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BACKGROUND AND OBEJECTIVE: The prevalence of sleep-disordered breathing (SDB) in patients with chronic heart failure seems to be remarkably high, but existing studies are based on small cohorts of patients who were not receiving guideline-based drug treatment for heart failure. The aim of this study was to investigate the prevalence of SDB in patients with ischemic (ICM) or non-ischemic (DCM) cardiomyopathy. PATIENTS AND METHODS: A total of 647 consecutive patients (130 females, 517 males; mean age 63.23 10.4 years) in stable, symptomatic chronic heart failure (NYHA class at least II) and with impaired systolic left ventricular function (ejection fraction ≤ 40%) were screened by cardiorespiratory polygraphy for the presence and type of SDB. Sleep apnea was classified as obstructive (OSA) or central (CSA) according to the majority of events, and as ICM or DCM according to the results of current left heart catheterization. SDB was defined according to the apnea-hypopnea index (AHI) as: no SDB: ≤ 5/h, mild: 6 -14/h, moderate: 15 - 29/h, and severe ≥ 30/h. RESULTS: Prevalence of SDB was 70% among DCM and 82% among ICM patients (p < 0.05). Central sleep apnea was found in 32% of DCM and 46% of ICM patients, obstructive sleep apnea in 38% of DCM and 36% of ICM patients. Moderate (15.7% vs. 9.9%, p < 0.05) and severe central sleep apnea (24.4% vs. 15.5%, p < 0.05) was documented more often in ICM than DCM patients. Severity of obstructive sleep apnea was similar in ICM and DCM patients. ICM patients were older than DCM patients (66.4 11 years vs. 66.0 9.0 years, p < 0.01) and in general presented with a greater impairment of cardiopulmonary function. CONCLUSIONS: There is a high prevalence of SDB in patients in chronic heart failure. Central sleep apnea can be documented particularly in ICM patients and seems to be a marker for the severity of heart failure. Because of their prognostic implications, risk stratification and identification of patients eligible for specific SDB treatment, screening for such disorders should be part of every heart failure work-up.

The purpose of this review is to summarize current knowledge about the link between sleep-disordered breathing (SDB) and cardiovascular and cerebrovascular diseases. Obstructive sleep apnoea (OSA) is a well-established risk factor for systemic arterial hypertension, and its treatment with continuous positive airway pressure leads to a decrease in daytime and night-time blood pressure profiles. Pulmonary arterial hypertension occurs in 20–30% of OSA patients and is usually mild. It is not yet clear if OSA per se leads to pulmonary hypertension or if the coexistence of chronic obstructive pulmonary disease with daytime and/or sleep-related hypoxaemia is required to provoke a persistent rise in pulmonary artery pressure. Furthermore, OSA is associated with nocturnal cardiac arrhythmias, especially cyclical fluctuations of the heart rate in response to recurrent apnoeas. Atrioventricular conduction blocks and ventricular premature beats are less often observed and seem to be confined to patients with severe OSA and those with accompanying ischaemic heart disease. The association between OSA and vaso-occlusive disease (i.e. atherosclerosis) is less clear. However, accumulating experimental and epidemiological data support such a link. Thus, OSA may lead to coronary artery disease (CAD) and stroke by promoting atherosclerosis. Correspondingly, patients with CAD or acute stroke show a high prevalence of SDB. Cheyne—Stokes respiration (CSR) is a specific pattern of central sleep apnoea occurring in patients with advanced congestive heart failure (CHF). If present, CSR clearly has a negative impact on the clinical course of CHF. Although the optimal treatment strategy for CSR is less well defined than that for OSA, the successful reversal of CSR might increase overll survival in affected patients.

Aim: Evaluation of the prevalence and nature of sleep-disordered breathing (SDB) in patients with symptomatic chronic heart failure (CHF) receiving therapy according to current guidelines. Methods and results: We prospectively screened 700 patients with CHF (NYHA class ≥II, LV-EF ≤40%) for SDB using cardiorespiratory polygraphy (Embletta™). Furthermore, echocardiography, cardiopulmonary exercise and 6-min walk testing were performed. Medication included ACE-inhibitors and/or AT1-receptor blockers in at least 94%, diuretics in 87%, β-blockers in 85%, digitalis in 61% and spironolactone in 62% of patients. SDB was present in 76% of patients (40% central (CSA), 36% obstructive sleep apnoea (OSA)). CSA patients were more symptomatic (NYHA class 2.9±0.5 vs. no SDB 2.57±0.5 or OSA 2.57±0.5; pb0.05) and had a lower LV-EF (27.4±6.6% vs. 29.3±2.6%, pb0.05) than OSA patients. Oxygen uptake (VO2) was lowest in CSA patients: predicted peak VO2 57±16% vs. 64±18% in OSA and 63±17% in no SDB, pb0.05. 6-min walking distances were 331±111 m in CSA, 373±108 m in OSA and 377±118 m in no SDB (pb0.05). Conclusions: This study confirms the high prevalence of SDB, particularly CSA in CHF patients. CSA seems to be a marker of heart failure severity.

Rationale: This study investigates the influence of cardiac resynchronization therapy (CRT) on sleep disordered breathing (SDB) in patients with severe chronic heart failure (CHF). Methods and Results: A total of 100 consecutive patients with CHF eligible for CRT (NYHA class III, LBBB, QRS width 150 ms, EF 35%, LVEDD 60 mm) were screened for SDB using cardiorespiratory polygraphy (Embletta®) before device implantation. Mean age 64.8 9.8 years, CAD n 42, DCM n 54, valvular heart disease n 4, mean EF 25.7 6.8%, mean VO2peak 13.4 4.8 ml/kg/min, mean QRS width 185 18 ms. Central sleep apnea (CSA) was documented in 39 patients (39%) and obstructive sleep apnea (OSA) in 34 patients (34%). Only 27 patients (27%) had normal results during cardiorespiratory polygraphy. Twenty-two patients with CSA (central apnea index 15/hr) and 8 patients with OSA were reinvestigated 12 24 weeks after biventricular pacemaker implantation for apnea-hypopnea-index (AHI), NYHA classification, and peak oxygen uptake. Eleven patients demonstrated a significant improvement of CSA by CRT: AHI 32.0 vs 10.8, p 0.0001, EF (23.1 vs 27.8%, p 0.026), NYHA (2.9 vs 2.1 p 0.0002), and oxygen uptake (13.7 vs 17.4, p 0.01). In contrast, CSA remained unchanged in the other 11 patients (AHI 33.9/hr vs 30.7/hr, ns). All nonresponders were also nonresponders with respect to CRT (neither improvement of NYHA, EF nor of oxygen uptake after 3 months of CRT). OSA was not influenced by CRT (AHI 14.0 versus 12.0, p ns), despite good clinical response to CRT (NYHA 3.1 versus 2.3; VO2peak 13.7 versus 17.6 ml/kg/min, p 0.02). Conclusion: In appr. 50 % of patients with CRT, a short term improvement of heart failure symptoms and parameters correlates with a marked improvement in central sleep apnea. In patients who do not show a clinical improvement during the first 3 months of CRT, CSA does also not improve, which supports CSA being a marker for the severity of CHF. In contrast OSA is not influenced by CRT. Because of its pathophysiologic and prognostic significance and the availability of modern treatment options, cardiorespiratory screening should be routinely implemented in the evaluation of CRT patients.