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DRS ed Aritmie Cardiache Iper ed Ipocinetiche: la clinica
FRANCESCO PERNA, MD, PhD
Laboratorio di Elettrofisiologia CardiacaPoliclinico Gemelli, Università Cattolica del Sacro Cuore, Roma
Corso Multidisciplinare di Aggiornamento
“La Sindrome delle Apnee Notturne:una sfida diagnostico terapeutica”
Roma, 15 Novembre 2012
Nessuno
Conflitti di interesse
The Sleep Heart Health Study
Mehra R et al. Am J Respir Crit Care Med 2006;173:910–6
SDB and arrhythmiasEpidemiology
Important pathophysiological and
epidemiological relationships have been identified between OSA and clinically significantarrhythmias, including
bradyarrhythmias, SVA/atrial fibrillation
(AF) and sudden cardiac death (SCD).
SDB and arrhythmiasEpidemiology
• 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
2. Monahan K et al, J Am Coll Cardiol. 2009;54:1797–804.
1. Mehra R et al. Am J Respir Crit Care Med 2006;173:910–6
SDB and arrhythmiasPathophysiology
Chan KH and Wilcox I, Expert Rev Cardiovasc Ther 2010;8(7):981–994
- 65 mmHg- 65 mmHg
Atrial enlargement
Intrathoracicpressurechange due to airwayobstruction
Ventricular remodeling
Ventricular stiffness
Right heart overload
Acute changes
• Hypoxemia• Sympathetic surge• Parasympathetic surge• Myocardial ischemia• Intrathoracic pressure
fluctuations with cardiac wall stress
• Increased afterload
Chronic changes
• Oxidative stress, endot. dysf• Chronically increased
sympathetic activity• Hypertension• Atrial & ventricular
remodeling• Systemic inflammation• Hypercoagulability• LV syst & diast dysfunction
SDB and arrhythmiasPathophysiology
SDB and bradyarrhythmias
Diving reflexApnea-inducedhypoxemia causes:
– Peripheral resistance (Symp)
– Heart rate (PS)
Ludka O, Tex Heart Inst J 2011;38(4):340-343
• 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
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
• 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
SDB and bradyarrhythmias
Garrigue S et al, Circ 2007;115:1703-1709
SAS
NO SAS
Positive effect of CPAP on bradyarrhythmias in SDB patients
Simantirakis EN, Eur Heart J 2004;25:1070–1076
on CPAP
on CPAP
on CPAP
N°b
rady
card
ias
N°p
ause
s
% of pts with
pauses and
brady
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, 1037–1040
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, 1037–1040
“we have foundno clinical benefit from pacing in SA with the purpose of improvinga breathing disorder”
AOP should not be considered an alternative to CPAP in the treatment of patients with SA
SDB and bradyarrhythmias
• Most subjects with bradyarrhythmiasshould be investigated for OSA (Polysomnography)
• The first line of treatment for bradyarrhythmias in the setting of OSA is treatment of the OSA (CPAP)
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 pathophysiologicallink not known
SA can predict:- Lifetime risk of developing AF- Postoperative AF (CABG): x2- AF recurrence after electrical CV- AF recurrence after cath ablation
Gami AS et al, J Am Coll Cardiol 2007;49:565.Kanagala et al, Circulation 2003;107:2589-2594
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 pathophysiologicallink not known
SA can predict:- Lifetime risk of developing AF- Postoperative AF (CABG): x2- AF recurrence after electrical CV- AF recurrence after cath ablation
Gami AS et al, J Am Coll Cardiol 2007;49:565.Kanagala et al, Circulation 2003;107:2589-2594
No CPAP: 82%
CPAP: 42%
Control: 53%
SDB and atrial fibrillation
Monahan K et al, Am J Cardiol 2012;110(3):369–372
Response to antiarrhythmic drugs in AF patients with SDB
Chronically heightened sympathetic activity, even during the waking period, might also hinder pharmacologic rate-control strategies(Somers VK, J Clin Invest 1995;96(4):1897–1904)
OSA as a predictor of AF recurrenceafter catheter ablation
Ng CY et al, Am J Cardiol 2011; 108:47–51.
OSA patients 25% greater risk of AF recurrence after catheter ablation
Patel D et al, Circ Arrhythm Electrophysiol. 2010;3:445-451
CPAP improves PVAI success rates
• 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 IntervCard 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 fibrillationshould be monitored for the presence of SDB (polysomnography), which can be effectively treated by CPAP
SDB and atrial fibrillation
The Sleep Heart Health Studypatients
with SDBpatients
without SDB
Mehra R et al, Am J Respir Crit Care Med 2006; ;173:910-916.
SDB and ventricular arrhythmias
>25% with severe SA have complex ventricular ectopy>5% NSVTduring sleep. (x3 risk) Independent of related comorbidities
SDB and malignant ventricular arrhythmias in heart failure patients
Bitter T et al, European Heart Journal 2011;32:61–74
Time to first appropriate implantable defibrillator therapy
CPAP withdrawal and repolarization
Rossi V et al,European Heart Journal
2012;33: 2206–2213
SubtherapeuticCPAP
TherapeuticCPAP
Day-night pattern of SCD in OSA
Gami AS et al, N Engl J Med 2005;352:1206.
AHI
OSA is associated with an increased risk of SCD, particularly at night
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
58 yo maleBMI 26 Kg/m^2
NIDCMLVEF 30%>25000 PVCs, drug-refractory
Dryness of mouthSnoringDaytime sleepiness
Clinical case
Vitulano N et al, J Cardiovasc Med 2009 Dec 7
•AHI : 33/h
•SO2 <90%: 18.5% of the sleeping time
• SO2 <80%:5%
Clinical case – 2Polysomnography
Vitulano N et al, J Cardiovasc Med 2009 Dec 7
Ventricular ectopy during night time
Vitulano N et al, J Cardiovasc Med 2009 Dec 7
Baseline25550
CPAP12112
• 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
Conclusions
• 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
Further considerations
Recommended