Short-term variability of blood pressure during sleep in snorers with or without apnea.

In normal subjects, the level and variability of blood pressure decrease during non-rapid eye movement (non-REM) sleep. In contrast, sleep apnea is associated with large swings in nocturnal pressure. In this study, we evaluated a computer-derived index of all-night blood pressure variability in normotensive snorers with or without sleep apnea. We also examined this index in snorers receiving medical treatment for coexistent ischemic heart disease. Beat-to-beat blood pressure was recorded with a photoplethysmographic device (Finapres) throughout polysomnography. Subjects were categorized into four groups: those without cardiovascular disease without or with sleep apnea (> or = 15 apnea plus hypopnea per hour of sleep), and those with ischemic heart disease without or with sleep apnea. A frequency distribution histogram of all increases and decreases of blood pressure according to their amplitudes was drawn and the SD of the distribution used as an estimation of variability. Mean systolic and diastolic pressures during the total sleep time were not different among the four groups. In contrast, the SD of the distribution of systolic and diastolic pressure variations that were higher in the apneic than in the nonapneic groups (P < .05) correlated with apnea plus hypopnea (P < .0001) and transient electroencephalographic arousal number per hour of sleep (P < .0001). In both apneic and nonapneic subjects, blood pressure variability as assessed by SD decreased during stages 3 and 4 of non-REM sleep compared with stages 1 and 2 and REM sleep (P < .001). Blood pressure variability was similarly increased in apneic subjects with or without ischemic heart disease. We speculate that in apneic individuals with coexistent ischemic heart disease, pressure variability that is increased despite treatment with beta-blockers or calcium antagonists may be a risk factor for acute coronary events.

Evaluation of an ambulatory device, CID 102, in the diagnosis of obstructive sleep apnoea syndrome.

Diagnosis of obstructive sleep apnoea syndrome (OSAS) is usually performed during overnight polysomnography in the sleep laboratory. In an attempt to simplify the diagnostic strategy, we compared an ambulatory device, CID 102, with polysomnography during the same night in the laboratory in 50 consecutive patients referred for polysomnography. The CID 102 device monitors oxygen saturation, heart rate, body position and tracheal breath sounds. An acoustic pressure sensor is placed on the suprasternal notch. Signals coming from this sensor are amplified and analysed in three different channels, according to their frequency and energy. CID respiratory disturbance index is defined as the number, per hour of analysis time, of apnoeas lasting more than 10 s plus episodes of desaturation by 4% or more associated with pauses lasting from 7-10 s or snores. The polysomnographic data were recorded on paper (Reega 2000, Alvar) and analysed manually. Polysomnographic apnoea-hypopnoea index (AHIp) was defined as the number of apnoeas plus hypopnoeas per hour of sleep. The sensitivity, specificity, positive predictive value and negative predictive value of various CID respiratory disturbance index (> or = 5, > or = 10, > or = 15 and > or = 20 per hour) in diagnosing obstructive sleep apnoea syndrome were determined. When OSAS was diagnosed as AHIp > or = 15, sensitivity and specificity of a CID respiratory disturbance index > or = 5 were 73 and 62%, respectively. Positive predictive value of CID respiratory disturbance index > or = 10 for AHIp > or = 10 was 94%. CID 102 false negative patients had only hypopnoeas without any desaturation.(ABSTRACT TRUNCATED AT 250 WORDS)

[Obstructive sleep apnea syndrome in adults and cardiovascular risk]. / Syndrome d'apnées obstructives du sommeil de l'adulte et risque cardiovasculaire.

Sleep obstructive apnea syndrome (SOAS) is a common condition with a strong male predominance. Its incidence is more than 1 percent in the population as a whole. It exists in snorers. Both snoring and SOAS are linked to the presence of abnormalities (congenital or acquired) of the upper respiratory tract. The nocturnal cardiovascular consequences of SOAS are directly linked to apnea. Bradycardia occurs during apnea and tachycardia when ventilation restarts. Paroxysmal nocturnal hypertension is a constant feature. Even in individuals who are normotensive during the day, each restarting of ventilation is accompanied by peaking of blood pressure. The pulmonary artery pressure curve follows that of systemic blood pressure. Complications begin when SOAS has been present for several years: 1) Chronic: permanent systemic hypertension is common (56 percent of SOAS). It is often refractory to antihypertensive treatment. 2) Acute: the onset of myocardial infarction and of cerebrovascular accidents explains the heavy mortality of SOAS (37 percent at 8 years in untreated individuals with a number of episodes of apnea exceeding 20 per hour of sleep). Other acute complications are less common: acute pulmonary edema, nocturnal sudden death. These events may be prevented by treatment suppressing apnea: actuarial survival curves are then superimposable upon those of the population as a whole. Thus SOAS is a cardiovascular risk factor which is remarkably reversible by specific treatment, though which most often passes unrecognized.

[Fast rhythms in metabolic diseases in children]. / Les rythmes rapides dans les maladies métaboliques chez l'enfant.

The authors study fast EEG rhythms in amino acidopathies of the newborn and in progressive encephalopathy of the central nervous system in children, when an inborn error of metabolism has either been found or is suspected. In the first group: amino acidopathies (including phenylketonuria), fast rhythms on the EEG of the neonates are of low amplitude, spindle-like bursts of 7-13 Hz and usually located in rolandic areas. This activity progressively disappears. Later, fast rhythms of beta-frequency and low voltage are spread on the whole scalp with a normal EEG organisation. They are seen in the favourable or rather favourable development of children receiving a diet. In the second group: progressive encephalopathy of the central nervous system, fast rhythms of 14-24 Hz appearing at a rather late stage of the disease, while the normal background activity completely disappears. In neuro-axonal dystrophy, where they are considered as 'specific,' they are of very high voltage, i.e., 50-200 microV. The authors insist on the importance of EEG fast rhythms both in amino acidopathies of the newborn, as a contributive factor to diagnosis and prognosis, and in progressive encephalopathies of the central nervous system, as a valuable tool in the diagnosis of numerous affections.

[Study on focalized EEG paroxysms in children (author's transl)]. / Etude sur les paroxysmes EEG focalises de l'enfant.

The authors studied 111 children whose EEG showed paroxysmal foci on the lateral areas of the skull, often on the rolandic and temporal areas, but also on occipital, parietal and frontal areas. In 60% of the cases there was no clinical epileptic manifestation. In 25% of the cases those foci were responsible for epileptic seizures with good prognosis; in 15% of the cases they were associated with other epileptogenic processes responsible for epileptic fits of unfavorable evolution. The past history of these children had been studied in particular: hyperthermic convulsions and lateralisation difficulties were very frequent, but organic lesions were also found, which, although they did not seem to be directly responsible for the foci, were related to the organic lesion by a reactional or 'functional' factor.