Study Objectives: Obstructive sleep apnea (OSA) is associated with a range of cardiovascular sequelae and increased cardiovascular mortality. The aim of our study was to assess the prevalence of OSA in patients with symptomatic angina and angiographically verified coronary artery disease (CAD). In addition, we analyzed the association of OSA and other coronary risk factors with CAD and myocardial infarction. Methods: Overnight non-laboratory-monitoring-system recordings for detection of OSA was performed in 223 male patients with angiographically verified CAD and in 66 male patients with exclusion of CAD. A logistic regression analysis was performed to assess associations between risk factors and CAD and myocardial infarction. Results: CAD patients were found to have OSA in 30.5%, whereas OSA was found in control subjects in 19.7%. The mean apnea/hypopnea index (AHI) was significantly higher (p < 0.01) in CAD patients (9.9 ± 11.8) than in control subjects (6.7 ± 7.3). Body-mass-index (BMI) was significantly higher in patients with CAD and OSA than in patients with CAD without OSA (28.1 vs. 26.7 kg/m²; p < 0.001). No significant difference was found with regard to other risk factors and left ventricular ejection fraction (LVEF) between both groups. Hyperlipidemia (OR 2.3; CI 1.3–3.9; p < 0.005) and OSA defined as AHI ≥20 (OR 2.0; CI 1.0–3.8, p < 0.05) were independently associated with myocardial infarction. Conclusions: There is a high prevalence of OSA among patients with angiographically proven CAD. OSA of moderate severity (AHI ≥20) is independently associated with myocardial infarction. Thus, in the care of patients with CAD, particular vigilance for OSA is important.

Continuous positive airway pressure (CPAP) is the most widely used therapy for obstructive sleep apnoea (OSA). Despite its general efficacy, oxygen desaturation due to hypoventilation persists in some patients. The present study analysed the factors which are associated with this primary failure and, moreover, examined the effect of a bilevel positive airway pressure (BiPAP) trial. In a 15-month period, 13 patients with OSA (Group A) failed to respond to initial CPAP therapy defined by a remaining apnoea/hypopnoea index (AHI) of > or = 5 or a mean nocturnal SaO2 < 90%. These patients were compared to an age- and AHI-matched control group (Group B) successfully treated by CPAP. A logistic regression analysis was performed to identify factors which are associated with initial failure to CPAP. Patients of the CPAP-failure group were treated with nasal BiPAP in the control mode. These patients were significantly more obese than patients of the control group (mean body mass index 44.2 +/- 7.7 vs 31.2 +/- 6.3 kg m-2; P < 0.001). PaO2 at rest (P < 0.001) and at exercise (P < 0.005) was significantly lower in Group A patients. PaCO2 at rest (P < 0.001) was significantly higher in Group A patients and changed for the worse during exercise, whereas it improved in the control group. Group A patients spent significantly (P < 0.0001) more time with oxygen saturation < 90%. The percentage of time spent at < 90% of SaO2 was the only factor which was independently associated with the initial failure of CPAP (OR 1.13; 95% CI 1.0-1.2). After 3 months of treatment with BiPAP, the patients' blood gas values while awake improved significantly (P < 0.05) for PaO2 as well as for PaCO2. In conclusion, patients with OSA resistant to initial CPAP are morbidly obese with impaired awake blood gas values. The percentage of time spent at < 90% of nocturnal SaO2 is independently associated with initial failure of CPAP. BiPAP in the control mode is adequate for nocturnal ventilation, and improves awake blood gas values.

P Pr ro og gn no os st ti ic c aan na al ly ys si is s a an nd d p pr re ed di ic ct ti iv ve e r ru ul le e f fo or r o ou ut tc co om me e o of f h ho os sp pi it ta al l--t tr re ea at te ed d c co om mm mu un ni it ty y--a ac cq qu ui ir re ed d p pn ne eu um mo on ni ia a ABSTRACT: In community-acquired pneumonia (CAP) mortality may be reduced by early identification of patients requiring intensive care treatment. The purpose of this study was to determine prognostic factors of outcome in patients with CAP in order to establish a clinically applicable discriminant rule.Ninety three episodes of CAP in 92 patients were retrospectively reviewed with regard to epidemiological, clinical, laboratory and microbiological data. The prognostic analysis included a univariate as well as a multivariate approach, in order to identify parameters associated with death using the Cox regression hazard function in a backward stepwise selection model. The three parameters found to contribute most to the significance of the model were used in a discriminant rule for classification of outcome.The parameters found to be significantly different between survivors and nonsurvivors were heart rate, systolic and diastolic as well as mean blood pressures, leucocyte count, percentage of lymphocytes, and lactate dehydrogenase (LDH) values. The multivariate analysis revealed that heart rate, systolic arterial pressure, and LDH serum levels were most closely associated with fatal outcome. A prognostic rule composed of the variables heart rate ≥90 beats·min -1 , systolic arterial blood pressure ≤80 mmHg, and LDH ≥260 U·l -1 achieved a sensitivity of 77%, a specificity of 75%, and positive and negative predictive values of 42 and 93%, respectively. It was associated with a six fold increased risk of fatal outcome.In conclusion, heart rate, systolic blood pressure, and LDH values were most closely associated with death in a multivariate analysis. A discriminant rule consisting of these three variables achieved favourable classification results. The rule qualifies for further prospective validation, and may prove useful in the management of hospital-treated CAP.

Pulmonary hypertension is a potential complication of obstructive sleep apnoea. Most recent studies agree on a 15-20% prevalence [1]. The development of pulmonary hypertension is strongly linked to an obstructive ventilatory pattern, daytime hypoxaemia and hypercapnia, whereas the severity of obstructive sleep apnoea plays only a minor role [2]. However, some patients develop pulmonary hypertension despite normal waking arterial oxygen tension (Pa,O 2 ) levels [3]. In this group of patients, the nocturnal breathing disorder may be crucial for the development of pulmonary hypertension, since it has been hypothesized that episodic and recurrent hypertension, due to repeated apnoeas, could lead to permanent pulmonary hypertension [4].Transient and repetitive elevations in pulmonary artery pressure, with reference to atmospheric pressure, have been described [5]. While intravascular pulmonary artery pressure decreases during apnoea and increases at the resumption of breathing, transmural pulmonary artery pressure (Ppa,tm) (i.e. corrected for intrathoracic pressure swings) shows a trend toward a progressive increase throughout an apnoea and toward a decrease once ventilation has been resumed [6]. Several factors and mechanisms, mainly mechanical events or hypoxic vasoconstriction, have been proposed as contributing to the changes in the pulmonary artery pressure (Ppa,tm) within an apnoea cycle. Mechanical events are caused preferably by intrathoracic pressure swings [7]. Limitation of left ventricular filling and emptying at low intrathoracic pressure could contribute to an increase in pulmonary vascular resistance by increasing the pulmonary venous pressure and blood volume [8]. On the other hand, several studies have indicated an association between changes in oxygen saturation and changes in pulmonary artery pressure during an obstructive apnoea [4,9,10]. MARRONE et al. [11] showed that hypoxia is a major determinant of the slow changes in the transmural pulmonary artery pressure over the whole course of an apnoea. In addition, they found rapid changes in the Ppa,tm that was synchronous with intrathoracic pressure changes breathby-breath.The purpose of our study was to examine which factors contribute to the increase of the Ppa,tm in an apnoea. ABSTRACT: Changes in pulmonary artery pressure within an obstructive apnoea and elevations of transmural pulmonary artery pressure (Ppa,tm) towards the end of apnoea are well known. The purpose of our study was to examine which factors contribute to the increase of Ppa,tm in an apnoea. In addition, the time course of Ppa,tm and associated factors during a sleep study was investigated.We analysed the association of changes in arterial oxygen saturation (Sa,O 2 ), oesophageal pressure (Poes) to estimate intrathoracic pressure, systolic blood pressure (BPsys) to estimate left ventricular afterload, apnoea duration and the change in Ppa,tm (∆Ppa,tm) during the course of obstructive apnoeas. Consecutive apnoeas in nonrapid eye movement (NREM)-sleep at the beginning, the middle ...

The study was conducted at a tertiary care and teaching hospital with about 200 beds for internal medicine. The objective was to determine the diagnostic yield and value in directing antibiotic therapy of a routine microbial approach in patients with community-acquired pneumonia referred to a tertiary care center. We studied 93 episodes in a retrospective study. 69/93 (74%) cases were treated with at least one empirical antibiotic therapy prior to admission. Microbial investigation was performed in 83/93 cases (89%). An etiological agent was established in 19/83 (23%) cases including 7/50 (14%) by blood culture and 12/52 (23%) by serology. Bronchoscopy with 18 protected specimen brush and 20 bronchoalveolar lavage examinations was definitely diagnostic in only 1/25 (4%) cases, and this case was also identified by blood culture. 5/25 (20%) were probably diagnostic. Three pathogens, Streptococcus pneumoniae, Mycoplasma pneumoniae and Legionella pneumophila, accounted for 15/19 (79%) of the identified agents. The diagnostic results directed a change in antibiotic therapy in 6/19 (32%) of cases with definitely proven pathogens. 4/19 (21%) of cases would have been treated with an inappropriate regimen without diagnostic results. The diagnostic yield of routine microbial investigation in pretreated patients is low. The routine approach reveals its limited value especially in patients with severe courses. The role of bronchoscopy remains to be defined for patients with severe (and pretreated) community-acquired pneumonia.