Patients with obstructive sleep apnoea syndrome (OSAS) are subject to an increased cardiovascular morbidity including myocardial infarction and stroke. Platelets play an important role in the pathogenesis and triggering of acute cardiovascular syndromes. So far, the influence of OSAS on platelet function is not fully understood. Platelet aggregability to epinephrine, collagen, arachidonic acid, and adenosine diphosphate in vitro was measured in 17 consecutive male patients (53.0±2.1 yrs) with polysomnographically verified OSAS and compared with that of 15 male controls (50.1±3.6 yrs) at 20:00 h, 24:00 h, and 06:00 h. In addition, the long‐term effects of continuous positive airway pressure (CPAP) therapy on platelet aggregability was assessed after 6 months. Platelet aggregation in vitro induced by epinephrine showed a slight increase overnight in the untreated OSAS patients ( ns) whereas it decreased slightly ( ns) in the controls and in the treated OSAS patients. Pretherapeutic platelet aggregability was significantly lowered by CPAP therapy both at 24:00 h (64.0±6.5 versus 55.3±6.7%, p<0.05) and at 06:00 h (64.1±6.5 versus 45.8±7.6%; p=0.01). Platelet aggregability during sleep in the controls resembled that found in patients with OSAS during CPAP therapy. The results suggest that obstructive sleep apnoea syndrome contributes, at least in part, to platelet dysfunction and that long‐term continuous positive airway pressure treatment may reduce platelet aggregability.

There is conclusive evidence that obstructive sleep apnoea syndrome (OSAS) influences right heart haemodynamics and can also induce pulmonary hypertension. It is not known, however, whether right ventricular dysfunction can occur in patients with OSAS in the absence of lung disease.We studied 107 patients (94 males, 13 females, mean age 55±11 yrs) with polysomnographically verified OSAS in whom clinically significant lung disease was excluded. Right ventricular ejection fraction (RVEF) was determined by radionuclide ventriculography. In addition, pulmonary function tests, arterial blood gas analysis and right heart catheterization were performed. RVEF was impaired in 19 patients (18%). Eighteen (95%) had signs or symptoms consistent with mild right ventricular failure. Patients with or without impaired RVEF did not differ with respect to body mass index, age or lung function. Stepwise multiple logistic regression analysis revealed that RVEF was significantly associated with the apnoea/hypopnoea index (r=-0.68; p=0.0009) and the extent of nocturnal oxyhaemoglobin saturation (r=0.42; p=0.035), but not with age, body mass index, blood gas analysis, gender, lung function, pulmonary artery pressure and left ventricular ejection fraction.We conclude that in patients with otherwise unexplained right ventricular failure, obstructive sleep apnoea syndrome may underlie the right ventricular dysfunction. Eur Respir J 1997; 10: 2079-2083 Obstructive sleep apnoea syndrome (OSAS) is a common condition characterized by repeated pauses (apnoeas) or reductions (hypopnoeas) in breathing during sleep [1]. It is caused by a complete or partial upper airway obstruction, which leads to increasing pleural pressure swings, decreases in oxyhaemoglobin saturation and subsequent arousal from sleep, whereupon airway patency is restored and airflow resumes.These mechanisms seem to be responsible for a series of secondary physiological events, which in turn give rise to the clinical complication of the syndrome and probably associated cardiovascular disease [2,3].While episodic nocturnal pulmonary hypertension in OSAS is well described [4,5], the consequences of OSAS with respect to the function of the right ventricle are less well studied [6][7][8][9]. Right ventricular dysfunction occurring in patients with OSAS has generally been attributed to concomitant chronic obstructive lung disease, hypercapnia, or at least mild hypoxia [8,[10][11][12]. As yet, no direct association between OSAS and right ventricular dysfunction is known. To examine this question, the prevalence of right ventricular dysfunction and parameters possibly influencing right ventricular function were studied in a group of OSAS patients in whom an intrinsic pulmonary disorder was excluded. Methods Study designOne hundred and seven consecutive patients (94 males, 13 females) referred to our sleep laboratory for snoring, suspected OSAS, or excessive daytime sleepiness with a mean age of 55±11 yrs (range 28-74) and a mean body mass index (BMI) of 31-52 kg·m -2 (rang...

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Continuous blood pressure (BP) measurement allows the investigation of transient changes in BP and thus may give insights into mechanisms of BP control. We validated a continuous, non-invasive BP measurement based on the pulse transit time (PTT), i.e., BP(PTT), by comparing it with the intra-arterial BP (BP(i.a.)) measurement. Twelve subjects (five females and seven males) were included. BP(i.a.) was obtained from the radial artery using a system from ReCor Medical. Systolic and diastolic BP were calculated using the PTT (BP(PTT), SOMNOscreen). (PTT) was determined from the electrocardiogram and the peripheral pulse wave. The BP was modulated by application of increasing doses of dobutamine (5, 10, 20 μg/kg body mass). Systolic BP(PTT) and systolic BP(i.a.) correlated significantly (R = 0.94). The limits of agreement in the Bland-Altman plot were ± 19 mmHg; the mean values differed by 1 mmHg. The correlation coefficient for the diastolic BP measurements was R = 0.42. The limits of agreement in the Bland-Altman plot were ± 18 mmHg, with a mean difference of 5 mmHg in favour of the BP(PTT). The study demonstrates a significant correlation between the measurement methods for systolic BP. The results encourage the application of PTT-based BP measurement for the evaluation of BP dynamics and pathological BP changes.

It is feasible to automatically measure SDB severity using a pacemaker trans-thoracic impedance sensor. Advanced SDB was frequently undiagnosed in this cohort of pacemaker patients.