Obstructive sleep apnoea (OSA) occurs because of recurrent narrowing and occlusion of the velopharynx (VP) during sleep. The speci®c cause of OSA is unknown. Cephalometric radiography, ®breoptic nasopharyngoscopy, acoustic re¯ec-tion techniques, and computerized tomography have limitations (dynamic and tridimensional evaluation) in the mechanism of occlusion investigation. Static and dynamic examination of the soft tissue structures surrounding the upper airway during the respiratory cycle in wakefulness and sleep, can lead to a better understanding of the process.Ultrafast magnetic resonance imaging (one image per 0.8 s) was used to study the upper airway and surrounding soft tissue in 17 patients with OSA during wakefulness and sleep, and in eight healthy subjects whilst awake.The major ®ndings of this investigation in the 25 subjects were as follows: 1) the VP was smaller in apnoeic patients, only during part of the respiratory cycle; 2) the variation in VP area during the respiratory cycle was greater in apnoeic patients than in controls, particularly during sleep, suggesting an increased compliance of the VP in these patients; 3) VP narrowing was similar in the lateral and anterior-posterior dimensions, both in controls and apnoeic patients while awake; apnoeic patients during sleep have a more circular VP upon reaching the minimum area; 4) there was an inverse relationship between dimensions of the lateral pharyngeal walls and airway area, probably indicating that lateral walls are passively compressed or stretched as a result of changes in the airway calibre; and 5) soft palate and parapharyngeal fatpads were larger in apnoeic patients, although their role in the genesis of OSA is uncertain.It was concluded that changes in the velopharynx area and diameter during the respiratory cycle are greater in apnoeic patients than in normal subjects, particularly during sleep. This suggests that apnoeic patients have a more collapsible velopharynx, this being the main mechanism of obstruction. Eur Respir J 2001; 17: 79±86. Obstructive sleep apnoea (OSA) occurs because of recurrent narrowing and occlusion of the upper airway during sleep [1], and the site of obstruction is most commonly at the level of the velopharynx (VP). Unfortunately, the speci®c cause of this obstruction is unknown [2±4]. Cephalometric analysis [5,6], which provides information on the morphology of the upper airway, does not allow dynamic evaluation. Fibreoptic nasopharyngoscopy with the Mu È ller manoeuvre [4,7,8] allows a dynamic evaluation of the pharyngeal airway, but is usually performed with the patient awake, and the changes in pressure and shape during the manoeuvre are not necessarily representative of the physiological changes during quiet breathing. Acoustic re¯ection has been used to demonstrate increased effective compliance of the pharynx during wakefulness in OSA patients in response to changes in pharyngeal intraluminal pressure and lung volume [9,10]. A major limitation of the acoustic re¯ection technique is its inabi...
Objective: To analyse the association between serum C-peptide and coronary artery disease in the general population. Methods: Follow-up study of 6630 adults from the general population. They were stratified into group 1 (no insulin resistance: C-peptide < third tercile and glycaemia < 100 mg/dL), group 2 (initial insulin resistance: C-peptide ⩾ third tercile and glycaemia < 100 mg/dL) and group 3 (advanced insulin resistance: glycaemia ⩾ 100 mg/dL). Results: After 3.5 years of follow-up, group 2 had a higher incidence of myocardial infarction (relative risk (RR) = 4.2, 95% confidence interval (CI) = 1.7-10.6) and coronary artery disease (RR = 3.5, 95% CI = 1.9-6.6) than group 1. Group 3 also had increased incidences of both diseases. In multivariable analysis of the entire population, groups 2 and 3 showed significant risks of myocardial infarction and coronary artery disease (RR > 3 and RR > 2, respectively). However, when people with diabetes were excluded, the increased risks were corroborated only in group 2 for myocardial infarction (RR = 2.8, 95% CI = 1.1-6.9; p = 0.025) and coronary artery disease (RR = 2.4, 95% CI = 1.3-4.6; p = 0.007). Conclusion: Elevated C-peptide is associated with the incidence of myocardial infarction and coronary artery disease in the general population. It can be an earlier predictor of coronary events than impaired fasting glucose.
C-reactive protein (CRP) is produced by the macrophages in the liver and adipocytes and is integrated in the acute-phase response pathway. Being a nonspecific marker of inflammation, it increases in response to inflammation. The results of recent studies that have analyzed the role of CRP have not yet influenced current clinical practice. When used in combination with other established biomarkers for the prediction of the first major cardiovascular event or death, CRP does not improve the risk stratification obtained with the current guidelines. The reduction of CRP levels itself or as a statin-related pleiotropic effect has been assessed in different scenarios, including the acute phase of myocardial infarction; secondary prevention of cardiovascular diseases; special patient populations, such as diabetic patients; and finally in a primary prevention study (JUPITER [Justification for the Use of statins in primary Prevention: an Intervention Trial Evaluating Rosuvastatin]). Risk stratification in all the examined scenarios was related to serum LDL-C levels; in other words, the degree of cardiovascular risk was always lipid dependent.
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