The Effect of Sleep Disordered Breathing on Cardiovascular Disease

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1 The Effect of Sleep Disordered Breathing on Cardiovascular Disease Juan G. Flores MD Pulmonary, Critical Care and Sleep Medicine Dupage Medical Group Director of Edward Sleep Lab

2 Disclaimers or Conflicts of Interest:

3 Educational Objectives: Describe the various types of sleep disordered breathing Discuss the pathophysiology of sleep disordered breathing in the setting of cardiovascular disease Review currently accepted treatment options for sleep disordered breathing

4 Sleep Disordered Breathing Obstructive Sleep Apnea (OSA) Central Sleep Apnea Cheynes-Stokes Breathing (CSB) Complex Sleep Apnea Alveolar Hypoventilation Syndrome (AHS)

5 OSA Definition Physiologic spectrum ranging from increased upper airway resistance to complete airway collapse Repetitive events leading to cessation of airflow and associated desaturations AHI>5 if symptomatic AHI>15 with or without symptoms

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8 OSA Symptoms Nocturnal symptoms: Witnessed apneas, snoring, gasping Frequent awakenings, GERD Nocturia Daytime symptoms: hypersomnia/fatigue, morning headaches Irritability/mood instability, depression work/school/marital problems Loss of libido/impotence

9 OSA Risk Factors Gender (M>F 2:1) Obesity (fat deposition and distribution) Neck size Upper airway/soft tissue abnormalities Craniofacial anomalies (micrognathia) Smoking, alcohol and hypnotics Ethnicity/race (Asians)

10 Young T et al. N Engl J Med 1993;328: OSA Prevalence

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14 Cardiovascular effects of OSA Increased sympathetic activity Induced by hypoxia, hypercapnia Alterations in cardiac output due to intrathoracic pressure swings Autonomic dysfunction Elevated plasma/urine catecholamines Oxidative stress Inflammation, endothelial dysfunction

15 Effect of Negative Intrathoracic Pressure

16 Southwest J Pulm Crit Care 2012;5:

17 OSA and Hypertension Absence of nocturnal BP dip Severity of OSA directly correlates with effect on BP AHI 5-15 had 2x risk of HTN AHI > 15 had 3x risk of HTN HTN more pronounced in patients with daytime hypersomnia due to OSA OSA is independent risk factor for HTN

18 Peppard PE et al. N Engl J Med 2000;342: OSA and HTN

19 Effect of CPAP HTN: modest reduction Mean reduction in SBP 2.6 mmhg More effective in resistant HTN and in pts with daytime hypersomnolence Largest benefit in pts with severe OSA Extended treatment leads to additional benefit More effective than supplemental oxygen

20 OSA and CAD Severe OSA is an independent risk factor Due to decreases in HDL, increased CRP, hyperglycemia, insulin resistance Can, et al. Chest :233. Exacerbates pre-existing CAD Higher rate of re-infarction Previous MI also leads to worsening of OSA/SDB Gami AS et al. N Engl J Med 2005;352:

21 CAD: Effect of CPAP those with severe OSA had lower incidence of fatal and nonfatal cardiovascular events Events: MI, CVA, ACS Benefits from CPAP noted in those with nightly use of >4hrs/night Cardiovascular incidents in OSA pts using CPAP was similar to those w/o OSA

22 OSA and Atrial Fibrillation Causes include: Hyperadrenergic state Hypoxia, hypercapnia (acidosis) Increased negative intrathoracic pressures affecting thin-walled atria due to fluctuations in transmural pressures OSA is modifiable risk factor for recurrent AF Prevalence of OSA in pts with AF 30-80%

23 OSA and Arrhythmias Bradycardia, asystole noted in 18% Enhanced vagal tone and parasympathetics Not associated with intrinsic AV nodal dysfunction Ventricular ectopy (NSVT, bigeminy, PVC s, etc) More prevalent in pts with severe OSA (AHI >30)

24 Atrial Fibrillation: Effect of CPAP decreases rate of recurrent afib in those with previous cardioversion Higher arrhythmia-free survival rate off antiarrhythmics Fein, et al. J Am Coll Cardiol 2013; 62:300. Other arrhythmias (bradycardia, asystole, VT): Prospective study revealed near complete resolution after prolonged use Ryan, et al. Thorax2005; 60:781

25 OSA and PAH 20% prevalence of PAH in those with moderate to severe OSA Severity of PAH is mild in absence of coexisting pulmonary disease or CHF Etiology: Pulm vasoconstriction due to increased sympathetics Hypoxia-induced vascular remodeling PA smooth muscle hypertrophy Increased LV afterload Bradley, et al. Chest 2001; 119:

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