2/19/2013. Cardiovascular Disease Prevention International Symposium. Cardiovascular Disease and Sleep Apnea. Still Controversial?

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1 Cardiovascular Disease Prevention International Symposium Cardiovascular Disease and Sleep Apnea February 16, 2013 Jonathan A. Fialkow, M.D., FACC, FAHA Medical Director, Clinical Cardiology, Baptist Cardiac & Vascular Institute Miami, Florida Premise OSA and Cardiovascular Diseases have many of the same risk factors, Ex, age, male gender, obesity OSA associated with numerous conditions that are known to increase risk for CVD, Ex. Type 2 DM and metabolic syndrome, hypertension Is there a causality between OSA and cardiovascular disease? Still Controversial? From: Sleep Apnea and Cardiovascular Disease: Title and subtitle BreakAn American Heart Association/American College of Cardiology Foundation Scientific Statement From the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing In Collaboration With the National Heart, Lung, and Blood Institute National Center on Sleep Disorders Research (National Institutes of Health) Figure Legend: Partial and complete airway obstruction resulting in hypopnea and apnea, respectively. Reprinted from Hahn PY, Somers VK. Sleep apnea and hypertension. In: Lip GYH, Hall JE, eds. Comprehensive Hypertension. St. Louis, MO: Mosby; 2007: Copyright Elsevier Used with permission. J Am Coll Cardiol. 2008;52(8): doi: /j.jacc

2 OSA on Polysomnogram 2

3 AHI Signs/symptoms of OSA Snoring Gasping or choking from sleep Excessive daytime sleep Daytime fatigue Cognitive dysfunction(memory, concentration) Change in mood (irritable) Unrefreshed Sleep 3

4 The Meat of the Disorder 4

5 From: Sleep Apnea and Cardiovascular Disease: American Heart Association/American College of Cardiology Foundation Scientific Statement From the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing In Collaboration With the National Heart, Lung, and Blood Institute National Center on Sleep Disorders Research (National Institutes of Health) Figure Legend: Schematic outlining proposed pathophysiological components of OSA, activation of cardiovascular disease mechanisms, and consequent development of established cardiovascular disease. J Am Coll Cardiol. 2008;52(8): doi: /j.jacc Cardiovascular Effects of Apnea Tends to result in decreased blood O2 and increased CO2 Hypoxia independently associated with CVD Nervous system responds by increasing heart rate and blood pressure and constricting blood vessels in periphery Mueller Manuever: airway closure, increased negative intra-thoracic pressure resulting in increased transmural cardiac pressures Alteration in heart rate and BP variability 5

6 OSA and Hypertension Sleep Heart Study, over 6000 patients, showed linear relationship between mean systolic and diastolic BP and OSA severity. Prevalence of hypertension linearly increased with the presence and severity of OSA Canadian population-based study found each apneic event per hour increased odds of HTN by 1% and each 10% reuction in nocturnal oxygen saturation increased the likelihood of hypertension developing by 13% 50% of OSA patients have hypertension compared with 30% of general public JNC-7 lists sleep apnea as significant cause of secondary HTN Nieto FJ, et.al, JAMA 2000;283 Lavie P, et.al, BMJ 2000:320 6

7 Pleural Pressure Decrease in pleural pressure with inspiration and increases with positive airway pressure Transmural pressure of heart-intracardiac pressure minus extracardiac pressure Each inspiration increases transmyocardial pressure PAP decreases preload and afterload. Mechanical consequences of OSA 7

8 Atrial Fibrillation Obesity and hypoxemia are independent predictors of A-fib in pts < 65 82% recurrence of A-fib if OSA untreated after cardioversion 50% of pts presenting for cardioversion have OSA Mechanisms: LA stretch more common in OSA, recurrent hypoxemia, significant cathechol swings, arousals, low sats.nightly for YEARS Gami,et.al Circulation 2004:110: From: Obstructive Sleep Apnea, Obesity, and the Risk of Incident Atrial Fibrillation J Am Coll Cardiol. 2007;49(5): doi: /j.jacc Incidence of AF Based on Presence or Absence of OSA Cumulative frequency curves for incident atrial fibrillation (AF) for subjects <65 years of age with and without obstructive sleep apnea (OSA) during an average 4.7 years of follow-up. p = Apoor S., et.al, J Am Coll Cardiol. 2007;49(5): From: Obstructive Sleep Apnea, Obesity, and the Risk of Incident Atrial Fibrillation J Am Coll Cardiol. 2007;49(5): doi: /j.jacc Figure Legend: Incidence of AF Based on the Severity of OSA and Obesity Cumulative frequency of incident atrial fibrillation (AF) during an average 4.7 years of follow-up, based on interactions between the body mass index (BMI) and the apnea-hypopnea index (AHI). An AHI 40 represents severe OSA. A BMI <25 represents normal weight, a BMI 25 to 30 kg/m 2 represents overweight, and a BMI >30 kg/m 2 represents obesity. Apoor S, et.al, J Am Coll Cardiol, 2007;49(5):

9 Coronary Artery Disease OSA associated with increased risk of MI and CVA independent of other variables OSA worsens other CVA risk factors Mechanisms: recurrent hypoxia, decreased coronary blood flow, arousals, apnea leading to increased negative intrathoracic pressure, systemic inflammation, coagulation and endothelial dysfxn improved with CPAP 9

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11 Congestive Heart Failure Prospective study of patients with LV failure found concurrent sleep apnea in 50%. Untreated associated with increased mortality risk Randomized trials with CPAP show improvement in cardiac function, sympathetic activity and QOL No clear evidence yet that treating OSA in CHF decreases mortality but studies are suggestive Javaheri S, et.al., Int J Cardiol 2006:106 Cloward TV, Et.al, Chest 2003 From: Sleep Apnea and Cardiovascular Disease: American Heart Association/American College of Cardiology Foundation Scientific Statement From the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing In Collaboration With the National Heart, Lung, and Blood Institute National Center on Sleep Disorders Research (National Institutes of Health) Figure Legend: Schematic outlining possible mechanisms underlying development of CSA and the possible feedback from CSA resulting in exacerbation of heart failure (16). Reproduced with permission. J Am Coll Cardiol. 2008;52(8): doi: /j.jacc Cerebrovascular Accident 750,000 CVAs per year 72% of patients with CVA have OSA OSA precedes onset of CVA Results from similar CV causes of hypertension, inflammation, oxidation, etc. Also assoc. with central sleep apnea (40%) Severe central SA> 2 weeks after large CVA has poor outcomes (similar to cardiac dysfunction) SA improves in 50% during recovery phase 11

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13 \. Sleep and Metabolic Abnormalities 13

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15 Obesity Trends* Among U.S. Adults BRFSS, 1990, 1999, 2009 (*BMI 30, or about 30 lbs. overweight for 5 4 person) No Data <10% 10% 14% 15% 19% 20% 24% 25% 29% 30% 15

16 Sleep Duration and Cardiometabolic Risk Knutson,Kristen, BPRCEM, Vol 24,Issue 5 Oct 2010 pg

17 Role of Adiposity Abdominal obesity key part of metabolic syndrome definition and key driver of syndrome Adipose tissue hypoxia may trigger inflammation tenable that OSA-induced hypoxia may promote metabolic dysfunction Leptin (responsible for appetite and energy consumption)resistance may promote ventilatory depression Vgontzas AN, et. Al Sleep Med. Rev. 9, (2005) Sleep Apnea and Inflammation Inflammation plays key role in endothelial dysfunction, insulin resistance, lipid peroxidation forerunners of atherosclerosis OSA shown to increase activation of neutrophils, lymphocytes,monocytes and platelets, activation of NF-kB, increased CRP,TNF, IL-6, PAI-1, fibrinogen, cell adhesion molecules and decreased adiponectin, all independent of obesity Lavie L., et. al, Prog, Cardiovasc Dis. 51(4) Trakada G, et al Sleep Med Clinics 2, (2007) 17

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19 CPAP for Metabolic Syndrome 86pts with mod-severe OSA and metabolic syndrome Double blind, placebo controlled (sham CPAP) 3 month crossover Results: 20% had resolution of Met. Syndrome Significant BP reduction with treatment (sleep fragmentation? Nocturnal hypoxemia-sympathetic overdrive?) TC/HDL improved, TG and non-hdl improved Lower HgbA1c, BMI, abdominal fat (CT scan) Sharma,et.al, N Engl J Med 2011;365: Effect of CPAP Pepperell, et. al Lancet 2001: BP decreased 2.5mgHG sleep or awake with CPAP. Est. CVA risk reduction of 20% and CAD 15% Yaneko, et al NEJM 2003: pts with EF<45% rx with CPAP improved daytime QOL, decrease daytime BP and HR, LVEF increased from 25 to 34% Summary/Cauality? OSA increases risk of cardiovascular diseases. Pts with OSA should be regularly screened for these potential complications Pts with cardiovascular diseases should be screened for OSA OSA is significant cause for secondary HTN, occurs in half of pts with OSA Ischemic heart disease is more common in pts with OSA and may increase risk of fatal and non-fatal CV events 19

20 Summary Pts with heart failure should be assessed for OSA. Treatment for sleep-disordered breathing may improve cardiac function and QOL OSA commonly associated with A-fib and untreated OSA impairs success of cardioversion and maybe ablation CPAP improves multiple cardiometabolic risk factors independent of other treatments/interventions Longer term and additional trials are still needed 20

21 Slow Wave Sleep and risk Strong association between sleep disordered breathing (OSA, sleep deprivation and/or short sleep duration) and HTN Indicies of breathing disturbance, level of hypoxia, sleep duration, arousal index were NOT independently assoc. with HTN risk (slow wave sleep linked to cognitive skills, positive glucose metabolism, slow HR and BP) Fung M., Hypertension, 111,1744. Authors conclude, This article adds to the growing body of literature that associates sleep architecture with metabolic and physiological changes that may reflect altered neurohormones and inflammatory markers They add, Further studies are necessary to confirm these observations, elucidate the causal pathways and determine whether modifications in slow-wave sleep improve HTN 21

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