Obstrüktif Uyku Apnesi Şiddeti ve PR Süresi Arasındaki İlişki

Year 2016, Volume: 19 Issue: 1, 27 - 31, 04.04.2016

Harun Karamanlı Fatih Aygün Recep Akgedik

Abstract

Giriş: Obstriktif uyku
apnesi (OSA) şiddeti ile elektrokardiyogramdaki PR süresinin genişlemesi
arasındaki ilişki ve PR süresini etkileyebilecek OSA şiddet indeksleri ile
ilişkisi araştırılmıştır.

Hastalar ve Yöntem: Bu çalışma;
kliniğimizde Ocak 2013 ve Ağustos 2014 tarihleri arasında, OSA tanısı almış 85
kişiyi içermektedir. Polisomnografi (PSG) raporları alanında uzman hekim
tarafından değerlendirildi. Şiddetli uyku apne hastalığı olan bireyler grup 1
olarak adlandırılırken, orta, hafif uyku apne hastalığı olan bireyler grup 2
olarak belirlendi.

Bulgular: Çalışmaya
katılan tüm bireylerin yaş dağılımı; minimum 20 yıl, maksimum 85 yıldır
(ortalama ± standart sapma 45.5 ± 13.2 y). Bu kişilerin 51’i (%60) erkek, 34’ü
(%40) kadındır. Polisomnografi şiddetli OSA tanısı alan bireyleri içeren grup
1’de PR süresi 163.1 ± 35.2 milisaniye (ms) iken grup 2’de 147.8 ± 29.3
milisaniye olduğu görüldü.

Sonuç: Şiddetli OSA tanısı alan
bireylerin, hafif ve orta şiddette OSA tanısı alan bireylere göre PR
sürelerinin yüksek olduğu görüldü. Sonucun istatiksel olarak anlamlı olduğu
tespit edildi (p< 0.05, p= 0). OSA şiddeti göstergesi ve
hipoksi-reoksijenizasyon parametreleri olan AHI (apne-hipopne indeksi), ODI
(oksijen desaturasyon indeksi); arousal değerleri PR uzamasında katkı
sağladığına inanmaktayız.

Keywords

PR aralığı süresi, obstrüktif uyku apnesi

Relationship Between Severity of Obstructive Sleep Apnea and PR Interval

Abstract

Introduction:
Relationship between obstructive sleep apnea (OSA)
and electrocardiogram and OSA severity index relationship that may affect the
PR interval were studied.

Patients
and Methods: This study included 85 people who had OSA
diagnosed at our clinic between January 2013 and August 2013. Their
polysomnography (PSG) reports were evaluated by physicians who are expert in
their fields. Individuals with severe OSA diseases were categorized as group 1,
and individuals with mild to moderate OSA were categorized as group 2.

Results: Age
distribution of individuals who participated to the study ranged from 20 years
to 85 years (mean ± standard deviation, 45.5 ± 13.2 years). Fifty-one (60%) of
those individuals were men, and 34 (40%) of them were women. The PR interval
for the group who had severe OSA on PSG (group 1) was 163.1 ± 35.2 ms, and it was
147.8 ± 29.3 in group 2.

Conclusion: It was observed that
individuals having severe OSA had higher PR intervals than individuals who had
mild to moderate OSA. It was determined that results were statistically
significant (p< 0.05, p= 0.032). We believe that apnea-hypopnea index,
oxygen desaturation index, and arousal values, which are indications of OSA
severity and parameters of hypoxia-reoxygenation, contribute to PR
prolongation.

Keywords

PR interval time, sleep apnea obstructive

References

• 1. Bonsignore MR, Marrone O, Insalaco G, Bonsignore G. The cardiovascular effects of obstructive sleep apnoeas: analysis of pathogenic mechanisms. Eur Respir J 1994;7:786-805.
• 2. Fletcher EC, DeBehnke RD, Lovoi MS, Gorin AB. Undiagnosed sleep apnea in patients with essential hypertension. Ann Intern Med 1985;103:190-5.
• 3. Peker Y, Hedner J, Norum J, Kraiczi H, Carlson J. Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7-year follow-up. Am J Respir Crit Care Med 2002;166:159-65.
• 4. Gami AS, Howard DE, Olson EJ, Somers VK. Day-night pattern of sudden death in obstructive sleep apnea. N Engl J Med 2005;352:1206-14.
• 5. Huikuri HV, Castellanos A, Myerburg RJ, Sudden death due to cardiac arrhythmias. N Engl J Med 2001;345:1473-82.
• 6. O’Driscoll DM, Meadows GE, Corfield DR, Simonds AK, Morrell MJ. Cardiovascular response to arousal from sleep under controlled conditions of central and peripheral chemoreceptor stimulation in humans. J Appl Physiol (1985) 2004;96:865-70.
• 7. Otto ME, Belohlavek M, Romero-Corral A, Gami AS, Gilman G, Svatikova A, et al. Comparison of cardiac structural and functional changes in obese otherwise healthy adults with versus without obstructive sleep apnea. Am J Cardiol 2007;99:1298-302.
• 8. Chung M-H, Kuo TBJ, Hsu N, Chu H, Chou K-R, Yang CCH. Sleep and autonomic nervous system changes - enhanced cardiac sympathetic modulations during sleep in permanent night shift nurses. Scand J Work Environ Health 2009;35:180-7.
• 9. Bitter T, Horstkotte D, Oldenburg O. [Sleep disordered breathing and cardiac arrhythmias: mechanisms, interactions, and clinical relevance]. Dtsch Med Wochenschr 2011;136:431-5.
• 10. Maeno K, Kasagi S, Ueda A, Kawana F, Ishiwata S, Ohno M, et al. Effects of obstructive sleep apnea and its treatment on signal-averaged P-wave duration in men. Circ Arrhythm Electrophysiol 2013;6:287-93.
• 11. Somers VK, Dyken ME, Mark AL, Abboud FM. Parasympathetic hyperresponsiveness and bradyarrhythmias during apnoea in hypertension. Clin Auton Res 1992;2:171-6.
• 12. Armour JA, Richer LP, Pagé P, Vinet A, Kus T, Vermeulen M, et al. Origin and pharmacological response of atrial tachyarrhythmias induced by activation of mediastinal nerves in canines. Auton Neurosci 2005;118:68-78.
• 13. Budeus M, Hennersdorf M, Felix O, Reimert K, Perings C, Wieneke H, et al. Prediction of atrial fibrillation in patients with cardiac dysfunctions: P wave signal-averaged ECG and chemoreflexsensitivity in atrial fibrillation. Europace 2007;9:601-7.
• 14. Burstein B, Nattel S. Atrial fibrosis: mechanisms and clinical relevance in atrial fibrillation. J Am Coll Cardiol 2008;51:802-9.