Struma ovarii complicating pregnancy. Case report and literature review.

A 19-year-old woman at 12th week of pregnancy was referred to our hospital with severe acute abdominal pain, nausea and vomiting. Patient's abdomen was untreatable. Routine examinations, except neutrophilic leukocytosis, were normal. Ultrasound imaging showed the presence of intrauterine pregnancy corresponding to amenorrhea and a right complex ovarian mass, with well defined margins without papillary projection, 14x12 cm in diameter. No free fluid was evident. Due to untreatable abdomen and suspecting torsion of the ovarian tumor the patient underwent laparotomy under general anesthesia. The pregnant uterus was normal. The right ovary had increased volume for a cystic-solid mass of the size of 14 cm with smooth surface and twisted on the vascular peduncle. A right adnexectomy was performed. Intraoperative frozen section was negative for malignancy and postoperative histological examination revealed a struma ovarii without atypia of the follicular cells. Postoperative course was normal. The patient was discharged after three days and she delivered at term a normal baby. Mostly struma ovarii represents an incidental finding during cesarean section, but in rare case it may be cause of complications such as torsion, rupture, hypertiroidism and rarely may be a malignant tumor. The AA describe literature data on struma ovarii diagnosed in pregnancy.

Reticulocytes in untreated obstructive sleep apnoea.

BACKGROUND AND AIM: The short, repetitive hypoxaemic episodes observed in obstructive sleep apnoea (OSA) may determine small augmentations in mature red blood cells. It is unknown whether they affect reticulocyte release. This study explored whether the number and degree of maturation of circulating reticulocytes may be altered in OSA, possibly through the effect of erythropoietin. METHODS: Fifty male adult patients with suspected OSA, normoxic during wakefulness, were studied. After nocturnal polysomnography, a blood sample was withdrawn for blood cells count, erythropoietin, iron and transferrin determination. Reticulocyte concentration and degree of immaturity [high (H), medium (M), or low (L)] were also determined. Immature reticulocyte fraction (IRF) was calculated as (M+H) percentage of reticulocytes. RESULTS: A wide range of OSA severity was found [apnoea/hypopnoea index (AHI): 44.3 +/- 30.4, range 0.3-105; sleep time spent at oxyhaemoglobin saturation <90%: 18.1 +/- 22.2%, range 0-81%]. Both reticulocyte count and IRF slightly exceeded the normal range. Patients with a reticulocyte concentration > 2% had higher EPO levels (p < 0.05), but not worse nocturnal desaturations, than those with values < 2%. By contrast, subjects with IRF < 15% showed worse desaturations (p < 0.05), but similar EPO concentrations, when compared to subjects whose IRF was < 10%. At univariate analysis, reticulocyte count correlated to erythropoietin, while IRF to transferrin saturation, BMI and OSA severity. At multiple regression, only lowest nocturnal oxygen saturation remained a significant contributor to IRF (r2 0.223, p < 0.05). CONCLUSIONS: This data suggests that hypoxaemia due to OSA could influence the release of immature reticulocytes, but this effect is not mediated by erythropoietin.

Baroreflex control of heart rate during sleep in severe obstructive sleep apnoea: effects of acute CPAP.

Baroreflex control of heart rate during sleep (baroreflex sensitivity; BRS) has been shown to be depressed in obstructive sleep apnoea (OSA), and improved after treatment with continuous positive airway pressure (CPAP). Whether CPAP also acutely affects BRS during sleep in uncomplicated severe OSA is still debatable. Blood pressure was monitored during nocturnal polysomnography in 18 patients at baseline and during first-time CPAP application. Spontaneous BRS was analysed by the sequence method, and estimated as the mean sequence slope. CPAP did not acutely affect mean blood pressure or heart rate but decreased cardiovascular variability during sleep. Mean BRS increased slightly during CPAP application (from 6.5+/-2.4 to 7.5+/-2.9 ms x mmHg(-1)), mostly in response to decreasing blood pressure. The change in BRS did not correlate with changes in arterial oxygen saturation or apnoea/hypopnoea index. The small change in baroreflex control of heart rate during sleep at first application of continuous positive airway pressure in severe obstructive sleep apnoea was unrelated to the acute resolution of nocturnal hypoxaemia, and might reflect autonomic adjustments to positive intrathoracic pressure, and/or improved sleep architecture. The small increase in baroreflex control of heart rate during sleep may be of clinical relevance as it was accompanied by reduced cardiovascular variability, which is acknowledged as an independent cardiovascular risk factor.

Preference for fixed or automatic CPAP in patients with obstructive sleep apnea syndrome.

BACKGROUND: The aims of this study were to compare compliance to treatment with fixed CPAP and with autoCPAP, subjective preference for type of CPAP treatment, and factors associated to preference for autoCPAP in patients with OSAS. PATIENTS AND METHODS: Twenty-two subjects were studied in a randomized, single blind cross-over fashion. They were treated for one month by fixed CPAP (Elite Sullivan V, ResMed, Sydney, Australia) and one month by autoCPAP (Autoset T, ResMed, Sydney, Australia). RESULTS: Four subjects who stated a preference for fixed CPAP and four who expressed no preference were pooled together; fourteen preferred autoCPAP. Compliance to treatment using the two machines did not differ in the first group (3.8 (1.9) vs. 3.8 (1.5)h/day, fixed vs autoCPAP), but was higher with autoCPAP in the second group (4.8 (1.8) vs 5.5 (1.5)h/day, P<0.05). Baseline apnea/hypopnea index (AHI) was high in both groups, but was higher in the second group P<0.02. First treatment was always fixed CPAP in patients who preferred fixed CPAP, while it was either in the other subjects. CONCLUSIONS: Compliance to autoCPAP differs among OSAS patients. As long as factors predicting higher compliance to autoCPAP are not found, a trial with autoCPAP in patients poorly compliant to fixed CPAP may be warranted.

Effects of fixed compared to automatic CPAP on sleep in Obstructive Sleep Apnoea Syndrome.

BACKGROUND: Automatic CPAP has been developed to improve CPAP efficiency and compliance. Continually matching the effective pressure may be associated to more frequent arousals that could disturb sleep. The aim of the present study was to compare sleep architecture after one month's home therapy with CPAP or with an AutoCPAP device. METHODS: Twenty OSAS patients (18 M / 2 F) after polysomnographic study with CPAP titration received either an automatic (AutoSet T, ResMed, Sydney, Australia) or a fixed level CPAP machine in a random, single blind fashion for one month. At the end of the home treatment period polysomnography was repeated while CPAP was administered by the same machine used at home. RESULTS: There was no significant difference between groups in terms of age (50.0 vs 45.5, NS), sex, BMI (38.3 vs 35.1, NS), RDI (45.4 vs 48.0, NS), and CPAP effective level (9.8 vs 10.8, NS). After one month of therapy the correction of sleep respiratory disturbances and of sleep structure was satisfactory in both groups. No difference in any polysomnographic variable or in subjective sleepiness was found at re-evaluation. CONCLUSIONS: The results of this study demonstrate that on average CPAP administered by a fixed CPAP machine and by the AutoSet T autoCPAP device has similar effects in improving respiratory function during sleep, nocturnal sleep architecture, and subjective daytime sleepiness after a one-month therapy. As autoCPAP devices are more expensive than fixed CPAP machines, their prescription should be considered only after a clear demonstration of an increase in compliance to treatment by these devices.

Blood pressure responsiveness to obstructive events during sleep after chronic CPAP.

The aim of this study was to investigate whether chronic continuous positive airway pressure (CPAP) affects blood pressure (BP) responsiveness to obstructive events occurring on the first night of CPAP withdrawal in obstructive sleep apnoea (OSA) after chronic treatment. Thirteen male subjects with severe OSA underwent nocturnal polysomnography with beat-by-beat BP monitoring before treatment and after 4.9 +/- 3.4 months of home CPAP (mean daily use 5.1 +/- 1.7 h). Variations in oxyhaemoglobin saturation (deltaSa,O2), systolic (deltaPs), and diastolic (deltaPd) BP within nonrapid eye movement apnoeas and hypopnoeas were measured on a sample of pre- and post-treatment events. In addition, a pretreatment sample was selected for deltaSa,O2 to match post-treatment events. The higher the mean deltaSa,O2 was in the full pretreatment sample, the more deltaSa,O2, deltaPs and deltaPd were attenuated after treatment. Mean deltaPs decreased from 47.3 +/- 8.5 in the full pretreatment sample to 42.2 +/- 6.9 in the selected pretreatment sample, to 31.5 +/- 5.9 mmHg in the post-treatment sample. The post-treatment value differed significantly from both the pretreatment values. The corresponding values for mean deltaPd were 27.0 +/- 3.5, 24.0 +/- 3.1 and 19.6 +/- 3.7 mmHg, with all values differing significantly from each other. Chronic continuous positive airway pressure is followed by a decrease in apnoea/ hypopnoea-related blood pressure swings, possibly secondary to both reduced severity of event-related hypoxaemia and decreased responsiveness to obstructive events secondary to chronic prevention of nocturnal intermittent hypoxaemia.

Airway inflammation in nonasthmatic amateur runners.

Elite athletes show a high prevalence of symptoms and signs of asthma, but no study has assessed the acute effects of endurance exercise on airway cells in nonasthmatic athletes. We measured exhaled nitric oxide (NO) and collected samples of induced sputum after 3% NaCl aerosol administration for 20 min in nonasthmatic middle-aged amateur runners after the Fourth Palermo International Marathon and 6--9 wk later (habitual training period) at baseline. After the marathon, exhaled NO (n = 9 subjects) was higher [27 +/- 9 parts/billion (ppb)] than at baseline (12 +/- 4 ppb; P < 0.0005). Polymorphonuclear neutrophil (PMN) counts in induced sputum were much higher in runners (91.2 +/- 3.6% of total cells postmarathon and 78.7 +/- 9.1% at baseline) than in sedentary control subjects (9.9 +/- 5.9%; P < 0.001). Expression of L-selectin and CD11b/CD18 in sputum PMNs was lower after the race than at baseline and inversely related to the amount of exhaled NO (r = -0.66 and -0.69, respectively; P < 0.05). Our data indicate that sputum PMNs are increased in nonasthmatic runners both after a marathon and at baseline and suggest that NO may modulate exercise-associated inflammatory airway changes.

Evaluation of the POLYMESAM system in the diagnosis of obstructive sleep apnea syndrome.

The reliability of a POLYMESAM (PM) instrument in the detection of ventilatory disorders and in the diagnosis of obstructive sleep apnea syndrome (OSAS) was evaluated in 50 subjects suspected for OSAS, simultaneously studied by polysomnography (PSG) in a sleep laboratory. Recordings were analysed by separate scorers, blinded to the results of the paired recording. The number of central (Ac), obstructive (Ao) or mixed apneas (Am), of hypopneas (H), and the total number of ventilatory disorders (AH) per hour of time in bed (TIB) calculated on the two recordings were significantly correlated. Bland and Altman analysis showed a good agreement between AH/TIB, Ac/TIB, Am/TIB and mean AH duration; a lower Ao/TIB at PM was mirrored by a higher H/TIB. Forty-two subjects had OSAS according to an apnea/hypopnea index (AHI) > or = 10 at PSG. Due to low sleep efficiency, AH/TIB was substantially lower than AHI. However an AH/TIB > or = 5 at PM showed a sensitivity of 100% and a specificity of 71.4%, while an AH/TIB > or = 10 showed a sensitivity of 95.2% and a specificity of 100%. In conclusion, PM proved reliable for recognition of the characteristics of ventilatory disorders and for diagnosis of OSAS.

Influence of sampling interval on the evaluation of nocturnal blood pressure in subjects with and without obstructive sleep apnoea.

Blood pressure (BP) variability during sleep is high in obstructive sleep apnoea syndrome (OSAS). How BP sampling interval affects the estimate of mean nocturnal BP in OSAS and control subjects was investigated. Nine subjects with apnoea/hypopnoea index (AHI) <5 and 18 OSAS patients with AHI >30 underwent nocturnal polysomnography with beat-by-beat BP monitoring. Mean nocturnal BP was evaluated averaging: a) all systolic (Ps) and diastolic (Pd) BP values; b) Ps and Pd sampled every 5, 10, 15, 20, and 30 min. The sampling starting point was repeatedly shifted, and several mean BP estimates for each sampling interval were obtained. Differences (deltaPs and deltaPd) between means obtained by sampling BP and by averaging all BP values were calculated. In both groups deltaPs and deltaPd scatter increased as sampling interval increased; their variance was always higher in OSAS subjects (p<0.001). Over 95% of deltaPs and deltaPd were <5% of the beat-by-beat mean values at all sampling intervals in controls, but this occurred only at sampling intervals < or =10 min in OSAS subjects. To conclude, for each blood pressure sampling time, a larger number of inaccurate nocturnal mean blood pressure estimates are obtained in obstructive sleep apnoea syndrome than in control subjects. Obstructive sleep apnoea syndrome subjects require more frequent blood pressure measurements to obtain a similar accuracy in nocturnal blood pressure evaluation.

Blood pressure and heart rate during periodic breathing while asleep at high altitude.

The ventilatory and arterial blood pressure (ABP) responses to isocapnic hypoxia during wakefulness progressively increased in normal subjects staying 4 wk at 5,050 m (Insalaco G, Romano S, Salvaggio A, Braghiroli A, Lanfranchi P, Patruno V, Donner CF, and Bonsignore G; J Appl Physiol 80: 1724-1730, 1996). In the same subjects (n = 5, age 28-34 yr) and expedition, nocturnal polysomnography with ABP and heart rate (HR) recordings were obtained during the 1st and 4th week to study the cardiovascular effects of phasic (i.e., periodic breathing-dependent) vs. tonic (i. e., acclimatization-dependent) hypoxia during sleep. Both ABP and HR fluctuated during non-rapid eye movement sleep periodic breathing. None of the subjects exhibited an ABP increase during the ventilatory phases that correlated with the lowest arterial oxygen saturation of the preceding pauses. Despite attenuation of hypoxemia, ABP and HR behaviors during sleep in the 4th wk were similar to those in the 1st wk. Because ABP during periodic breathing in the ventilatory phase increased similarly to the ABP response to progressive hypoxia during wakefulness, ABP variations during ventilatory phases may reflect ABP responsiveness to peripheral chemoreflex sensitivity rather than the absolute value of hypoxemia, suggesting a major tonic effect of hypoxia on cardiorespiratory control at high altitude.

Myocardial ischemia during sleep.

The role of sleep in the pathogenesis of coronary ischaemic events such as myocardial infarction, transient myocardial ischaemia, or cardiac sudden death, is unclear. This review will analyse the available data on the subject according to: (i) the autonomic and cardiovascular changes during sleep that may potentially favour myocardial ischaemia; (ii) the evidence of a circadian distribution of coronary events; and (iii) the factors possibly involved in the pathogenesis of nocturnal angina. Available data suggest that myocardial ischaemia may occur by different mechanisms in non-rapid eye movement (NREM) (decreased coronary perfusion pressure) and rapid eye movement (REM) sleep (increased myocardial oxygen demand). Coronary events show a major peak of occurrence between 6.00 a.m. and noon; however, the myocardial ischaemic threshold, defined as the heart rate value at which myocardial ischaemia develops, may be lower at night than during the daytime, suggesting an unexpectedly higher susceptibility to myocardial ischaemia during sleep than during wakefulness. These data warrant further study on the pathophysiology of coronary circulation during sleep. Finally, some evidence is available that sleep disordered breathing may precipitate nocturnal angina especially in REM sleep, through decreased arterial oxygen content secondary to hypoventilation or true apnoeas. More data are needed to better understand the effects of sleep on the coronary circulation, and to improve the therapeutic approach of nocturnal angina.

Effects of high-altitude periodic breathing on sleep and arterial oxyhaemoglobin saturation.

This study aimed to investigate the effect of periodic breathing (PB) at high altitude on sleep structure and arterial oxygen saturation (Sa,O2). Five healthy subjects underwent polysomnographic studies at sea level, and during the first and the fourth week of sojourn at 5,050 m. Their breathing pattern, sleep architecture and Sa,O2 were analysed. PB was detected in the high-altitude studies during nonrapid eye movement (NREM) sleep and tended to increase from the first to the fourth week. Stages 3-4 were absent in four subjects at the first week, but only in one at the fourth week, irrespective of the amount of PB. The arousal index was 11.6+/-3.8 at sea level, 30.1+/-15.5 at the first week at altitude and 33.0+/-18.2 at the fourth week. At altitude, arousal index in NREM sleep was higher during PB than during regular breathing. In NREM sleep, the mean highest Sa,O2 levels in NREM epochs with PB were higher than in those with regular breathing by 2.8+/-1.7% at the first week and 2.9+/-1.5% at the fourth week (p<0.025). From the first to the fourth week, mean Sa,O2 increased significantly during wakefulness (5.6%), NREM (5.2% with regular breathing and 5.3% with PB) and rapid eye movement sleep (7.6%). The data demonstrate a slight role of periodic breathing in altering sleep architecture at high altitude and also show that periodic breathing induces only a minor improvement in arterial oxygen saturation during nonrapid eye movement sleep.

What is the evidence that obstructive sleep apnoea is an important illness?

Obstructive sleep apnoea (OSA) is described by some authors as a potentially lethal disease and by others as an almost harmless condition. Excessive daytime sleepiness, neuropsychological dysfunction, altered quality of life, cardiovascular disease (systemic and pulmonary hypertension, cardiac arrhythmias, stroke and ischaemic heart disease) and increased mortality have been described as OSA complications. There is little argument that OSA may determine sleepiness, alter cognitive functions, and worsen quality of life, although with great interindividual variability: this should induce OSA to be considered an important illness per se, since sleepiness in OSA was shown to lead to important consequences, like road traffic accidents. Besides, OSA may interact with coexisting cardiac and respiratory disease and favour the appearance of heart and respiratory failure. Therefore, OSA is certainly also worth careful consideration as an important aggravating factor of other diseases. The evidence that obstructive sleep apnoea is an independent risk factor for cardiovascular complications other than owing to the recurrent transient blood pressure surges associated with apnoeas during sleep, and for an increased mortality is more conflicting. More studies are necessary to identify which characteristics of obstructive sleep apnoea may be considered important markers of its severity and as risk factors for different possible complications.

Autonomic cardiac regulation in obstructive sleep apnea syndrome: evidence from spontaneous baroreflex analysis during sleep.

OBJECTIVE: To assess spontaneous baroreceptor-heart rate reflex sensitivity during sleep in patients with obstructive sleep apnea syndrome, a condition associated with increased cardiovascular morbidity and mortality and characterized by marked sympathetic activation, which is believed to originate from hypoxic chemoreceptor stimulation, although little is known of other possible mechanisms such as baroreflex impairment. DESIGN AND METHODS: In 11 patients with severe obstructive sleep apnea syndrome (mean+/-SD age 46.8+/-8.1 years, apnea/hypopnea index 67.9+/-19.1 h), who were normotensive or borderline hypertensive during wakefulness by clinic blood pressure measurements, finger blood pressure was monitored beat-by-beat non-invasively (Finapres) at night during polysomnography. Periods of wakefulness and sleep were identified based on electroencephalographic recordings. Baroreflex sensitivity was assessed by the sequence technique, as the slope of the regression line between spontaneous increases or reductions in systolic blood pressure (SBP) and the related lengthening or shortening in the RR interval, occurring over spontaneous sequences of four or more consecutive beats. The number of these sequences was also computed, as an additional index of baroreflex engagement by the spontaneous blood pressure fluctuations. The controls were age-related normotensive or borderline hypertensive subjects without sleep apnea who had been investigated in previous studies; in these subjects blood pressure was recorded intra-arterially over 24 h in ambulatory conditions and spontaneous baroreflex sensitivity was assessed by the sequence technique. RESULTS: In our patients the lowest nocturnal arterial oxygen saturation was 78.6+/-12.1% (mean+/-SD). During sleep, the number of pooled +RR/+SBP and -RR/-SBP sequences per hour was 20.3+/-2.7 per h in patients with sleep apnea and 27.1+/-2.1 /h in controls (means+/-SEM). The average baroreflex sensitivity during sleep periods was 7.04+/-0.8 ms/mmHg in sleep apnea patients and 10.05+/-2.1 ms/mmHg in controls. Both the pooled number of sequences and baroreflex sensitivity values of the sleep apnea patients were significantly (P < 0.01) less than the corresponding night values of control subjects. In the sleep apnea patients, at variance from controls, baroreflex sensitivity did not show any increase during sleep compared with its values during wakefulness (6.9+/-1.0 ms/mmHg). CONCLUSIONS: Our data provide evidence that spontaneous baroceptor reflex sensitivity is depressed in severe obstructive sleep apnea syndrome. This suggests that in such patients baroreflex dysfunction and not only chemoreceptor stimulation by hypoxia may be involved in the sympathetic activation which occurs during sleep. Such dysfunction may contribute to the higher rate of cardiovascular morbidity and mortality reported in these patients.

Cardiovascular and ventilatory response to isocapnic hypoxia at sea level and at 5,050 m.

To assess the effect of chronic hypoxic conditions on ventilatory, heart rate (HR), and blood pressure (BP) responses to acute progressive isocapnic hypoxia, we studied five healthy Caucasian subjects (3 men and 2 women). Each subject performed one rebreathing test at sea level (SL) and two tests at the Pyramid laboratory at Lobuche, Nepal, at the altitude of 5,050 m, 1 day after arrival (HA1) and after 24 days of sojourn (HA2). The effects of progressive isocapnic hypoxia were tested by using a standard rebreathing technique. BP, electrocardiogram, arterial oxygen saturation, airflow and end-tidal CO2 and O2 were recorded. For each subject, the relationships between arterial oxygen saturation and HR, systolic BP and minute ventilation (VE), respectively, were evaluated. At HA1, the majority of subjects showed a significant increase in VE and BP response and a decrease in HR response to progressive isocapnic hypoxia as compared to SL. At HA2, VE and BP responses further increased, whereas the HR response remained similar to that observed at HA1. A significant relationship between hypoxic ventilatory responses and both systolic and diastolic BP responses to progressive hypoxia was found. No significant correlation was found between hypoxic ventilatory and HR responses.

Respiration in NREM and REM sleep after upper airway surgery for obstructive sleep apnoea.

To verify whether upper airway surgery in obstructive sleep apnoea syndrome affects differently respiration in NREM and REM sleep, 22 patients were studied by polysomnography before and three months after surgical treatment. On the average, treatment improved respiration during both sleep states, but no significant interaction was found between sleep state and effect of surgical treatment. According to the response to treatment, three groups of patients were identified: the first group (N = 6), with an improvement in apnoea-hypopnoea index (AHI), percentage of sleep time spent in apnoea and hypopnoea (time in AH) and mean oxyhaemoglobin saturation (SaO2) in both NREM and REM sleep; the second group (N = 5), with an improvement in AHI only in NREM sleep, associated with improvement in mean SaO2 in both sleep states; the third group (N = 11), without any improvement in AHI and time in AH, either associated (N = 5) or not (N = 6) with an improvement in mean SaO2 in both sleep states. An increase in the percentage of hypopnoeas out of the total AHI after treatment could partly account for the apparent discrepancy between AHI and mean SaO2 behaviour in the subjects of the second group, but not in the patients of the third group who improved their mean SaO2. Mixed apnoeas occurred before surgery in six subjects; they remained numerous after surgery only in two subjects who did not show any SaO2 improvement. In conclusion, the degree of improvement in respiration after upper airway surgery was similar in every patient in NREM and REM sleep.

Respiratory sinus arrhythmia during obstructive sleep apnoeas in humans.

Respiratory sinus arrhythmia (RSA) reflects parasympathetic modulation of heart rate (HR) during the respiratory cycle. Since the time-course of RSA during obstructive sleep apnoea (OSA) is not known, an analysis was made of ECG in samples of consecutive OSA recorded in 5 patients during NREM sleep while breathing room air (OSA-AIR, mean lowest SaO2 83.0 +/- 6.5%) or supplemental oxygen (OSA +/- O2, mean lowest SaO2 91.7 +/- 2.2%), respectively. For each breath, HR at the transition from expiration to inspiration (HRei), and HR at maximal inspiration (HRie) were calculated, and the inspiratory increase in HR estimated as the ratio: HRie/subsequent HRie. Similarly, the expiratory decrease in HR was estimated as: HRie/subsequent HRei. RSA was identified by an inspiratory increase in HR (HRei/HRie < 1), and an expiratory decrease in HR (HRie/HRei > 1). OSA-AIR and OSA + O2 did not differ for duration or oesophageal pressure nadir. During OSA-AIR, the inspiratory increase in HR became progressively more marked from the first occluded to the first open breath, whereas during OSA + O2 it remained stable throughout the apnoeic cycle. The expiratory decrease in HR remained constant during the apnoeic phase, but was blunted in the first open breaths irrespective of O2 administration. In summary, hypoxia appeared to affect inspiratory, but not expiratory HR. Instead, the expiratory slowing of HR transiently disappeared in the immediate post-apnoeic phase, suggesting a possible effect of arousal or pulmonary inflation. These data suggest that the parasympathetic system may contribute to cardiovascular regulation during OSA.

[The surgical treatment of obstructive sleep apnea syndrome]. / La terapia chirurgica nella sindrome dell'apnea ostruttiva nel sonno (OSAS).

Studies concerning the anatomical abnormalities of upper airways in patients affected by Obstructive Sleep Apnea Syndrome (OSAS) allowed the corrective surgical treatments in this syndrome. To provide an improvement or a definitive recovery of OSAS, various surgical treatments, i.e. functional nasal surgery, palatal surgery [Partial resection of palate (RPP), Uvulopalatopharingoplasty (UPPP), Palatopharingoplasty (PPP), modified Palatopharingoplasty (modified PPP)], mandibular and base tongue surgery, have been performed in order to obtain an enlargement of upper airways. It has been reported that in RPP, UPPP, PPP and modified PPP partial or total uvula and soft palate resection is conduct; in our research we performed modified PPP. 44 OSAS patients, severe or moderately severe form (polisomnographic diagnosis), underwent surgical treatment: 5 patients underwent functional nasal surgery; 9 patients underwent modified PPP; 29 patients underwent nasal and palatal surgery; only 1 patient underwent base tongue surgery. 32 patients underwent polisomnographic records after surgery (two months later) and we evaluated Apnea Index (I.A.) and a SaO2 low (nadir) with statistic tests. The results have been positive. Therefore, we have now 7 normal, 2 mild form, 7 moderate form, 3 moderately severe form and 13 severe form OSAS patients. If, on the one hand, all these surgical treatments can be considered a good way of therapy, on the other, only tracheostomy represents today the unfailing surgical therapy.