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