DRS ed Aritmie Cardiache Iper ed Ipocinetiche: la clinica

Transcription

1 Corso Multidisciplinare di Aggiornamento La Sindrome delle Apnee Notturne: una sfida diagnostico terapeutica DRS ed Aritmie Cardiache Iper ed Ipocinetiche: la clinica FRANCESCO PERNA, MD, PhD Laboratorio di Elettrofisiologia Cardiaca Policlinico Gemelli, Università Cattolica del Sacro Cuore, Roma Roma, 15 Novembre 2012

2 Conflitti di interesse Nessuno

3 SDB and arrhythmias Epidemiology Important pathophysiological and epidemiological relationships have been identified between OSA and clinically significant arrhythmias, including bradyarrhythmias, SVA/atrial fibrillation (AF) and sudden cardiac death (SCD). The Sleep Heart Health Study Mehra R et al. Am J Respir Crit Care Med 2006;173:910 6

4 SDB and arrhythmias Epidemiology Sleep Heart Health Study (SHHS): Risk of AF x4 Risk of NSVT x3 Risk of complex PVCs x2 Odds of an arrhythmic event after a hypopneic or apneic episode x18 than after normal breathing 1. Mehra R et al. Am J Respir Crit Care Med 2006;173: Monahan K et al, J Am Coll Cardiol. 2009;54:

5 SDB and arrhythmias Pathophysiology Chan KH and Wilcox I, Expert Rev Cardiovasc Ther 2010;8(7):

6 Intrathoracic pressure change due to airway obstruction Atrial enlargement Ventricular remodeling Ventricular stiffness - 65 mmhg - 65 mmhg Right heart overload

7 SDB and arrhythmias Pathophysiology Acute changes Chronic changes Hypoxemia Sympathetic surge Parasympathetic surge Myocardial ischemia Intrathoracic pressure fluctuations with cardiac wall stress Increased afterload Oxidative stress, endot. dysf Chronically increased sympathetic activity Hypertension Atrial & ventricular remodeling Systemic inflammation Hypercoagulability LV syst & diast dysfunction

8 SDB and bradyarrhythmias Diving reflex Apnea-induced hypoxemia causes: Peripheral resistance (Symp) Heart rate (PS) Ludka O, Tex Heart Inst J 2011;38(4):

9 SDB and bradyarrhythmias OSA >> healthy subjects (5-50 %) Most patients: sinus bradycardia About 10%: asystole or AV block More likely with SpO2 drop 4% EP parameters: normal while awake CPAP may reverse the bradyarrhythmias

10 SDB and bradyarrhythmias OSA >> healthy subjects (5-50 %) Most patients: sinus bradycardia About 10%: asystole or AV block More likely with SpO2 drop 4% NO SAS SAS EP parameters: normal while awake CPAP may reverse the bradyarrhythmias 98 patients with pacemaker screened for SA w ESS & PSG 57 pts (59%) has SA 50% of HF pts 68% of AVB pts 58% of SND 21% had severe SA SAS should be systematically searched in these pts Whether treating SAS would have changed the need for pacing is unknown Garrigue S et al, Circ 2007;115:

11 Positive effect of CPAP on bradyarrhythmias in SDB patients N bradycardias N pauses on CPAP on CPAP % of pts with pauses and brady on CPAP Simantirakis EN, Eur Heart J 2004;25:

12 Atrial Overdrive Pacing (AOP) in the treatment of SDB This meta-analysis based on 10 randomized controlled trials indicates that AOP probably does reduce the AHI, but only by 4.65 episodes/h. This treatment effect is very modest, and is much smaller than that seen with CPAP. Baranchuk A et al, Europace (2009) 11,

13 Atrial Overdrive Pacing (AOP) in the treatment of SDB we have found no clinical benefit from pacing in SA with the purpose of improving a breathing disorder AOP should not be considered an alternative to CPAP in the treatment of patients with SA This meta-analysis based on 10 randomized controlled trials indicates that AOP probably does reduce the AHI, but only by 4.65 episodes/h. This treatment effect is very modest, and is much smaller than that seen with CPAP. Baranchuk A et al, Europace (2009) 11,

14 SDB and bradyarrhythmias Most subjects with bradyarrhythmias should be investigated for OSA (Polysomnography) The first line of treatment for bradyarrhythmias in the setting of OSA is treatment of the OSA (CPAP)

15 SDB and atrial fibrillation 1983: relationship between OSA and AF - observational study of 400 adults 1998: confirmed by 2 controlled studies More recently, prospective studies confirmed independent association Exact pathophysiological link not known SA can predict: - Lifetime risk of developing AF - Postoperative AF (CABG): x2 - AF recurrence after electrical CV - AF recurrence after cath ablation Kanagala Gami AS et al, Circulation J Am Coll Cardiol 2003;107: ;49:565.

16 SDB and atrial fibrillation 1983: relationship between OSA and AF - observational study of 400 adults 1998: confirmed by 2 controlled studies More recently, prospective studies confirmed independent association Exact pathophysiological link not known SA can predict: - Lifetime risk of developing AF - Postoperative AF (CABG): x2 - AF recurrence after electrical CV - AF recurrence after cath ablation Control: 53% No CPAP: 82% CPAP: 42% Kanagala Gami AS et al, Circulation J Am Coll Cardiol 2003;107: ;49:565.

17 SDB and atrial fibrillation Response to antiarrhythmic drugs in AF patients with SDB Monahan K et al, Am J Cardiol 2012;110(3): Chronically heightened sympathetic activity, even during the waking period, might also hinder pharmacologic rate-control strategies (Somers VK, J Clin Invest 1995;96(4): )

18 OSA as a predictor of AF recurrence after catheter ablation Patel D et al, Circ Arrhythm Electrophysiol. 2010;3: CPAP improves PVAI success rates OSA patients 25% greater risk of AF recurrence after catheter ablation Ng CY et al, Am J Cardiol 2011; 108:47 51.

19 SDB and atrial fibrillation SDB has been recognized as a predisposing factor to atrial tachyarrhythmias, especially AF Less strong association with atrial flutter OSA does not predict AFL recurrence after ablation (van Oosten E et al, J Interv Card Electrophysiol 2011) At present, there is no clear evidence for differentiating medical treatment for nighttime as compared with daytime atrial fibrillation. Individuals with nocturnal onset of atrial fibrillation should be monitored for the presence of SDB (polysomnography), which can be effectively treated by CPAP

20 SDB and ventricular arrhythmias patients with SDB patients without SDB The Sleep Heart Health Study >25% with severe SA have complex ventricular ectopy >5% NSVT during sleep. (x3 risk) Independent of related comorbidities Mehra R et al, Am J Respir Crit Care Med 2006; ;173:

21 SDB and malignant ventricular arrhythmias in heart failure patients Time to first appropriate implantable defibrillator therapy Bitter T et al, European Heart Journal 2011;32:61 74

22 Rossi V et al, European Heart Journal 2012;33: CPAP withdrawal and repolarization Subtherapeutic CPAP Therapeutic CPAP

23 Day-night pattern of SCD in OSA AHI OSA is associated with an increased risk of SCD, particularly at night Gami AS et al, N Engl J Med 2005;352:1206.

24 SDB and ventricular arrhythmias SDB may reduce/eliminate protective effects of sleep on ventricular irritability (arrhythmia suppression) Increased incidence of myocardial infarction, LV remodeling, systolic and diastolic dysfunction CPAP therapy is recommended in heart failure patients with coexisting OSA on behalf of an enhanced prognosis Studies suggest a positive effect on ventricular irritability, but conclusive evidence for a protective effect of CPAP on the occurrence of malignant arrhythmias in patients with OSA is lacking

25 Clinical case 58 yo male BMI 26 Kg/m^2 NIDCM LVEF 30% >25000 PVCs, drug-refractory Dryness of mouth Snoring Daytime sleepiness Vitulano N et al, J Cardiovasc Med 2009 Dec 7

26 Clinical case 2 Polysomnography AHI : 33/h SO 2 <90%: 18.5% of the sleeping time SO 2 <80%:5% Vitulano N et al, J Cardiovasc Med 2009 Dec 7

27 Ventricular ectopy during night time Baseline CPAP Vitulano N et al, J Cardiovasc Med 2009 Dec 7

28 Conclusions Diagnosis of SDB should be considered in patients presenting with cardiac arrhythmias, especially if: Patients have nocturnal arrhythmias Arrhythmia is refractory to standard therapy Heart Failure is present Other clinical indicators of OSA are present Polysomnography should be then performed in most patients with cardiovascular disease including cardiac arrhythmias Early treatment of OSA can reduce arrhythmias and improve symptoms and may have the potential confer a mortality benefit

29 Further considerations Whether sleep apnea treatment is capable of reducing risk for atrial and ventricular fibrillation and sudden death and for mortality has not been established definitively Future research (large scale prospective trials) is required, first, to identify patient subgroups in which OSA imparts a heightened risk of poor arrhythmic outcomes and to evaluate the role of OSA therapy in modulating such risk