Dr Andrew Rosenstengel
Sleep/Respiratory Physician
Holy Spirit Northside
Obstructive sleep apnoea (OSA) is a common disorder associated with repetitive episodes of reduced airflow through the upper airway (hypopnoeas) or complete upper airway obstruction (apneas) associated with reduced blood oxygen levels (desaturations). This condition is more prevalent in obese patients. These patients are in turn more likely to suffer from cardiovascular disease as well as diseases that increase cardiac risk, such as diabetes and hypertension. A large number of observational studies have displayed an association between OSA and cardiovascular disease, independent of obesity. Accumulating evidence suggests that treating sleep apnoea, especially severe sleep apnoea, in these patients with continuous positive airway pressure (CPAP) may mitigate cardiac risk.
Recurrent hypoxemia, sympathetic nervous system stimulation, increased inflammation and metabolic change can all be seen in OSA. These changes are thought to be triggers for increased cardiovascular risk. Sympathetic nervous stimulation can increase heart rate and blood pressure, with severe sleep apnoea provoking the greatest changes.
Hypertension is prevalent inpatients with obstructive sleep apnoea, with the prevalence increasing with the severity of sleep apnoea. CPAP has been shown to induce modest but real and significant reductions in blood pressure. A much higher incidence of atrial fibrillation is seen in patients with obstructive sleep apnoea and patients with atrial fibrillation are more likely to have OSA. Limited data suggest that treatment for atrial fibrillation in the form of cardioversion or ablation may be more successful if co-morbid OSA is effectively treated. Other rhythm disturbances such as bradycardia or asystole can be seen in OSA due to increased vagal tone. These abnormal rhythms often resolve with effective CPAP therapy.
Pulmonary hypertension is also commonly seen in patients with severe OSA, and heart failure has an increased incidence in this group as well.
Summary:
There is a strong association between sleep apnoea, especially severe sleep apnoea, and cardiac disease. Patients with known cardiac disease may benefit from questioning about symptoms of sleep apnoea and may prompt investigation for sleep disordered breathing. Treatment of obstructive sleep apnoea with CPAP therapy has been shown to be effective in improving cardiac outcomes and reducing risk in certain populations with cardiac disease.
Impact of OSA on cardiovascular events after coronary artery bypass surgery.
Uchôa CH, Danzi-Soares Nde J, Nunes FS, de Souza AA, Nerbass FB, Pedrosa RP, César LA, Lorenzi-Filho G, Drager LF. University of São Paulo, Sao Paulo, Brazil.Chest. 2015 May;147(5):1352-60.
BACKGROUND: The impact of OSA on new cardiovascular events in patients under going coronary artery bypass graft (CABG) surgery is poorly explored.
METHODS: Consecutive patients referred for CABG underwent clinical evaluation and standard polysomnography in the preoperative period. CABG surgery data, including percentage of off-pump and on-pump CABG, number of grafts, and intraoperative complications, were collected. The primary end point was major adverse cardiac or cerebrovascular events (MACCEs) (combined events of all-cause death, myocardial infarction, repeated revascularization, and cerebrovascular events). Secondary end points included individual MACCEs, typical angina, and arrhythmias. Patients were evaluated at 30 days (short-term) and up to 6.1 years (long term) after CABG.
RESULTS: We studied 67 patients (50 men; mean age, 58 ± 8 years; mean BMI, 28.5 ±4.1 kg/m2). OSA (apnea-hypopnea index ≥ 15 events/h) was present in 56% of the population. The patients were followed for a mean of 4.5 years (range, 3.2-6.1years). No differences were observed in the short-term follow-up. In contrast, MACCE (35% vs 16%, P = .02), new revascularization
(19% vs 0%, P = .01), episodes of typical angina (30% vs 7%, P = .02), and atrial fibrillation (22% vs 0%, P =.0068) were more common in patients with than without OSA in the long-term follow-up. OSA was an independent factor associated with the occurrence of MACCE, repeated revascularization, typical angina, and atrial fibrillation in the multivariate analysis.
CONCLUSIONS: OSA is independently associated with a higher rate of long-term cardiovascular events after CABG and may have prognostic and economic significance in CABG surgery.
Sleep apnea and asymptomatic carotid stenosis: a complex interaction.
Ehrhardt J, Schwab M, Finn S, Guenther A, Schultze T, Witte OW, Rupprecht S. Jena University Hospital, Germany Chest. 2015 Apr;147(4):1029-36.
BACKGROUND: Carotid arteriosclerosis and sleep apnea are considered as independent risk factors for stroke. Whether sleep apnea mediates severity of carotid stenosis remains unclear. Sleep apnea comprises two pathophysiologic conditions: OSA and central sleep apnea (CSA). Although OSA results from upper airway occlusion, CSA reflects enhanced ventilatory drive mainly due to carotid chemoreceptor dysfunction.
METHODS: Ninety-six patients with
asymptomatic extracranial carotid stenosis of ≥50% underwent polysomnography to (1) determine prevalence and severity of sleep apnea for different degrees of carotid stenosis and (2) analyze associations between OSA and CSA, carotid stenosis severity, and other arteriosclerotic risk factors.
RESULTS: Sleep apnea was present in 68.8% of patients with carotid stenosis. Prevalence and severity of sleep apnea increased with degree of stenosis (P ≤.05) because of a rise in CSA (P ≤ .01) but not in OSA. Sleep apnea (OR, 3.8; P ≤.03) and arterial hypertension (OR, 4.1; P ≤ .05) were associated with stenosis severity, whereas diabetes, smoking, dyslipidemia, BMI, age, and sex were not. Stenosis severity was related to CSA (P ≤ .06) but not to OSA. In addition, CSA but not OSA showed a strong association with arterial hypertension (OR, 12.5; P ≤.02) and diabetes (OR, 4.5; P ≤ .04).
CONCLUSIONS: Sleep apnea is highly prevalent in asymptomatic carotid
stenosis. Further, it is associated with arteriosclerotic disease severity as well as presence of hypertension and diabetes. This vascular risk constellation seems to be more strongly connected with CSA than with OSA, possibly attributable to carotid chemoreceptor dysfunction. Because sleep apnea is well treatable, screening should be embedded in stroke prevention strategies.
Hypertension
Association of severe OSA and elevated blood pressure despite antihypertensive medication use.
Walia HK, Li H, Rueschman M, Bhatt DL, Patel SR, Quan SF, Gottlieb DJ, Punjabi NM, et al Cleveland Clinic, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH, USAJ Clin Sleep Med. 2014 Aug 15;10(8):835-43. Comment in J Clin Sleep Med. 2014 Aug 15;10(8):845-6.
RATIONALE: We hypothesized that untreated severe obstructive sleep apnea (OSA) is associated with elevated ambulatory blood pressure (BP) in subjects with high cardiovascular disease (CVD) risk despite medical management.
METHODS: Data from the baseline examination of the Heart Biomarker Evaluation in Apnea Treatment (Heart BEAT) study, a 4-site randomized controlled trial were analyzed. Individuals with moderate-severe OSA (apnea hypopnea index, AHI =15-50) and cardiovascular risk were recruited from cardiology practices. Those with hypertension were included. Intensive antihypertensive regimen (IAR) was defined as ≥ 3 anti hypertensives including a diuretic. Definitions were controlled BP (BP < 130/80), uncontrolled elevated BP (BP ≥ 130/80 not on IAR) and resistant elevated BP (BP ≥ 130/80 mm Hg despite IAR). Associations of untreated severe OSA (AHI ≥ 30) and uncontrolled and resistant elevated BP were evaluated using logistic regression analyses adjusted for age, sex, race, body mass index, smoking status, diabetes, and CVD.
RESULTS: Among the 284 participants (mean age 63.1 ± 7.2 years, 23.6% with severe OSA), 61.6% had controlled BP, 28.5% had uncontrolled elevated BP, and 9.9% had resistant elevated BP. Among participants prescribed IAR, resistant elevated BP was more prevalent in those with severe compared to moderate OSA (58.3% vs.28.6%, p = 0.01). Participants with severe OSA had a 4-fold higher adjusted odds of resistant elevated BP (OR 4.1, 95% CI: 1.7-10.2), a finding not reproduced in the absence of IAR use.
CONCLUSIONS: Among patients with increased cardiovascular risk and moderate to severe OSA, untreated severe compared to moderate OSA was associated with elevated BP despite IAR suggesting untreated severe OSA contributes to poor BP control despite aggressive medication use.
Influence of sleep apnea severity on blood pressure variability of patients with hypertension.
Steinhorst AP, Gonçalves SC, Oliveira AT, Massierer D, Gus M, Fuchs SC, Moreira LB, Martinez D, Fuchs FD. Graduate Program in Medicine: Cardiology, School of Medicine, Universidade Federal do Rio Grande do Sul, Brazil. Sleep Breath. 2014 May;18(2):397-401.
PURPOSE: Obstructive sleep apnea (OSA) is a risk factor for the development of hypertension and cardiovascular disease. Apnea overloads the autonomic cardiovascular control system and may influence blood pressure variability, a risk for vascular damage independent of blood pressure levels. This study investigates the hypothesis that blood pressure variability is associated with OSA.
METHODS: In a cross-sectional study, 107 patients with hypertension underwent24-h ambulatory blood pressure monitoring and level III polysomnography to detect sleep apnea. Pressure variability was assessed by the first derivative of blood pressure over time, the time rate index, and by the standard deviation of blood pressure measurements. The association between the apnea-hypopnea index and blood pressure variability was tested by univariate and multivariate methods.
RESULTS: The 57 patients with apnea were older, had higher blood pressure, and had longer duration of hypertension than the 50 patients without apnea.
Patients with apnea-hypopnea index (AHI) ≥ 10 had higher blood pressure variability assessed by the standard deviation than patients with AHI < 10 during sleep (10.4 ± 0.7 versus 8.0 ± 0.7, P = 0.02) after adjustment for age, body mass, and blood pressure. Blood pressure variability assessed by the time rate index presented a trend for association during sleep (P = 0.07). Daytime blood pressure variability was not associated with the severity of sleep apnea.
CONCLUSION: Sleep apnea increases nighttime blood pressure variability inpatients with hypertension and may be another pathway linking sleep abnormalities to cardiovascular disease.
Arrhythmias
Positive pressure therapy in patients with cardiac arrhythmias and obstructive sleep apnea.
Dediu GN, Dumitrache-Rujinski S, Lungu R, Frunz S, Diaconu C, Barto D, Bogdan MA. Romania Pneumologia. 2015 Jan-Mar;64(1):18-22.
BACKGROUND: Positive pressure therapy (CPAP) in patients with cardiac arrhythmias and obstructive sleep apnea (OSAS) may have favorable effects by correcting intermittent hypoxemia and sympathetic activation.
OBJECTIVE: To assess the effect of CPAP added to pharmacological treatment in the rate control and prevention of arrhythmias recurrence in patients with OSA.
MATERIALS AND METHODS: Prospective, interventional study study which included patients diagnosed with OSAS (cardio respiratorypolygraphy, AHI>5/hour), and arrhythmias (ECG, Holter ECG), divided in two groups: group A (pharmacological therapy only) and group B (pharmacological therapy and CPAP). The patients were evaluated at enrollment (T0), at 3 and 6 months (T3 and T6) regarding the type, severity and recurrence of cardiac arrhythmias.
RESULTS: 36 patients (31 men), mean age: 63.2 ± 12 years were enrolled. In group A: 7 patients with ventricular extra systoles, 8 with permanent atrial fibrillation, 1 patient with atrial flutter and 2 patients with paroxystic supraventricular tachycardia. In group B: 8 patients with ventricular extra systoles, 5 with permanent atrial fibrillation, 2 patients with recurrent episodes of atrial fibrillation and 3 with paroxystic supraventricular tachycardia. A positive correlation (r: 0.74, p < 0.001) between Oxygen Desaturation Index and AHI was found. At T6, 12 patients from group B, and 18from group A were evaluated. In group B, the mean heart rate in patients with atrial fibrillation was 69/min., lower than in group A (82/min.), no cases with recurrent atrial fibrillation were found, and more patients with class II Lown ventricular extra systoles passed in class I Lown, compared to group A. In group B, heart rate statistically correlated with AHI (r: 0.53, p < 0.005).
CONCLUSION: In patients with OSAS, adding CPAP to pharmacological therapy has favorable effects on preventing recurrences, heart rate control in patients with atrial fibrillation and in reducing frequency and/or severity of ventricular extra systoles.
Incidence and risk of atrial fibrillation in sleep-disordered breathing without coexistent systemic disease.
Chao TF, Liu CJ, Chen SJ, Wang KL, Lin YJ, Chang SL, Lo LW, Hu YF, Tuan TC, Chen TJ, Chiou CW, Chen SA.Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taiwan Circ J. 2014;78(9):2182-7. Epub 2014 Jul 23.
BACKGROUND: Although the link between sleep-disordered breathing (SDB) and atrial fibrillation (AF) has been reported, a population-based longitudinal cohort study was lacking. The goal of the present study was to investigate the AF risk carried by SDB, using the National Health Insurance Research Database in Taiwan.
METHODS AND RESULTS: From 2000 to 2001, a total of 579,521 patients who had no history of cardiac arrhythmias or significant comorbidities were identified. Among them, 4,082 subjects with the diagnosis of SDB were selected as the study group, and the remaining 575,439 subjects constituted the control group. The study endpoint was the occurrence of new-onset AF. During a follow-up of 9.2±2.0 years, there were 4,023 patients (0.7%) experiencing new-onset AF. The occurrence rate of AF was higher in patients with SDB compared to those without it (1.3% vs.0.7%, P<0.001). The AF incidences were 1.38 and 0.76 per 1,000 person-years for patients with and without SDB, respectively. After an adjustment for age and sex, SDB was a significant risk factor of AF with a hazard ratio of 1.536. The AF risk increased with increasing clinical severity of SDB, represented by the requirement of continuous positive airway pressure use.
CONCLUSIONS: SDB itself, without the coexistence of other systemic diseases, was a risk factor of AF.
