BTG - Obstructive Sleep Apnea Exacerbates Heart Failure - Continuous Positive Airway Pressure May Reverse Cardiomyopathy
BTG - Obstructive Sleep Apnea Exacerbates Heart Failure - Continuous Positive Airway Pressure May Reverse Cardiomyopathy
Obstructive sleep apnea (OSA) occurs in about one-third of heart-failure patients, and its presence is associated with poor outcome.1 The Sleep Heart Health Study (SHHS) has found that OSA patients are at 2.38 times greater risk of heart failure.2 OSA may worsen heart failure in the following ways:3,4 inflammatory and oxidative—hypoxia, serum inflammatory, and oxidative markers (high sensitivity C-reactive protein (hs-CRP), plasminogen activator inhibitor (PAI)-1); neurohumoral—arousal index, arousals per hours sleep and sympathetic activation (elevated urinary catecholamines); mechanical—repetitive bouts of negative intra-thoracic pressure and greater left ventricular muscle stress; thrombotic—increased levels of clotting factors and platelet aggregation; and endothelial— increased markers for endothelial dysfunction and injury.
Both untreated OSA patients and heart failure patients are at increased risk of nocturnal death from cardiac ischemia and ventricular arrhythmia. Ryan et al. studied the interaction between OSA and ventricular arrhythmia in heart failure patients.5 They tested the effects of continuous positive airway pressure (CPAP) therapy on ectopic ventricular arrhythmias in a randomized controlled trial of 18 heart failure patients who had >10 ventricular ectopies per hour of sleep.Ventricular premature beats (VPB) were counted if they were premature, =0.12 seconds in duration, morphologically different to those arising from sinus beats, and had no premature P wave. Couplets and ventricular tachycardia were few and were not analyzed.
The CPAP-treated heart failure patients experienced a 58% reduction in VPBs (see Figure 1), as well as a reduction in daytime systolic pressure (by 4.6mmHg) and increased left ventricular ejection fraction and overnight urinary norepinephrine. It should be noted that this was a small study, and that the occurrence of ventricular extrasystoles does not in itself portend a life-threatening condition.Another recent study compared the effects of a month of CPAP treatment with medical treatment alone in patients with OSA and co-existing heart failure.6 Both the CPAP and the control patients were receiving optimal medical therapy. In the CPAP group,OSA was eliminated and there were significant reductions in mean daytime systolic blood pressure (p=0.02), heart rate (p=0.007), and left ventricular end-systolic dimension (p=0.009). There was also improved left ventricular ejection fraction, from 25% to 33.8% (p<0.001).This effect has been confirmed by a similar, larger study.7
CPAP May Provide Clear Cardiovascular Benefits to Cardiac Patients
In addition to reducing the detrimental effects of OSA, CPAP may also benefit the cardiac patient by: eliminating the exaggerated negative intra-thoracic pressure that occurs during apnea events, thereby reducing the left ventricle transmural pressure gradient and improving left ventricular ejection fraction and venous return; increasing lung volume and assisting inspiratory muscle function; reducing hypoxia and normalizing the balance of oxygen demand and supply to the heart; eliminating the pressor effect of hypoxia, hypercapnia and arousal, and the downward resetting of sympathetic outflow, thus reducing nocturnal catecholamine levels; and reducing both nocturnal and daytime blood pressure and heart rate.
CPAP May Also Playa Preventive Role
Young middle-aged OSA patients who have no other signs of cardiovascular disease show significant early signs of atherosclerosis. These signs are proportionate to the severity of their OSA.8 This suggests that OSA may play an independent role in the early pathophysiology of atherosclerosis, and that early CPAP treatment may ameliorate its progression.Kaneko points out that medical therapy alone does not improve any of the nocturnal effects of OSA—intermittent hypoxia, impairment of cardiac output, myocardial ischemia, and sympathetic pressor effects—to the same degree as CPAP.6 Furthermore, he suggests that long-term CPAP use may actually foster a sustained improvement in cardiac betaadrenergic function and myocardial contractility.
- Wilcox I, McNamara S G,Wessendorf T et al., “Prognosis and sleep disordered breathing in heart failure”, Thorax (1998);53 (Suppl 3): pp. S33–S36.
- Shahar E,Whitney C W, Redline S et al.,“Sleep-disordered breathing and cardiovascular disease: cross sectional results of the Sleep Heart Health Study”, Am J Respir Crit Care Med (2001);163: pp. 19–25.
- Ferreira S,Winck J, Bettencourt P,“Heart failure and sleep apnea: to sleep perchance to dream”, Eur J Heart Fail (2005); E-pub.
- Naughton M T, “The link between obstructive sleep apnea and heart failure: underappreciated opportunity for treatment”, Curr Cardiol Rep (2005); 7: pp. 211–215.
- Ryan C M, Usui K, Floras J S et al., “Effect of continuous positive airway pressure on ventricular ectopy in heart failure patients with obstructive sleep apnea”, Thorax (2005); 60: pp. 781–785.
- Kaneko Y, Floras J S, Usui K et al.,“Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea”, N Engl J Med (2003); 348: pp. 1233–1241.
- Mansfield D R, Gollogly N C, Kaye DM et al.,“Controlled trial of continuous positive airway pressure in obstructive sleep apnea and heart failure”, Am J Respir Crit Care Med (2004); 169: pp. 361–366.
- Drager LF, Bortolotto LA, Lorenzi MC et al., “Early signs of atherosclerosis in obstructive sleep apnea”, Am J Respir Crit Care Med (2005);172: pp. 613–618.
