the operation room. See our earlier reports [34,35] for other effects of the surgery such as a reduction in desaturation and an improvement in oxygen saturation.
The surgery lowered the mean AHI from 73.8 to 33.2 events/h, p < 0.001. The SD was 10.3 and 20.4 events/h, respectively. Figure 1 illustrates the individual AHI reductions and a five-number summary of pre- and postoperative AHIs. Figure 2 shows the scatterplot and correlation of preoperative AHI vs. mean heart rate. The correlation for the data showed that preoperative mean heart rate was not related to the AHI in these very severe OSA patients, r = −0.043, p = 0.83, two-tailed test. The surgery reduced the mean heart rate from 68.6 ± 7.3 to 62.7 ± 7.5 beats/min (p < 0.001). The mean heart rate reduction was 5.9 beats/min, with a 95% confidence interval of 3.4 to 8.4 beats/min. Figure 3 illustrates the individual mean heart rate reductions and a five-number summary of pre- and post-operative mean heart rates. A Spearman correlation for the data showed that the postoperative proportion difference in mean heart rate was not related to any of these parameters (AHI, hypopnea in AHI ratio, desaturation index, and mean SpO2), r = (−0.1652, −0.3404, −0.1566, and −0.1447), p = (0.4103, 0.0823, 0.4353, and 0.4714), respectively (Figure 4, Figure 5, Figure 6 and Figure 7).

5. Discussion

An elevated heart rate, serving as a risk factor of mortality and a predictive measurement for various medical conditions such as cardiovascular diseases [1,2,3,4,5,6,7,8], presents in severe OSA patients [9,10,11], and may help patients with several cardiovascular conditions if reduced [2,7]. In our results of the subgroup of very severe OSA, the non-framework multilevel surgery reduced the mean heart rate from 68.6 ± 7.3 to 62.7 ± 7.5 beats/min with a mean heart rate reduction of 5.9 beats/min, despite the unfavorable anatomy of the narrow retroglossal space and confined framework. Our sample size of 27 is small and consists of patients treated by a single surgeon, limiting the generalizability of the results. However, the results illustrate an effect size that is big enough to show significance. The heart rate reduction of 5.9 beats/min was inferior to Lin’s 8.7 beats/min 6 months after maxillary–mandibular advancement [45] but better than Sumi’s 4.5 beats/min after 3- to 4-day use of nasal CPAP [11], Mayer’s 3.4 beats/minute after 6 months of nasal CPAP therapy [37], de Paula Soares’s 2.4 beats/min 6 to 9 months after lateral pharyngoplasty [46], and those reporting no change in mean heart rate after their treatments (e.g., see [47,48,49], including Van der Cruyssen’s patients after maxillary–mandibular advancement [49]). Because the lack of detailed information in the literature made statistical analysis impossible, this was just the order of the mean heart rate reductions (so as to enable the AHI comparisons below). Care must be taken when interpreting these comparisons due to possible different OSA severities in the databases and the effect size of the treatment (e.g., mean AHI reduction) across studies. The mean AHI reduction in the present study was 40.5 events/h, which was worse than Mickelson’s 42.2 events/h [44] but better than Walker’s 38.2 events/h [50] and Vilaseca’s 14.4 events/hour [23] in patients with very severe OSA.
Mean heart rate in sleep is affected by not only the medical conditions mentioned above, but also other controllable or uncontrollable variables. Mean heart rate in sleep may increase after short-term heavy physical activity, such as in cyclists after a two-week period of intensified training [51]. However, mean heart rate may drop during good-quality sleep of stages 3 and 4 (e.g., see [52]). For each person, studies found an intrinsic night-to-night variation under controlled submaximal physical activity to be about 5–8 beats/min [53,54,55,56]. The difficulty in controlling the intrinsic variation and individual physical activity before each PSG is a limitation of the present study. Apart from treatment effect, this probably contributed to the variation in the mean heart rate reduction in Figure 3.
OSA is characterized by the recurrent collapse of the upper airway in sleep, leading to chronic intermittent hypoxia. Chronic intermittent hypoxia has been well reported to elevate circulating epinephrine levels [57,58,59,60,61], which have a strong positive relationship with platelet aggregation [57,58,59,60]. Elevated serum epinephrine levels result in an elevated heart rate in OSA [57,58,59,60,61]. Studies showed that treatment of OSA by nasal CPAP decreases the epinephrine level and platelet aggregability and restores the physiological periodic pattern of platelet aggregability [57,62]. Future studies are needed to investigate whether heart rate reduction goes through the same mechanism of decreasing epinephrine level and platelet aggregability following multilevel surgery in very severe OSA patients.
An elevated heart rate is associated with a higher risk of developing hypertension and atherosclerosis (e.g., see [2] for a review). The mean heart rates in patients with refractory hypertension (uncontrolled hypertension despite the administration of at least five antihypertensive drugs [63]) rise more [64] than those with resistant hypertension (hypertension with no identifiable cause in which blood pressure levels remain uncontrolled despite using at least three antihypertensive drugs (including a diuretic, if tolerated) at full doses [63]). Compared to resistant hypertension, patients with refractory hypertension have an even greater prevalence and severity of OSA [64]. More severe OSA may have hypertension that is more difficult to treat. This may be due to the fact that a higher sympathetic tone in patients with very severe OSA can cause more hyperinsulinemia and insulin resistance which can eventually promote the development of atherosclerosis [2]. Moreover, the hemodynamic disturbances related to a higher heart rate directly affect the arterial wall, promoting further development of atherosclerotic plaques [2]. Future long-term studies are needed to confirm whether the heart rate reduction remains in the long run following multilevel surgery, and whether it reduces the incidence of developing atherosclerosis, or helps to treat hypertension.

6. Conclusions

Despite the unfavorable anatomy in very severe OSA patients, non-framework surgery reduced the mean heart rate from 68.6 to 62.7 beats/min with a mean heart rate reduction of 5.9 beats/min. The results suggest that this surgery may reduce the risk of consequences and mortality associated with an elevated mean heart rate. We will disclose these findings to our future patients with very severe OSA who refuse or cannot use a CPAP device or reject direct skeletal surgery. We will also inform them of the thus far undetermined contributors to the reduction, variation, and potential risks.

Author Contributions

E.I.H. conceptualized the study, analyzed the PSGs, ran the analysis, and wrote the primary draft of the manuscript. C.-K.L., C.-M.L., Y.-C.H., and J.-A.S. registered the patients, read the PSGs, and revised the manuscript. S.-Y.H. and Y.-C.L. registered the patients, interpreted the data, and provided essential comments on the manuscript. All authors have read and agreed to the published version of the manuscript.

Funding

This study did not receive any external funding.

Conflicts of Interest

The authors declare no conflict of interest.

References

  1. Greenland, P.; Daviglus, M.L.; Dyer, A.R.; Liu, K.; Huang, C.-F.; Goldberger, J.J.; Stamler, J. Resting Heart Rate is a Risk Factor for Cardiovascular and Noncardiovascular Mortality: The Chicago Heart Association Detection Project In Industry. Am. J. Epidemiol. 1999, 149, 853–862. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  2. Palatini, P.; Julius, S. Elevated Heart Rate: A Major Risk Factor for Cardiovascular Disease. Clin. Exp. Hypertens. 2004, 26, 637–644. [Google Scholar] [CrossRef] [PubMed]
  3. Kannel, W.B.; Kannel, C.; Paffenbarger, R.S.; Cupples, L. Heart rate and cardiovascular mortality: The Framingham study. Am. Heart J. 1987, 113, 1489–1494. [Google Scholar] [CrossRef]
  4. Gillman, M.W.; Kannel, W.B.; Belanger, A.; D’Agostino, R.B. Influence of heart rate on mortality among persons with hypertension: The Framingham Study. Am. Heart J. 1993, 125, 1148–1154. [Google Scholar] [CrossRef]
  5. Palatini, P.; Julius, S. Association of tachycardia with morbidity and mortality: Pathophysiological considerations. J. Hum. Hypertens. 1997, 11, 19–27. [Google Scholar]
  6. Benetos, A.; Rudnichi, A.; Thomas, F.; Safar, M.; Guize, L. Influence of Heart Rate on Mortality in a French Population. Hypertension 1999, 33, 44–52. [Google Scholar] [CrossRef]
  7. Diaz, A.; Bourassa, M.G.; Guertin, M.-C.; Tardif, J.-C. Long-term prognostic value of resting heart rate in patients with suspected or proven coronary artery disease. Eur. Heart J. 2005, 26, 967–974. [Google Scholar] [CrossRef] [PubMed]
  8. Tverdal, A.; Hjellvik, V.; Selmer, R. Heart rate and mortality from cardiovascular causes: A 12 year follow-up study of 379 843 men and women aged 40-45 years. Eur. Heart J. 2008, 29, 2772–2781. [Google Scholar] [CrossRef] [Green Version]
  9. Cicek, D.; Gokay, S.; Lakadamyali, H.; Sapmaz, I.; Muderrisoglu, H. Effect of Obstructive Sleep Apnea on Heart Rate, Heart Rate Recovery and QTc and P-wave Dispersion in Newly Diagnosed Untreated Patients. Am. J. Med. Sci. 2012, 344, 180–185. [Google Scholar] [CrossRef]
  10. Kawano, Y.; Tamura, A.; Watanabe, T.; Kadota, J. Influence of the severity of obstructive sleep apnea on heart rate. J. Cardiol. 2010, 56, 27–34. [Google Scholar] [CrossRef] [Green Version]
  11. Sumi, K.; Chin, K.; Takahashi, K.; Nakamura, T.; Matsumoto, H.; Niimi, A.; Mishima, M. Effect of nCPAP therapy on heart rate in patients with obstructive sleep apnoea-hypopnoea. QJM Int. J. Med. 2006, 99, 545–553. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  12. Wang, X.; Ouyang, Y.; Wang, Z.; Zhao, G.; Liu, L.; Bi, Y. Obstructive sleep apnea and risk of cardiovascular disease and all-cause mortality: A meta-analysis of prospective cohort studies. Int. J. Cardiol. 2013, 169, 207–214. [Google Scholar] [CrossRef] [PubMed]
  13. Konecny, T.; Khoo, M.; Edelhofer, P.; Park, J.; BukartykM, J.; Covassin, N.; Venkataraman, S.; Karim, S.; ChahalM, A.; Kara, T.; et al. Increased heart rate with sleep disordered breathing in hypertrophic cardiomyopathy. Int. J. Cardiol. 2020. [Google Scholar] [CrossRef] [PubMed]
  14. Lacedonia, D.; Carpagnano, G.E.; Sabato, R.; Storto, M.M.L.; Palmiotti, G.A.; Capozzi, V.; Barbaro, M.P.F.; Gallo, C. Characterization of obstructive sleep apnea-hypopnea syndrome (OSA) population by means of cluster analysis. J. Sleep Res. 2016, 25, 724–730. [Google Scholar] [CrossRef] [Green Version]
  15. Campanini, A.; De Vito, A.; Frassineti, S.; Vicini, C. Role of skin-lined tracheotomy in obstructive sleep apnoea syndrome: Personal experience. Acta Otorhinolaryngol. Ital. 2004, 24, 68–74. [Google Scholar]
  16. Haviv, Y.; Bachar, G.; Aframian, D.J.; Almoznino, G.; Michaeli, E.; Benoliel, R. A 2-year mean follow-up of oral appliance therapy for severe obstructive sleep apnea: A cohort study. Oral Dis. 2014, 21, 386–392. [Google Scholar] [CrossRef]
  17. Lavie, P.; Lavie, L.; Herer, P. All-cause mortality in males with sleep apnoea syndrome: Declining mortality rates with age. Eur. Respir. J. 2005, 25, 514–520. [Google Scholar] [CrossRef] [Green Version]
  18. Veasey, S.C.; Guilleminault, C.; Strohl, K.P.; Sanders, M.H.; Ballard, R.D.; Magalang, U.J. Medical Therapy for Obstructive Sleep Apnea: A Review by the Medical Therapy for Obstructive Sleep Apnea Task Force of the Standards of Practice Committee of the American Academy of Sleep Medicine. Sleep 2006, 29, 1036–1044. [Google Scholar] [CrossRef]
  19. Maimon, N.; Hanly, P.J. Does Snoring Intensity Correlate with the Severity of Obstructive Sleep Apnea? J. Clin. Sleep Med. 2010, 6, 475–478. [Google Scholar] [CrossRef]
  20. Brown, E.C.; Cheng, S.; McKenzie, D.K.; Butler, J.E.; Gandevia, S.C.; Bilston, L. Respiratory Movement of Upper Airway Tissue in Obstructive Sleep Apnea. Sleep 2013, 36, 1069–1076. [Google Scholar] [CrossRef] [Green Version]
  21. Olaithe, M.; Bucks, R.S. Executive Dysfunction in OSA before and After Treatment: A Meta-Analysis. Sleep 2013, 36, 1297–1305. [Google Scholar] [CrossRef] [PubMed]
  22. Cohen, R. Obstructive sleep apnea: Oral appliance therapy and severity of condition. Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endodontol. 1998, 85, 388–392. [Google Scholar] [CrossRef]
  23. Vilaseca, I.; Morelló, A.; Montserrat, J.M.; Santamaría, J.; Iranzo, A. Usefulness of Uvulopalatopharyngoplasty with Genioglossus and Hyoid Advancement in the Treatment of Obstructive Sleep Apnea. Arch. Otolaryngol. Head Neck Surg. 2002, 128, 435–440. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  24. Lee, L.-A.; Huang, C.; Chen, N.-H.; Wang, C.-L.; Fang, T.-J.; Li, H.-Y. Severity of Obstructive Sleep Apnea Syndrome and High-Sensitivity C-Reactive Protein Reduced After Relocation Pharyngoplasty. Otolaryngol. Neck Surg. 2011, 144, 632–638. [Google Scholar] [CrossRef] [PubMed]
  25. Lee, L.-A.; Yu, J.-F.; Lo, Y.-L.; Chen, Y.-S.; Wang, D.-L.; Cho, C.-M.; Ni, Y.-L.; Chen, N.-H.; Fang, T.-J.; Huang, C.-G.; et al. Energy Types of Snoring Sounds in Patients with Obstructive Sleep Apnea Syndrome: A Preliminary Observation. PLoS ONE 2012, 7, e53481. [Google Scholar] [CrossRef] [PubMed]
  26. Shiba, T.; Takahashi, M.; Sato, Y.; Onoda, Y.; Hori, Y.; Sugiyama, T.; Bujo, H.; Maeno, T. Relationship between Severity of Obstructive Sleep Apnea Syndrome and Retinal Nerve Fiber Layer Thickness. Am. J. Ophthalmol. 2014, 157, 1202–1208. [Google Scholar] [CrossRef]
  27. Huynh, N.T.; Emami, E.; Helman, J.I.; Chervin, R.D. Interactions between sleep disorders and oral diseases. Oral Dis. 2013, 20, 236–245. [Google Scholar] [CrossRef] [Green Version]
  28. Gay, P.C.; Herold, D.L.; Olson, E.J. A Randomized, Double-blind Clinical Trial Comparing Continuous Positive Airway Pressure with a Novel Bilevel Pressure System for Treatment of Obstructive Sleep Apnea Syndrome. Sleep 2003, 26, 864–869. [Google Scholar] [CrossRef] [Green Version]
  29. Otake, K.; Sasanabe, R.; Hasegawa, R.; Banno, K.; Hori, R.; Okura, Y.; Yamanouchi, K.; Shiomi, T. Glucose Intolerance in Japanese Patients with Obstructive Sleep Apnea. Intern. Med. 2009, 48, 1863–1868. [Google Scholar] [CrossRef] [Green Version]
  30. Li, H.-Y.; Wang, P.-C.; Lee, L.-A.; Chen, N.-H.; Fang, T.-J. Prediction of Uvulopalatopharyngoplasty Outcome: Anatomy-Based Staging System Versus Severity-Based Staging System. Sleep 2006, 29, 1537–1541. [Google Scholar] [CrossRef]
  31. Suh, G.D. Evaluation of Open Midline Glossectomy in the Multilevel Surgical Management of Obstructive Sleep Apnea Syndrome. Otolaryngol. Neck Surg. 2012, 148, 166–171. [Google Scholar] [CrossRef] [PubMed]
  32. Fritscher, L.G.; Mottin, C.C.; Canani, S.; Chatkin, J.M. Obesity and Obstructive Sleep Apnea-Hypopnea Syndrome: The Impact of Bariatric Surgery. Obes. Surg. 2007, 17, 95–99. [Google Scholar] [CrossRef] [PubMed]
  33. Parati, G.; Lombardi, C.; Narkiewicz, K. Sleep apnea: Epidemiology, pathophysiology, and relation to cardiovascular risk. Am. J. Physiol. Integr. Comp. Physiol. 2007, 293, R1671–R1683. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  34. Huang, E.I.; Huang, S.-Y.; Lin, Y.-C.; Lin, C.-M.; Lin, C.-K.; Huang, Y.-C.; Su, J.-A. Increasing Hypopnea in Sleep Breathing Disturbance Improves Postoperative Oxygen Saturation in Patients with Very Severe Obstructive Sleep Apnea. Appl. Sci. 2020, 10, 6539. [Google Scholar] [CrossRef]
  35. Huang, E.I.; Kuo, C.-L.; Chou, Y.-T.; Lin, Y.-C.; Huang, S.-Y. Modified Z-palatoplasty with one-layer closure in one-stage multilevel surgery for severe obstructive sleep apnea. Auris Nasus Larynx 2018, 45, 791–795. [Google Scholar] [CrossRef]
  36. Khoo, M.C.; Belozeroff, V.; Berry, R.B.; Sassoon, C.S.H. Cardiac Autonomic Control in Obstructive Sleep Apnea. Am. J. Respir. Crit. Care Med. 2001, 164, 807–812. [Google Scholar] [CrossRef]
  37. Mayer, J.; Becker, H.; Brandenburg, U.; Penzel, T.; Peter, J.; Wichert, P. Blood Pressure and Sleep Apnea: Results of Long-Term Nasal Continuous Positive Airway Pressure Therapy. Cardiology 1991, 79, 84–92. [Google Scholar] [CrossRef]
  38. Pleava, R.; Mihaicuta, S.; Șerban, C.; Ardelean, C.L.; Marincu, I.; Gaita, D.; Frent, S. Long-Term Effects of Continuous Positive Airway Pressure (CPAP) Therapy on Obesity and Cardiovascular Comorbidities in Patients with Obstructive Sleep Apnea and Resistant Hypertension—An Observational Study. J. Clin. Med. 2020, 9, 2802. [Google Scholar] [CrossRef]
  39. Peker, Y.; Hedner, J.; Norum, J.; Kraiczi, H.; Carlson, J. Increased Incidence of Cardiovascular Disease in Middle-aged Men with Obstructive Sleep Apnea. Am. J. Respir. Crit. Care Med. 2002, 166, 159–165. [Google Scholar] [CrossRef]
  40. Kohler, M.; Stoewhas, A.-C.; Ayers, L.; Senn, O.; Bloch, K.E.; Russi, E.W.; Stradling, J.R. Effects of Continuous Positive Airway Pressure Therapy Withdrawal in Patients with Obstructive Sleep Apnea: A randomized controlled trial. Am. J. Respir. Crit. Care Med. 2011, 184, 1192–1199. [Google Scholar] [CrossRef]
  41. Li, H.-Y.; Li, K.K.; Chen, N.-H.; Wang, C.-J.; Liao, Y.-F.; Chen, N. Three-dimensional computed tomography and polysomnography findings after extended uvulopalatal flap surgery for obstructive sleep apnea. Am. J. Otolaryngol. 2005, 26, 7–11. [Google Scholar] [CrossRef] [PubMed]
  42. Hessel, N.S.; De Vries, N. Results of uvulopalatopharyngoplasty after diagnostic workup with polysomnography and sleep endoscopy: A report of 136 snoring patients. Eur. Arch. Otorhinolaryngol. 2003, 260, 91–95. [Google Scholar] [CrossRef] [PubMed]
  43. Caples, D.S.M.; Rowley, J.A.; Prinsell, D.J.R.; Pallanch, J.F.; Elamin, M.M.B.; Katz, D.S.G.; Harwick, J.D. Surgical Modifications of the Upper Airway for Obstructive Sleep Apnea in Adults: A Systematic Review and Meta-Analysis. Sleep 2010, 33, 1396–1407. [Google Scholar] [CrossRef] [PubMed]
  44. Mickelson, S.A.; Rosenthal, L. Midline Glossectomy and Epiglottidectomy for Obstructive Sleep Apnea Syndrome. Laryngoscope 1997, 107, 614–619. [Google Scholar] [CrossRef]
  45. Lin, C.-H.; Chin, W.-C.; Huang, Y.-S.; Wang, P.-F.; Li, K.K.; Pirelli, P.; Chen, Y.-H.; Guilleminault, C. Objective and subjective long term outcome of maxillomandibular advancement in obstructive sleep apnea. Sleep Med. 2020, 74, 289–296. [Google Scholar] [CrossRef]
  46. Soares, C.F.D.P.; Cavichio, L.; Cahali, M.B. Lateral pharyngoplasty reduces nocturnal blood pressure in patients with obstructive sleep apnea. Laryngoscope 2014, 124, 311–316. [Google Scholar] [CrossRef]
  47. Narkiewicz, K.; Kato, M.; Phillips, B.G.; Pesek, C.A.; Davison, D.E.; Somers, V.K. Nocturnal Continuous Positive Airway Pressure Decreases Daytime Sympathetic Traffic in Obstructive Sleep Apnea. Circulation 1999, 100, 2332–2335. [Google Scholar] [CrossRef] [Green Version]
  48. Roche, F.; Court-Fortune, I.; Pichot, V.; Duverney, D.; Costes, F.; Emonot, A.; Vergnon, J.M.; Geyssant, A.; Lacour, J.R.; Barthélémy, J.C. Reduced cardiac sympathetic autonomic tone after long-term nasal continuous positive airway pressure in obstructive sleep apnoea syndrome. Clin. Physiol. 1999, 19, 127–134. [Google Scholar] [CrossRef]
  49. Van Der Cruyssen, F.; Vuylsteke, P.; Claerhout, M.; Bulcke, M.V.; Timmermans, L.; Delsupehe, K. The effect of maxillary-mandibular advancement surgery on two-dimensional cephalometric analysis, polysomnographic and patient-reported outcomes in 32 patients with sleep disordered breathing: A retrospective cohort study. Oral Maxillofac. Surg. Cases 2019, 5, 100112. [Google Scholar] [CrossRef]
  50. Walker, E.B.; Frith, R.W.; Harding, D.A.; Cant, B.R. Uvulopalatopharyngoplasty in severe idiopathic obstructive sleep apnoea syndrome. Thorax 1989, 44, 205–208. [Google Scholar] [CrossRef] [Green Version]
  51. Jeukendrup, A.; Hesselink, M.; Snyder, A.; Kuipers, H.; Keizer, H. Physiological Changes in Male Competitive Cyclists after Two Weeks of Intensified Training. Int. J. Sports Med. 1992, 13, 534–541. [Google Scholar] [CrossRef] [PubMed]
  52. Penzel, T.; Kantelhardt, J.W.; Lo, C.-C.; Voigt, K.; Vogelmeier, C. Dynamics of Heart Rate and Sleep Stages in Normals and Patients with Sleep Apnea. Neuropsychopharmacology 2003, 28, S48–S53. [Google Scholar] [CrossRef] [PubMed]
  53. Waldeck, M.R.; Lambert, M.I. Heart Rate during Sleep: Implications for Monitoring Training Status. J. Sports Sci. Med. 2003, 2, 133–138. [Google Scholar] [PubMed]
  54. Brisswalter, J.; Legros, P. Daily Stability in Energy Cost of Running, Respiratory Parameters and Stride Rate among Well-Trained Middle Distance Runners. Int. J. Sports Med. 1994, 15, 238–241. [Google Scholar] [CrossRef] [PubMed]
  55. Lamberts, R.P.; Lemmink, K.A.P.M.; Durandt, J.J.; Lambert, M.I. Variation in Heart Rate during Submaximal Exercise: Implications for Monitoring Training. J. Strength Cond. Res. 2004, 18, 641–645. [Google Scholar]
  56. Mosko, S.S.; Dickel, M.J.; Ashurst, J. Night-to-Night Variability in Sleep Apnea and Sleep-Related Periodic Leg Movements in the Elderly. Sleep 1988, 11, 340–348. [Google Scholar] [CrossRef] [Green Version]
  57. Sanner, B.; Konermann, P.D.M.; Tepel, M.; Groetz, J.; Mummenhoff, C.; Zidek, W. Platelet function in patients with obstructivesleep apnoea syndrome. Eur. Respir. J. 2000, 16, 648–652. [Google Scholar] [CrossRef] [Green Version]
  58. Larsson, P.T.; Wallén, N.H.; Hjemdahl, P. Norepinephrine-induced human platelet activation in vivo is only partly counteracted by aspirin. Circulation 1994, 89, 1951–1957. [Google Scholar] [CrossRef] [Green Version]
  59. Mills, P.J.; Kennedy, B.P.; Loredo, J.S.; Dimsdale, J.E.; Ziegler, M.G. Effects of nasal continuous positive airway pressure and oxygen supplementation on norepinephrine kinetics and cardiovascular responses in obstructive sleep apnea. J. Appl. Physiol. 2006, 100, 343–348. [Google Scholar] [CrossRef]
  60. Sukegawa, M.; Noda, A.; Sugiura, T.; Nakata, S.; Yoshizaki, S.; Soga, T.; Yasuda, Y.; Iwayama, N.; Nakai, S.; Koike, Y. Assessment of continuous positive airway pressure treatment in obstructive sleep apnea syndrome using 24-hour urinary catecholamines. Clin. Cardiol. 2005, 28, 519–522. [Google Scholar] [CrossRef]
  61. Oga, T.; Chin, K.; Tabuchi, A.; Kawato, M.; Morimoto, T.; Takahashi, K.; Handa, T.; Takahashi, K.; Taniguchi, R.; Kondo, H.; et al. Effects of Obstructive Sleep Apnea with Intermittent Hypoxia on Platelet Aggregability. J. Atheroscler. Thromb. 2009, 16, 862–869. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  62. Hui, D.S.; Ko, F.W.-S.; Fok, J.P.; Chan, M.C.; Li, T.S.; Tomlinson, B.; Cheng, G. The Effects of Nasal Continuous Positive Airway Pressure on Platelet Activation in Obstructive Sleep Apnea Syndrome. Chest 2004, 125, 1768–1775. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  63. Calhoun, D.A.; Jones, D.; Textor, S.; Goff, D.C.; Murphy, T.P.; Toto, R.D.; White, A.; Cushman, W.C.; White, W.; Sica, D.; et al. Resistant Hypertension: Diagnosis, Evaluation, and Treatment. A scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research. Hypertension 2008, 51, 1403–1419. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  64. Martínez-García, M.A.; Navarro-Soriano, C.; Torres, G.; Barbé, F.; Caballero-Eraso, C.; Lloberes, P.; Diaz-Cambriles, T.; Somoza, M.; Masa, J.F.; González, M.; et al. Beyond Resistant Hypertension. Hypertension 2018, 72, 618–624. [Google Scholar] [CrossRef]
Applsci 10 08094 g001 550
Figure 1. Individual apnea–hypopnea index (AHI) changes revealed a significant reduction after the surgery. Each boxplot displays a five-number summary: the minimum, the maximum, the median, and the first and third quartiles.
Figure 1. Individual apnea–hypopnea index (AHI) changes revealed a significant reduction after the surgery. Each boxplot displays a five-number summary: the minimum, the maximum, the median, and the first and third quartiles.
Applsci 10 08094 g001
Applsci 10 08094 g002 550
Figure 2. Scatter plot and correlation of preoperative AHI vs. mean heart rate. This shows that preoperative mean heart rate was not related to AHI in the very severe obstructive sleep apnea (OSA) patients in this study.
Figure 2. Scatter plot and correlation of preoperative AHI vs. mean heart rate. This shows that preoperative mean heart rate was not related to AHI in the very severe obstructive sleep apnea (OSA) patients in this study.
Applsci 10 08094 g002
Applsci 10 08094 g003 550
Figure 3. Individual mean heart rate changes revealed a significant reduction after the surgery. The surgery reduced the mean heart rate from 68.6 ± 7.3 to 62.7 ± 7.5 beats/minute (p < 0.001). Each boxplot displays a five-number summary: the minimum, the maximum, the median, and the first and third quartiles. There was an outlier in the postoperative mean heart rates.
Figure 3. Individual mean heart rate changes revealed a significant reduction after the surgery. The surgery reduced the mean heart rate from 68.6 ± 7.3 to 62.7 ± 7.5 beats/minute (p < 0.001). Each boxplot displays a five-number summary: the minimum, the maximum, the median, and the first and third quartiles. There was an outlier in the postoperative mean heart rates.
Applsci 10 08094 g003
Applsci 10 08094 g004 550
Figure 4. Scatter plot and correlation of change in AHI (defined here as (postoperative–preoperative)/preoperative AHI) vs. change in mean heart rate (defined here as (postoperative–preoperative)/preoperative mean heart rate). This shows that the change in mean heart rate was not related to the change in AHI.
Figure 4. Scatter plot and correlation of change in AHI (defined here as (postoperative–preoperative)/preoperative AHI) vs. change in mean heart rate (defined here as (postoperative–preoperative)/preoperative mean heart rate). This shows that the change in mean heart rate was not related to the change in AHI.
Applsci 10 08094 g004
Applsci 10 08094 g005 550
Figure 5. Scatter plot and correlation of proportion change in hypopnea/AHI (defined here as (postoperative–preoperative)/preoperative fraction of hypopnea in AHI) vs. change in mean heart rate (defined here as (postoperative–preoperative)/preoperative mean heart rate). This shows that the change in mean heart rate was not related to the proportion change in hypopnea/AHI.
Figure 5. Scatter plot and correlation of proportion change in hypopnea/AHI (defined here as (postoperative–preoperative)/preoperative fraction of hypopnea in AHI) vs. change in mean heart rate (defined here as (postoperative–preoperative)/preoperative mean heart rate). This shows that the change in mean heart rate was not related to the proportion change in hypopnea/AHI.
Applsci 10 08094 g005
Applsci 10 08094 g006 550
Figure 6. Scatter plot and correlation of change in desaturation index (defined here as (postoperative–preoperative)/preoperative desaturation index) vs. change in mean heart rate (defined here as (postoperative–preoperative)/preoperative mean heart rate). This shows that the change in mean heart rate was not related to the change in desaturation index.
Figure 6. Scatter plot and correlation of change in desaturation index (defined here as (postoperative–preoperative)/preoperative desaturation index) vs. change in mean heart rate (defined here as (postoperative–preoperative)/preoperative mean heart rate). This shows that the change in mean heart rate was not related to the change in desaturation index.
Applsci 10 08094 g006
Applsci 10 08094 g007 550
Figure 7. Scatter plot and correlation of change in mean SpO2 (defined here as (postoperative–preoperative)/preoperative mean SpO2) vs. change in mean heart rate (defined here as (postoperative–preoperative)/preoperative mean heart rate). This shows that the change in mean heart rate was not related to the change in mean SpO2.
Figure 7. Scatter plot and correlation of change in mean SpO2 (defined here as (postoperative–preoperative)/preoperative mean SpO2) vs. change in mean heart rate (defined here as (postoperative–preoperative)/preoperative mean heart rate). This shows that the change in mean heart rate was not related to the change in mean SpO2.
Applsci 10 08094 g007
Table
Table 1. Results for patients receiving various surgeries. Order is numbered according to the surgery date. a: modified Z-palatoplasty (ZPP); A: uvulopalatopharyngoplasty (UPPP); b: tongue-base glossectomy; c: septomeatoplasty; d: bilateral endoscopic sinosurgery; e: adenoidectomy; Preop: preoperative; Postop: postoperative; AHI: apnea–hypopnea index.
Table 1. Results for patients receiving various surgeries. Order is numbered according to the surgery date. a: modified Z-palatoplasty (ZPP); A: uvulopalatopharyngoplasty (UPPP); b: tongue-base glossectomy; c: septomeatoplasty; d: bilateral endoscopic sinosurgery; e: adenoidectomy; Preop: preoperative; Postop: postoperative; AHI: apnea–hypopnea index.
Case #Age (years)SexRemarksPreop AHI(/h)Postop AHI(/h)Preop Mean Heart Rate (Beats/min)Postop Mean Heart Rate (Beats/min)
125maleabce79.429.174.968.2
234maleabcd660.879.474.8
758maleabcd62.677.679.570.1
1443maleab87.75769.558.4
1644maleab69.79.661.464
2148maleabcd62.960.87764.9
2263maleAbc65.743.864.754.2
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Share and Cite

MDPI and ACS Style

Huang, E.I.; Huang, S.-Y.; Lin, Y.-C.; Lin, C.-M.; Lin, C.-K.; Huang, Y.-C.; Su, J.-A. A Non-Framework Multilevel Surgery May Reduce Mean Heart Rate in Patients with Very Severe Obstructive Apnea Having Confined Retroglossal Space and Framework. Appl. Sci. 2020, 10, 8094. https://doi.org/10.3390/app10228094

AMA Style

Huang EI, Huang S-Y, Lin Y-C, Lin C-M, Lin C-K, Huang Y-C, Su J-A. A Non-Framework Multilevel Surgery May Reduce Mean Heart Rate in Patients with Very Severe Obstructive Apnea Having Confined Retroglossal Space and Framework. Applied Sciences. 2020; 10(22):8094. https://doi.org/10.3390/app10228094

Chicago/Turabian Style

Huang, Ethan I., Shu-Yi Huang, Yu-Ching Lin, Chieh-Mo Lin, Chin-Kuo Lin, Ying-Chih Huang, and Jian-An Su. 2020. "A Non-Framework Multilevel Surgery May Reduce Mean Heart Rate in Patients with Very Severe Obstructive Apnea Having Confined Retroglossal Space and Framework" Applied Sciences 10, no. 22: 8094. https://doi.org/10.3390/app10228094

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop