Σύνδρομο σπνικής άπνοιας. Ποιός o ρόλος ηοσ ζηη γένεζη και ανηιμεηώπιζη ηων αρρσθμιών;

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1 Σύνδρομο σπνικής άπνοιας. Ποιός o ρόλος ηοσ ζηη γένεζη και ανηιμεηώπιζη ηων αρρσθμιών; E.N. Σημανηηράκης MD, FESC Επίκ. Καθηγηηής Καρδιολογίας Πανεπιζηημιακό Νοζοκομείο Ηρακλείοσ

2 Epidemiology 4% 2% 24% 9% 4% of men and 2% of women aged have diagnosed sleep apnea 24% of men and 9% of women aged have undiagnosed sleep-disordered breathing Young T et al. N Eng J Med 1993;328:

3 Sleep Apnea Syndrome Apnea is the cessation of airflow at the nose or the mouth for at least 10 seconds, followed by arousal and oxygen desaturation of at least 4 %. Hypopnea is a 50% reduction in airflow for at least 10 seconds, followed by arousal and/or oxygen desaturation of at least 4%. Types of SAS Obstructive Sleep Apnea Central Sleep Apnea Mixed Sleep Apnea

4 Obstructive Sleep Apnea OSA is described as repetitive episodes of complete or partial upper airway obstruction during sleep (respiratory efforts persist) As a result affected persons have unrestful sleep and excessive daytime sleepiness

5 Central Sleep Apnea The second most common breathing disorder during sleep. Loss of inspiratory airflow, but it occurs because of a loss of phasic diaphragmatic activity (both airflow and respiratory efforts are absent) Affects more than 50% of patients with CHF

6 Sleep Apnea Syndrome Cardiovascular Consequences

7 Sleep Apnea Syndrome Main Pathophysiological Characteristics that may affect CVS Negative intrathoracic pressure Apnoea induced hypoxia Arousals

8 Sleep Apnea Syndrome Other Pathophysiological Effects Endothelial dysfunction (endothelin 1 etc) Increase in inflammatory mediators (CRP, Interleukin 6, oxidative stress) Increase in coagulation factors (Fibrinogen, PA inhibitor)

9 Sleep Apnea Syndrome Arrhythmias Sinus arrest Sinoatrial block Atrioventricular block Supraventricular tachycardia Atrial fibrillation Ventricular Arrhythmias

10 Sleep Apnea Syndrome Mechanisms of Rhythm Disturbances Hypoxia, Hypercapnia ANS disturbances Increased negative intrathoracic pressure Increased inflammation markers

11 Sleep Apnea Syndrome Rhythm Disturbances - Mechanisms CSR-CSA provokes ventricular ectopy that is most pronounced during the hyperpnoic phase Mechanisms Increased sympathetic activity Increased HR Negative intra-thoracic pressure Increase in inflammatory indices Leung RST. et al, Sleep 2004

12 Sleep Apnea Syndrome Predisposition factors for arrhythmias The severity of the syndrome Excessive obesity Severe arterial blood desaturation Harbison J, Chest 2000;118:591-5

13 Normal Sleep Rhythm Disturbances ECG Incidence VPS in nolmals 0-12% VT in nolmals 0-4% Guilleminault C, Am J Cardiol 1983:52

14 Sleep Apnea and Arrhythmias Rhythm Disturbances In individuals with sleep-disordered breathing, the entire spectrum of arrhythmias appears to be increased 20% 18% 20% 16% 14% 12% 11% 10% Overall8% 46-58% 8% 7% 7% 6% Sinus Brady/pauses 4% % 4% 3% 2% 0% Reported rates of cardiac arrhythmias in patients with SA AF 49% VT 2% Sinus arrest AVB II Sinus brady AT PAF VT PVC Guilleminault C, Am J Cardiol 1983:52

15 Incidence of cardiac arrhythmias in SAS patients Limitations The vast majority of published data are based on 18-24h Holter recordings There is much discrepancy regarding the incidence of arrhythmic episodes Reported incidence of brady-arrhythmic episodes and sinus pauses ranges from 5%-50% in various studies

16 The aim of this study was to clarify the incidence of brady- and tachy-arrhythmias, their relation to the severity of the disease, other anthropometric and clinical parameters and whether they exhibit intra-individual variation evaluate rhythm disturbances in OSAHS patients before and after CPAP treatment by using ILR in order to monitor cardiac rhythm for at least 16 months investigate the acute and mainly, the long-term impact of CPAP treatment on the occurrence of cardiac rhythm disturbances in such patients European Heart Journal 2004; 25:

17 Total follow-up period:16 months 23 patients 83% with severe OSAHS 17% with moderate OSAHS Exclusion criteria hypertension, diabetes mellitus, SSS, AV-conduction abnormalities, indications of CAD, DCM, HCM, valvular heart disease, history of respiratory failure or lung disease that might have led to structural or functional pulmonary dysfunction, or use of cardioactive medication, hypnotics or drugs affecting sleep

18 Weekly fluctuations of cardiac pauses and bradycardic episodes in SAS patients ILR compared to Holter monitoring revealed cardiac rhythm disturbances in 47% vs 13% of patients Median number of bradycardias per patient decreased drastically from 5.5 for the 8- week pre-treatment period to 0.5 for the 8-week period following treatment (P=0,028) Median number of pauses per patient also showed a downward trend, falling from 1 for the 8-week pre-treatment period to 0 for the post-treatment period (P=0,089) European Heart Journal 2004; 25:

19 12 seconds of asystole doue to CHB in a patient with severe SAS Reveal Recording

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22 Paced patients and SAS There is a high prevalence of SAS in paced patients (up to 59%) Garrigue et al, Ciculation 2007 Pacemaker s sensor (MV) allows monitoring of respiratory cycles, detecting apnoic events on a 24-h basis Pacemaker s Holter provides high quality recordings of cardiac rhythm disturbances on a 24-h basis

23 Paced patients and SAS Clinical Implications Screening and monitoring SDB in patients having a PM with a MV sensor with low cost Detection of Cheyne-Stokes respiration in patients with CHF Assessment of therapeutic effect of pacing or CPAP Prospective exploration of the relationship between respiratory events and cardiac rhythm disturbances

24 AOP at 15 bpm over mean nocturnal HR reduced AHI by more than 50%

25 AOP at 15 bpm over mean nocturnal HR reduced AHI by more than 50%

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27 Comments Main differences in basic characteristics The discrepancy of our results and those of Garrigue Garrigue et et al al. are attributed insimantirakis the different et al. study population 1. Mild impairment of LVF 1. Normal LVF 2. Mixed type of SAS 2. Obstructive type of SAS Our findings are in agreement with four recently published studies that included patients with similar characteristics Pepin J-L et al. European Respiration Journal 2005 Luthje L, et al. Am J Respir Crit Care Med Unteberg C et al. European Heart Journal 2005 Krahn AD,et al, JACC 2006; 47:379-83

28 Incidence of AF based on presence or absence of OSA in patients <65 years old Incidence of AF based on body mass index in OSA patients<65 years old Obesity and the magnitude of nocturnal oxygen desaturation (consequence of OSA) are independent risk factors for incident AF in individuals <65 years of age Neither obesity nor OSA, predicted incident AF in subjects 65 years old JACC 2007;49:565 71

29 Proportion of patients with OSA was significantly higher in the AF group than in the general cardiology group (49% versus 32%, P=0.0004) OSA is strikingly more prevalent in patients with AF than in high-risk patients with multiple other cardiovascular diseases Circulation 2004;110:

30 Recurrence rate of AF at 12 months 82% in 27 untreated or inappropriately treated subjects with OSA 42% in the treated OSA group (P=0.013) 53% in the control group without known OSA (P=0.009) Patients with untreated OSA have a higher recurrence of AF after cardioversion than patients without a polysomnographic diagnosis of sleep apnea Appropriate treatment with CPAP in OSA patients is associated with lower recurrence of AF Circulation 2003;107:

31 Comparison of AF recurrence after catheter ablation in pts with OSA and non-osa controls Pts with OSA have significantly greater AF recurrence rates after pulmonary vein isolation. Am J Cardiol 2011

32 116 of 153 pts who underwent AF ablation were identified as having OSA During a mean follow-up period of 18.8±10.3 months, 51 patients (33%) experienced AF recurrences after the ablation Concomitant OSA increased the risk 261% while the use of CPAP reduced the risk of recurrence 59% (p<0.05 and p<0.01, respectively). Naruse Y et al, Heart Rhythm 23/11/2012

33 Patients with OSA have a peak in SCD during the sleeping hours, in contrast to the nadir of SCD during this period in patients without OSA and in the general population (46% vs 21% vs 16%) N Engl J Med 2005;352:

34 RR for SCD from midnight to 6 a.m. in patients with OSA is proportional to the severity of OSA 1.87 in mild-to-moderate OSA 2.61 in severe OSA N Engl J Med 2005;352:

35 CSA is highly prevalent in patients with asymptomatic LV dysfunction Severe CSA is associated with impaired cardiac autonomic control (heart rate variability was markedly depressed in patients with CSA) increased cardiac arrhythmias Circulation 2003;107:

36 In pts with CHF, CSA and OSA are independently associated with an increased risk for ventricular arrhythmias and appropriate cardioverter-defibrillator therapies. Bitter T et al, Eur H J 2011

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38 Ventricular arrhythmias in patients with and those without sleep-disordered breathing according to the time of day. Patients with an ICD and SDB have a striking increase in the onset of life-threatening ventricular arrhythmic events during sleeping hours. Heart Rhythm 2011

39 In these pts if device interrogation reveals a predominance of nocturnal onset of arrhythmias, SDB screening is highly recommended. Whether or not treatment of SDB reduces the risk of appropriate ICD therapy, awaits to be investigated. Heart Rhythm 2011

40 In CHF patients, sleep apnoea induces cardiac electrical instability manifested as TWA, reflecting increased risk of nocturnal SCD.

41 Distribution of ST-segment changes according to changes in sleep stages. Pts with Brugada syndrome have a high prevalence of SDB even in the setting of normal BMI. 56% ST-segment changes occurred during or within 1 minute after an episode of apnea or hypopnea. Am J Cardiol 2011

42 The higher incidence of nocturnal death in pts with Brugada syndrome may be conceivably related to comorbid SDB. Autonomic instability encountered in rapid eye movement sleep and arousals could potentiate the risk of arrhythmias. Am J Cardiol 2011

43 Conclusions Cardiac rhythm disturbances are frequent in patients with SAHS Although many well known pathophysiological mechanisms are responsible, their prognostic significance is not clear In any case, the effective treatment of the syndrome, alleviates the SDB-related arrhythmias

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