Correlation Between Salivary Alpha-Amylase Level and Heart Rate Variability in Pediatric Subjects with Sleep-Disordered Breathing

Se-Hwan Hwang; Heung-Ku Lee; Rae-Hyung Kim; Soo-Hyung Lee; Gibeom Ko; Chan-Soon Park

doi:10.18787/jr.2016.23.1.24

Journal List > J Rhinol > v.23(1) > 1044360

Go to TopGo to Top Go to BottomGo to Bottom

TOOLS

Hwang, Lee, Kim, Lee, Ko, and Park: Correlation Between Salivary Alpha-Amylase Level and Heart Rate Variability in Pediatric Subjects with Sleep-Disordered Breathing

Original Article

J Rhinol 2016;23(1):24-30.

Published online: 10 January 2016

DOI: https://doi.org/10.18787/jr.2016.23.1.24

Correlation Between Salivary Alpha-Amylase Level and Heart Rate Variability in Pediatric Subjects with Sleep-Disordered Breathing

Se-Hwan Hwang, MD, Heung-Ku Lee, MD, Rae-Hyung Kim, MD, Soo-Hyung Lee, MD, Gibeom Ko, MD, Chan-Soon Park, MD

Department of Otolaryngology-Head and Neck Surgery, College of Medicine, The Catholic University of Korea, Seoul, Korea

교신저자：박찬순, 16247 경기도 수원시 팔달구 중부대로 93 가톨릭대학교 의과대학 성빈센트병원 이비인후-두경부외과학교실 Tel: +82-31-249-8304, Fax: +82-31-257-3752, E-mail: pcs0112@catholic.ac.kr

Received 12 October 2015 Revised 15 December 2015 Accepted 22 February 2016

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background and Objectives

The aim of this study was to evaluate the relationship between salivary alpha-amylase (sAA) and heart rate variability (HRV) indices in SDB children based on objective parameters of polysomnography (PSG).

Materials and Method

This prospective study enrolled 67 children who underwent a physical examination and full-attended in-lab PSG with continuous electrocardiographic signal. The sAA were measured at night before PSG and in the early morning after PSG.

Results

The subjects were divided into control [n=26, apnea-hypopnea index (AHI)≤1] and obstructive sleep apnea syndrome (OSAS, n=41, AHI＞1) groups; the OSAS group was subdivided into mild (1＜ AHI≤5), moderate (5＜ AHI≤10), and severe (10＜ AHI) groups. The severe OSAS group was significantly different from the control and other OSAS subgroups in terms of the ratio between the low- and high-frequency components (LF/HF ratio) among the HRV indices. The LF/HF ratio was positively correlated with the sAA ratio and sAA subtraction (r=0.271; r=0.347).

Conclusion

TAlthough both HRV and sAA were useful methods of predicting severe OSAS in children, a weak correlation between HRV and sAA was shown in pediatric OSAS subjects. Therefore, HRV and sAA may be independent parameters revealing different aspects of pediatric OSAS.

Keywords: Child, Heart rate, Saliva, Alpha-Amylases, Sleep apnea syndromes, Correlation, Polysomnography.

References

1). Bixler EO, Vgontzas AN, Lin HM, Liao D, Calhoun S, Vela-Bueno A, et al. Sleep disordered breathing in children in a general population sample: prevalence and risk factors. Sleep. 2009; 32:731–6.

2). Guilleminault C, Eldridge FL, Simmons FB, Dement WC. Sleep apnea in eight children. Pediatrics. 1976; 58:23–30.

3). Ng DK, Wong JC, Chan CH, Leung LC, Leung SY. Ambulatory blood pressure before and after adenotonsillectomy in children with obstructive sleep apnea. Sleep Med. 2010; 11:721–5.

4). Marcus CL, Greene MG, Carroll JL. Blood pressure in children with obstructive sleep apnea. Am J Respir Crit Care Med. 1998; 157:1098–103.

5). Miman MC, Kirazli T, Ozyurek R. Doppler echocardiography in adenotonsillar hypertrophy. Int J Pediatr Otorhinolaryngol. 2000; 54:21–6.

6). Gorur K, Doven O, Unal M, Akkus N, Ozcan C. Preoperative and postoperative cardiac and clinical findings of patients with adenotonsillar hypertrophy. Int J Pediatr Otorhinolaryngol. 2001; 59:41–6.

7). Constantin E, McGregor CD, Cote V, Brouillette RT. Pulse rate and pulse rate variability decrease after adenotonsillectomy for obstructive sleep apnea. Pediatr Pulmonol. 2008; 43:498–504.

8). Mo JH. Obstructive Sleep Apnea and Systemic Diseases. J Rhinol. 2013; 100:8–13.

9). Chung YS. Pathogenesis of Obstructive Sleep Apnea. J Rhinol. 2009; 100:87–9.

10). Hakim F, Gozal D, Kheirandish-Gozal L. Sympathetic and cate-cholaminergic alterations in sleep apnea with particular emphasis on children. Front Neurol. 2012; 3:7.

11). Park DH, Shin CJ, Hong SC, Yu J, Ryu SH, Kim EJ, et al. Correlation between the severity of obstructive sleep apnea and heart rate variability indices. J Korean Med Sci. 2008; 23:226–31.

12). Kwok KL, Yung TC, Ng DK, Chan CH, Lau WF, Fu YM. Heart rate variability in childhood obstructive sleep apnea. Pediatr Pulmonol. 2011; 46:205–10.

13). Deng ZD, Poon CS, Arzeno NM, Katz ES. Heart rate variability in pediatric obstructive sleep apnea. Conf Proc IEEE Eng Med Biol Soc. 2006; 1:3565–8.

14). Park CS, Guilleminault C, Hwang SH, Jeong JH, Park DS, Maeng JH. Correlation of salivary cortisol level with obstructive sleep apnea syndrome in pediatric subjects. Sleep Med. 2013; 14:978–84.

15). Park CS, Guilleminault C, Park HJ, Cho JH, Lee HK, Son HL, et al. Correlation of salivary alpha amylase level and adenotonsillar hypertrophy with sleep disordered breathing in pediatric subjects. J Clin Sleep Med. 2014; 10:559–66.

16). Oh JI, Lee SH. Obstructive Sleep Apnea Syndrome in Children. Hanyang Med Rev. 2013; 100:246–52.

17). Nater UM, Rohleder N. Salivary alpha-amylase as a non-invasive biomarker for the sympathetic nervous system: current state of research. Psychoneuroendocrinology. 2009; 34:486–96.

18). Kwok KL, Yung TC, Ng DK, Chan CH, Lau WF, Fu YM. Heart rate variability in childhood obstructive sleep apnea. Pediatr Pulmonol;. 2011.

19). Guilleminault C, Connolly S, Winkle R, Melvin K, Tilkian A. Cy-clical variation of the heart rate in sleep apnoea syndrome. Mechanisms, and usefulness of 24 h electrocardiography as a screening technique. Lancet. 1984; 1:126–31.

20). Gula LJ, Krahn AD, Skanes A, Ferguson KA, George C, Yee R, et al. Heart rate variability in obstructive sleep apnea: a prospective study and frequency domain analysis. Ann Noninvasive Electrocardiol. 2003; 8:144–9.

21). Yang A, Schafer H, Manka R, Andrie R, Schwab JO, Lewalter T, et al. Influence of obstructive sleep apnea on heart rate turbulence. Basic Res Cardiol. 2005; 100:439–45.

22). Roche F, Gaspoz JM, Court-Fortune I, Minini P, Pichot V, Duverney D, et al. Screening of obstructive sleep apnea syndrome by heart rate variability analysis. Circulation. 1999; 100:1411–5.

23). Narkiewicz K, Montano N, Cogliati C, van de Borne PJ, Dyken ME, Somers VK. Altered cardiovascular variability in obstructive sleep apnea. Circulation. 1998; 98:1071–7.

24). Aydin M, Altin R, Ozeren A, Kart L, Bilge M, Unalacak M. Cardiac autonomic activity in obstructive sleep apnea: time-dependent and spectral analysis of heart rate variability using 24-hour Holter electrocardiograms. Tex Heart Inst J. 2004; 31:132–6.

25). Filaire E, Portier H, Massart A, Ramat L, Teixeira A. Effect of lecturing to 200 students on heart rate variability and alpha-amy-lase activity. Eur J Appl Physiol. 2010; 108:1035–43.

26). Nater UM, La Marca R, Florin L, Moses A, Langhans W, Koller MM, et al. Stress-induced changes in human salivary alpha-amylase activity–associations with adrenergic activity. Psychoneuroendocrinology. 2006; 31:49–58.

Table 1.

Basic demographic, anthropometric, conventional polysomnographic date

		Control (n=26)	OSAS (n=41)	p value
Gender	Male (%)	9 (34.6)	30 (73.2)	0.002
	Female (%)	17 (65.4)	11 (26.8)	0.002
Age		7.5±2.8	6.9± 3.4	0.179
BMI		18.3±3.2	18.1±3.9	0.459
Sleep parameters	Total sleep time (min)	471.2±45.9	468.7±39.5	0.643
	Sleep latency (min)	13.2±11.1	17.3±14.7	0.210
	Sleep efficiency (%)	93.8±6.7	91.6±7.4	0.081
Sleep stage duration (% of total sleep time)	N1	5.5±3.0	8.2±5.0	0.012
	N2	48.9±5.9	45.0±5.9	0.011
	N3	26.2±5.6	28.3±6.3	0.169
	REM	19.4±4.7	18.7±5.5	0.576
Respiratory parameters	AHI	0.2±0.3	13.2±22.1	＜0.0001
	Lowest O2 saturation	89.7±18.9	88.9±6.7	0.001

N (%) tested by chi-square test. Mean± SD tested by t-test and wilcoxon rank sum test. BMI: body mass index

Table 2.

The measurements regarding the sAA and HRV between the control and OSAS groups

		Control (n=26)	OSAS (n=41)	p value
Time-domain	Average RR interval	762.5±77.8	734.8±100.6	0.254
	SNDD	95.6±26.6	112.2±45.8	0.200
	SNDD index	70.8±25.1	88.6±43.6	0.078
	RMSSD	68.5±32.2	90.8±64.8	0.163
	NN50 count	9870.9±7152.8	10965±6635.8	0.625
	pNN50	26.7±19.4	29.4±19.7	0.586
	HRV Triangular index	17.9±6.0	19.4±7.8	0.519
Frequency-domain	TP	9060.6±2132.2	9993.5±3261.7	0.249
	VLF	3693.2±1335.9	4036.1±2283.6	0.989
	LF	2350.3±747.5	2819±1135.7	0.108
	HF	2765.2±1419.2	2936.4±1297.3	0.432
	LF/HF ratio	1.0±0.4	1.1±0.6	0.783
sAA	n-sAA	140.429±108.764	125.915±92.51	0.719
	m-sAA	60.111±51.777	65.0781±50.232	0.643
	sub-sAA	–80.318±79.376	–60.134±72.425	0.167
	r-sAA	0.476±0.195	0.582±0.336	0.303

Mean± SD tested by t-test and wilcoxon rank sum test

Table 3.

The measurements regarding the sAA and HRV according to the OSA severity subgroups

		Control 0≤ AHI≤1 (n=26)	Mild 1<AHI＜5 (n=19)	Moderate 5≤ AHI ＜10 (n=7)	Severe 10≤ AHI (n=15)	p value
Time-domain	Average RR interval	762.5±77.8	769.5±86.8	710.4±125	706.8±97.8	0.135
	SNDD	95.6±26.6	116.4±50.7	94.7±20.8	115.5±48.7	0.413
	SNDD index	70.8±25.1	94.5±51.7	75.1±21.0	88.2±42.2	0.287
	RMSSD	68.5±32.2	101.9±79.8	78.1±31.8	84.1±58.3	0.427
	NN50 count	9870.9±7152.8	13110.8±6153.7	7844.3±5281.4	9991.9±7267.3	0.275
	pNN50	26.7±19.4	36.7±19.3	20.4±11.8	25.8±18.9	0.214
	HRV Triangular index	17.9±6.0	21.0±6.5	15.0±6.0	19.7±9.4	0.210
Frequency-domain	TP	9060.6±2132.2	10141.9±2347.1	8258.3±2736.5	10634.9±4171.2	0.391
	VLF	3693.2±1335.9	3790.7±1427.4	3106.4±1302.7	4747.9±3170.2	0.611
	LF	2350.3±747.5	2547.2±739.4	2329.3±946.0	3355.7±1405.1	0.099
	HF	2765.2±1419.2	3503.8±1311.6	2616.3±988.2	2442.7±1216.6	0.084
	LF/HF ratio	1.0±0.4	0.8±0.3	0.9±0.3	1.6±0.7	0.002 ^a,b,c
sAA	n-sAA	140.429±108.764	151.843±114.392	122.269±85.251	94.775±50.544	0.675
	m-sAA	60.111±51.777	55.373±44.806	68.037±70.85	77.911±46.579	0.364
	sub-sAA	–80.318±79.376	–96.47±86.661	–54.232±42.504	–16.864±27.226	0.005 ^a,b,c
	r-sAA	0.476±0.195	0.44±0.28	0.472±0.246	0.813±0.323	0.003 ^a,b,c

p value: p value of difference between normal verse Mild verse Moderate verse Severe by ANOVA test and Kruskal-Wallis test, followed by post hoc Dunn's test. a: normal verse severe, b: mild verse severe, c: moderate verse severe

Table 4.

The correlation with AHI in the OSAS group

	AHI
	r	p value
LF/HF ratio	0.574	0.01
sub-sAA	0.37	0.016
r-sAA	0.38	0.013

Spearman's correlation

Table 5.

The correlation between sAA parameters and LF/HF ratio

	Total group		OSAS group
	LF/HF ratio		LF/HF ratio
	r	p value	r	p value
sub-sAA	0.347	0.005	0.441	0.005
r-sAA	0.271	0.032	0.305	0.059

Spearman's correlation

Table 6.

The evaluation of the effective screening parameters of LF/HF ratio and r-sAA to identify the severe OSAS group in all patients

	Cut off value	Sensitivity % (95%CI)	Specificity % (95%CI)	PPV % (95%CI)	NPV% (95%CI)	AUC (95%CI)	p value
LF/HF ratio	＞1.0989	80.0 (51.9–95.7)	70.8 (55.9–83.0)	46.2 (29.5–63.6)	91.9 (78.1–98.3)	0.80 (0.68–0.89)	＜0.0001
r-sAA	＞0.7383	66.7 (38.4–88.2)	88.5 (76.6–95.6)	58.8 (32.9–81.6)	90.0 (78.2–96.7)	0.81 (0.70–0.90)	＜0.0001

Receiver operating characteristic. curve 95% CI: 95% confidence interval, PPV: positive predictive value, NPV: negative predictive value, AUC: area under the curve

TOOLS

Similar articles