No abstract

Obstructive sleep apnoea (OSA) is linked with increased cardiovascular morbidity and mortality, possibly through an enhancement of atherosclerotic vascular changes. Up to now, however, only a few studies have tried to evaluate the occurrence of atherosclerosis in patients with OSA.In the present study, ultrasonography of the large extracranial vessels was performed in a group of consecutively admitted OSA patients (n535) and a control group of non-OSA patients (n535). Common carotid artery-intima media thickness (CCA-IMT) was measured at the far wall of both proximal carotid arteries. Furthermore, the presence of plaques and stenoses of the extracranial vessels was determined. All measurements were carried out blinded to the status of the patients.In the OSA group, CCA-IMT was significantly increased when compared with the non-OSA patients and was related to the degree of nocturnal hypoxia. Additionally, the formation of plaques was more pronounced and extracranial vessel stenosis was more common in the OSA patients.In conclusion, these findings are in favour of an independent influence of obstructive sleep apnoea on atherosclerotic changes of the arterial wall, and represent further strong arguments for obstructive sleep apnoea being a risk factor on its own for the emergence of cardiovascular disease.

We investigated incidence, age distribution in relation to etiology, and localization of spontaneous intracerebral hematoma in 100 consecutive cases. Incidence in the total population of the Giessen area was estimated to be > 11/100,000 inhabitants/yr and increased with age. There was a trend toward higher incidence in males. Overall mortality was 27%, 22% of 58 patients aged <70 years and 33% of 42 patients aged >70 years. Hypertensive putaminal hematoma showed the highest mortality rate (42%, 10 of 24 cases). Chronic alcoholism and anticoagulant medication influenced the mortality rate unfavorably. We found the following localizations and etiologies to have a specific relation with age: 1) lobar hematomas from vascular malformations, group aged <40 years; 2) hypertensive putaminal hematomas and hypertensive thalamic hematomas, group aged 40-69 years; and 3) lobar hematomas, group aged >70 years. Alcoholism was an additional factor in 38% of the 13 middle-aged men with hypertensive putaminal hematomas. Fourteen cases of spontaneous intracerebral hematoma were possibly due to cerebral amyloid angiopathy. Six of these 14 patients had recurrent lobar hematomas, but only three of the six could be histologically investigated. In these three cases, cerebral amyloid angiopathy was proven. (Stroke 1990;21:1412-1418)

Considering the significant benefit for patients with preoperative compared to intraoperative IABP and the absence of vascular problems after IABP insertion, the results of this study indicate a more liberal indication for IABP in high-risk patients before coronary bypass surgery.

In the present study the effects of intravenously administered corticotropin-releasing hormone (CRH) on the release of proopiomelanocortin (POMC) derivatives such as adrenocorticotropic hormone (ACTH), β-lipotropin (β-LPH) and β-endorphin (β-END) as well as direct effects of CRH on pain sensitivity were examined. In 16 healthy volunteers we studied the effects of 100 µg intravenously administered CRH in absence or presence of 12 mg naloxone on heat or pressure pain sensitivity, using a double-blind, cross-over and placebo-controlled design. To evaluate analgesic effects of CRH via release of POMC derivatives, we determined plasma concentrations of β-END-immunoreactive material (IRM), authentic β-END (β-END(1–31)) and β-LPH IRM, in parallel with heat and pressure pain tolerance thresholds before and 15 and 30 min after treatment with CRH (or placebo), and 5 min after naloxone (or placebo) administration which was administered 40 min after CRH (or placebo) injection. CRH increased levels of β-END IRM, β-END(1–31) and β-LPH IRM. As compared to β-END IRM levels measured by a commercial RIA kit, the β-END(1–31) levels determined by a highly specific two-site RIA, proved to be remarkably small. Furthermore, CRH did not induce increases of heat pain tolerance thresholds, but of pressure pain tolerance thresholds, which, however, were not reversible by naloxone. Neither β-END nor β-LPH IRM nor β-END(1–31) levels correlated with heat or pressure pain tolerance thresholds. We conclude that CRH does not modulate heat, but pressure pain; POMC derivatives like β-END IRM, β-END(1–31) or β-LPH do not mediate this effect.