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 Table of Contents  
ORIGINAL ARTICLE
Year : 2020  |  Volume : 8  |  Issue : 2  |  Page : 69-73

Predictors of impending cardiac arrhythmias by electrocardiographic markers in proven obstructive sleep apnea patients


1 Department of General Medicine, Sri Manakula Vinayagar Medical College and Hospital, Puducherry, India
2 Department of General Medicine, Mahatma Gandhi Medical College and Hospital, Puducherry, India

Date of Submission19-Mar-2020
Date of Decision06-Jun-2020
Date of Acceptance18-Jun-2020
Date of Web Publication4-Aug-2020

Correspondence Address:
Dr. J Karthik
Department of General Medicine, Sri Manakula Vinayagar Medical College and Hospital, Kalitheerthalkuppam, Puducherry - 605 107
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/heartindia.heartindia_12_20

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  Abstract 


Background: Obstructive sleep apnoea is proved to be one of the causes of sudden cardiac death due to undocumented transient cardiac arrhythmias.So we studied the changes in various electrocardiographic parameters (P wave duration, QRS duration and Tpeak to Tend interval) and its association with increasing severity of OSA by AHI to predict the risk of impending cardiac atrial and ventricular arrhythmias in these patients.
Objective: This study compares the risk of impending cardiac arrhythmias by electrocardiographic parameters with the increasing severity of obstructive sleep apnoea by AHI (apnoea-hypopnea index) in polysomnnography.
Methodology: The study was conducted in a rural based teaching tertiary care hospital in Puducherry,India. The electrocardiogram(ECG) of the 30 proven OSA patients were analysed for parameters like P wave duration, QRS duration and peak of T wave to end of T wave interval. Any deviation from the normal duration is recorded and compared with the severity of OSA by AHI to estimate the risk of arrhythmogenicity
Results: Out of 30 OSA patients in the study group 7 (23.3%) were found to have mild OSA [i.e AHI= 5 TO 14 events/hr] , 6 (20%) were found to have moderate OSA [i.e AHI=15 to 29 events/hr] and 17(56.7%) were found to have severe OSA[i.e AHI=30 and above]. The p value is significant [<0.001] for electrocardiographic parameters like Tp-Te interval and P wave duration in patients with AHI more than 15 events/hr [i.e moderate and severe OSA] and p value for QRS duration is 0.162 .
Conclusion: We concluded that the increase in duration of P wave, QRS duration and prolongation of Tp-Te interval in electrocardiogram is associated with increasing severity of obstructive sleep apnoea tends to possess significant risk of developing impending cardiac atrial and ventricular arrhythmias respectively which can be attributed to one of the causes of sudden cardiac death in OSA patients.

Keywords: Apnea hypopnea index, obstructive sleep apnea, P-wave duration, QRS duration, Tp-Te interval


How to cite this article:
Badrinath A K, Viswanathan K N, Babu S S, Yogaraja V, Karthik J. Predictors of impending cardiac arrhythmias by electrocardiographic markers in proven obstructive sleep apnea patients. Heart India 2020;8:69-73

How to cite this URL:
Badrinath A K, Viswanathan K N, Babu S S, Yogaraja V, Karthik J. Predictors of impending cardiac arrhythmias by electrocardiographic markers in proven obstructive sleep apnea patients. Heart India [serial online] 2020 [cited 2020 Oct 31];8:69-73. Available from: https://www.heartindia.net/text.asp?2020/8/2/69/291352




  Introduction Top


Obstructive sleep apnea (OSA) is the most common type of sleep apnea caused by complete or partial obstruction of the upper airway. It is characterized by repetitive shallow pauses in breathing in spite of efforts to breathe normally. If the symptoms are present in day time also, then it is referred to as OSA syndrome (OSAS). Symptomatic OSAS has been proven to be a risk factor for hypertension, heart failure, and vascular dysfunction and has been proposed to be causally related to both nonfatal and fatal coronary and cerebrovascular events. Preliminary data suggest that there is also a relationship between sleep-disordered breathing, cardiac arrhythmias, and sudden cardiac death.[1]

OSA has mainly been associated with premature atrial complex short runs, sinus bradycardia, sinus pauses, premature ventricular complexes, and paroxysmal atrial fibrillation (PAF), while central sleep apnea (CSA) has mainly been associated with atrial fibrillation. There is also evidence for a close temporal relationship between arrhythmias and OSA.

Searches of bibliographical databases revealed that several mechanisms seem to underpin the association between OSA and cardiac arrhythmias: (1) intermittent hypoxia associated with autonomic nervous system activation and increased oxidative stress, which may lead to cardiac cellular damage and alteration in myocardial excitability, (2) recurrent arousals, resulting in sympathetic activation and coronary vasoconstriction, and (3) increased negative intrathoracic pressure which may mechanically stretch the myocardial walls, and thus, promote acute changes in myocardial excitability as well as structural remodeling of the myocardium.[2],[3],[4]

The Tp-Te is a measure of cardiac transmural dispersion of repolarization, which is explained by a gradient of action potential duration from subendocardial M cells (longest) to epicardial cells (shortest). A prolonging of the Tp-Te interval to >100 ms in electrocardiogram (ECG) is proposed to be associated with increased vulnerability for the occurrence of early after depolarizations, and thus, ventricular tachycardia and sudden cardiac death.[5],[6]

The QT interval represents the electrocardiographic correlate of ventricular depolarization and repolarization, including the vulnerable period for reentry tachycardia, and it is considered a marker of ventricular electrical instability and a risk factor for the occurrence of malignant cardiac arrhythmias and sudden cardiac death. Previous studies explained pathophysiologic mechanisms suggest that apneic episodes in OSA are associated with significant QT prolongation (>120 ms) due to increased vagal activity.[7],[8],[9]

A prolonged P-wave duration (>120 ms) has been reported to be a prognostic factor for the occurrence of PAF, a condition linked to obstructive sleep apnea (OSA). Patients with OSA have been shown to have electrical abnormalities in electrophysiological mapping studies, such as longer P-wave duration, prolonged conduction times and longer sinus node recovery, as well as mechanical alterations, such as atrial enlargement and interatrial and intraatrial electromechanical delay, compared with controls. These observations suggest that patients with OSA may have an increased susceptibility to develop atrial fibrillation.[10],[11],[12],[13]


  Materials and Methods Top


Study area and design

A cross-sectional study conducted at the rural-based teaching tertiary care hospital in Puducherry from March 2019 to September 2019 for a period of 7 months. This study had been cleared by the Institutional Research and Ethics Committee.

Study participants

Patients chosen for study after getting informed consent were those all patients who are admitted with OSA and diagnosed based on polysomnography between the age group of 20–70 years. Those using medications such as antihistamines and beta blockers, OSA patients with known coronary artery disease, OSA patients with known chronic kidney disease, OSA patients with infection/sepsis/dyselectrolytemia were excluded since these factors can provoke arrhythmogenesis.

Methodology

The ECG of the 30 proven OSA patients were analyzed for parameters such as P-wave duration (normal is <100 ms), QRS duration (80–120 ms), and peak of T-wave to end of T-wave interval (Tp-Te <100 ms). Any deviation from the normal duration is recorded and compared with the severity of OSA by apnea hypopnea index (AHI) to estimate the risk of impending arrhythmogenicity.

Statistical analysis

Data were entered into the Microsoft excel data sheet and were analyzed using the SPSS 22 version software (IBM, Armonk, New york, USA). Categorical data were represented in the form of frequencies and proportions. The Chi-square test was used as the test of significance for the qualitative data. Continuous data were represented as mean and standard deviation. Independent t-test was used as the test of significance to identify the mean difference between two quantitative variables. MS Excel and MS Word were used to obtain the various types of graphs such as bar diagram.


  Results Top


A total of 30 OSA patients were selected in this study. Among 30 OSA patients, 24 were male and 6 were female [Table 1]. Majority of patients were in the mean age group of 47.4 years [Table 2]. Among the behavioral characteristics studied, 16.7% were alcoholic and 46.7% were smoker. Among 30 OSA patients, the mean BMI was 30.4 kg/m2.
Table 1: Baseline characteristics of the study population

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Table 2: Descriptive statistics of various parameters

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Out of 30 OSA patients in the study group, 7 (23.3%) were found to have mild OSA (i.e., AHI = 5 TO 14 events/h), 6 (20%) were found to have moderate OSA (i.e., AHI = 15 to 29 events/h], and 17 (56.7%) were found to have severe OSA (i.e., AHI = 30 and above).

  • The interquartile range for Tp-Te interval, QRS duration, and P-wave duration was 80–120 ms, 80-100 ms, and 100-110 ms, respectively. The mean value was 106.3 ms, 99 ms, and 102 ms, respectively
  • Among 7 mild OSA patients (AHI = 5 to 14 events/h), the mean percentage of Tp-Te interval, QRS duration, and P-wave duration were 0%, 10.7%, and 10.7%, respectively
  • Among 6 moderate OSA patients (AHI = 15 to 29 events/h), the mean percentage of Tp-Te interval, QRS duration, and P-wave duration was 15.2%, 9.8%, and 11.0%, respectively
  • Among 17 severe OSA patients (AHI more than or equal to 30 events/h), the mean% of Tp-Te interval, QRS duration, and P-wave duration were 4.4%, 23.3%, and 9.5%, respectively [Table 3].


The P < 0.001 for electrocardiographic parameters such as Tp-Te interval and P-wave duration in patients with AHI more than 15 events/h (i.e., moderate and severe OSA) and P value for QRS duration is 0.162 [Table 4].
Table 3: Comparison of electrocardiogram parameters and severity of obstructive sleep apnea

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Table 4: No of patients in varying AHI severity with abnormal various ECG parameters

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  • The Tp-Te interval is significantly prolonged in patients with severe OSA (AHI >30 events/h) with P < 0.001 [Table 4] when compared with moderate and mild OSA [Figure 1]
  • The QRS duration is prolonged only in 7 out of 30 patients with severe OSA (AHI >30 events/h) with no statistical significance (P = 0.162) [Table 4]
  • The P-wave duration is significantly prolonged in 13 out of 30 patients with severe OSA (AHI >30 events/h) with P < 0.001 [Table 4].
Figure 1: Line diagram showing the relationship between various electrophysiological predictors of impending arrhythmias and severity of obstructive sleep apnea

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  Discussion Top


Although causality between OSA and arrhythmia has yet to be established, emerging data have identified the range of mechanistic pathways that may increase the propensity of cardiac arrhythmogenesis in OSA. These pathways are complex, multidirectional, and potentially synergistic. OSA and AF have shared the risk factors and consequences (i.e., increasing age, obesity, and hypertension) that may act together to increase cardiovascular risk.

OSA-related autonomic nervous system fluctuations typified by enhanced parasympathetic activation during respiratory events and sympathetic surges subsequent to respiratory events, which contribute to augmented arrhythmic propensity. Other more immediate pathophysiologic influences of OSA-enhancing arrhythmogenesis include intermittent hypoxia, intrathoracic pressure swings leading to atrial stretch, and hypercapnia. Intermediate pathways by which OSA may trigger arrhythmia include increased systemic inflammation, oxidative stress, enhanced prothrombotic state, and vascular dysfunction. Long-term OSA-associated sequelae such as hypertension, atrial enlargement and fibrosis, ventricular hypertrophy, and coronary artery disease also predispose to cardiac arrhythmias. These factors can lead to a reduction in atrial effective refractory period, triggered and abnormal automaticity, and promote slowed and heterogeneous conduction; all of these mechanisms increase the persistence of reentrant arrhythmias.[1],[2],[3],[4]

In our study, the prevalence of prolongation of T-peak to T-end interval (>100 ms) among 30 OSA patients was significantly higher with significant P < 0.001, this study results was very similar with other study done by Panikkath et al. in 2011[5] and by Kors et al.in 2008[6] and Watanabe et al. in 2004.[7] However, our study showed a higher prevalence when compared to other studies. In this study, the prolongation of Tp-Te interval was seen in females also since the incidence of OSA is very low in females. Tp-Te interval corresponds with transmural dispersion of repolarization in the ventricular myocardium. The early after depolarizations can lead to reentry and its perpetuation, resulting in polymorphic ventricular tachycardia or ventricular fibrillation. Hence, a prolonged Tp-Te interval could increase the risk of ventricular arrhythmogenesis.[5],[6]

Prolonged P-wave duration (>100 ms) is seen in severe OSA patients having AHI more than 15 events/h with significant P value < 0.001 which was studied also by Kanagala R et al. in 2003 and by Gami et al. in 2004 indicating atrial conduction delay, a potent precursor of atrial fibrillation were studied only in male population, whereas our study showed significant results in female participants also [Figure 1].[10],[11],[12],[13],[14],[15]

The prolongation of QRS duration is not statistically significant with P value of 0.162 among 30 OSA patients. Previous studies done by Dhingra in 2005[8] and by Morin et al. in 2009[9] shown that patients develop greater left ventricular hypertrophy in response to OSA, leading to greater QRS prolongation which could lead to the high risk of developing ventricular tachyarrhythmias.


  Conclusion Top


Among 30 OSA patients, the prevalence of prolonged Tp-Te interval and prolonged P-wave duration was more in severe OSA (i.e., with AHI >30 events/h) which attributes to the high risk of developing ventricular tachyarrhythmias due to dispersion of transmural cardiac repolarization and atrial tachyarrhythmias due to atrial conduction abnormalities, respectively. Our study also showed significant results in the female population with OSA when compared to other studies.

Tp-Te interval and prolonged P-wave duration were statistically significant (P < 0.001) and independently associated with increased risk of SCD (sudden cardiac death) among participants with severe OSA (i.e., with AHI >30 events/h), whereas even though prolongation of QRS duration (>120 ms) was seen in severe OSA patients, but no statistical significance could be obtained (i.e., P = 0.162) in this study.

Prolonged P-wave duration in severe OSA suggests that OSA may cause an atrial conduction delay, possibly by left atrial overload or remodeling by its related pathophysiological effects, leading to an increased risk of atrial fibrillation. The effect of changes in QRS duration and Tp-Te interval in OSA patients increases the risk of impending ventricular tachyarrhythmias.

Hence, risk stratification to be made to those patients and warrants immediate evaluation in larger populations to prevent the impending risk of cardiac arrhythmias by periodic holter monitoring and regular follow-up. This may be modifiable by alleviating OSA with CPAP (continuous positive airway pressure) therapy and home BiPAP (Bilevel positive airway pressure) therapy.

Limitations

The first was the relatively small number of participants (sample size = 30) since the feasibility of getting proven OSA patients without the factors mentioned in the above exclusion criteria is very difficult.

The statistical correlation was significant only for Tp-Te interval with P < 0.001, whereas no significant correlation was obtained for QRS duration (P = 0.162) in this study.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Ethical Approval

This study cleared by institutional ethics committee.



 
  References Top

1.
Namtvedt SK, Randby A, Einvik G, Hrubos-Strøm H, Somers VK, Røsjø H, et al. Cardiac arrhythmias in obstructive sleep apnea (from the Akershus Sleep Apnea Project). Am J Cardiol 2011;108:1141-6.  Back to cited text no. 1
    
2.
Koshino Y, Satoh M, Katayose Y, Yasuda K, Tanigawa T, Takeyasu N, et al. Association of sleep-disordered breathing and ventricular arrhythmias in patients without heart failure. Am J Cardiol 2008;101:882-6.  Back to cited text no. 2
    
3.
Peng Y, Yuan G, Overholt JL, Kumar GK, Prabhakar NR. Systemic and cellular responses to intermittent hypoxia: Evidence for oxidative stress and mitochondrial dysfunction. Adv Exp Med Biol 2003;536:559-64.  Back to cited text no. 3
    
4.
Prabhakar NR, Kumar GK. Oxidative stress in the systemic and cellular responses to intermittent hypoxia. J Biochem 2004;385:217-21.  Back to cited text no. 4
    
5.
Panikkath R, Reinier K, Uy-Evanado A, Teodorescu C, Hattenhauer J, Mariani R, et al. Prolonged Tpeak-to-tend interval on the resting ECG is associated with increased risk of sudden cardiac death. Circ Arrhythm Electrophysiol 2011;4:441-7.  Back to cited text no. 5
    
6.
Kors JA, Ritsema van Eck HJ, van Herpen G. The meaning of the Tp-Te interval and its diagnostic value. J Electrocardiol 2008;41:575-80.  Back to cited text no. 6
    
7.
Watanabe N, Kobayashi Y, Tanno K, Miyoshi F, Asano T, Kawamura M, et al. Transmural dispersion of repolarization and ventricular tachyarrhythmias. J Electrocardiol 2004;37:191-200.  Back to cited text no. 7
    
8.
Dhingra R, Ho Nam B, Benjamin EJ, Wang TJ, Larson MG, D'Agostino RB Sr., et al. Cross-sectional relations of electrocardiographic QRS duration to left ventricular dimensions: The Framingham Heart Study. J Am Coll Cardiol 2005;45:685-9.  Back to cited text no. 8
    
9.
Morin DP, Oikarinen L, Viitasalo M, Toivonen L, Nieminen MS, Kjeldsen SE, et al. QRS duration predicts sudden cardiac death in hypertensive patients undergoing intensive medical therapy: The LIFE study. Eur Heart J 2009;30:2908-14.  Back to cited text no. 9
    
10.
Gami AS, Pressman G, Caples SM, Kanagala R, Gard JJ, Davison DE, et al. Association of atrial fibrillation and obstructive sleep apnea. Circulation 2004;110:364-7.  Back to cited text no. 10
    
11.
Gami AS, Hodge DO, Herges RM, Olson EJ, Nykodym J, Kara T, et al. Obstructive sleep apnea, obesity, and the risk of incident atrial fibrillation. J Am Coll Cardiol 2007;49:565-71.  Back to cited text no. 11
    
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Khan A, Latif F, Hawkins B, Tawk M, Sivaram CA, Kinasewitz G. Effects of obstructive sleep apnea treatment on left atrial volume and left atrial volume index. Sleep Breath 2008;12:141-7.  Back to cited text no. 12
    
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Kanagala R, Murali NS, Friedman PA, Ammash NM, Gersh BJ, Ballman KV, et al. Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation 2003;107:2589-94.  Back to cited text no. 13
    
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Guilleminault C, Connolly SJ, Winkle RA. Cardiac arrhythmia and conduction disturbances during sleep in 400 patients with sleep apnea syndrome. Am J Cardiol 1983;52:490-4.  Back to cited text no. 14
    
15.
Somers VK, Dyken ME, Clary MP, Abboud FM. Sympathetic neural mechanism in obstructive sleep apnea. J Med Physiol 1995;96:1897-904.  Back to cited text no. 15
    


    Figures

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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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