Original Research—Sinonasal Disorders
Otolaryngology–
Effects of Nasal Septum Deviation and
Septoplasty on Cardiac Arrhythmia Risk
Sinan Uluyol, MD1, Saffet Kilicaslan, MD1, Mehmet Hafit Gur, MD1,
Nermin Erdas Karakaya, MD1, Ipek Buber, MD2, and
Sedef Gulcin Ural, MD3
No sponsorships or competing interests have been disclosed for this article.
Abstract
Objective. Upper airway obstruction (UAO) can result in car-
diac complications, including arrhythmias and sudden cardiac
death. Nasal septum deviation (NSD) is a common cause of
UAO. The aim of this study was to assess the risk of cardiac
arrhythmias in patients with NSD. To assess this risk, we
measured noninvasive indicators of atrial arrhythmia (P-wave
dispersion [Pd]) and ventricular arrhythmia (corrected QT
dispersion [QTcd]) and compared these values between
NSD patients and healthy subjects.
Study Design. Prospective study.
Settings. Tertiary referral center.
Subjects and Methods. This study included 53 consecutive
patients who had underwent septoplasty due to marked
NSD. Electrocardiographic records were used to determine
Pd and QTcd values preoperatively and 6 months postopera-
tively. Fifty-three consecutive age- and sex-matched subjects
without any UAO were also examined as a control group.
Results. Preoperative Pd and QTcd values were significantly
higher in NSD patients than in the control group (Pd: 57.40
6 14.21 vs 34.11 6 7.12 milliseconds, P \ .001; QTcd:
81.77 6 16.39 vs 50.25 6 11.51 milliseconds, P \ .001,
respectively). In addition, Pd and QTcd values were signifi-
cantly greater in preoperative NSD patients when compared
with the same patients postoperatively (Pd: 57.40 6 14.21
vs 36.32 6 8.9 milliseconds, P = .013; QTcd: 81.77 6 16.39
vs 55.76 6 11.4 milliseconds, P = .012, respectively).
Conclusion. In conclusion, NSD patients are at risk for both
atrial and ventricular cardiac arrhythmias; however, septo-
plasty in these patients can relieve UAO and reduce the risk
of arrhythmias.
Keywords
airway obstruction, atrial arrhythmia, cardiac arrhythmia,
electrocardiography, nasal septum, ventricular arrhythmia
Received December 16, 2015; revised February 24, 2016; accepted
March 11, 2016.
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Head and Neck Surgery
2016, Vol. 155(2) 347–352
Ó American Academy of
Otolaryngology—Head and Neck
Surgery Foundation 2016
Reprints and permission:
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DOI: 10.1177/0194599816642432
http://otojournal.org
C
ardiac complications due to upper airway obstruc-
tion (UAO) have been previously investigated.
Studies revealed a strong association between UAO
and heart rhythm disorders.1,2 Factors thought to contribute
to cardiovascular morbidity in individuals with UAO are
enhanced oxidative stress, sympathetic nervous system acti-
vation, and exaggerated negative intrathoracic pressure
swings.2,3 One of the most common causes of UAO is nasal
septum deviation (NSD).4,5 The prolongation of P-wave dis-
persion (Pd) has been observed in adult patients with adeno-
tonsillar hypertrophy and obstructive sleep apnea (OSA).6,7
However, the risk of arrhythmia in NSD patients has not
been studied in detail.
QT and Pd dispersion parameters can indicate abnormal-
ities in the autonomic nervous system and cardiac function.
Pd is defined as the difference between the longest and
shortest P wave durations recorded from multiple electrocar-
diogram (ECG) leads. Pd reflects the inhomogeneous propa-
gation of sinus impulses. Thus, Pd has been performed in
the assessment of the risk for atrial fibrillation, which is
characterized by inhomogeneous and discontinuous atrial
conduction.8,9 QT dispersion is defined as the difference
between the longest and shortest QT intervals on the 12-
lead ECG. Heart rate–corrected QT dispersion (QTcd) is an
indirect measure of the heterogeneity of ventricular depolar-
ization, which may contribute to ventricular arrhythmias.10
Increased QTcd has been shown to be correlated with
the risk of arrhythmic death in a variety of cardiac or
noncardiac disorders.11 Therefore, the use of QT dispersion
to evaluate an individual’s susceptibility to ventricular
arrhythmias has become a standard for many noncardiac
conditions.12-15
1
Department of Otolaryngology, Van Training and Research Hospital, Van,
Turkey
2
Department of Cardiology, Pamukkale University Medical Faculty, Denizli,
Turkey
3
Department of Anesthesiology, Van Training and Research Hospital, Van,
Turkey
Corresponding Author:
Sinan Uluyol, MD, Van Bölge Eğitim ve Arasxtrıma Hastanesi KBB Kliniği,
Ipekyolu Caddesi, Hava Yolu Kavsxağı 1. Kilometre, 65300 Edremit Van/
Turkey.
Email: sinanuluyol@hotmail.com
348
The aim of this study was to quantify the risk of atrial
and ventricular arrhythmias in NSD patients and to examine
the effect of septoplasty on arrhythmia risk in these patients
by measuring Pd and QTcd values during the pre- and post-
operative periods.
Materials and Methods
This study adhered to the guidelines of the Helsinki
Declaration of the World Medical Association and was
approved by the research ethics committee at Van Training
and Research Hospital (no. 2015/7). Written informed con-
sent was obtained from all participants prior to the study.
The prospective study involved 53 consecutive patients
(18 women and 35 men) who underwent septoplasty due to
marked C- or S-shaped NSD from November 2014 to
March 2015. The control group was composed of 53 con-
secutive healthy age- and sex-matched subjects (20 female,
33 male) without NSD or other UAO reasons.
All participants were evaluated with the same systematic
protocol. For the diagnosis of presence or absence of NSD
or other UAO, a detailed otorhinolaryngologic examination
was made—including Mallampati classification, Friedman
tongue position, anterior rhinoscopy, and endoscopic nasal,
nasopharyngeal and hypopharyngeal examinations—and
obstructive symptoms were questioned with the Epworth
Sleepiness Scale (ESS).
We excluded patients with mild NSD, isolated unilateral
NSD, NSD with turbinate hypertrophy, UAO-related con-
ditions (ie, airway masses, vocal cord paralysis, adenotonsil-
lar hypertrophy, or OSA), a history of cardiac disease
(ie, arrhythmia, heart valve disorders, previous cardiac sur-
gery, myocardial infarction, congestive heart failure, bundle
branch block, or cardiomyopathy), medical conditions that
may have disrupted the cardiac conduction systems (ie,
hypertension, diabetes mellitus, hyperlipidemia, or thyroid
disease), long-term drug usage for chronic disease, and
tobacco use.
To identify patients with OSA for the purpose of exclu-
sion, we examined patients with portable overnight poly-
somnography (Itamar Watch-Pat200; Itamar Medical,
Caesarea, Israel), and we evaluated patient scores from the
ESS, the Mallampati classification, and Friedman tongue
position. Polysomnography examination was performed
only in the study group. Patients with an apnea-hypopnea
index .5, an ESS score .10, a Mallampati score .1, and a
Friedman tongue position of 2, 3, or 4 were excluded. The
ESS is a simple and validated questionnaire for assessing
subjective daytime sleepiness in the context of sleep disor-
ders. The ESS is a self-administered questionnaire contain-
ing 8 items that patients are asked to score on a scale of 0
to 3 (0, no chance of napping; 1, small chance of napping;
2, moderate chance of napping; and 3, strong chance of nap-
ping). Scores were totaled, with a range of 0 to 10 defined
as normal.16,17
Operations were performed under general anesthesia.
Killian’s incision was preferred. The incision was usually
situated on the concave side of the septum. The cartilaginous
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Otolaryngology–Head and Neck Surgery 155(2)
and bony nasal septum was exposed from both sides by the
elevation of mucoperichondrial and mucoperiosteal flaps.
Deviated structures were removed with cutting forceps or
Ballenger’s knife. Sufficient cartilage and bone were pre-
served for structural support. Internal nasal splints were
applied following transseptal suturing. Only the patients in
the study group underwent septoplasty; participants in the
control group did not undergo any surgery.
Electrocardiographic records were used to determine Pd
and QTcd values in NSD patients and the control group pre-
operatively and 6 months postoperatively. A standard 12-
lead ECG 50-mmV recording was performed following a
10-minute rest in the supine position. All recordings were
performed during spontaneous breathing. All measurements
were repeated 3 times and taken in the same quiet room.
Prior to analysis, a single blinded investigator calculated the
mean of 3 consecutive interval measurements. Pd was mea-
sured from the first sign of upward departure from the base-
line to the point of return to the baseline. The difference
between the longest and shortest P-waves in any of the 12
leads was defined as Pd (milliseconds). The QT interval
was measured starting from the onset of the QRS complex
until the end of the T-wave. QTcd dispersion was measured
as the difference between the maximum and minimum QT
intervals (milliseconds) with heart rate correction, according
to Bazett’s formula.18
Measurements were statistically compared through SPSS
20.0 for Windows (SPSS Inc, Chicago, Illinois). Continuous
variables are presented as mean 6 SD. Qualitative values
were compared via the chi-square test. Significant differ-
ences between the NSD and control groups were detected
through a 2-tailed t test; significant differences among the
control group and the pre- and postoperative NSD groups
were detected through analysis of variance. A P value \.05
was taken to indicate statistical significance.
Results
The study group included 53 patients with marked NSD (18
women, 35 men) and a mean age of 38.03 6 12.52 years
(range, 18-54 years). The control group included 53 healthy
subjects (20 women, 33 men) with a mean age of 41 6
15.76 years (range, 20-58 years). The age and sex distribu-
tion of the patients did not differ significantly between
groups (Table 1). Both Pd and QTcd values were signifi-
cantly higher in the preoperative NSD group as compared
with the control group (Pd, P \ .001; QTcd, P \ .001).
Among NSD patients, preoperative Pd and QTcd values
were significantly higher than postoperative values (Pd, P =
.013; QTcd, P = .012). Furthermore, postoperative Pd and
QTcd values in NSD patients did not differ significantly
than values observed in the control group (Pd, P = .31;
QTcd, P = .28). Table 2 presents the Pd and QTcd values.
Discussion
UAO is characterized by the partial or complete closure of
the upper airway. NSD is a common cause of recurrent and
chronic UAO and a possible risk factor for OSA.4,19-21
Uluyol et al 349

Nasal airflow resistance constitutes a significant part of
airway resistance; thus, small changes in the nasal patency
affect total airway resistance.20,22
Mechanical UAO can lead to hypoxia, hypercapnia, and
significant changes in intrathoracic pressure. All these fac-
tors may affect sympathetic and parasympathetic activation,
as well as cardiac autonomic responses.23 Although the
exact mechanisms underlying the link between UAO and
cardiac arrhythmias are not well known, they could be simi-
lar to the mechanisms relating OSA to various cardiovascu-
lar diseases. Autonomic dysfunction, sympathetic nervous
system activation, and hypoxia are believed to be the
common pathophysiologic factors involved in arrhythmo-
genesis.24,25 Suppression of cardiac efferent vagal tone and
an increase in sympathetic neural outflow may initiate
arrhythmias directly by causing abnormal cardiac remodel-
ing of the atrium and ventricle26,27 or indirectly by affecting
heart rate, blood pressure, and coronary blood flow.28,29
Hypoxia and oxygen-derived free radicals can also damage
cardiac myocytes and affect myocyte ion exchange, thereby
increasing the likelihood of functional deterioration as well
as facilitating arrhythmogenesis.3,25,30,31
Several studies have recognized that UAO, specifically
OSA, can contribute to cardiovascular morbidity. Although
the role of nasal obstruction in the pathogenesis of OSA has
Table 1. Demographic Characteristics.
Study Group Control Group
(n = 53) (n = 53)
Age, y
Mean 6 SD 38.034 6 12.52 41 6 15.76
Range 18-54 20-58
Sex, n
Women 18 20
Men 35 33
a
Two-tailed t test.
b
Chi-square test.
been well studied,32,33 to our knowledge there has not been
any published study evaluating the risk of arrhythmia in
NSD patients by noninvasive markers. Nasal obstruction
and mouth breathing could contribute to UAO through sev-
eral mechanisms. First, nasal obstruction causes the mouth
to open for the patient to breathe. This leads to a backward
rotation of the jaw, displacing the base of tongue posteriorly
and lowering the hyoid, which leads to increased pharyngeal
collapse. Second, nasal obstruction and mouth breathing
cause increased resistance upstream, which leads to
increased downstream resistance through the loss of nasal
ventilatory reflexes.23,34 It is confirmed that upper airway
patency activates the nasal mechanosensitive receptors and
leads to a direct positive effect on spontaneous ventilation,
higher resting breathing frequency, and higher minute venti-
lation.35 Nasal obstruction and mouth breathing reduce the
activation of these receptors, leading to (1) deactivation of
the nasal ventilatory reflex; (2) inhibition of respiratory rate,
minute ventilation, and muscle tone; and (3) an increase of
bronchoconstriction, which can trigger respiratory events in
susceptible individuals with subclinical OSA or exacerbate
apnea episodes.20,36 It has been suggested that the treatment
of NSD can be beneficial to overcome or prevent OSA.37
Although the effects of chronic UAO disorders—such as
adenotonsillar hypertrophy in childhood and OSA on the
cardiopulmonary system—have been researched and the
mechanisms have been demonstrated, the cardiopulmonary
effect of pure NSD has not been investigated adequately.
Therefore, it is difficult to explain the exact mechanisms
underlying the relationship between NSD and arrhythmo-
P Value genesis. Fidan and Aksakal noticed that pulmonary arterial
pressure is higher in patients with marked NSD and
.25a
decreases significantly after septoplasty.38 Literature has
revealed that increased pulmonary artery pressure associated
with hypoxia and pulmonary vasoconstriction may result in
.38b
hypertrophy of the right cardiac ventricle, which can then
lead to right cardiac failure.39 Derin et al carried out a pro-
spective study to investigate any impact of NSD on cardiac
arrhythmias by performing 24-hour rhythm Holter analysis

Table 2. Pd and QTcd Values.

Preoperative Values Postoperative Values

NSD (n = 53) Control (n = 53) P Valuea NSD (n = 53) P Valueb P Valuec

Pd
ms 57.40 6 14.21 34.11 6 7.12 \.001 36.32 6 8.9 .013 .31
Range 31-79 14-51 17-55
QTcd
ms 81.77 6 16.39 50.25 6 11.51 \.001 55.76 6 11.4 .012 .28
Range 57-112 30-73 28-81
Abbreviations: NSD, nasal septum deviation; Pd, P-wave dispersion; QTcd, heart rate–corrected QT dispersion.
a
Analysis between preoperative NSD and control groups.
b
Analysis between preoperative and postoperative NSD groups.
c
Analysis between postoperative NSD and control groups.

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350
before and after septoplasty, and they reported that septo-
plasty decreased ventricular and supraventricular extrasys-
toles.40 In an experimental study, hypoxia was shown to
induce extrasystoles, and the improvement of hypoxia has
been shown to decrease extrasystole occurrence.25 These
studies partially reveal and represent the possible effects of
nasal obstruction on cardiopulmonary function.
Recently, in a large prospective study, the predictive
value of QTcd was assessed in 1839 American Indians fol-
lowed up for 3.7 6 0.9 years. QTcd was reported as a sig-
nificant and independent predictor, with a 34% increase of
cardiovascular mortality for each 17-millisecond increase,
and the authors emphasized that QTcd .58 milliseconds
was associated with a 3.2-fold increased risk of cardiovascu-
lar mortality.41 Reported values of QT dispersion vary
mostly between 30 and 60 milliseconds in normal subjects,
with average values around 70 milliseconds also being
reported.11 In a meta-analysis of 6827 healthy subjects, the
average Pd value was reported as 33.46 6 9.65 milliseconds
(range, 7 6 2.7 to 58.56 6 16.24 milliseconds).42 Also, a
dispersion value 40 milliseconds was found to be signifi-
cantly specific and sensitive in patients with atrial fibrilla-
tion when compared with healthy controls.43 Although there
is no validated limit values to assess arrhythmia risk by
QTcd and Pd, the values considered by the large
population-based studies41-43 above could be accepted as
limit values. Mechanical UAO due to NSD can lead to inhi-
bition of nasal ventilatory reflex, hypoxia, hypercapnia,
autonomic dysfunction, sympathetic nervous system activa-
tion, disturbances in coronary blood flow, and generation of
oxygen-derived free radicals that could contribute to facili-
tate arrhythmogenesis. Therefore, we evaluated Pd and
QTcd—useful and noninvasive markers for the prediction of
arrhythmias—to quantify the risk of atrial and ventricular in
patients with NSD.
In this study, we observed substantial differences
between NSD patients and healthy controls. Pd and QTcd
values were higher in patients with NSD than in the healthy
subjects. We detected a significant reduction and normaliza-
tion in Pd and QTcd values after septoplasty in NSD
patients. These results suggest that NSD, a common cause
of UAO, facilitates arrhythmogenesis. Furthermore, septo-
plasty proved to be beneficial in NSD patients by eliminat-
ing UAO and reducing arrhythmia risk by withdrawing
sympathetic activation and enhancing parasympathetic tone.
It is important for physicians to accurately diagnose UAO
pathologies, such as NSD, in patients with cardiac arrhyth-
mia or other cardiac diseases. Treatment of NSD may be
useful following assessment in these patients. However, it is
important to recognize that NSD may predispose individuals
to future cardiac problems.
The strength of our study is the assessment of the risk of
atrial and ventricular arrhythmias in patients with NSD and
the effect of septoplasty on arrhythmia risk by measuring
noninvasive markers (Pd and QTcd) for the first time. There
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Otolaryngology–Head and Neck Surgery 155(2)
are several limitations to our study. First, this study included
a relatively small number of patients. Additional larger
population-based studies with long-term clinical follow-up
data are needed to accurately identify the potential effects
of NSD and septoplasty on cardiac arrhythmia risk.
However, inclusion of patients with bilateral marked septal
deviation limits the interpretation and generalizability to all
patients with septal deviation in the present study. The main
limitation is the lack of rhinomanometry examinations. This
type of information could determine the nasal airway resis-
tance more accurately.
Conclusions
This study is novel, as it assessed specific ECG markers
indicative of atrial or ventricular arrhythmic risk. In the 2
outcomes measures—Pd and QTcd—preoperative NSD
patients showed significantly higher values than the control
group, and these values ‘‘normalized’’ to levels similar to
those of the controls at 6 months postoperatively. These
results indicate the significant association between nasal
obstruction and arrhythmia risk. In conclusion, patients with
marked NSD should be encouraged to do septoplasty sooner
for prevention of future cardiac problems. Additional larger
population-based studies are needed to verify our prelimi-
nary results.
Author Contributions
Sinan Uluyol, wrote the article, performed surgeries, revised arti-
cle, final approval of the version to be published, integrity of any
part of the work; Saffet Kilicaslan, wrote article, designed study,
analysis of data, final approval of the version to be published,
integrity of any part of the work; Mehmet Hafit Gur, conception
and design, drafting the work, final approval of the version to be
published, integrity of any part of the work; Nermin Erdas
Karakaya, conception and design, revising article, final approval
of the version to be published, agreement to be accountable for all
aspects; Ipek Buber, designed work, analysis of data, drafting the
article, final approval of the version to be published, agreement to
be accountable for all aspects; Sedef Gulcin Ural, analysis of
data, revising article, final approval of the version to be published,
agreement to be accountable for all aspects
Disclosures
Competing interests: None.
Sponsorships: None.
Funding source: None.
References
1. Bitter T, Fox H, Gaddam S, Horstkotte D, Oldenburg O.
Sleep-disordered breathing and cardiac arrhythmias. Can J
Cardiol. 2015;31:928-934.
2. Leung RS. Sleep-disordered breathing: autonomic mechanisms
and arrhythmias. Prog Cardiovasc Dis. 2009;51:324-338.
3. Gozal D, Kheirandish-Gozal L. Cardiovascular morbidity in
obstructive sleep apnea: oxidative stress, inflammation, and
much more. Am J Respir Crit Care Med. 2008;177:369-375.
Uluyol et al
4. Ishii L, Godoy A, Ishman SL, Gourin CG, Ishii Ml. The nasal
obstruction symptom evaluation survey as a screening tool for
obstructive sleep apnea. Arch Otolaryngol Head Neck Surg.
2011;137:119-123.
5. Osborn JL, Sacks R. Chapter 2: nasal obstruction. Am J Rhinol
Allergy. 2013; 27(suppl 1):S7-S8.
6. Kocabasx A, Salman N, Ekici F, Cetin I, Akcan FA. Evaluation
of cardiac functions and atrial electromechanical delay in chil-
dren with adenotonsillar hypertrophy. Pediatr Cardiol. 2014;
35:785-792.
7. Jazi MH, Amra B, Yazdchi MR, Jahangiri M, Tabesh F,
Gholamrezaei A. P wave duration and dispersion in Holter
electrocardiography of patients with obstructive sleep apnea.
Sleep Breath. 2014;18:549-554.
8. Dilaveris PE, Gialafos JE. P-wave dispersion: a novel predic-
tor of paroxysmal atrial fibrillation. Ann Noninvasive
Electrocardiol. 2001;6:159-165.
9. Dilaveris P, Batchvarov V, Gialafos J, Maik M. Comparison
of different methods for manual P wave duration measurement
in 12-lead electrocardiograms. Pacing Clin Electrophysiol.
1999;22:1532-1538.
10. Pye M, Quinn AC, Cobbe SM. QT interval dispersion: a non-
invasive marker of susceptibility to arrhythmia in patients with
sustained ventricular arrhythmias? Br Heart J. 1994;71:
511-514.
11. Malik M, Batchvarov VN. Measurement, interpretation and
clinical potential of QT dispersion. J Am Coll Cardiol. 2000;
36:1749-1766.
12. Akbal A, Kurtaran A, Gürcan A, et al. P-wave and QT disper-
sion in spinal cord injury. Intern Med. 2014;53:1607-1611.
13. Izci F, Hocagil H, Izci S, Izci V, Koc MI, Acar RD. P-wave
and QT dispersion in patients with conversion disorder. Ther
Clin Risk Manag. 2015;11:475-480.
14. Seyfeli E, Duru M, Kuvandik G, Kaya H, Yalcin F. Effect of
obesity on P-wave dispersion and QT dispersion in women. Int
J Obes (Lond). 2006;30:957-961.
15. Guntekin U, Gunes Y, Tuncer M, Gumrukcuoglu HA, Kaya Y.
The effect of altitude on P-wave and QT duration and disper-
sion. Pacing Clin Electrophysiol. 2008;31:889-892.
16. Johns MW. A new method for measuring daytime sleepiness:
the Epworth sleepiness scale. Sleep. 1991;14:540-545.
17. Johns MW. Reliability and factor analysis of the Epworth
Sleepiness Scale. Sleep. 1992;15:376-381.
18. Bazett H. An analysis of the time-relations of electrocardio-
grams. Heart. 1920;7:353–370.
19. Liistro G, Rombaux Ph, Belge C, Dury M, Aubert G,
Rodenstein DO. High Mallampati score and nasal obstruction
are associated risk factors for obstructive sleep apnea. Eur
Respir J. 2003;21:248-252.
20. Michels Dde S, Rodrigues Ada M, Nakanishi M, Sampaio AL,
Venosa AR. Nasal involvement in obstructive sleep apnea syn-
drome. Int J Otolaryngol. 2014;2014:717419
21. Verse T, Pirsig W. Impact of impaired nasal breathing on
sleep-disordered breathing. Sleep Breath. 2003;7:63-76.
22. Ferris BG Jr, Mead J, Opie LH. Partitioning of respiratory
flow resistance in man. J Appl Physiol. 1964;19:653-658.
Downloaded from oto.sagepub.com at INDIAN RIVER STATE COLLEGE on August 5, 2016
351
23. Olsen KD, Kern EB, Westbrook PR. Sleep and breathing dis-
turbance secondary to nasal obstruction. Otolaryngol Head
Neck Surg. 1981;89:804-810.
24. Somers VK, Dyken ME, Clary MP, Abboud FM. Sympathetic
neural mechanisms in obstructive sleep apnea. J Clin Invest.
1995;96:1897-1904.
25. O’Connor PJ, Merrill GF. Ventricular arrhythmias caused by
repeat exposure to hypoxia are dependent on duration of reox-
ygenation. FASEB J. 1995;9:387-391.
26. Wiklund U, Olofsson BO, Franklin K, Blom H, Bjerle P,
Niklasson U. Autonomic cardiovascular regulation in patients
with obstructive sleep apnoea: a study based on spectral analy-
sis of heart rate variability. Clin Physiol. 2000;20:234-241.
27. McNicholas WT, Bonsigore MR. Sleep apnoea as an indepen-
dent risk factor for cardiovascular disease: current evidence,
basic mechanisms and research priorities. Eur Respir J. 2007;
29:156-178.
28. Ringler J, Garpestad E, Basner R, Weiss JW. Systemic blood
pressure elevation after airway occlusion during NREM sleep.
Am J Respir Crit Care Med. 1994;150:1062-1066.
29. Weiss JW, Remsburg S, Garpestad E, Ringler J, Sparrow D,
Parker JA. Hemodynamic consequences of obstructive sleep
apnea. Sleep. 1996;19:388-397.
30. Sano K, Watanabe E, Hayano J, et al. Central sleep apnoea
and inflammation are independently associated with arrhyth-
mia in patients with heart failure. Eur J Heart Fail. 2013;15:
1003-1010.
31. Gramley F, Lorenzen J, Jedamzik B, et al. Atrial fibrillation is
associated with cardiac hypoxia. Cardiovasc Pathol. 2010;19:
102-111.
32. Young T, Finn L, Kim H. Nasal obstruction as a risk factor for
sleep-disordered breathing: the University of Wisconsin Sleep
and Respiratory Research Group. J Allergy Clin Immunol.
1997;99:S757-S762.
33. Liistro G, Rombaux Ph, Belge C, Dury M, Aubert G,
Rodenstein DO. High Mallampati score and nasal obstruction
are associated risk factors for obstructive sleep apnea. Eur
Respir J. 2003;21:248-252.
34. Wilhoit SC, Suratt PM. Effect of nasal obstruction on upper
airway muscle activation in normal subjects. Chest. 1987;92:
1053-1055.
35. Milicić D, Mladina R, Djanić D, Prgomet D, Leović. Influence
of nasal fontanel receptors on the regulation of tracheobron-
chal vagal tone. Croat Med J. 1998;39:426-429.
36. Tanaka Y, Honda Y. Nasal obstruction as a cause of reduced
PCO2 and disordered breathing during sleep. J Appl Physiol
(1985). 1989;67:970-972.
37. Nakata S, Noda A, Yasuma F, et al. Effects of nasal surgery
on sleep quality in obstructive sleep apnea syndrome with
nasal obstruction. Am J Rhinol. 2008;22:59-63.
38. Fidan V, Aksakal E. Impact of septoplasty on pulmonary
artery pressure in patients with markedly deviated septum. J
Craniofac Surg. 2011;22:1591-1593.
39. Potsic WP, Pasquariello PS, Baranak CC, Marsh RR, Miller
LM. Relief of upper airway obstruction by adenotonsillectomy.
Otolaryngol Head Neck Surg. 1986;94:476-480.
352
40. Derin S, Akın F, S xahan M, Altun I, _ Sxahin C, Elicxora SS
x.
Impact of markedly nasal septal deviation on 24-hour rhythm
Holter findings. Kulak Burun Bogaz Ihtis Derg. 2015;25:284-288.
41. Okin PM, Devereux RB, Howard BV, Fabsitz RR, Lee ET,
Welty TK. Assesment of QT interval and QT dispersion for pre-
diction of all-cause and cardiovascular mortality in American
Indians: the Strong Heart Study. Circulation. 2000;101:61-66.
Downloaded from oto.sagepub.com at INDIAN RIVER STATE COLLEGE on August 5, 2016
Otolaryngology–Head and Neck Surgery 155(2)
42. Nussinovitch U. Meta-analysis of p-wave dispersion values in
healthy individuals: the influence of clinical characteristics.
Ann Noninvasive Electrocardiol. 2012;17:28-35.
43. Dilaveris PE, Gialafos EJ, Sideris SK, et al. Simple electrocar-
diographic markers for the prediction of paroxysmal idiopathic
atrial fibrillation. Am Heart J. 1998;135:733-738.