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    ABSTRACT: To construct an algorithm for the diagnosis of sleep apnea/hypopnea syndrome (SAHS) based on the optimized sequential use of nocturnal pulse oximetry and respiratory polygraphy (AutoSet, AS) in patients suspected of SAHS. Simultaneous performance of pulse oximetry and AS in 145 patients highly suspected of SAHS (at least two of the following signs or symptoms: chronic snoring, observations of repeated apneic events, and abnormal daytime drowsiness). SAHS was diagnosed when the apnea/hypopnea index (AHI) was greater than or equal to 10, based on AS findings. The diagnostic algorithm was obtained by calculating the prevalence of SAHS, calculating the best diagnostic cutoff point for a desaturation index greater than or equal to 4% (ID4%) based on the AHI; analyzing the positive predictive value (PPV) and negative predictive value (NPV) for the cutoff and the correlation and agreement between ID4% and the AHI depending on the presence and severity of SAHS. The overall prevalence of SAHS was 83.4%. The best cutoff point was obtained using ID4% greater than or equal to 10 (sensitivity 82%; specificity 83%). The PPV and NPV for the prevalence calculated were 0.95 and 0.29, respectively. The correlation between ID4% and AHI was 0.84; overall agreement was 0.93. For patients who did not have SAHS, the PPV was 0.49, and the NPV was 0.35; both gradually increased in cases of mild, moderate and severe SAHS (to 0.90 and 0.95, respectively, for severe SAHS). Using these data we created a diagnostic algorithm according to which an ID4% greater than or equal to 30 for nocturnal pulse oximetry (sensitivity 72%, specificity 100%) would indicate that AS testing would be unnecessary. An ID4% less than 30, on the other hand, would lead to further testing (AS, or polysomnography in the event of a negative AS), based on the high prevalence of SAHS in our series. The sequential use of nocturnal pulse oximetry and AS allows substantial savings of polysomnographic testing in groups at high risk of SAHS.
    Archivos de Bronconeumología 03/2003; 39(2):74-80. · 1.37 Impact Factor
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    ABSTRACT: Chronic intermittent hypoxia, a characteristic feature of sleep-disordered breathing, induces hypertension through augmented sympathetic nerve activity and requires the presence of functional carotid body arterial chemoreceptors. In contrast, chronic sustained hypoxia does not alter blood pressure. We therefore analyzed the biosynthetic pathways of catecholamines in peripheral nervous system structures involved in the pathogenesis of intermittent hypoxia-induced hypertension, namely, carotid bodies, superior cervical ganglia, and adrenal glands. Rats were exposed to either intermittent hypoxia (90 seconds of room air alternating with 90 seconds of 10% O2) or to sustained hypoxia (10% O2) for 1 to 30 days. Dopamine, norepinephrine, epinephrine, dihydroxyphenylacetic acid, and 5-hydroxytyptamine contents were measured by high-performance liquid chromatography. Expression of tyrosine hydroxylase and its phosphorylated forms, dopamine beta-hydroxylase, phenylethanolamine N-methyltransferase, and GTP cyclohydrolase-1 were determined by Western blot analyses. Both sustained and intermittent hypoxia significantly increased dopamine and norepinephrine content in carotid bodies but not in sympathetic ganglia or adrenal glands. In carotid bodies, both types of hypoxia augmented total levels of tyrosine hydroxylase protein and its phosphorylation on serines 19, 31, 40, as well as levels of GTP cyclohydrolase-1. However, the effects of intermittent hypoxia on catecholaminergic pathways were significantly smaller and delayed than those induced by sustained hypoxia. Thus, attenuated induction of catecholaminergic phenotype by intermittent hypoxia in carotid body may play a role in development of hypertension associated with sleep-disordered breathing. The effects of both types of hypoxia on expression of catecholaminergic enzymes in superior cervical neurons and adrenal glands were transient and small.
    Hypertension 01/2004; 42(6):1130-6. · 6.87 Impact Factor
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    ABSTRACT: Objective To construct an algorithm for the diagnosis of sleep apnea/hypopnea syndrome (SAHS) based on the opti-mized sequential use of nocturnal pulse oximetry and respi-ratory polygraphy (AutoSet®, AS) in patients suspected of SAHS Methods Simultaneous performance of pulse oximetry and AS in 145 patients highly suspected of SAHS (at least two of the following signs or symptoms: chronic snoring, ob-servations of repeated apneic events, and abnormal daytime drowsiness). SAHS was diagnosed when the apnea/hypopnea index (AHI) was greater than or equal to 10, based on AS findings. The diagnostic algorithm was obtained by calcula-ting the prevalence of SAHS, calculating the best diagnostic cutoff point for a desaturation index greater than or equal to 4% (ID4%) based on the AHI; analyzing the positive predic-tive value (PPV) and negative predictive value (NPV) for the cutoff and the correlation and agreement between ID4% and the AHI depending on the presence and severity of SAHS Results The overall prevalence of SAHS was 83.4%. The best cutoff point was obtained using ID4% greater than or equal to 10 (sensitivity 82%; specificity 83%). The PPV and NPV for the prevalence calculated were 0.95 and 0.29, respectively. The correlation between ID4% and AHI was 0.84; overall agreement was 0.93. For patients who did not have SAHS, the PPV was 0.49, and the NPV was 0.35; both gradually increased in cases of mild, moderate and severe SAHS (to 0.90 and 0.95, respectively, for severe SAHS). Using these data we created a diagnostic algorithm accor-ding to which an ID4% greater than or equal to 30 for noc-turnal pulse oximetry (sensitivity 72%, specificity 100%) would indicate that AS testing would be unnecessary. An ID4% less than 30, on the other hand, would lead to further testing (AS, or polysomnography in the event of a negative AS), based on the high prevalence of SAHS in our series Conclusions The sequential use of nocturnal pulse oxi-metry and AS allows substantial savings of polysomnograp-hic testing in groups at high risk of SAHS
    Archivos de Bronconeumología 01/2003; 39(02):74-80. · 1.37 Impact Factor